Sr.

Contents Page No.

No.

1 Medicine 1-153

2 Pediatrics 154-246

3 Obstetrics and Gynaecology 247-309

4 Dermatology 310-338

5 Psychiatry 339-361

6 ENT 362-397

7 Ophthalmology 392-450

8 Surgery 451-511

9 Orthopaedics 512-556

10 ANAESTHESIOLOGY 557-581

11 Pathology 582-609

12 DENTRISTRY 610-646
 Index
1. Medicine
Sr. No. Contents Page No.
1 Fever 2
2 CAP 6
3 Bronchial Asthama 8
4 Pleural Effusion 11
5 COPD 13
6 Bronchiectasis 15
7 Lung abcess 17
8 Pneumothorax 19
9 Lung Cancer 21
10 Pulmonary Embolism 23
11 Hypertension 25
12 Heart Failure 30
13 Ischaemic Heart Disease 32
14 Acute Rheumatic Fever 35
15 Infective Endocarditis 36
16 Diabetes mellitus 40
17 Thyroid 52
18 Cerebrovascular Accident 55
19 Sub-archnoidHaemorrhage 57
20 Pyogenic Meningitis 58
21 Tubercular Mengitis 60
22 Viral Meningitis 61
23 Viral Encephalitis 63
24 Epilepsy 65
25 GBS (Guillainbarre syndrome) 68
26 Apthous ulcer 69
27 Oesophageal candidiasis 70
28 Dyspepsia 71
29 Gastro-oesophageal Reflux 72
30 Peptic ulcer disease 73
31 Vomiting 76
32 Constipation 77
33 Irritable Bowel Syndrome 78
Sr. No. Contents Page No.
34 Ulcerative Colitis 79
35 Amoebic liver abscess 81
36 Pyogenic Liver Abscess 83
37 IntesitinalProtozoal Infection 85
38 Ascitis 89
39 Hepatitis 90
40 Hepatic Coma 92
41 Nephrotic Syndrome 93
42 Acute Nephritic Syndrome 94
43 Acute Renal failure 95
44 Chronic kidney disease 97
45 Malaria 99
46 Dengue 107
47 Leptospirosis 111
48 Influenza A- H1N1 113
49 Diarrhoeal Diseases 116
50 Rheumatoid Arthritis 121
51 Snake bite 123
52 Scorpion Sting 127
53 Dog Bite 129
54 Poisoning 132
55 Alcohol Intoxication 135
56 Anaemia 136
57 Heat Stroke 138
58 Tuberculosis (RNTCP) 142
59 Leprosy (NLEP) 151
 2. Pediatrics
Sr. No. Contents Page No.
1 Emergency Management in Pediatrics 155
2 Neonatal Resuscitation Guidelines 167
3 Guidelines For Management Of Normal Newborn 169
4 Care of at Risk Neonates 175
5 Care of Sick Neonates 177
6 Management of Low Birth Weight Babies 181
7 Neonatal Sepsis 185
8 Treatment Of Respiratory Distress In Newborn 189
9 Meconium Aspiration Syndrome 191
10 Bleeding Neonate 193
11 Jaundice in the Newborn 196
12 Management of Surgical Neonate 201
13 Vitamin A Deficiency 202
14 Rickets 203
15 Management of Children with SAM 204
16 Mumps 207
17 Case Management of Children with Sever Acute Malnutrition (SAM) 209
18 Fever with Rash 214
19 Enteric fever / Typhoid 216
20 Acute Meningoencephalities 217
20 Tuberculous Meniingities 219
21 Acute Respiratory Infection 221
22 Bronchial Asthama 226
23 Breath holding spell 228
24 Bronchiolitis 229
25 Empyema 230
26 Approach to Fever 231
27 Acute Flaccid Paralysis (AFP) 232
28 Febrile seizures 235
29 Acute Nephritis 237
30 Nepharotic Syndrome 238
30 Congestive Heart Failure (CHF) 240
31 PICA 242
32 Nocturnal Enuresis 243
33 Thrush / Candiasis 244
34 Congenital Hypothyroidism 245
35 Urinary Tract Infection (UTI) (UTI) 246
 3. Obstetrics and Gynaecology
Sr. No. Contents Page No.
1 Normal Pregnancy 248
2 Normal Labour 253
3 Clinical Care for high risk pregnancy 257
4 Obstetric complications 265
5 Medical disorders complicating pregnancy 285
6 Comprehensive Abortion Care 295
7 Common gynecological problems 298

4. Dermatology
Contents Page No.
Sr. No.
1 Infections of Skin 311
Bacterial
Viral
Fungal
Parasitic

2 Non infectious Skin Conditions 319

Urticaria
Psoriasis
Lichen Planus
PityriasisRosea
Pityriasis Alba
Acne
Miliaria
Eczema / Dermatitis
Atopic Dermatitis

3 Sexually Transmitted infections (STI) 324

Syphilis
Chancroid
LymphoGranuloma Venereum (LGV)
Gonorrhoea
Chlamydial infection
Bacterial Vaginosis
Trichomoniasis
Candidiasis
Wart
Herpes Genitalis

4 Syndromic management of STDS 329

5 HIV AIDS 331

 5. Psychiatry
Sr. No. Contents Page
No.
1 Mental illness- Introduction 340
2 Evaluation: History and MSE 341
3 Schizophrenia 342
4 Bipolar Mood Disorder 344
5 Major Depressive Disorder 347
6 Anxiety Disorder 349
7 Somatization Disorder 351
8 Organic Brain Syndrome 352
9 Drug Abuse And Substance use disorder 354
10 Intellectual Subnormality 356
11 Child and Adolescent Psychiatry 358
12 Psychiartric Emergencies 360
13 Procedure For Admission to A Mental Hospitel 361
 6. Ent
Sr. No. Contents Page No.
1 Acute Otitis Media 363
2 Chronic suppurative Otitis Media 366
3 Acute Parotis 367
4 Furuncle 368
5 Otomycosis 369
6 Neck Swellings 370
7 Atrophic Rhinities 371
8 NasalMyasis 372
9 Forign body in the Nose 373
10 Deviated nasal septum 374
11 Nasal obstruction 375
12 Tonsillitis 376
13 Adenoiditis 377
14 Peritonsillar abscess 378
15 Acute Pharyngitis 379
16 Hoarsness of voice 380
17 Stridor 381
18 Facial Palsy 382
19 Sensory Neural Hearing Loss 384
20 Vertigo 386
21 Fracture Involving Nasal Bone 388
22 Fracture Involving Maxilla 389
23 Penetrating neck injury 391
24 Blunt External Laryngeal Trauma 393
25 Epistaxis 394
26 Premalignant lesion of oral cavity 395
27 Acute upper airway obstruction 396
28 Deaf mutism 397
 7. Ophthalmology
Sr. Contents Page
No. No.
1 Lid 399
2 Dacryocystitis 402
3 Conjunctiva 405
4 Cornea / Ulcer 409
5 Sclera 412
6 Uveitis 414
7 Glaucoma 416
8 Cataract 421
9 Ophthalmitis 425
10 Retinal Detachment 428
11 Refractive Error 429
12 Diabetic Retinopathy 434
13 Ocular injuries 437
14 Ocular Emergencies 441
15 Pediatric Ocular Problems 443
16 Low Vision 448
17 Eye Banking 449
 8. Surgery
Sr. No. Contents Page No.
1 452
Abdominal Pain
2 456
Wounds & Abscess Management
3 458
Head Injury
4 460
Chest Injury
5 465
Abdominal Injury
6 466
Gangrene
7 468
Burn
8 470
Dressings
9 472
Breast
10 477
Congenital Anomalies
11 488
Venous Thromboembolism
12 490
Varicose Veins
13 492
Genito Urinary Disorder
14 493
Ano-rectal diseases
15 497
Tracheostomy
499
16 Urinary Catheterization
17 506
Triage
 9. Orthopaedics
Sr. No. Contents Page No.
1 Infections in Orthopaedics 513
2 Arthritis 516
3 Congenital Disroderrs 518
4 Metabolic Disorders of Bone 520
5 Regional Conditions 521
6 Common Spine Disorders 524
7 General fracture management 526
8 Poly Trauma 530
9 Pelvic Injury 531
10 Fractures of upper limb 533
11 Fractures of lower limb 539
12 Dislocatons 544
13 Ligamentous injuries 547
14 Spinal trauma 548
15 Mangled Extremeties ( amputation) 552
16 Common Fractures in children 553
17 Bone Tumors 554

10. Anaesthesiology
Sr. Contents Page
No. No.
1 Introduction: General Protocol of Anaesthesia 558
2 Protocol of Difficult Air way 567

3 Pre AnaesthesiaCheck up Protocol 568

4 Conduct of Anaesthesia 569
5 Complications of Anaesthesia 570
6 Regional Anaesthesia Clinical Protocol 571
7 Cardio Pulmonary Resuscitation 573
8 Anaesthesia Obstetric Protocol 577
9 Spinal Anaesthesia 580
 11. Pathology
Sr. No. Contents Page No.
1 Introduction 583
2 Haematology 584
3 Serology 595
4 Biochemistry 598
5 Histopathology 599
6 Cytology study 600
7 Blood Bank 601
8 Normal Lab Values 603
9 Laboratory tests performed at PHC/RH/SDH/DH 609

12. Dentistry
Sr. No. Contents Page No.
1 Dental Caries 611
2 Diseases of Dental Pulp &Periapical Tissues 614
3 Periodontal Diseases 619
4 Spread of Oral Infection 625
5 Oral Mucosal Diseases 627
6 Premalignant lesions and conditions 630
7 Orofacial Pain 635
8 Traumatic injuries to teeth 636
9 Discoiouration of Teeth 638
10 Maxillofacial Injuries 639
11 Temporomandibular Joint disorders 642
12 Dental Impactions 645
 Abbrevations Used
Sr.No. Abbreviation Forms
1 ASHA Accredited Social Health Activist
2 AFB Acid Fast Bacillus
3 AIDS Acquired Immuno Deficiency Syndrome
4 AMTSL Active Management of Third Stage of Labor
5 AFP Acute Flaccid Paralysis
6 ARF Acute Renal Failure
7 ARDS Acute Respiratory disease syndrome
8 ARDS Acute Respiratory Distress Syndrome
9 ANC Ante Natal Care
10 APH Ante Partum Hemorrhage
11 ARV Anti Rabies Vaccine
12 ART Anti Retroviral Treatment
13 ASV Anti Snake Venom
14 ATT/AKT Anti Tuberculosis Treatment
15 ARM Artificial Rupture of Membranes
16 BSL Blood Sugar Level
17 BUN Blood Urea Nitrogon
18 BMI Body Mass Index
19 CRP C Reactive Protein
20 CRT Capillary Refill Time
21 CPD Cephalo Pelvic Disproportion
22 CPK ceratinizephospho kinase
23 CVA CerebvoVasculan Accident
24 CIN Cervical Intra epithelial Neoplasia
25 CS Cesarean Section
26 COPD Chronic Obstructive Pulmonary Disease
27 CRF Chronic Renal Failure
28 CAP Community Acquired Pneumonia
29 CQS Complete Blood Count
30 CT Scan Computerized Tomography
31 CTEV Congenital TalipesEquinoVarus
32 CCF Congestive Cardiac Failure
33 CPAP Continuous Positive Ambulatory Pressure
34 CMV CytoMegalo Virus
Sr.No. Abbreviation Forms
35 DHF Dengue Hemorrhagic fever
36 DNS Dextrose Normal Saline
37 D&C Dilatation and Curettage
38 DOT Directly Observed Treatment
39 DMARDS Disease Modifying Anti Rheumatic Drugs
40 DIC Disseminated Intra vascular Coagulation
41 DIC Disseminated Intravascular Coagulation
42 DUB Dysfunctional Uterine Bleeding
43 ECG Electro Cardiograph
44 EEG Electro Encephalon Graph
45 ELISA Enzyme Linked Immuno Assay
46 EBV Epstein Barr Virus
47 ESR Erythrocyte Sedimentation Rate
48 ESR Erythrocyte Sedimentation Role
49 EDD Expected Date Of Delivery
50 FBM Expressed Breast Milk
51 XDRTB Extensive Drug Resistant Tuberculosis
52 F-IMNCI Faculty based Integrated Management of Newborn Child and
Infant
53 FHR Fetal Heart Rate
54 FHS Fetal Heart Sound
55 FNAC Fine Needle Aspiration cytology
56 FRU First Referral Unit
57 FRU First Referral Unit
58 FFP Fresh Frozen Plasma
59 GERD Gastro Esophageal Reflux Disease
60 GIT Gastro Intestinal Tract
61 GDM Gestational Diabetes Mellitus
62 GFR Glomerular Filteration Rate
63 HA Health Assistant
64 HCC
65 HDN Hemolytic Disease of Newborn
66 HE Hepatic Encephalopathy
67 HSV Herpes Simplex Virus
68 HDL High Density Lipids
69 HCG Human Chorionic Gonadotropins
Sr.No. Abbreviation Forms
70 ADCV Human Diploid Cell Vaccine
71 HIV Human Immune Deficiency Virus
72 HPV Human Papilloma Virus
73 HTN Hypertension
74 HSG HystroSalpingoGraphy
75 IG Immunoglobulin
76 IVF In Vitro Fertilization
77 IVC Inferior Vena Cava
78 IDDM Insulin Dependent Diabetes Mellitus
79 ICTC Integrated Counseling and Testing Centre
80 IMNCI Integrated Management of Newborn Child and Infant
81 ICU Intensive Care Unit
82 ICCU Intensive Coronary Care Unit
83 IPPR Intermittent Positive Pressure Respiration
84 IHBD Intra Hepahic Biliary Duct
85 IUD Intra Uterine Death
86 IUGR Intra Uterine Growth Retardation
87 IUI Intra Uterine Insemination
88 IDA Iran Deficiency Anemia
89 IFA Iran Folic Acid
90 IBS Irritable Bowel syndrome
91 IHD Ischemic Heart Disease
92 JVP Jugular Venus Pressure
93 KMC Kangaroo Mother Care
94 KFT Kidney Function Test
95 LMP Last Menstrual Period
96 LVH Left Ventricular Hypertrophy
97 LFT Liver Function Test
98 LBW Low Birth Weight
99 LDL Low Density Lipids
100 LRTI Lower Respiratory Tract Infections
101 LSCS Lower Segment Cesarean Section
102 MRI Magnetic Resonance Imaging
103 MVA Manual Vacume Aspiration
104 MCV Mean Cell Volume
105 MCHC Mean Corpuscular Hemoglobin Concentration
Sr.No. Abbreviation Forms
106 MMR Vaccine Measles, Mumps, Rubella Vaccine
107 MTP Medical Termination of Pregnancy
108 MAM Medium Acute Malnutrition
109 MOHFW Ministry of Health and Family Welfare
110 MDRTB Multi Drug Resistant Tuberculosis
111 MPW Multi Purpose Worker
112 MI Myocardial Infration
113 NACP National Aids Control Programme
114 NICU Neonatal Intensive Care Unit
115 NBSU New Born Stabilization Unit
116 NGO Non Government Organization
117 NSAID Non Steroidal Anti Inflammatory Drug
118 OC Oral Contraceptive
119 ORS Oral Rehydration Salt
120 PCV Pack Cell Volume
121 PEF Peak Expiratory Flow
122 PEFR Peak Expiratory Flow Rate
123 PID Pelvic Inflammatory disease
124 PUD Peptic Ulcer Disease
125 PMN Poly Morpho Nuclear
126 PCR Polymerase Chain Reaction
127 PEEP Positive End Expiratory Pressure
128 PEP Post Exposure Prophylaxis
129 PET Scan
130 PPH Post Partum Hemorrhage
131 PROM Premature Rupture of Membranes
132 PID Prolapse Intervertebral disc
133 PT Prothrmbin Time
134 PPD Purified Prohine Derivative
135 RDT Radical Drug Treatment
136 RF Renal Failure
137 RNTCP Revised National Tuberculosis Control Programme
138 RVH Right Ventricular Hypertrophy
139 RL Ringer Lactate
140 SAM Sever Acute Malnutrition
141 STD Sexually Transmitted Disease
Sr.No. Abbreviation Forms
142 STI Sexually Transmitted Infections
143 SGA Small for Gestational Age
144 SNCU Special New Born Care Unit
145 SLR Test Straight Leg Raising Test
146 SAH Sub Arachnoid Hemorrhage
147 SVC Superior Vena Cava
148 TSH Thyroid Stimulating Hormone
149 TIA Transient Ischemic Attack
150 UC Ulcerative Colitis
151 USG Ultra Sonography
152 URTI Upper Respiratory Tract Infections
153 VLBW Very Low Birth Weight
154 VIA Visual Inspection of Cervix with Acetic Acid
155 WHO World Health Organization
MEDICINE

Page 1
 1. FEVER
Body temperature is controlled by the hypothalamus.
The normal core body temperature is 36.5-37.5C
2. Causes
(97.7-99.5F).The morning temperature of >98.9F
Malaria
and the evening temperature of >99.9F defines
Sepsis
fever. Abscess
Brucellosis
1. Definition Lymphoma
Since an oral temperature is 0.5F (0.3C) to 1F Night sweats Characteristic of Tuberculosis, but
(0.6C) lower than a rectal or tympanic temperature: sweating from any cause is usually worse at
Rectal temperature 100.4F - Core temperature night.
Recurrent fever Cholecystitis, Cholangitis and
Tympanic temperature 100.4F - Core Temperature Urinary tract infection with obstruction or
Oral temperature 99.5F-99.9F calculi.
Headache Fever due to any cause can produce
Axillary temperature 99.0F-99.5F headache. If severe and with photophobia
Note: suspect- Meningitis.
Delirium Common in elderly and young ones.
This is not absolute, remember that fever is a
relative condition. Muscle pain Myalgia classical of viral fever,
Have a lower threshold for fever at 6am or 6pm. Influenza, Malaria, Leptospirosis and
Keep antipyretics and recent intake in mind Brucellosis.
when considering fever.
Feeling hot-does not necessarily imply fever. 3. Evaluation of Febrile Patient
Rigors profound chills accompanied by Although fever is a normal response, prolonged
chattering of teeth &severe shivering implies a episodes can cause damage so always evaluate for
rapid rise in body temperature. stability of patient (regardless of what you think is
the cause).

Table 1: Evaluation of fever patient

1.Temperature Axillary temperature >990F
2.White Blood Cell Count >12,000 or <4,000 or
>10% bands
3.Heart Rate >90 bpm*
4.Respiratory Rate >24 bpm^ or PaCO2<32mm Hg
Sepsis = SIRS** + infection
Severe sepsis = SIRS** + infection + end organ damage
Septic shock = Severe sepsis + refractory hypotension
(<90 mm Hg or 40% below baseline)
* beats per minute
^ breaths per minute
**SIRS- systemic inflammatory response syndrome
3.1. Fever Pattern 3.2. Relation to Pulse
It is important to note that the cycle of fever pattern is Liebermeisers rule: For everyone degree rise of
often not very helpful in determining the cause of the temperature above normal, the pulse will increase by
disease. 8-10 beats per minute.
Possible exceptions are: Tertian and quartan Malaria, Fagets Sign: The exception to Liebermeisers Rule.
Abscesses, Pel-Ebstein fever and drug fever.

Page 2
This Relative bradycardia may be useful when
present, although it is associated with a substantial
6. Common associated
differential diagnosis, including Typhoid fever, symptoms
Rickettsial diseases, Yellow fever, Legionnaire's
disease, Psittacosis, Leptospirosis, Drug fever, i.Fever only
Brucellosis, Mycoplasma infections, Neoplasm and ii.Neurologic
Factitious fever. iii. Abdominal
iv. Pulmonary
4. Types of fever v. Rash
vi. Haemorrhage
Continuous fever - Does not fluctuate more than vii. Bone and joint
1C in 24 hr. e.g. Lobar Pneumonia, Typhoid viii. Gynaecologic
fever, Brucellosis, Urinary tract infection.
Intermittent fever- Temperature elevation for a
certain period then returning back to normal. eg. 6.1 Fever only
Malaria, Pyaemia, Septicemia. Malaria
Quotidian- Periodicity of 24 hr- Plasmodium Typhoid fever
Falciparum Malaria. Dengue
Tertian fever- 48 hr periodicity- Plasmodium Leptospirosis
Vivax and Ovale. Rickettsia
Quartan fever - 72 hr periodicity-Plasmodium Relapsing fever
Malaria Other viral illnesses
Remittent fever- Temprature remains above HIV
normal throughout the day with fluctuations
more than 1C in 24 hr eg. Infective
Endocarditis. 6.2 Neurologic symptoms
Fever, headache, altered mental status, convulsions,
5. Hints to be obtained from coma
Cerebral malaria
history Meningitis
Encephalitis
(Since Presentation can be non- specific) Chronic Meningitis: TB, Cryptococcal
Meningitis
Detailed fever history Rabies
Medication review Japanese Encephalitis
Family illnesses West Nile Encephalitis
Ethnicity HIV
Detailed history of past surgeries Toxoplasmosis
Recent sick contacts and TB contacts/risks HIV dementia
Host factors (Immunocompromised) Trypanosomiasis (Sleeping Sickness)
Recent travel
Environmental exposures associated with jobs
or hobbies 6.3 Abdominal symptoms
Animal exposure Fever, abdominal pain
Unusual dietary habits Typhoid
High risk behavior Infectious colitis: Shigella, E. coli, salmonella,
Sexual history including Contraceptives Campylobacter, Ameba
Gynecologic history Amebic liver abscess
Hypersensitivities to environmental Abdominal TB
agents/medicines or family history of such Appendicitis, Pyelonephritis
diseases HIV

Page 3
 6.4 Fever and rash i. Urinary tract infection
Fever and skin rash ii. Pelvic inflammatory disease
iii. Sexually transmitted disease
Chicken pox
Measles
Dengue 7.3. Abdominal symptoms
Other viruses Diarrhoea with or without blood, weight loss
and abdominal pain
i. Gastroenteritis
6.5 Haemorrhagic symptoms ii. Intra-abdominal sepsis
Hematemesis, melena, epistaxis, petechiae, purpura, iii. Inflammatory bowel disease
puncture site bleeding iv. Malignancy
Dengue
Relapsing fever
Ebola, Lassa, Marburg 7.4. Skin rash-appearance &
Yellow fever distribution will give a clue
i. Macular - Measles, Rubella, Toxoplasmosis
ii. Haemorrhagic - Meningococcal, Viral
6.6 Bone and Joint haemorrhagic fever
Fever with joint or bone pain
iii. Vesicular - Chicken Pox, Shingles, Herpes
Sickle cell disease
Simplex
Septic arthritis iv. Nodular - Erythema nodosum- TB & Leprosy
Osteomyelitis v. Erythematous - Drug rash and Dengue fever.
Pyomyositis
Rheumatic fever 7.5 Joint symptoms-
Chickungunya Joint pain, swelling or limitation of movement is
Brucellosis suggestive of active arthritis
i. Distribution-mono, oligo, polyarticular
ii. Appearance-fleeting-Rheumatic fever
6.7 Gynaecological symptoms iii. Oligoarthritis-infective, Kochs
Fever, pelvic pain, vaginal discharge
iv. Polyarticular-Rheumatoid arthritis, Osteoarthritis
PID v. Axial skeleton involvement
Tubo-ovarian abscess Spondyloarthropathy, Psoratic
Postpartum endometritis
Septic abortion
8. Hints to obtain from
7. Symptom Analysis of Fever examination
i. Verify presence of fever- true/factitious Vital Signs: Monitor all of the vital signs for
ii. Duration-acute/chronic stability
iii. Mode of onset- abrupt/gradual General appearance: Do they look sick?
iv. Progression- continuous/intermittent Anxious? Do they have altered sensorium?, look
v. Severity- how it affects the daily work /physical for pallor, icterus, cyanosis, clubbing and
activities? lymphadenopathy.
vi. Relieving and aggravating factors Oral examination: Oral cavity infections, dental
vii. Treatment received and outcome examination, gum examination, sinuses
viii. Associated symptoms- localising features. Cardio vascular examination: Any murmurs
Respiratory examination: Bronchial sounds,
7.1. Respiratory tract symptoms Decreased breath sounds, Adventitious sounds
i. Sore throat, nasal discharge, sneezing-URTI Central nervous system examination: Fundus
ii. Sinus pain & headache- Sinusitis examination, Mental Status, Encephalopathy,
iii. Cough, sputum, wheeze or breathlessness-LRTI
look for any neurological deficit.
Per abdomen: Tenderness, Organomegaly,
7.2. Genitourinary Symptoms Ascites
Frequency of micturition, loin pain, vaginal or Skin: Rashes, Nail Exam, Wounds/Decubitus
urethral discharge suggesting Ulcers

Page 4
 Musculoskeletal examination: Joint examination, Sputum Cultures
Muscle tenderness. Skin biopsy
Genital/pelvic examination and rectal
examination. 10.3. ESR
Look for indwelling devices. Normal: Men = Age/2, Women = Age+10/2
Elevated in:
9. Differential diagnosis Acute or Chronic Inflammation
Infection (TB, UTI/Prostatitis, Endocarditis, Infection
Abscess, Line Infection, Sinusitis, Meningitis, Tissue Injury
Arthritis, Osteomyelitis, Wound infectious, Thyroid Disease
Diarrhea) Azotemia
Inflammatory (Rheumatic Disorders, An elevated ESR does not rule in or out disease
Vasculitis) As opposed to the ESR, the CRP increases more
Drug Fever (Beta-Lactam antibiotics, quickly with an acute process, and decreases for
Amphotrecin B, Chemotherapy, Drug quickly when the underlying state resolves.
Interactions)
Thrombotic (DVT/PE/MI) ESR > 100
Neurologic (Hypothalamic disorder, Spinal Cord T - TB
Injuries, ICH) O - Osteoarthritis
Endocrine (Thyrotoxicosis, Adrenal E - Endocarditis
Insufficiency, Subacute Thyroiditis) V - Vasculitis (Temporal Arteritis)
Gastrointestinal (IBD, Pancreatitis, A - Abscess
Cholecystitis) N - Neoplasm (especially Lymphoma, Plasma
Malignancy Cell dyscariasis)

10. Fever Workup 10.4. Blood cultures

10.1 Minimum in all patients
CBC with differential and micro review
Blood smear- for malarial parasites
CXR PA and Lateral. Add Decubitus if needed.
Infiltrates negative if dry
Urine analysis (with Microscopy) and Urine
Culture
2 sets of blood cultures + Cultures from any
central catheter
Electrolytes and Metabolic Panel, LFTs,
Hepatitis Panel, HIV Test
10.2 Other Specific procedures/labs
to obtain data
Autoimmune Workup (RF, ANA, etc as history
guide, ESR, CRP)
Specific Viral Serologies
Lumbar Puncture, Thoracentesis, Arthrocentesis,
Paracentesis
CT Scan of Head
CT PE Protocol/Dopplers of extremities
Echocardiogram
Stool Cultures - Gram Stain, Clostridium difficle
toxin etc
The bacteriologic burden is highest in the blood
stream approximately 1 hour before fever spikes.
So collect blood cultures 1 hour before fever
spike.
If you are suspecting Endocarditis, tell the lab to
continue following the cultures for at least 4
weeks.
11. Treatment of Fever Itself
Give empiric Antibiotics when there is high
suspicion of the source of infection or if the
source is unknown and the patient is unstable.
Tab Paracetamol 500mg orally 4 times a day for
most fevers with discomfort.
Dont always lower the temperature so readily.
This decreases your ability to know when to draw
cultures and may lower the patients defense
mechanism. Once workup has been performed (and
possibly repeated) then temperature can be lowered.
However, have low threshold for lowering the
temperature when there is a hypermetabolic state that
would be damaging (i.e concurrent MI, CVA) or if
the patient is very symptomatic.

Page 5
 2. COMMUNITY ACQUIRED PNEUMONIA
[CAP]
Other presentations may include headache and
1. Introduction myalgia
Pneumonia is an infection of pulmonary
Certain etiologies, such as legionella, also may
parenchyma that causes them to function
produce gastrointestinal symptoms
abnormally
Signs -
Classified as typical or atypical, although the
clinical presentations are often similar. Tachycardia
Approximately 20-33% of episodes result in
hospitalization Tachypnoea

Typical: Up to 70% usually caused by Streptococcus Dullness to percussion of chest, crackles or rales
pneumoniae on auscultation, bronchial breath sounds, tactile
fremitus, and egophony (E to A changes)
Atypical: 30-40%(My Lungs Contain Viruses)
Patients with typical pneumonia are more likely
Mycoplasma pneumoniae to present with dyspnea and bronchial breath
sounds on auscultation
Legionella pneumophila
Chlamydia pneumoniae 3. Radiological imaging
Viruses: Influenza, Adenovirus 1) Chest x ray (PA and Lateral)
2. Clinical features Lobar consolidation more common in typical
pneumonia
Symptoms:
Bilateral, diffuse infiltrates commonly seen in
Cough, fever, chills, fatigue, dyspnea, rigors, and atypical pneumonia
pleuritic chest pain
If performed early in the course of the disease,
cough may be persistent and dry, or it may may be negative
produce sputum

Figure 1 - Chest X-Ray PA VIEW - CAP

2) CT scan- Could be performed in patients 4. Laboratory Diagnosis
with a negative chest radiograph when there is a high
clinical suspicion for pneumonia and to rule out other Complete blood count, sputum, gram stain and
pathologies. cultures, blood sugars, blood urea, serum creatinine.

Page 6
 Cap Amoxicillin 1gm thrice a day x 5 days plus
5. Treatment TabAzithromycin/Clarithromycin as above
Initial treatment of CAP is based on physical doses
examination findings, laboratory results and patient OR
characteristics. After examination you must decide Cap Amoxicillin and Clavulunate 2gm twice a
whether to treat patient on OPD basis or to admit the day x 5 days plus a tab
patient. Azithromycin/Clarithromycin as above doses
OR
Patients with any one of following features must be
Tab Levofloxacin 750mg OD, OR
admitted
Moxifloxacilline 400mg OD, OR Gemifloxacin
Respiratory rate >30/min 320mg OD x 5-7 days
Systolic BP<90mmHg or diastolic <60mmHg OR
New onset confusion or impaired level of Tab Cefpodoxime 200mg BD or Tab
consciousness Cefuroxime 500mg BD Plus macrolide
Comorbid illness- Diabetes, Ischaemic Heart antibiotics
Disease, Alcoholics, Immunocompromised,
Multilobar pneumonia 5.4. Inpatients
Therapy for pneumonia is empiric because specific - I.V. Cefotaxime 1-2 gm 8 hrly or
pathogens usually are not identified at the time
treatment is initiated. - I.V. Ceftriaxone 1-2 gm OD or
- I.V. Ampicilin 1-2 gm 4-6 hrly or
5.1. Duration of therapy
- I.V. Ampicillin Sulbactum 2 gm 8 hrly x 4 days
S. pneumoniae: 7-10 days or until afebrile 3 days
Mycoplasma/Chlamydia pneumoniae: 10-14 plus
days, up to 21 days Tab Azithromycin or in severe cases I.V.
Legionella: 10-21 days Azithromycin 1gm on day one and then 500mg
OD next 4 days orTab levofloxacin,
5.2. CAP, not hospitalized moxifloxacinas above.
No comorbidities After clinically stable (T<100.00F, HR<100
beats/min, RR<24/min, SBP>90mmsg, O2
Cap Amoxycillin 500mg three times a day x 5 sat>90%) and able to tolerate oral intake, may be
days switched to oral antibiotics for remainder of
Tab Azithromycin 500mg PO x 1, then 250mg therapy
once a day -5 days OR
Tab Clarithromycin 500mg twice a day -5 -7 PPV23 is recommended for all adults65 years
days OR of age and in younger patients with a number of
Cap Doxycycline 100mg twice a day -10 days conditions that increase the risk of invasive
pneumococcal disease.
5.3. CAP, not hospitalized
With comorbidities 6. Complications
Lung abscess, pleural effusion, empyema. These
patients need to be referred to district hospital.

Page 7
 3. BRONCHIAL ASTHMA
1. Introduction
Asthma is defined as a chronic inflammatory disease
of airway that is characterized by increased
responsiveness of tracheobronchial tree to a
multiplicity of stimuli.
2. Precipitating factors
Childhood infections Respiratory syncytial
virus
Allergen exposure Allergy to feathers, animal
danders, dustmites, molds
NSAID, aspirin, beta blocker, sulfite containing
topical ophthalmic solution, food preserving
agent
Wood and vegetable dust, industrial chemicals
and plastic
Exercise, emotional stress.
3. Symptoms
Dysponea, cough and wheezing
Sense of constriction in the chest
Cough that produces thick, stringy mucus.
Increase mucus production, typically tenacious
mucus.
4. Signs
Tachyponea, tachycardia, mild systolic hypertension
Respiration become audibly harsh, rhonchi heard on
auscultation.
In severe cases - Accessory muscle become visibly
active, Paradoxical pulse, Cyanosis, Silent chest. In
some severe cases patients may land in to respiratory
failure.
5. Investigation
Sputum and blood examination for eosinophilia
Chest X-ray showing hyperinflated lungs
Simple spirometry shows air flow limitation with
deceased FEV1, FEV1 / FVC and PEF.
Short acting inhaled 2 agonist (SABA) Salbutamol 100mcg/metered dose 1-2 puffs, Levosalbutamol
50mcg/metered dose 1-2 puffs as needed, Terbutaline
Peak expiratory flow- by using peak expiratory
flow meter >20% of diurnal variation on 3 days
in a week for 2 week.
Diagnosis of asthma is established by
demonstrating reversible airway obstruction.
Reversibility is defined as 12%
a increase in
FEV1 15 minutes after two puffs of a
adrenergic agonist (salbutamol) on spirometry.
6. Treatment
Drug treatment: Classified in to:
6.1. Controller: To be taken on longterm basis
to control asthma through their anti-inflammtory
effects
(a) Inhaled corticosteroids(ICS)
Beclomethasone 200mcg/metered dose twice a day
OR
Budesonide 200-400 mcg/metered dose twice a day
OR
Fluticasone- 100-250mcg/metered dose twice a day
(b) Systemic corticosteroids
Oral Prednisone or Prednisolone once daily for 5 to
10 days
(c) Leukotriene modifier
Tab Montelukast 10mg once a day X 5 days.
(d) Long acting inhaled 2 agonist-
-Salmeterol (MDI 21ug/puff, 2 puff 12 hourly OR
- Formeterol (1 to 2 puffs 12 hourly)
(e) Theophylline-Tab Deryphylline 150 mg twice a
day X 5 days.
6.2. Reliever: Used on or as needed basis to
quickly relieve symptoms by their bronchodilator
properties. These are:
Page 8
 Systemic glucocorticoid - Tab Prednisolone 40-60mg/day

Short acting oral 2 agonist - Tab Salbutamol 2-4mg/day

Anti cholinergic - Ipratropium inhaler

Theophylline - 100-300mg three times a day

6.3. Combinations available as Formoterol/Budesonide 1-2 puffs twice daily

Salbutamol/Beclomethasone.
inhaler and rotacaps Inhaled drugs are preferred over oral due to less dose,
Salmeterol/Fluticasone 1-2 puffs twice daily less side effects, quick onset of action.

OCS
LABA LABA LABA
ICS ICS ICS ICS
Low dose Low dose High dose High dose
Short acting 2 agonist as required for symptom relief
Mild persistent Moderate Severe persistent Very severe
Mild intermittent
persistent persistent
Figure-1: Step wise approach to asthma therapy according to the severity of asthma and ability to control
symptoms.

ICS = Inhaled corticosteroid; Bradycardia or arrhythmia

LABA = Long acting 2 agonist Confusion, coma.
OCS = Oral corticosteroid
7. Acute severe asthma: (Status 7.3. Treatment
asthamaticus) Oxygen 40-60 % nasally to achieve oxygen
Can be fatal and must be treated promptly. saturation >90%
Inj Hydrocortisone-200mg I.V. stat and then
7.1. It is characterized by 100mg 8 hrly
Severe dyspnoea Salbutamol (2.5-5mg) and Ipratropium Bromide
Respiratory rate 25/min (0.5mg) alternately inhaled through the
Heart rate 110/min. nebulizer.
Inability to complete sentence in single breath. Inj. Aminophylline 500mg in 500 ml of 5%
PEF (peak expiratory flow)35-50% predicted Dextrose over 12 hours if patient is not receiving
theophylline previously.
7.2. Life threatening features Inj. Ampicillin 500 mg 6 hrly till patient is stable
PEF<33% predicted and then oral Ampicillin 500 mg TDS X 5 days.
SpO2<92% silent chest In very severe cases patient may require
ventilatory support.
Cyanosis
Normal or raised PaCO2 (suggests impending
respiratory failure) Refer to higher center with above life threatening
signs.
Feeble respiratory effort

Page 9
Rotahaler Spacer Metered dose inhaler

Figure 2 Types of Devices used in Bronchial Asthma

Page 10
 4. PLEURAL EFFUSION
A pleural effusion is an abnormal excess amount of Cancer
fluid in the pleural space Liver disease (Cirrhosis)
End-stage renal disease
1. Symptoms Nephrotic syndrome
Breathlessness Congestive heart failure
Cough Pulmonary embolism
Fever Constrictive pericarditis
Pleuritic chest pain Lupus and other autoimmune conditions

2. Signs 4. Investigations
Decreased breath sounds 4.1. Chest X-ray film
Stony dullness on percussion P-A view, lateral decubitus, lateral view
Decreased vocal resonance
Blunting of CP angle, Ellis S shaped in large
3. Common Causes effusions

Tuberculosis
Pneumonia

Figure 1: Chest radiograph showing left-sided pleural effusion

Figure 2: Massive right pleural effusion with shift of mediastinum towards left

4.2. Ultrasound 4.3. Blood tests

Useful in small amounts of fluid, loculated, CBC, ESR, Renal and liver function blood tests:
septations

Page 11
4.4. Thoraco centesis 5. Treatment
Once a pleural effusion is identified on imaging, a Management of common pleural effusions
fluid sample is usually taken to determine the pleural
effusion's character and seriousness, a procedure 5.1. Tuberculosis
called thoraco centesis.
Is the commonest cause of pleural effusion?
A sample of fluid is removed with a needle inserted
between the ribs Straw coloured effusion
Cell count - lymphocyte predominance
Pleural fluid tests: routine, microscopy cytology and Pleural fluid protein > 3g/dl
ADA (Adenosine diaminase) levels
Cob web formation
There are two different types fluid ADA level is high.
Transudative OR Exudative Tubercular pleural effusion is treated as per RNTCP
guidelines
i. Transudative: clear fluid
Clear fluid, low protein content, cell count is low. 5.2. Para pneumonic effusion
eg. Congestive cardiac failure, liver cirrhosis,
Nephrotic syndrome. Chest X-ray consolidation features along with
effusion
ii. Exudative: Cell count predominantly neutrophilic
Straw coloured, high protein content, cell count Appropriate antibiotics
is high. Thoracocentesis toensure that empyema has not
By the gross characteristics of the fluid. developed
Frankly purulent fluid indicates an empyema.
A putrid odor suggests an anaerobic empyema. 5.3. Malignant effusion
A milky, opalescent fluid suggests a chylothorax,
Cytology positive
resulting most often from lymphatic obstruction
Refer to higher centre
by malignancy or thoracic duct injury by trauma
Treatment of underlying cause in heart failure,
Grossly bloody fluid result from trauma, malignancy,
nephroticsyndrome, liver cirrhosis

Page 12
 5. CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD)
cause cough with expectoration on most days for at
1. Introduction least 3 months a year for more than 2 consecutive
COPD is a chronic lung disease characterized by years.
airflow limitation that is not fully reversible.
ii. Emphysema
It includes chronic bronchitis and emphysema.
It is defined as distension of air spaces distal to the
i. Chronic Bronchitis terminal bronchiole with destruction of alveolar
This is a condition associated with excessive septa.
tracheobronchial mucus production sufficient to

Table-1: Differentiating features between Emphysema and Bronchitis

Features Predominant emphysema (Pink Predominant bronchitis (Blue
puffer) bloater)
1. Age of onset 6th decade 5th decade
2. Cough After dyspnea Before dyspnea
3. Dyspnea Severe Mild
4. Sputum Scanty, mucoid Copious, purulent
5. Infections Less common Common
6. Respiratory insufficiency Often terminal Repeated attacks
7. Chest x-ray Hyperinflation +/- bullous changes; Increased bronchovascular marking;
small heart large heart
8. PaCO2 (mm Hg) 35-40 50-60
PaO2 (mm Hg) 65-75 45-60
9. Pulmonary hypertension Mild Moderate to severe
10. Cor pulmonale Preterminal stage Common
11. Diffusing capacity Decreased Normal to slight reduction

Table-2: Differences between Pink puffer and Blue bloater

Pink puffer Blue bloater

1. Course Progressive dyspnea Intermittent dyspnea

2. Sputum Scanty Profuse

3. Polycythaemia Uncommon Common

4. X-ray Attenuated peripheral vessels Normal peripheral vessels

5. pCO2 Normal Increased

6. Alveolar gas transfer Reduced Normal

2. Etiology 3. Signs
Smoking (active and passive), Smoke from biomass Sitting and bending forward with hands on
fuel (firewoods, burnt plastics) knees(tripod position).

Page 13
Pursed lip breathing Inhaled bronchodilators include -
Cyanosis Ominous sign Short acting beta agonists -Salbutamol, 1-2 puffs
three times a day, terbutaline 1.5mg three times a day
Forced expiratory time Normal - 4 secs, COPD - 6
secs and above Long acting beta agonis (Salmeterol, Formoterol), 1-
2 puffs twice a day
Barrel chest
Short acting anticholinergics (Ipratropium) 1-2 puffs,
Hyper resonant chest 2-3 times a day
Diminished breath sound and bilateral wheeze Long acting anticholinergic (Tiotropium) 1-2 puffs
Spirometry showing obstruction (Fev1 / Fvc < 70%) once a day.
even after bronchodilator confirms the diagnosis of (d) Theophylline
COPD.
Inj Aminophylline 250mg in 500 ml of 5 % Dextrose
4. Treatment slowly over 8-10 hrs in acute attacks.
Tab Theophylline 100-300mg three times a day
4.1. Non pharmacological
Side effects: tachycardia, nausea, arrhythmias and
Rehabilitation convulsions
Exercise
Nutrition (e) Glucocorticoids
Education Inhaled corticosteroids should be given in severe
Avoid smoking COPD or in those with repeated exacerbation.

4.2. Pharmacological Fluticasone 1-2 puffs twice a day

(a) Oxygen therapy Budesonide 1-2 puffs twice a day

(b) Antibiotics Systemic corticosteroids should be given only in

patients with acute exacerbationof COPD.
Antibiotics are required as infection often precipitates
acute attacks. Inj benzyl penicillin 10 lakhs units 6 Tab Prednisolone 30-40 mg /day for 8-10 days in
hrly 5-7 days or Inj ampicillin 500mg 6 hrly 5-7 days tapering doses

(c) Bronchodilators 5. Complications

Inhaled bronchodilators are preferred to oral i. Pneumothorax
formulations in view of better efficacy and lesser side ii. Respiratory failure
effects. iii. Cor pulmonale

Page 14
 6. BRONCHIECTASIS
1. Defination 3. Symptoms
Bronchiectasis is chronic, irreversible dilation and Cough with production of large quantities of purulent
distortion of the bronchi caused by inflammatory and often foul-smelling sputum.
destruction of the muscular and elastic components of Fever, generalized malaise, weight loss, Hemoptysis
the bronchial walls. It may be focal or diffuse. It is Dry bronchiectasis; usually involve the upper lobes
categorized as cylindrical, tubular, varicose or cystic.
Recurrent pneumonia
2. Etiology 4. Signs
Conditions associated with the development of
bronchiectasis Early phases or dry variety: normal
Severe or secondary infection: persisting
2.1. Post infection crackling rales in the same part of lung
Later stage: Emphysema and cor pulmonale.
Bacterial pneumonia Moist crackles at lung bases
Tuberculosis Halitosis, skin pallor
Pertussis
Measles 5. Laboratory tests
Influenza
Fungus Sputum for Gram stain, C&S, and acid-fast
bacteria (AFB)
2.2. Proximal airway obstruction CBC with differential (leukocytosis with left
shift, anemia).
Foreign body aspiration Serum protein electrophoresis to evaluate for
Benign airway tumors hypogammaglobulinemia.
Antibody test for aspergillosis.
2.3. Abnormal host defense Sweat test in patients with suspected cystic
Ciliary dyskinesia (Kartageners syndrome) fibrosis.
Alpha 1 antitrypsin deficiency
6. Evaluation
2.4 Immuno deficiency
6.1. Chest x-ray:
HIV, Hypogamaglobulenimia
Increased in size and numberof ronchovascular
2.5 Genetic disorders markings (quiet nonspecific). Presence of Tram-
track indicates dilated airways suggestive of
Cystic fibrosis bronchiectasis.

6.2. CT or HRCT:
High sensitivity and specificity

Page 15
 Figure 1- HRCT showing Bronchiectasis
Tram track sign: The bronchial wall is thicken and
visible; the bronchi lose the trend of narrowing from
proximal end to distal end.
Signet ring sign: Dilated bronchi appear as ring
structures with internal diameters greater than those
of their accompany pulmonary artery branches.
7. Differential diagnosis
Differentiate from:
Chronic bronchitis, Lung abscess, Tuberculosis
Congenital pulmonary cyst.
8. Treatment
8.1.Non-Pharmacologic Therapy
Chest physiotherapy helps the Postural drainage
and enhances removal of respiratory secretions.
Adequate hydration, mucolytic administration
8.2. Acute General Treatment
Supplemental oxygen for hypoxemia.
The choice of antibiotics should be accurate by
the results of sputum culture and drug sensitivity
test.
Empirical therapy - Antipseudomonal
antibiotics. Cipofloxacin and Gentamicin or
Antibiotic therapy is based on the results of
sputum, Gram stain, and C&S
Bronchodilators are useful in patients with
demonstrable airflow obstruction.
8.3. Chronic Treatment
Avoidance of tobacco.
Maintenance of proper nutrition and hydration
Prompt identification and treatment of infections.
Pneumococcal vaccination and annual influenza
vaccination
Page 16
 7. LUNG ABSCESS
1. Introduction
A lung abscess is an infection of the lung
parenchyma resulting in a necrosis and cavitation
of lung.
Commonest site is right lung and involves the
posterior segment of the right upper lobe, the
superior segment of the lower lobe, or both
The bacterial infection may reach the lungs in
several ways that most common is aspiration of
oro-pharyngeal contents.
2. Microbiology
The most common anaerobes are
Peptostreptococcus, Bacteroids, Fusobacterium
species & Microaerophilic streptococcus.
Other organisms that may infrequently cause
lung abscess include Staphylococcus aureus,
Streptococcus pyogens, Streptococcus
pneumoniae (rarely), Hemophilus influenza,
Actinomyces species, Nocardia species, & Gram
negative bacilli (Pseudomonas)
Mycobacterial tuberculosis is a common cause.
Non-bacterial pathogens may also cause lung
abscesses. Parasites [Paragonimus, Entamoeba]
Fungi [Aspergillus, Cryptococcus, Histoplasma,
Blastomyces, Coccidioides] seen in
immunocompromised patients.
3. Clinical presentation
Figure 1- X-Ray Showing Lung Abscess
Symptoms are generally insidious and
prolonged, occurring for weeks to months
Fever, chills, and sweats
Cough
Sputum production (purulent with foul odor)
Pleuritic chest pain
Hemoptysis
Dyspnea
Malaise, fatigue, and weakness
Tachycardia and tachypnea
Dullness to percussion, whispered pectoriloquy, and
bronchophony
4. Lab.Studies
CBC- leukocytosis
Sputum for gram stain, culture & sensitivity.
If T.B. is suspected, acid fast bacilli stain &
mycobacterial culture is requested.
Blood culture may be helpful in establishing the
etiology.
Obtain sputum for ova & parasite whenever a
parasitic cause for lung abscess is suspected.
5. Radiological imaging
5.1. CXR
Lung abscesses are most commonly found in the
posterior segment of the right upper lobe. They
appear as irregularly sharp cavity with an air-fluid
level inside.
Page 17
5.2. CT Scan
- An abscess is rounded radio-lucent lesion with a
thick wall & ill-defined irregular margins.
Figure 2 CT-SCAN Showing Lung Abscess
6. Medical care
Antibiotic therapy:
IV Clindamycin 600mg 3 times a day, till
afebrile then oral 300mg four times a day for 7
days.
Alternative is IV Amoxycillin/Clavulanate
1.2gm thrice a day or I.V. Ampicillin
/sulbactum 1.5gm thrice a day then to oral
Amoxicillin/Clavulanate for 7 days, with I.V.
Metronidazole 500mg 8 hrly is an effective drug
against anaerobic bacteria for 7 days.
In hospitalized patients who have aspirated and
developed a lung abscess, antibiotic therapy
should include coverage against staph aureus and
Enterobacter and Pseudomonas species and as
per the identified pathogen.
Cephalosporins that have gram-positive, gram-
negative, and anaerobic coverage, may be used
when a polymicrobial infection is suspected as
cause of lung abscess.
Duration of therapy is generally for 4-6 weeks to
as long as 14 weeks.
Antibiotic treatment should be continued until the
chest radiograph has shown either the resolution of
lung abscess or the presence of a small stable lesion.
Patients with poor response to antibiotic therapy
include bronchial obstruction with a foreign body or
neoplasm or infection with a resistant bacteria,
Mycobacteria, or fungi.
7. Complication
Rupture into pleural space causing empyema, Pleural
fibrosis, bronchopleural fistula.
Page 18
 8. PNEUMOTHORAX

Stature.
1. Definition
3.2 Secondary spontaneous - less
The presence of air within the pleural cavity.
common
2.Classification Chronic bronchitis &emphysema, (35%).
Asthma,(0.8).
2.1.Spontaneous Suppurative pneumonia like staphylococci,
klebsiella, HIV (2-4%).
Primary. TB of lungs.
Secondary.
3.3 Traumatic Iatrogenic
2.2.Traumatic Paracentesisthoracis, (28%).
Central venous cannulation, (22%).
Non-iatrogenic. Barotrauma (mechanical ventilation).
Iatrogenic. Tracheostomy.

3.4 Traumatic non iatrogenic

2.1 Spontaneous
Pneumothorax occuring in the absence of trauma may
be described as spontaneous.
Presents in 3 ways:
Open Pneumothorax- air moves freely in & out
of pleural space during breathing.
Closed pneumothorax- no movement of air from
the pleural space due to closure of the
communication, air slowly gets absorbed & the
lung re-expands.
Tension pneumothorax- a check valve
mechanism is produced; this allows air to enter
pleura & accumulate to raise the intrapleural
pressure above the atmospheric pressure and
leads to compression on lung & shifting of
mediastinum to opposite side.
a. Primary spontaneous
pneumothorax
Commonly occurs in healthy subjects with no
h/o of pre-existing lung disease.
Disease of young adult.
b. Secondary spontaneous
pneumothorax
Coexisting structural or functional abnormality
in the lung.
3. Causes of Pneumothorax
3.1 . Primary spontaneous
Apical blebs (90%).
pneumothorax
Open & closed chest injury, (road traffic
accident).
Stab or gun shot wounds.
Rib fractures.
4. Symptoms
Small pneumothorax is asymptomatic.
Chest pain - Sharp unilateral associated with
shortness of breath is commonest presentation.
Sharp & stabbing Chest pain exacerbated by
deep inspiration & postural change.
Anxious, restless, tachypnoeic, struggling for
breath, rapid low volume pulse & hypotension.
May large pneumothorax produce respiratory
distress, signs of shock.
Closed pneumothorax usually does not produce
severe symptoms.
Tension pneumothorax medical emergency.
5. Physical signs
Small pneumothorax difficult to detect on
physical examination.
Absence or diminished breath sounds on affected
side.
Chest movement diminished on affected side
Decreased vocal fremitus.
Hyper resonant percussion note.
Ipsilateral enlargement of chest due to decrease
elastic recoil of the collapsed lung.
Shift of mediastinum on opposite side.

Page 19
 Increased JVP. ECG- Diminished anterior QRS amplitude.
Respiratory distress. Radiographic appearances.
Diaphoresis.s
Cyanosis. X-ray chest-sharply defined lung edge convex
Hypotension. outwards separated from chest wall by translucency
Crepitus is seen if there is associated with no lung markings &mediastinal displacement
subcutaneous emphysema. depending upon the extent of pneumothorax.

6. Diagnosis

Plain X-ray film of the chest showing

hyperleucency without any lung
markings on right side of the chest
(Pneumothorax)

Figure 1 X-Ray Showing Pneumothorax

If pneumothorax small but patient mild

7. Differential diagnosis
Transmural myocardial infarction-ECG changes
& left sided pneumothorax changes resolve once
re-expansions.
Emphysema confused with pneumothorax but x-
ray main diagnostic tool.
Massive emphysematous bulla or congenital
cyst, when ruptures may confused with
pneumothorax but previous x-ray, lateral
decubitus view helpful in differentiating upper
lobe bulla/cyst.
8. Complications
Recurrence, Haemopneumothorax, Pyopneumothorax
and Respiratory failure when tension pneumothorax
present.
9. Treatment
T/T depends on cause, size, degree of physiological
derangement Primary pneumothorax-smaller without
pleural air leak may resolve spontaneously.
symptomatic, admit the pt& administer high.
flow oxygen, resulting nitrogen gradient will
speed resorption.
If pneumothorax larger than 15% to 20% or
more than mildly symptomatic, insert a
thoracostomy tube.
Secondary pneumothorax- pts are symptomatic
& require lung re-expansion.
Often bronchopleural fistula persists & larger
thoracostomy tube & suction are required.
Iatrogenic pneumothorax--due to barotrauma
from mechanical ventilation always persistent air
leak & should be managed with a chest tube &
suction.
Tension pneumothorax--decompress the affected
hemithorax immediately with a14 gauge needle
attached to a fluid filled syringe, release of air
with clinical improvement confirms the
diagnosis. Seal chest wound with an occlusive
dressing & arrange the placement of a
thoracostomy tube.

Page 20
 9. LUNG CANCER

1. Definition 3. Risk factors

Uncontrolled growth of malignant cells in one or Smoking: Smokers have 10 fold or greater
both lungs and tracheo-bronchial tree. increase in risk.
Radiation Exposure.
2. Epidemiology Family history: 1st degree relatives 2 to 3 fold
increase risk.
Lung cancer was initially thought to be
Environmental/ Occupational Exposure:
infrequent in India.
Asbestos, arsenic, chromium, mustard gas,
Rare below age 40.
nickel, Radon, polycyclic & hydrocarbons.
Increasing until age 80 after which rate tapers
Scarring.
off.
Probability developing lung cancer
approximately 8% & 6% in males & females.
4. Signs and Symptoms

Table No. 1
Signs & symptoms Range of frequency
Cough (persistent for > than 2 weeks) 8-75%
Weight loss 0-68%
Dyspnoea 3-60%
Chest pain (poorly localized deep chest discomfort) 20-49%
Hemoptysis (seen more in central tumours) 6-35%
Bone pain 6-25%
Clubbing 0-20%
Fever 0-20%
Weakness 0-10%
SVC syndrome 0-4%
Dysphagia 0-2%
Wheezing & stridor 0-2%
Large cell Carcinoma 10-15%,
undifferentiated, giant or clear ce
5. Types of Lung Cancer
5.2. Small cell Carcinoma (20-25%,
5.1. Non small cell carcinoma oat, intermediate cell)
Squamous Cell Carcinoma (25-40%, epidermoid
derived). 6. Diagnosis
Adenocarcinoma (25-40%, bronchial, acinar, History and Physical exam: Physical signs like
papillary, solid, broncioalveolar). clubbing, lymphadenopathy, hoarseness of voice
(vocal cord palsy on indirect larygoscopy) along with
chest x ray signs of mass lesion and. collapse which
are pointers towards the diagnosis of malignancy.

Page 21
Non resolving pneumonia in an elderly individual or Chest X-ray identifies nodules usually >1cm
in smoker, lung malignancy needs to be excluded. HRCT Chest- mass lesion along with its
morphology and vascularity can be better
6.1. Diagnostic tests visualised

Figure 1: Chest X ray showing Left parahilar lung mass

Bronchoscopy - It is the most useful Focal neurologic signs, papilledema.

investigation. Soft tissue mass.
Pleural tapping - cytological examination of the Hematocrit < 40%in men, <35%in women.
pleural fluid is necessary to establish the Elevated alkaline phosphatase, GGT, SGOT,
diagnosis. calcium levels.
Esophageal compression dysphagia.
6.2. Staging tests Laryngeal nerve paralysis hoarseness.
CT chest/abdomen. Symptomatic nerve paralysis - Horners
Bone scan. syndrome.
Bone marrow aspiration. Cervical/thoracic nerve invasion - Pancoast
PET scan helpful in staging to determine tumour.
degree of metastases Lymphatic obstruction _- pleural effusion.
MRI/CT brain useful in looking at CNS Vascular obstruction - SVC syndrome.
involvement. Pericardial/cardiac extension - effusion,
tamponade.
7. Clinical findings suggestive of
metastatic disease 8. Treatment
Medical, surgical and radiation therapy modalities
Lymphadenopathy [>1 cm]. considered according to the type and stage of the
Bone tenderness. cancer.
Hepatomegaly [>13cm span].

Page 22
 10. PULMONARY EMBOLISM
1. Introduction
Thrombosis that originates in the venous system and
embolizes to the pulmonary arterial circulation .DVT
in veins of leg above the knee (>90%), DVT
elsewhere (pelvic, arm, calf veins, etc.), Cardiac
thrombi.
Risk factors-obesity, smoking, OC pills, surgery,
trauma, malignancy, thrombophilia.
2. Signs and symptoms
Massive PE Severe dyspnoea, hypotension,
cyanosis, tachycardia.
Moderate PE- cough, pleuritic pain,hemoptysis
fever.Other signs are anxiety agitation, raised JVP,
loud P2, right ventricular heave.
ECG Findings
Figure-1: ECG changes seen in Pulmonary Embolism
Sometimes patients are asymptomatic.
Differential Diagnosis - Myocardial ischemia-angina,
myocardial infarct, pneumonia, pericarditis,
congestive heart failure etc.
3. Investigations
Chest xray- atelectasis, westermark sign
increased lucency in area of embolism,
Hamptons hump-peripheral wedge shaped
density above diaphragm, pleural effusion.
ECG- Sinus tachycardia, Classic S1Q3T3
pattern, signs of RV strain-Rin V1 V2 with t
inversion.
ABG - hypoxia, hypocapnia, respiratory
alkalosis Normal does not rule out PE.
Page 23
 D-dimer is raised (high sensitivity but poor
specificity).
4.Treatment
CT Pulmonary Angiography is gold standard.
V/Q Lung scan identifies areas of lung that are
ventilated but not perfused.
US Venous Doppler to detect deep venous
thrombosis.
Thrombolysis in massive PE. Inj streptokinase
2.5 lakhs bolus then 1.0 lakh per hour.
Unfractionated heparin 80u/kg bolus then
18u/kg/hr with goal of PTT 46-70 secs.
LMWH-inj enoxaparin 1 mg/kg 12 hrly. To
overlap with warfarin and to continue it for 3-6
months.
Page 24
 11. HYPERTENSION

Blood pressure is lateral pressure exerted by column

of blood on the walls of artery when it flows through 4.2. Basic investigations for initial
it. evaluation: Always includes
Hematocrit / Hb.
1. Definition
Serum BUN, Creatinine.
Hypertension - Defined as any one of the
following: Serum potassium.

Systolic blood pressure > 140 mmHg and / or Fasting blood sugar.
Diastolic blood pressure >90 mmHg, Total cholesterol, S Triglycerides.
Patient taking antihypertensive medications. Urine analysis for albumin, blood, glucose.
Essential HT: When the cause is not known (90 ECG for left ventricular hypertrophy and ST-T
to 95 % cases).
changes.
Secondary HT: Specific organ dysfunction is Fundoscopy for HT retinopathy.
detected (5 to 10 % cases).
4.3. Investigations usually included
2. Symptoms depending on cost & other
Often asymptomatic (silent killer). factors
Due to Elevated pressure: Headache (Occipital), i. TSH
vomiting, giddiness, breathlessness, palpitations. ii. Complete blood count.
Due to Vascular disease: Cerebrovascular iii. HDL, LDL cholesterol.
accident, Acute Myocardial Infarction.
iv. Serum calcium, phosphorus.-
Due to Underlying disease: symptoms of
underlying organ affected. v. Serum Uric Acid.
vi. Chest X-ray - Cardiomegaly.
3. Signs
vii. USG renal system - cortical scarring, shrunken
Blood vessels Bruits over carotid. size, obstructive uropathy.
Abdominal Bruit To rule out reno-vascular viii. Echocardiography LVH, Diastolic
hypertension. dysfunction, Ejection Fraction.
Spells of sweating, tachycardia 4.4. Special tests to screen for
Pheochromocytoma.
secondary HT(only in indicated
Tremors, neck swelling Thyroid Disorder.
cases)
Snoring, Daytime somnolence Obstructive Renovascular disease: renal doppler, MR
sleeps Apnoea. angiography, DTPA scan.
Asymmetry of pulses, Radiofemoral delay Renal parenchymal: kidney biopsy.
Takayasu Disease, Coarctation of Aorta.
Pheochromocytoma: 24 hr urine metanephrine
4. How to investigate? & catecholamines.
Cushings syndrome: Sr cortisol,
4.1. Accurate BP measurement dexamethasone suppression test.
The average of two or more seated blood pressure Aldosteronism: plasma aldosterone:renin ratio.
during each of two or more outpatient visits.

Page 25
4.5. Annual tests in hypertensive Fundoscopy.
subjects 5. How to treat?
Hemogram.
Renal profile. 5.1. Goal BP 150/90 mm Hg in elderly and
140/90 mmHg in all others (including DM, CKD).
Lipid profile.
5.2. Life style changes
Urinalysis.
ECG.

Table 1: Lifestyle changes to manage hypertension

Modification Aim
Weight reduction Attain and maintain BMI < 25 kg/m2
Adopt DASH eating plan Diet rich in fruits, vegetables & low-fat dairy products with
reduced content of saturated and total fat
Dietary sodium reduction < 4.8-7.4 g NaCl/d
Physical activity Regular aerobic activity- brisk walking for 30 min/d

5.3. Guidelines for management

Table 2: Hypertension management guidelines
Lifestyle
BP Classification SBP mmHg DBP mmHg Drug Therapy
Modification
Normal <120 and <80 Encourage No
Prehypertension 120-139 or 80-89 Yes No
Stage 1 Hypertension 140-159 or 90-99 Yes Single Agent
Stage 2 Hypertension 160 or 100 Yes Combo

Page 26
 5.4. Treatment protocol
Figure 1: Treatment Protocol for HT Age > 30 Yr.

History & Physical examination

Confirmation of diagnosis by
BP > 140/90 mm of Hg.

Educate Patient on nutrition, saltrestrictions, physical activity

de-addiction and regular follow up. ( Refer to Health Workers Manual )

Start the Treatment

Age 60 Yr. Age < 60 Yr.

Goal of Treatment Goal of Treatment
BP < 150/90 mm Hg. BP < 140/90 mm Hg.

1) IF BP is 140-160 1) IF BP is 140-100
Start CCB Start ACE inhib.*( Not recommended in Renal Failure)
T. Amlodipine 5mg OD T. Enalpril 5 mg OD

Goal achieved Goal achieved

Cont. Rx Cont. Rx

Goal Not Achieved Goal Not Achieved

T. Enalpril 10 mg OD
T. Amlodipine 10 mg OD

Goal achieved Goal achieved

Cont. Rx Cont. Rx

Goal Not Achieved

Goal Not Achieved

Goalachieved
Goalachieved Cont. Rx
Cont. Rx
T. Enalpril + T. Hydrochlorthizide
T. Amlodipine + T. Hydrochlorthizide 5 mg OD + 12.5 mg OD
5 mg OD + 12.5 mg OD

Goal not achieved

Goal Not Achieved

Page 27
 Goalachieved
Cont. Rx
Age 60 Yr.
Goal of Treatment
BP < 150/90 mm Hg.
Age < 60 Yr.
Goal of Treatment
BP < 140/90 mm Hg.
2) If BP is>160 mm of Hg

2) If BP is>160 mm of Hg
Start

T. Amlodipine + T. Hydrochlorthizide
Start
5 mg (OD) + 12.5 mg (OD)
T. Enalpril + T. Hydrochlorthizide
Goal achieved 5 mg (OD) + 12.5 mg (OD)
Cont. Rx
Goal achieved
Goal not achieved Cont. Rx

Goal not achieved

T. Amlodipine + T. Hydrochlorthizide
10 mg (OD) + 25 mg (OD)
T. Enalpril + T. Hydrochlorthizide
10 mg (OD) + 25 mg (OD)
Goal achieved
Cont. Rx
Goal achieved
T. Amlodipine + T. Hydrochlorthizide + T. Enalpril cont. Rx
10 mg OD + 25 mg OD + 5mg OD
Goal not Achieved

Goal not Achieved

T. Enalpril + T. Hydrochlorthizide + T. Amlodipine
10 mg OD + 25 mg OD + 5mg OD
Goal achieved
Cont. Rx
Goal achieved
Goal not Achieved Cont. Rx

Goal not Achieved

T. Amlodipine + T. Hydrochlorthizide + T. Enalpril
10 mg OD + 25 mg OD + 10mg OD
T. Enalpril + T. Hydrochlorthizide + T. Amlodipine
10 mg OD + 25 mg OD + 10mg OD
Refer to DH

Goal Achieved Refer to DH

Cont. Rx
Goal Achieved
Cont. Rx
Goal not achieved
Goal not achieved

Page 28
 If age < 30 yr & BP> 140/90 - immediately refer
to DH (District hospital).
6. Vigilance for End Organ
When patient is on drug if systolic BP is < 100 Damage in hypertensive
mm of Hg withhold the drugs (anti-hypertensive
drugs) and refer to DH. patients
BP >160/100, Start min 2 anti-hypertension Congestive heart failure.
If initial BP is > 200/100 refer to DH after a shot IHD.
of Inj. Frusemide 60 mg stat. Chronic kidney Disease.
If Sr. Creatinine > 1.5mg% refer to DH. Stroke.
Hypertensive Retinopathy.
5.5. Hypertension in Pregnancy
Tablet Methyl Dopa -500mg-1000mg/Day in 7. When to refer?
three divided dose.
Tablet Nifedepine Extended Release Preparation Annual Work-up of known Hypertensive
30- 60 mg OD/BD. subjects.
Other drugs that can be given-Labetalol, Young Hypertensive/ secondary HT.
Hydralizine, Beta Blocker. Resistant Hypertension (Target BP not achieved
ACE inhibitors and ARBS avoided. with 3 drugs including diuretics).
Pregnant subjects.
Hypertensive emergencies (BP > 180/ 110 mm
Hg with e/o end organ damage).

Page 29
 12. HEART FAILURE
1. Introduction
It and congestion in the veins that drains into it.
2. Types of heart failure
The heart consists of two distinct parts; right and left
receiving blood from different venous system and
perfusing distinct parts of the body; the right heart
perfusing Heart Failure is a condition where the heart
is unable to perform its functions optimally; leading
to decreased perfusion of the tissues supplied by the
lungs for gaseous exchange and the left heart
perfusing the systemic circulation.
Hence there are two types of heart failure.
Right heart failure.
Left heart failure.
2.1 Right Heart Failure
The right receives blood from the systemic veins and
pumps blood into the pulmonary artery through the
pulmonary valve.
Hence the cause of Right heart failure would be;
increased pressure in the pulmonary artery
(Pulmonary Hypertension) or pulmonary valve
stenosis.
Causes of Pulmonary Hypertension:
i. Chronic obstructive Pulmonary disease (COPD)
seen commonly in smokers. Cor Pulmonale.
ii. Mitral valve stenosis seen in Rheumatic heart
diseases.
Clinical features of Right heart failure:
As the right heart receives blood from the systemic
veins, the main clinical features involves features of
congestion in the systemic venous system.
i. Raised Jugular Venous Pressure with engorged
superficial neck veins.
ii. Tender Hepatomegaly: Painful, soft liver
palpable in the right hypochondrium.
iii. Dependent Oedema: Pitting oedema
demonstrable on the shin of the tibia and ankles.
When to Suspect Right Heart Failure:
i. Right heart failure should be suspected if the
clinical features are present like swelling in the
legs and engorged neck vein.
ii. Also, once the features can be demonstrated on
clinical examination, the underlying causes of
right heart failure should be looked for; e.g.
History of smoking and signs of COPD, or signs
of Mitral Valve Disease.
Investigations for Right Heart Failure:
The diagnosis of Right Heart failure is a clinical one.
Investigations are basically to diagnose the
underlying cause of right heart failure.
Treatment of Right Heart Failure:
Right heart failure is not a medical emergency and
doesnot cause immediate fatality. There is no direct
treatment of Right Heart failure. This condition is
alleviated by effective treatment of the cause of
failure.
Hence attempts should be made to manage COPD
effectively, like:
Antibiotics in acute exacerbation.
Effective bronchodilation using inhalers and oral
long acting Xanthines (Deriphyllin).
Low flow oxygen inhalation which is the
treatment of choice for Cor Pulmonale.
Effective treatment of Mitral stenosis including
Low salt diet, Diuretics, and Digoxin.
When to Refer a Case of Right Heart Failure to
Higher Centre:
A case of right heart failure needs to be referred for
specialized treatment only for management of non
responsive chronic obstructive airway disease. Incase
the cause of right heart failure is Mitral valve disease
which is not amenable to medical management, such
cases should be referred to a cardiac centre for
definitive management of the condition.
2.2. Left Heart Failure:
[Pulmonary Oedema]
The left heart receives blood from the pulmonary
vein and pumps blood in the systemic circulation.
Causes of left heart failure:
i. Systemic Hypertension is the commonest
cause for left ventricular failure
ii. Valvular heart diseases: Aortic stenosis, Aortic
regurgitation and Mitral regurgitation are all
causes or acute left heart failure.
iii. Myocardial infarction involving significant
part of left ventricle can cause L.V.failure.
Page 30
 Clinical features:
i. Sudden onset breathlessness is the main
symptom.
ii. There may be continuous cough with pink
frothy sputum.
iii. The patient will be very anxious and restless.
iv. The patient will choose to be in the sitting
position and unable to lie down.
v. On auscultation of the chest, crepitations will
be heard most prominently in the bases.
vi. General examination will reveal high blood
pressure which is the commonest cause.
vii. Such patients are likely to present with
cyanosis. (Bluish discoloration of tonque, lip,
oral mucosa and fingers and toes.
Investigations:
Left ventricular failure is a medical emergency and
time should not be wasted in any investigation.
However after stabilizing the patient investigations
may be carried out to find the underlying cause.
Treatment:
Left heart failure or Pulmonary oedema is a medical
emergency and speed of administration of treatment
is of paramount significance.
i. The patient should be treated in the propped up
position using a backrest or raised head end of
the bed.
ii. High flow Oxygen inhalation should be given.
iii. Sedation preferably with Morphine 10mg I.V or
Pentazocin 30 mg is the management of choice.
If these powerful narcotics are not available, any
form of sedation will be of help.
iv. Intravenous Frusemide (Lasix) 60mg I.V should
be administered.
v. Acute reduction of blood pressure must be done
if the cause of left heart failure is Hypertension:
I.V. infusion of Nitroglycerine (5 microg/kg) by
BP monitoring, should be tried for the purpose.
vi. Anti platelets, statins to be continued.
When to Refer the Patient:
Treatment of left heart failure must be attempted at
the peripheral level. Once stabilized the patient may
be referred to higher centre for management of the
underlying cause.
Failure of the patients breathlessness to resolve, may
require, endotracheal intubation or non invasive
positive pressure ventilation and patient should be
referred to such a centre if facilities for the same is
not available.
Page 31
 13. ISCHAEMIC HEART DISEASE AND
ACUTE CORONARY SYNDROME
1. Introduction
1.1. Ischemic heart disease (IHD)
It is a condition in which there is an inadequate
supply of blood and oxygen to a portion of the
myocardium. It typically occurs when there is an
imbalance between myocardial oxygen supply and
demand.
1.2. Patients with ischemic heart
disease fall into two large
groups.
i. Patients with chronic coronary artery disease
(CAD) who most commonly present with
stable angina.
ii. Patients with acute coronary syndromes
(ACSs).
a. Patients with acute myocardial infarction (MI)
with ST-segment elevation on their
presenting electrocardiogram (ECG).
b. With unstable angina (UA) and non-ST-
segment elevation MI.
2. Stable Angina
2.1. Clinical Presentation
Chest pain Retrosternal, dull aching, constricting or
burning, radiating to neck, jaw, shoulders or arms
usually precipitated by exertion or stress and relieved
by rest or nitrates. Angina is crescendo and
decrescendo in nature and typically last for 2-5
minutes.
The physical examination is often normal in patients
when asymptomatic. Examination during an anginal
attack and transient left ventricular failure, there can
be a third, fourthheart sound, and systolic murmur of
mitral regurgitation.
2.2. Investigations
CBC, Urine, Blood sugar, Lipidprofile, and Xray
chest PA view may be helpful.
ECG taken at that time may show ST elevation or
depression or T inversion. In between anginal
episodes, the ECG may be normal.
A treadmill stress test would confirm angina in over
95% of these cases in referral hospital.
Echocardiography to measure left ventricular
function and rule out segmental dyskinesia
suggestive of earlier myocardial infarction.
2.3. Treatment
Daily exercise, Stop smoking,Dietary modification
low cholesterol, low fat diet with high roughage.
Control of hypertension, Diabetes Mellitus and
Dyslipidemia.
Drug Treatment
Tab Aspirin 75 mg once daily.
Tab Clopidogrel 75 mg per day.
Tab Atorvastatin 40 mg per day.
Nitrates -Sublingual glyceryl trinitrate300-500
microgram tds or Isosorbide dinitrate 10 mg
thrice a day. If there is headache lower dose of 5
mg twice or thrice daily can be tried.
Betablockers - Tab Metoprolol 50 200 mg /
day (PO in divided dose).
Potassium channel activators- Nicorandril 10mg
BD.
Calcium channel blockers like Tab Amlodepine
5-10 mg OD.
Refer for coronary angiogram and revascularisation
therapy.
3. Unstable Angina and Non-
ST-Segment Elevation
Myocardial Infarction
Page 32
UA is defined as angina pectoris or equivalent
ischemic discomfort with at least one of three
features:
(1) It occurs at rest (or with minimal exertion),
usually lasting >10 minutes.
(2) It is severe and of new onset (i.e., within the prior
46 weeks); and/or
(3) It occurs with a crescendo pattern (i.e., distinctly
more severe, prolonged, or frequent than previously).
3.1. Clinical Presentation
Chest pain, typically located in the substernal region
or sometimes in the epigastrium that radiates to the
neck, left shoulder, and/or the left arm.
3.2. Electrocardiogram
ST-segment depression, transient ST-segment
elevation, and/or T-wave inversion.
3.3. Cardiac Biomarkers
CPK-MB and troponin raised in Non ST segment
elevated MI.
3.4. Treatment
Bed rest.
Sublingually Nitroglycerin .3-.6 mg stat can
repeat after 5 min - 3 Doses.
If symptoms persist, intravenous Nitroglycerin
infusion at dose of 5-10. microgm/min. once
pain has resolved Oral isosorbitrate dinitrate 10
mg BD can be given.
Asprin initial dose of325 mg followed by
150mg/day lifelong.
Clopidogrel -Loading dose of 300mg followed
by 75 mg/.day for 2 years.
Tab Atorvastatin 40mg / day lifelong.
Intravenous beta blocker metoprolol 5-15 mg
over 5 mins followed by tab metoprolol 50-
100mg/day in divided doses with BP check.
Unfractionated Heparin (UFH) bolus 6070
U/kg (maximum 5000 U) IV followed by
infusion of 1215 U/kg per h (initial maximum
1000 U/h) titrated to A PTT 5070 s.
or
Enoxaparin 1 mg/kg SC every 12 hr.
4. ST segment elevated
Myocardial Infarction
4.1. Clinical Presentation
Chest Pain- commonly occurs at rest, severe, and
lasts longer. Typically, the pain involves the central
portion of the chest and/or the epigastrium, and, on
occasion, it radiates to the arms, abdomen, back,
lower jaw, and neck.
Sudden-onset breathlessness, Sweating, loss of
consciousness, a confusional state.
Sensation of profound weakness, the appearance of
an arrhythmia, an unexplained drop in arterial
pressure.
4.2. Laboratory Findings
CBC, Blood sugar, lipid profile, Xray chest.
Cardiac markers-CPK-MB elevated.
TrpT,I released within 4-6 hours and elevated for
2 weeks.
Electrocardiogram Convex ST segment
elevation with either peaked upright or inverted
T waves. Q waves if necrosis occurs.
Echocardiogram - regional wall motion
abnormality.
4.3. Complications
Arrhythmias.
Acute Heart failure.
Rupture of papillary muscle.
Embolism leading to stroke.
Ventricular remodelling.
Ventricular aneurysm.
4.4. Treatment
Bed rest.
Oxygen therapy-2-4L/min.
Sublingually Nitroglycerin .3-.6 mg stat can
repeat after 5 min - 3 Doses if symptoms persist,
intravenous Nitroglycerin infusion at dose of 5-
10 microgm/min. once pain has resolved Oral
isosorbitratedinitrate 10 mg BD can be given.
Aspirin 325mg and then 150mg OD.
Clopidogrel 300mg and then 75mg BD.
Page 33
 Atorvastatin 80mg and then 40mg HS. Stool softeners Bisacodyl (Dulcolax) 10 mg at
night.
Reperfusion therapy: If presenting within 12
hours of chest pain with ECG showing ST Message
elevation > 1 mm then give Inj. Streptokinase 1.5
Acute myocardial infarction is an emergency
million units over 1 hour (contraindications- a
whatever treatment possible should be started at the
history of cerebrovascular hemorrhage at any
center and patient should be transferred to District
time, a nonhemorrhagic stroke or other
Hospital or any hospital where ICU facility is
cerebrovascular event within the past year,
available in a cardiac ambulance. Patient should not
marked hypertension at any time during the acute
be allowed to walk for even short distances and
presentation, suspicion of aortic dissection, and
absolute Bed Rest is important. Treatment of
active internal bleeding).
complications like Heart failure, Arrythmias may
Beta blockers: ), Metoprolol 25 to 50 mg BD, need expert opinion.
Atenolol 25 to 100 mg OD(if pulse rate > Coronary Angiography and revascularisation therapy
60/mm, BP > 90/60 mm Hg ,lung fields clear). should be advised.
ACE inhibitors Enalapril 2.5 20 mg / day in
divided doses twice a day.

Page 34
 14. ACUTE RHEUMATIC FEVER (ARF)

Acute rheumatic fever (ARF) is a multisystem

1. Introduction disease resulting from an autoimmune reaction to
infection with group A streptococcus.

2. Criteria for diagnosis of ARF

Major manifestations Carditis (Pancarditis)
Polyarthritis (Migratory)
Chorea
Erythema marginatum
Subcutaneous nodules
Minor manifestations Clinical: fever, polyarthralgia
Laboratory: elevated erythrocyte sedimentation rate or leukocyte
count
Electrocardiogram: prolonged P-R interval
Supporting evidence of a preceding Elevated or rising anti-streptolysin O or
streptococcal infection within the last 45 days
other streptococcal antibody, or
A positive throat culture, or
Rapid antigen test for group A streptococcus, or
Recent scarlet fever

Two major or one major and two minor precipitating group A streptococcal infection.
manifestations plus evidence of preceding group A Penicillin is the drug of choice and can be given
streptococcal infection. orally [as phenoxymethyl penicillin, 500 mg (250 mg
for children 27 kg) PO twice daily, or Amoxicillin 50
3. Investigations mg/kg (max 1 g) daily, for 10 days] or as a single
White blood cell count, Erythrocyte sedimentation dose of 1.2 million units (600,000 units for children
rate, C-reactive protein, Blood cultures if 27 kg) IM Benzathine Penicillin G.
febrile, Electrocardiogram, Chest x-ray if clinical or 4.2 Aspirin in initial dose of 80100 mg/kg per
echocardiographic evidence of carditis, day in children (48 g/d in adults) in 45 divided
Echocardiogram (consider repeating after 1 month if doses is used for the treatment of arthritis, arthralgia,
negative). Throat swab (preferably before giving and fever for 4 weeks.
antibiotics)culture for group A streptococcus.
4.3 Inj. Benzathine Penicillin G 1.2 IU (6 lakhs
Anti-streptococcal serology: both anti-streptolysin O units for children 27 kg) IM every 3 weeks as
and anti-DNase B titres, if available. prophylactic dose up to the age of 25 years.
4. Treatment 5. When to refer
4.1 Antibiotics Evidence of Congestive cardiac failure, Arrhythmia.
All patients with Acute rheumatic Fever (ARF)
should receive antibiotics sufficient to treat the

Page 35
 15. INFECTIVE ENDOCARDITIS

1. Definition Streptococci, Pneumococci Enterococci,

Staphylococcus aureus, Coagulase-negative
Infective endocarditis is a form of endocarditis, or staphylococci. Fastidious gram-negative coccobacilli
inflammation, of the inner tissue of the heart (such as (HACEK group i.e. Haemophilus species,
its valves) caused by infectious agents. The agents Aggregatibacter Aphrophilus, Cardiobacterium,
are usually bacterial, but other organisms can also be Eikenella, Kingella), Gram-negative bacilli,Candida
responsible. spp.
Infection most commonly involves heart valves either
native or prosthetic.
3. Clinical Manifestations
2. Organisms Causing Major (Symtoms and signs)
Symptoms- Fever, chills, arthralgia, Fatigue.
Clinical Forms of
Endocarditis
Figure 1: Signs of Infective EndcarditisSigns

Page 36
 haemorrhages,conjuctival
4. Diagnosis haemorrhages,Janeway lesion
iv. Immunological
Modified Dukes Criteria phenomenon;(glomerulonephritis;Oslernodes;
Roths spots;rheumatoid factor)
4.1 Major Criteria v. Microbiological evidence positive blood
cultures but not meeting major criteria or
i. Positive blood culture serological evidence of active infection with
Two separate positive blood cultures with organism consistent with infective
microorganism(s) typical for infective endocarditis.
endocarditis:viridians.
streptococci,streptococcus bovis HACEK Documentation of 2 major / one major and 3 minor/5
group, staphylococcus aureus, community minor criteria allow a diagnosis Infective
acquired enterococci endocarditis.
or
Persistently positive blood culture defined as
5. Investigations
presence of micro organism consistent with
infective endocarditis from blood cultures
drawn >12 hrs apart. CBC-Anaemia,Leucocytosis.
or Urine-Microscopic haematuria.
Single positive blood culture for coxiella Elevated ESR, Elevated CRP.
burnetti or phase one IgG antibody titer of >1 : Blood culture 3 sets of two bottle blood. culture
800. from different venipuncture site separated from
one another by atleast one hour over 24 hours.
ii. Echocardiographic evidence of endocardial Echocardiography.
involvementTypicalvalvular
lesions;vegetations,abscess,or new partial 6. Complications
dehiscence of a prosthetic valveNew Valvular
regurgitation. Blood clots or emboli that travel to brain,
kidneys, lungs, or abdomen.
4.2 Minor Criteria Brain abscess.
Congestive heart failure.
i. Predisposition;predisposingheart condition or Glomerulonephritis.
intravenous drug use. Jaundice.
ii. Temperature greater than 38.0 C. Neurological changes.
iii. Vascular phenomenon;major arterial Rapid or irregular heartbeats, including atrial
emboli,septic pulmonary infarcts,mycotic fibrillation.
aneurisms,intracranial Severe valve damage.
Stroke.

Page 37
 7. Treatment
Table 1: Antimicrobial Therapy

Organism Drug (Dose, Duration

Penicillin-susceptible streptococci
Moderately penicillin-resistant streptococci
Enterococci
Staphylococci (native valve)
Staphylococci (prosthetic valves)
Inj. Penicillin G (23 mU IV q4h for 4 weeks) or
Inj. Ceftriaxone (2 g/d IV as a single dose for 4 weeks) plus
Inj. Vancomycin (15 mg/kg IV q12h for 4 weeks)
Inj. Penicillin G (45 mU IV q4h) or ceftriaxone (2 g IV qd)
for 6 weeks plus
Inj. Gentamicin (3 mg/kg qd IV or IM as a single dosee or
divided into equal doses q8h for 6 weeks) Plus
Inj. Vancomycin (15 mg/kg 12 hourly) as noted above for 4
weeks
Inj. Penicillin G (45 mU IV q4h) plus
Inj. Gentamicin (1 mg/kg IV q8h), both for 46 weeks
Inj. Vancomycin (15 mg/kg IV q12h for 46 weeks)
Inj. Vancomycin (15 mg/kg IV q12h for 68 weeks) plus
Inj. Gentamicin (1 mg/kg IM or IV q8h for 2 weeks) plus
Rifampin (300 mg PO q8h for 68 weeks)

8. Prevention
High Risk cardiac lesions where antibiotic
prophylaxis is needed.

1. Prosthetic heart valve.

2. Prior endocarditis.
3. Unrepaired cyanotic congenital heart disease.
4. Completely repaired cyanotic heart disease
within 6 months.
5. Incompletely repaired cyanotic heart disease
with residual defects.

Page 38
 Table: 2: Antibiotic Regimens for Prophylaxis of Endocarditis in Adults with High-Risk Cardiac
Lesion

A. Standard oral regimen

1. Amoxicillin: 2 g PO 1 h before procedure

B. Inability to take oral medication

1. Ampicillin: 2 g IV or IM within 1 h before procedure

C. Penicillin allergy

1. Clarithromycin or azithromycin: 500 mg PO 1 h before procedure

2. Cephalexin: 2 g PO 1 h before procedure

3. Clindamycin: 600 mg PO 1 h before procedure

D. Penicillin allergy, inability to take oral medication

1. Cefazolin or ceftriaxone: 1 g IV or IM 30 min before procedure

2. Clindamycin: 600 mg IV or IM 1 h before procedure

Message- If any valvular heart disease or prosthetic valve patient develops fever, infective
endocarditis should be thought of apart from other normal causes of fever.

Page 39
 16. DIABETES MELLITUS
Genetic defects of insulin action.
1. Introduction
Diseases of exocrine pancreas Trauma,
Diabetes mellitus is a clinical syndrome characterized
Pancreatitis, Pancreatectomy, Cystic fibrosis,
by hyperglycemia due to absolute or relative
Fibrocalculous Pancreatic diabetes,
deficiency of insulin.
Haemochromatosis.
Gestational Diabetes Mellitus (GDM) Onset /
2.Classification of Diabetes Recognition of glucose intolerance in pregnancy.
Mellitus
2.1. Type 1 Diabetes Mellitus 3. Diagnosis of DiabetesMellitus
Autoimmune pancreatic B cell destruction; absolute Symptoms of Diabetes Mellitus and Random
insulin deficiency. Blood Sugar > 200 mg% (mg / dl)
Fasting blood sugar > 126 mg % on more than
2.2. Type 2 Diabetes Mellitus one occasion.
Characterized by peripheral tissue Insulin Resistance
/ Relative Insulin deficiency. 2 hours Plasma glucose > 200 mg% during oral
glucose tolerance test with glucose 75g
2.3. Other Specific Types glucose.

Genetic defects of B cell function Maturity

Onset Diabetes in Young (MODY).

Table 1: Criterion for Diagnosis based on blood glucose levels

Normal Glucose Prediabetic Diabetes mellitus

Impairedglucose
tolerance

FPG <100mg/dl 100-125 mg/dl >126 mg/dl

2hr PG <140mg/dl 141-199 mg/dl >200 mg/dl

A1C (Glycosulated <5.6% 5.7-6.4% >6.5 mg/dl

Hemoglobin)

4. Clinical symptoms
Common symptomsare
Other symptoms are tiredness, fatigue, pruritis vulvae
1. Polyuria {increased frequency of micturition), giddiness, burning over feet, and can present with
2. Polydipsia (increased thirst), complications of diabetes.
3. Polyphagia (increased appetite),
4. Weight loss. Table -2: Major differentiating features of Type 1 and
Type 2 diabetes are as follows-

Page 40
5. Management
Type 1 Diabetes Mellitus:

5.1 Type 1 Diabetes Mellitus e) glucosidase inhibitors - acarbose, voglibose,

miglitol
Strict meal plan * Carbohydrate: 50 - 60% * f) DPP4 inhibitors- sitagliptin, vidagliptin
Protein: 10 20% * Fat: 30% (If patient is
dyslipidemic, fat should be 15%) * Caloric Parenteral agents
intake: 30Kcal / kg 1. Insulin
Physical exercise 2. GLP-1 receptor agonist- Liraglutide,Exenatide

Only Insulin (a) Bi-guanides

Dose- 500mg-2000mg/day.
5.2 Type 2 Diabetes Mellitus:
Contra-indications to Bi-guanide therapy: 1. Renal
Strict meal plan failure when creatine clearance < 40 ml / min 2.
Physical exercise Arteriography or intravenous urography as
Oral hypoglycemic agents intravenous iodinated products may precipitate lactic
acidosis on patients with bi-guanides 3. Advanced
Insulin
liver cell failure 4.Alcoholism 5.Cardiac diseases
Oral Hypoglycemic Agents: 6.Diabetes with significant acute and late
complications 7.Pregnancy 8. Old age > 70 years.
a) Biguanides - Metformin
b) Sulphonylureas - Glibenclamide, Glipizide,
Glimeperide,, Gliclazide
(b) Sulphonylureas
c) Glinides (nonsulphonylurea secretogouge) - Mechanism of action- Increases insulin secretion
repaglinide from the beta cells through the ATP sensitive K
channels.
d) Thiazolidinediones pioglitazone

Page 41
 Table-3: Sulphonylurea drugs with dosage and side effects

Drug Dose Side effets

Glibenclamide 1.25-20 mg Hypoglycaemia, weight gain
Glimeperide 1-8 mg Hypoglycaemia
Glipizide 2.5 -25 mg Hypoglycaemia
Gliclazide 30-240 mg Hypoglycaemia

Contraindications for sulphonylurea therapy
1. Insulin dependent diabetes mellitus (IDDM)
2. Pregnancy
3. Patients with severe infections
4. Allergic reactions
5. Significant liver and kidney disease
6. Patients undergoing surgery
(c) Glinides-(Nonsulphonylureas)
Increase insulin secretion
Dose-Repaglinide 0.5-3 mg/day.
(d) Thiazolidinediones-These are insulin sensitisers
Pioglitazone is commonly used.
thereby increasing insulin secretion only with the
intake of food. They do not cause hypoglycaemia.
Dose- vidagliptin 50 mg BD, Sitagliptin 100mg OD.
Insulin
Consider insulin as initial therapy in patients
with:
Fasting plasma glucose > 250 - 300 mg/dl since
more rapid glycemic control will reduce glucose
toxicity to islet cells, improve insulin secretion
secretogoue-
and possibly make oral hypoglycemic agents
more effective.
Lean patients or those with severe weight loss.
Underlying renal or hepatic disease.

Dose- 15- 45 mg/day. Hospitalized or acutely ill patients.

Side effects- Weight gain, congestive cardiac failure, If response to oral hypoglycemics is not
fractures, adequate. Consider insulin as initial therapy

(e) Glcosidase inhibitors Decreases intestinal Pregnancy

glucose absorbtion and reduce postprandial Types of Insulin
hyperglycemia.
1. Rapid-acting insulin: aspart insulin and lispro
Dose- Acarbose -25 -100 mg/day to be taken with insulin
food. 2. Regular or Short-acting insulin
Voglibose-. 0.2- 0.3 thrice a day 3. Intermediate-acting insulin: lente insulin and
NPH insulin
(f) DPP 4 Inhibitors 4. Long-acting insulin: Insulin detemir and insulin
Mechanism of action They inhibit the enzyme glargine
DPP 4 and increase endogenous GLP-1 action

Figure-1: Treatment Protocol for DM Type II

History & Physical examination

RBS>140 mg/dlSuspect

Page 42
 Confirmation of diagnosis by
Fasting bllood sugar - >126 mg/dl OR
Post Prandial B.S->200 mgCC/dl OR
Random Blood Sugar -> 200 mg/dl

Educate Patient on Diet, Physical activity,

De-addiction Foot care and regular follow up.
(Refer to Health Workers Manual)

Take blood for Sr. Creatinine & Other investigation Urine

Start the albumin &Sugar treatment

Fasting B.S:> 126-200 or/and Fasting B.S:>200-300and/orPost Prandial B.S:

>300-350
Post Prandial B.S:> 200-300
Start with combination therapy
Start with monotherary Metformin + Sulphonyl Urea
Tab. Metformin 500mg BD 500mg BD (Glimiprideor Glipizide)
(1 mg OD) (2.5mg OD)

Evaluate after
15 days with Sr. Creat Report
> 1.5 mg%

If Sr. Creat is
< 1.5 mg% Urgent Referral to DH

Target to be achieved with therapy

Fasting 100 126 mg/dl

Target to be achieved with therapy

Fasting 100 126 mg/dl

Target achieved with given Target not achieved with giventherapy

therapy

Continue the Rx and regular follow up Step wise increase the dose of medicine
after 15-30 days.

Page 43
 Target achieved Target not achieved

Follow up after 15-30 days. Refer to DH

Steps to increase dose in: 3) 1 gm BD + 2 mg BD Or 5 mg BD (If target

A) Monotherapy:
I. Start with T. Metformin 500mg BD
( If target not achieved )
II. T. Metformin 750 mg BD
target not achieved )
III. T. Metformin 1 gm BD
target not achieved )
Refer the patients to DH.
B) Combination therapy:
Metformin + Glimepride OrGlipizide.
1) 500mg BD + 1mg OD Or 2.5mg BD
(If target not achieved)
2) 750mg BD + 1mg OD Or 2.5mg BD
(If target not achieved)
not achieved)
Refer the patients to DH.
* The main aim of this protocol to control raised
( If Blood sugar however not to complicate by
Hypoglycemia.
( If
Instruction: - Dont allow patients to fast while
on medication.
-Strict De-addiction state should be
maintained.
- If sudden rise in blood sugar
observed then urgent referral to District Hospital.

6. Check list

Page 44
 Microvascular complications
7. Complications of Diabetes
Mellitus Eye disease- Retinopathy, Macular edema.
7.1 Acute complications Neuropathy- Sensory and motor neuropathy (mono
and poly),
Hypoglycemia
Diabetic Ketoacidosis (DKA) Autonomic neuropathy
Diabetes and infections
Hyperosmolar Hyperglycemic coma (HHNKC). Nephropathy

7.2 Chronic complications Macrovascular complications

Coronary heart disease

8. Hypoglycemia
Cerebrovascular disease Hypoglycemia is a clinical emergency occurring in
Peripheral arterial disease diabetes characterized by either autonomic or
neuroglycopenic symptoms (or) biochemically
Other gastroparesis, sexual dysfunction, random blood sugar < 60mg, due to antidiabetic
dermatologic agent, food and activity mismatch.

Table-4: Clinical presentation of Hypoglycemia

8.1 Management Dextrose supplementation - Conscious: Oral

Glucose, Sugar, Fruit Juice, Unconscious: 50%
Draw blood sample immediately Dextrose 100ml IV Stat. Followed by 10%

Page 45
 Dextrose then by 5% DNS maintenance (or) Inj.
Glucagon 1mg im if not accessible to
intravenous route
Patient still remains unconscious - To rule out
cerebral edema, If present IV mannitol + Inj.
Dexamethasone 8mg IV
Stop the antidiabetic agents for 3 days in Type 2
Diabetic mellitus patients and recheck blood
sugars. In Type 1 Diabetic mellitus patients,
recheck blood sugars after 6 hrs and adjust
insulin dose accordingly.
Identify the cause of hypoglycemia
If recurrent hypoglycemia, rule out - Renal
function disorder, Liver function disorder
Repeat blood sugar value after hypoglycemia
correction and monitor blood sugars
Referral: If the patient remains unconscious
even after dextrose administration refer the
patient immediately to higher centre for further
evaluation.
Table 5
Important Note Patient Education:
Educate patient and his family members about
low blood sugars and symptoms
Never miss a meal after insulin / Oral
hypoglycemic agents
Be cautious of unaccustomed physical activity
To carry diabetic identity card
Always carry simple sugar (biscuits and toffee)
to avoid low sugar.
9. Diabetic Ketoacidosis (DKA)
Ketoacidosis is a major medical emergency and
remains a serious cause of morbidity, principally in
people with type 1 diabetes, which should be treated
in hospital.Patient should be referred to tertiary
health centre after the primary management.
9.1 Manifestation of DKA
Page 46
9.2 Investigations ABG for pH and bicarbonate
Urine sugar [positive]
Blood glucose [usually > 250 mg %] Urine acetone [positive]
Blood urea [may or may not be ] Chest X-ray
Serum creatinine [may or may not be ] ECG
Serum electrolyte [Na or , K or decreased] Ultrasonogram abdomen / KUB.
Serum bicarbonate < 10 mmol / l
9.3 Management of DKA

9.4 Referral Anuric

Elevated renal parameters
Refer the patient to a higher centre if:
Evidence of septicaemia
Patient is comatose
Hypotension requiring ionotropic support

Page 47
9.5 Complications of Diabetic Ketoacidosis

10. Hyperglycemic
Hyperosmolar Non-Ketotic
Coma (HHNKC)
10.2 Symptoms
It is an acute metabolic complication in middle aged
and elderly diabetics with high morbidity and Polyuria
mortality. Polydipsia
Severe hyperglycemia (Blood sugar > 600
10.1 Causes mg%)
Profound dehydration
Precipated by Elevated osmolality
Hemianopia, muscle fasciculation, seizures
Infection
Altered sensorium, coma
Trauma
Burns 10.3 Treatment
Infarction
Hyper-alimentation 1. Fluid replacement: normal saline at the rate of
Drugs like - Thiazide, Cimetidine, Phenytoin 2 litre in 1st 2 hours and 1 litre in another 2
and Parentral diuretics hours
2. Low dose insulin.
3. Correction of electrolytes and hyperosmolality.
4. Low-dose heparin to prevent vascular
thrombosis intravascular coagulation.

Page 48
 10.4 Distinguishing features
Table-6: Distinguishing features between DKA and HHNKC

Moderate worker 40 kcal/kg Ideal body weight

11. Medical Nutrition Therapy
A non-pharmacological mode of management of
diabetes. Medical Nutrition therapy is individualized
and should be a tailor made regimen. It is used as a
compliment for an oral glucose lowering agent /
insulin therapy.
Energy Recommendations:
This depends on body weight and physical
activity. 20 kcal/kg Ideal body weight
Sedentary worker 30 kcal/kg Ideal body weight
For heavy worker
In obese people - Reduce 500 kcal from the
calculated energy requirement
For under weight- Add 500 kcal to the calculated
energy requirement of the total kcal, 45 - 65 %
kcal from carbohydrate and 10-25 % kcal from
proteins
Fat recommendation - 500ml / month of a blend
of oils / individual Gingelly oil and any refined

Page 49
 vegetable oil could be used (or) Rice brand oil and any refined vegetable oil
Fibre recommendation - 14gm/1000kcal
12. Gestational Diabetes
provided.
Mellitus
Fluid recommendation - 8 to 10 glasses / day of
water except in LVF, CKD, Cirrhosis etc. Gestational Diabetes mellitus is defined as
carbohydrate intolerance of variable severity with
11.1 MNT in Gestational Diabetes onset or first recognition during the present
pregnancy.
Mellitus
12.1 Risk for gestational diabetes
30 kcal / kg Instant Body weight in first trimester
mellitus
30 kcal / kg Instant Body weight + 300 kcal/day
in II and III trimester Age more than 25 years
Protein - 1gm/kg Instant Body weight + 10gm Family history of diabetes mellitus
daily throughout pregnancy
History of unexplained fetal loss
Avoid hypocaloric diets in obese GDM
History of baby being large for gestational age
Provide compulsory bed time and evening snack
to avoid accelerated starvation and nocturnal History of congenitally malformed infant
hypoglycemia Maternal obesity
Gestational Diabetes mellitus:
History of Polycystic ovarian disease
Strict meal plan
Polyhydramnios
Physical exercise
Pre-eclampsia
Insulin
Unexplained intrauterine death
Other specific types
12.2 Methods of screening
Strict meal plan
Physical exercise Spot test: Fasting < 90 mg% [normal 2 hr post-
prandial < 120 mg%, random < 105 mg% values]
Insulin with or without oral hypoglycemic agents
ADA recommendation
Figure-2: Methods of Screening

Page 50
12.3 Diagnostic Criteria
WHO criteria (with 75 gm of glucose ) F - 95 mg %
1 hr - 180 mg % 2 hr - 155 mg % If any two values
equals or crosses normal value, it is termed as
Gestational Diabetes mellitus.
Important Note OGTT value should never be treated.
12.4 Treatment
1. Medical Nutrition Therapy [refer MNT] 2. Insulin
is essential if MNT fails to achieve euglycemia
Target Glycemic Level
Fasting glucose 90 mg %
2 hr postprandial 120 mg %
Monitoring Glycemic Control
Blood glucose fasting and postprandial every
three days till glycemia is achieved; then every
fortnightly, throughout first and second trimester.
Every week in third trimester.
Glycemic profile monitoring once in 1st and 2nd
trimester and then every month.
Page 51
 17. THYROID DISORDERS
* When full replacement is achieved then follow up
1. Hypothyroidism measurement at annual intervals and later by a 2 - 3
yearly interval
Hypothyroidism may be
* Ensure ongoing compliance.
1 Primary 1.4. Special treatment considerations
Common causes of which are autoimmune, iatrogenic
due to Iodine131, antithyroid or lithium treatment A hypothyroid woman should be euthyroid prior
and thyroidectomy to conception and during early pregnancy (effect
on fetal neuronal development). Thyroid profile
2 Secondary should be immediately done after confirmation
of pregnancy and in second and third trimester.
1. Pituitary disease
2. Hypothalamic disease. Dose of Thyroxine should be increased by 50%
during pregnancy and return to previous level
1.1. Symptoms after delivery
Elderly require less Thyroxine (less by upto
Coarse dry skin
20%) especially those with coronary artery
Hoarseness of voice disease, starting dose 12.5 mcg/day with similar
increments every 2 - 3 months until TSH level is
Facial puffiness, weight gain normalized.
Cardiac enlargement and/or pericardial effusion, In hypothyroidism due to low TSH (supra-
thyroid cause is suspected) detailed
Goiter with or without prolonged relaxation investigations are required and patient should be
phase of deep tendon reflexes. referred to a tertiary care level
Myxedema coma is a rare complication of severe Asses the response clinically and by serum TSH
hypothyroidism with hypothermia, hy- (serum T3 in suprathyroid type) at 8 weekly
poventilation, hyponatremia, hypoxia, intervals
hypercapnoea and hypotension. Once euthyroid state is restored, follow-up at 6 -
12 monthly intervals.
1.2. Diagnosis is confirmed by
1.5. Treatment of Myxedema coma
Low serum free T3 and T4
Warm blankets, mechanical ventilation for
Serum TSH raised respiratory failure.
Other investigation blood sugar level and lipid Correction of metabolic disturbances and treat
profile precipitating factors.
Drugs * L-Thyroxine 500 mcg IV bolus, then
1.3. Treatment 50-100mcg IV daily * If intravenous preparation
not available, the same dose is administered
Pharmacological through Ryles tube.
* Tab. L -Thyroxine- 1.6 mcg per kg body weight or * Once acute phase is over, maintain L-Thyroxine
Start with 50 100mcg/day as above.
* Dose to be adjusted based on TSH levels * Inj.Hydrocortisone 100 mg IV stat, 25-50 mg 8
* Goal is normal TSH (lower half of reference range hourly.
* Measure TSH levels after about 6 wks of instituting Caution: Avoid sedatives
therapy
* Adjust by 12.5 or 25 mcg increments if TSH is
high; decrement of the same if TSH is
suppressed.

Page 52
1.6. Patient Education
L-Thyroxine should be taken as a single daily
dose, ideally on awakening, at least 30 minutes
before breakfast.
Fibre and bran products (e.g., Isapghola husk)
may impair absorption, as also cholestyramine,
cholestipol, iron sulphate, sucralfate, aluminium
hydroxide
Metabolism of L-Thyroxine is increased by
Phenytoin, Rifampicin and carbamazepine.
2.1. Symptoms
Graves disease is characterized by diffuse goiter,
Ophthalmopathy and Dermopathy in varying
combinations.
Ophthalmopathy in Graves' disease; lid retraction,
periorbital edema, conjunctival injection, and
proptosis are marked
2.2. Diagnosis
Diagnosis is confirmed by low to undetectable serum
TSH and increased Serum free (FT3) and free (FT4)
Ultra sonography of neck
Thyroid scan (if available)
2.3. Treatment
Pharmacological
Explain to the patient that the treatment is life
long. Do not modify dose or stop treatment with-
out consultation.
Over treatment may lead to decreased bone
mineral density and adverse cardiac
complications.
2. Hyperthyroidism
Thyrotoxicosis is defined as the state of thyroid
hormone excess and is not synonymous with
hyperthyroidism, which is the result of excessive
thyroid function. However, the major etiologies of
thyrotoxicosis are hyperthyroidism caused by Graves'
disease, toxic MNG, and toxic adenomas
Adjunctive treatment * For adrenergic symptoms
such as sweating, tremor and tachycardia. Tab.
Propranalol 40 120 mg a day. Or atenolol 25
mg to 50 mg
Anti thyroid drug-
Tab. Propylthiouracil 100 150 mg every 6
8 hours or Tab. Carbimazole 10 20 mg every
8 12 hours; After euthyroid state is achieved
in 6 8 weeks once daily dosage. Review with
serum TSH and FT3 after 3 4 weeks treatment
has been initiated.
Once controlled reduce to the smallest effective
dose or continue initial dose combined with L-
Thyroxine
Drugs are given for an average of 2 years.
Definitive treatment is surgery/ablation of
thyroid tissue
Subtotal thyroidectomy in younger patients (<30
years) in whom antithyroid therapy has been
unsuccessful and in very large goiters.
Page 53
 Radioactive iodine (I131): Method of choice in
* Elderly * Younger patients who have
completed family with recurrent thyrotoxicosis
following surgery or when surgery is refused or
contraindicated. Caution Radioactive iodine
should never be given in pregnancy. In woman
of childbearing age if radioactive iodine is
planned, a pregnancy test should always be
carried out.
2.4. Pregnancy
In pregnant woman surgery should not be
performed in 1st or 3rd trimesters
Antithyroid drugs are less risky but may induce
hypothyroidism in the foetus and should be used
in the smallest necessary dose to keep serum
TSH and FT4 in normal range.
Propylthiouracil is preferred usual maintenance
is 200 mg/day. If > 300 mg/day required during
1st trimester, Subtotal thyroidectomy is indicated
in 2nd trimester
Propranolol should be avoided as it can cause
foetal growth retardation and neonatal
respiratory depression.
Ophthalmopathy: Refer to ophthalmologist. Initiate
therapy in mild cases with elevation of head at night,
diuretics to decrease edema, use of tinted sunglasses
and 1 % methyl cellulose eye drops to prevent drying
and refer patients with severe and progressive
exophthalmos to an ophthalmologist.
2.5. Toxic multinodular goiter
Radioactive iodine is the treatment of choice.
Large doses are usually required.
Treatment with antithyroid drugs given till
patient is euthyroid.
Propranalol may be useful before and after
radioactive iodine administration.
2.6. Thyrotoxic crisis or thyroid
storm
Refer to a tertiary care centre.
Life threatening hyperthyroidism with fever,
vomiting, diarrhoea, jaundice, delirium and
coma.
Usually precipitated by acute illness such as
stroke, infection, diabetic ketoacidosis, trauma,
patients undergoing surgery or radioactive iodine
treatment in a poorly prepared patient:
Tab. Propylthiourcil 600 mg loading dose, then
200 300 mg every 6 hours orally or through
Ryles tube. (or) Tab. Carbimazole 15 25 mg 6
hourly.
1 hour after the 1st dose of antithyroid drug,
saturated solution of Potassium iodide (SSKI) 5
drops every 5 hours. (or) Lugols iodine 10 drops
3 times a day. (or) Sodium iodide 1 g IV slowly.
Tab. Propranalol 40 60 mg 4 hourly or 0.5 2
mg IV every 4 hours.
Inj. Dexamethasone 2 mg IV 6 hourly
Continue iodides and dexamethasone until
normal metabolic stage is achieved and give sup-
portive treatment such as cooling, antipyretics,
antibiotics for infection, intravenous fluids, etc.
Once euthyroid status is achieved, manage as
already outlined.
Page 54
 18.Cerebrovascular Accidents
1. Definition
A stroke, or cerebrovascular accident, is defined by
this abrupt onset of a neurologic deficit that is
attributable to a focal vascular cause.
Thus, the definition of stroke is clinical, and
laboratory studies including brain imaging are used to
support the diagnosis.
The clinical manifestations of stroke are highly
variable because of the complex anatomy of the brain
and its vasculature. TIA (Transient Ischemic Attack)
is a brief episode of neurological dysfunction lasting
1 hr to 24 hrs without residual deficit. Stroke in
evaluation means when deficit worsens after patient
first presents.
Cerebral ischemia is caused by a reduction in blood
flow that lasts longer than several seconds. If the
cessation of flow lasts for more than a few minutes,
infarction or death of brain tissue results. When
blood flow is quickly restored, brain tissue can
recover fully and the patient's symptoms are only
transient.
Focal ischemia or infarction, conversely, is usually
caused by thrombosis of the cerebral vessels
themselves or by emboli from a proximal arterial
source or the heart.
Intracranial hemorrhage is caused by bleeding
directly into or around the brain; it produces
neurologic symptoms by producing a mass effect on
neural structures, from the toxic effects of blood
itself, or by increasing intracranial pressure.
2. Clinical features
Most of the patients are elderly.
There could be a history of hypertension,
diabetes, ischaemic heart disease
Past history of cerebrovascular accident may be
present.
Hemiplegia or hemiparesis: Paralysis or
weakness of right or left half of the body with
deviation of one side of the face seen.
Lower limb monoparesis or monoplegia.
Faciobrachial stroke : involving right or left
upper limb along with ipsilateral facial
weakness.
Rarely bilateral lower limb weakness in
unpaired anterior cerebral artery thrombosis.
Hemiplegia or hemiparesis may be accompanied
by motor aphasia(patient unable to speak) or
sensory aphasia (inability to comprehend) if
there is cortical involvement of dominant
hemisphere(right side in left handed people, left
side in 90% of right handed people).
Transient or permanent loss of central vision
due to involvement of ophthalmic artery a
branch of internal carotid artery.
Difficulty in swallowing, speaking due to bulbar
involvement could be a presentation. In cases
where patient has previously had
cerebrovascular accident, fresh infarct now
causing bilateral cortical involvement may lead
to dysphagia and dysarthria causing what is
known as peudobulbar palsy. On examination in
these patients jaw jerk is brisk.
Midbrain lesions have ocular involvement.
Sensory involvement occurs in stroke involving
thalamus or medulla.
The neurological deficit may be preceeded by
tingling numbness.
TIA - Transient Ischaemic Attack is a
neurological deficit that recovers completely
within 24 hours.
A focal deficit progressing over a period of
hours and is characteristic of thrombotic. stroke.
Any focal deficit preceded by a prolonged
headache could be due to infarct with
haemorrhagic conversion secondary to cerebral
venous sinuous thrombosis.
Focal deficit could be accompanied by
convulsions.
3. Examination
Patient may have bradycardia if he is on beta
blockers or due to raised intractanial pressure
secondary to cerebral oedema.
Blood pressure should be recorded and
monitored.
The power of all 4 limbs should be graded and
any improvement or deterioration in the power
should be recorded.
Reflexes on the involved side are brisk and
plantar reflex is extensor on the involved side.
History of headache, altered sensorium, fever,
vomiting.
4. Investigations
Non contrast CT scan brain to differentiate
between infarct and haemorrhage and site of
lesion.
Routine investigations like HB,CBC,ESR, liver
Page 55
 function test , renal function test, serum
electrolytes, fasting and post prandial glucose,
complete lipid profile.
ECG, X- ray chest, 2D echo especially in young
patients to rule out cardiac source of embolism.
Ideally MR angiography in cases of infarction to
look for the stenosis in intracranial vessels.
SOS MR venography if any doubt of cerebral
venous thrombosis.
5. Complications
Aspiration pneumonia
Deep vein thrombosis in lower limb
complicating further as pulmonary embolism.
Bed sore
6. Treatment
Blood pressure, blood glucose and temperature
of patients of acute cerebral infarction should be
controlled.
Anti - hypertensive medication. A blood
pressure of 150/90 mmhg can be maintained
initially to prevent cerebral ischaemia due to
hypoperfusion.
IV Mannitol 100cc 8 hourly in cases of
intracerebral bleed, in large infarcts, brainstem
infarction, cerebellar lesions and all patient
having altered sensorium. Serum electrolytes
and urine output should be monitored (on
mannitol.)
Tab Aspirin 75-150 mg od after lunch should be
started in cases of cerebral infarction. As
intracranial bleed is ruled out.
Tab atorvastatin 40mg OD H.S.
Antiepileptics (inj Eptoin 100mg tds) if
convulsions are present. But in case the bleed is
large and if the patient is going to be shifted to a
higher centre it may be advisable to give anti-
epileptics as the patients general condition might
worsen if he gets a convulsion.
Half an hour before ryles tube feeding
Domperidom should be administered. Ryles
tube feeding in strict propped up position.
Inj. Heparin (5000 IU IV bolus and then once a
day to keep PT (INR) 2 to 3 times of normal
value) for prophylaxis of deep vein thrombosis
in cases of cerebral infarction (not in intracranial
bleed) in patient of hemiplegia.
Physiotherapy.
Early detection and treatment of complications.
7. When to refer
All young patients of stroke, intracranial bleed
or infarction.
Patients diagnosed with cerebral venous
thrombosis.
Subarachnoid haemorrhage if seen on the CT.
Patient suspected to have AV malformation.
Large intracerebral bleeds who might require
evacuation to be transferred after stabilizing
blood pressure.
Page 56
 19. SUBARACHNOID HEMORRHAGE (SAH)
Excluding head trauma, the most common cause of
SAH is rupture of a saccular aneurysm. Other causes
include bleeding from a vascular malformation
(arteriovenous malformation or dural arterial-venous
fistula) and extension into the subarachnoid space
from a primary intracerebral hemorrhage.
1. Clinical features
Most unruptured intracranial aneurysms are
completely asymptomatic. Symptoms are usually due
to rupture and resultant SAH, although some
unruptured aneurysms present with mass effect on
cranial nerves or brain parenchyma. At the moment
of aneurysmal rupture with major SAH, the ICP
suddenly rises. This may account for the sudden
transient loss of consciousness that occurs in nearly
half of patients. Sudden loss of consciousness may be
preceded by a brief moment of excruciating
headache.
The most important characteristic is sudden onset or
as a change in the patient's usual headache pattern.
The headache is usually generalized, often with neck
stiffness and vomiting is common.
Although sudden headache in the absence of focal
neurologic symptoms is the hallmark of aneurysmal
rupture, focal neurologic deficits may occur. The
deficits that result can include hemiparesis, aphasia,
and abulia.
Occasionally, prodromal symptoms suggest the
location of a progressively enlarging unruptured
aneurysm.
A third cranial nerve palsy, particularly when
associated with pupillary dilation, loss of ipsilateral
(but retained contralateral) light reflex, and focal pain
above or behind the eye, may occur with an
expanding aneurysm at the junction of the posterior
communicating artery and the internal carotid artery.
Visual field defects can occur with an expanding
supraclinoid carotid or anterior cerebral artery
aneurysm.
Aneurysms can undergo small ruptures and leaks of
blood into the subarachnoid space, so-called sentinel
bleeds. Sudden unexplained severe headache at any
location should raise suspicion of SAH and be
investigated, because a major hemorrhage may be
imminent.
A detailed history should be sought for use of oral
contraceptive pills in young females to rule out SAH
secondary to cerebral venous thrombosis as could
occur in any procoagulant state.
2. Investigations
CT brain, MRI angiography and MRI venography to
rule out cerebral venous thrombosis which could
present as subarachnoid haemorrhage.
3. Treatment: Subarachnoid
Hemorrhage
1. Protecting the airway.
2. Managing blood pressure before and after
aneurysm treatment, with antihypertensive agent.
Preventing rebleeding prior to treatment.
3. Managing vasospasm, treating hydrocephalus.
4. Maintaining electrolyte balance and hydration
5. IV mannitol 100cc 8 Hourly to treat raised Intra
cranial pressure.
6. Treatment with the calcium channel
antagonist nimodipine (60 mg PO every 4 h)
improves outcome, perhaps by preventing
ischemic injury rather than reducing the risk of
vasospasm.
7. Volume expansion helps prevent hypotension,
augments cardiac output, and reduces blood
viscosity by reducing the hematocrit. This
method is called "triple-H" (hypertension,
haemodilution, and hypervolemic) therapy.
8. Acute hydrocephalus can cause stupor or coma.
It may clear spontaneously or require temporary
ventricular drainage. When chronic
hydrocephalus develops, ventricular shunting
is the treatment of choice.
4. When to refer
A patient diagnosed to be having SAH should be
transferred to a higher centre at the earliest after
stabilizing blood pressure for further management.
Page 57
 20. PYOGENIC MENINGITIS
Meningitis is a serious disease in which there is
inflammation of the meninges that cover the brain
and spinal cord.
Bacterial meningitis can be deadly and contagious
among people in close contact.
Viral meningitis tends to be less severe and most
people recover completely.
Fungal meningitis is a rare form of meningitis and
generally occurs only in people with weakened
immune system.
1. Clinical Presentation
Meningitis can present as either an acute
fulminant illness that progresses rapidly in a
few hours or as a subacute infection that
progressively worsens over several days.
The classic clinical triad of meningitis is fever,
headache, and nuchal rigidity. Nausea,
vomiting, and photophobia are also common
complaints.
Seizures occur as part of the initial presentation
of bacterial meningitis or during the course of
the illness in 2040% of patients. Generalized
seizure activity and status epilepticus may be due
to hyponatremia, cerebral anoxia.
Raised Intracranial Pressure (ICP) is an
expected complication of bacterial meningitis
and the major cause of obtundation and coma in
this disease.
Signs of increased ICP include a deteriorating
or reduced level of consciousness,
papilledema, dilated poorly reactive pupils,
sixth nerve palsy, decerebrate posturing.
Cushing reflex (bradycardia, hypertension,
and irregular respirations).
The rash of meningococcemia for
meningococcal meningitis, which begins as a
diffuse erythematous maculopapular rash
resembling a viral exanthem; however, the skin
lesions of meningococcemia rapidly become
petechial. Petechiae are found on the trunk and
lower extremities, in the mucous membranes and
conjunctiva, and occasionally on the palms and
soles.
On examination meningial signs are positive.
Meningeal signs (Can be found in any type of
meningitis)
i. Neck stiffness: Stiffness of neck & resistance to
passive movements, with pain & spasm on attempted
motion. The chin cannot be placed upon the chest.
ii. Kernigs sign:
With the hip flexed, the knee is extended.
Normally it can be done up to 135 degree. In
meningitis it is restricted due to spasm of
hamstrings.
iii. Brudzinskis sign:
Neck sign- on flexing the neck, there is flexion
of hips & knees.
Leg sign- on flexing one leg, other leg also
flexes.
iv. Straight leg raising test (SLR):
With the patient supine & both legs extended, one leg
is passively flexed at the hip keeping the knee
extended. Normally it can be lifted up to 90 degree. It
is restricted in meningitis.
2. Diagnosis
CSF Studies
The classic CSF abnormalities in bacterial meningitis
are (1) polymorphonuclear (PMN) leukocytosis
(>100 cells/L in 90%), (2) decreased glucose
concentration [<2.2 mmol/L (<40 mg/dL) and/or
CSF/serum glucose ratio of <0.4 in 60%,hence it is
mandatory that a blood glucose levels be estimated
simultaneously with the CSF study], (3) increased
protein concentration [>0.45 g/L (>45 mg/dL) in
90%], and (4) increased opening pressure (>180
mmH2O in 90%). CSF bacterial cultures are positive
in >80% of patients, and CSF Gram's stain
demonstrates organisms in >60%
3. Treatment
i. Intravenous fluids.
ii. Inj Mannitol 100mg 8 hourly to 6 hourly.
iii. Inj Dexamethasone 4mg 8 hourly but first
dose to be given 20 minutes before first dose
of antibiotics.
Page 58
iv. Antimicrobial therapy of
(Ceftriaxone 2g twice a day intravenously,
cefotaxime, or cefepime) A 2-week course of
intravenous antimicrobial therapy is
recommended for pneumococcal meningitis.
Or ampicillin IV 2 gm 4 hourly (total 12 gm per
day) for at least 3 weeks. Gentamicin is added in
critically ill patients (2 mg/kg loading dose, then
7.5 mg/kg per day given every 8 hrs. and
adjusted for serum levels and renal function).
The combination of Trimethoprim (1020
mg/kg per day) and Sulfamethoxazole (50100
mg/kg per day) given every 6 h may provide an
alternative in penicillin-allergic patients.
Vancomycin 2g 12 hourly is the drug of choice
for methicillin-resistant staphylococci and for
patients allergic to penicillin. (3 weeks).
For gram-negative bacillary meningitis, the
third-generation cephalosporins - cefotaxime
(2gm 4 hourly i.e. total 12 gm per day),
ceftriaxone (2gms 12 hourly), and ceftazidime
(2gms 8 hourly) - are efficacious for the
treatment of, with the exception of meningitis
due to P. aeruginosa, which should be treated
with ceftazidime, cefepime, or meropenem.
(2gms 8 hourly). A 3-week course of
intravenous antibiotic therapy is recommended
for meningitis due to gram-negative bacilli.
4. When to refer
i. Lumbar puncture requires to be done and facility
not available.
ii. Presence of any focal deficit.
Note: If meningitis is suspected empirical antibiotic
treatment has to be started immediately.
Page 59
 21. TUBERCULOUS MENINGITIS
1. Clinical Manifestations
The disease often presents subtly as headache
and slight mental changes after a prodrome of
weeks of low-grade fever, malaise, anorexia, and
irritability.
If not recognized, tuberculous meningitis may
evolve acutely with severe headache, confusion,
lethargy, altered sensorium, and neck rigidity.
Typically, the disease evolves over 12 weeks, a
course longer than that of bacterial meningitis.
Since meningeal involvement is pronounced at
the base of the brain, paresis of cranial nerves
(ocular nerves in particular) is a frequent finding,
and the involvement of cerebral arteries may
produce focal ischemia.
The ultimate evolution is toward coma, with
hydrocephalus and intracranial hypertension.
2. Diagnosis
CSF Studies
In adults, the mean white blood cell (WBC) count
(range, 0-4000 cells/L) with lymphocytic
predominance. The mean protein level in adults
averages 224 mg/dL (range, 20-1000 mg/dl). The
proportion with depressed glucose levels (< 45
mg/dL or 40% of serum glucose).
3. Treatment
IV fluids
Inj. Mannitol 100cc thrice a day to four times a
day, should be tapered and stopped to be
overlapped with oral glycerol 1oz three times a
day. Patient may have worsening of headache or
get signs of raised ICT, mannitol should be
reinstituted and tapered again.
For treatment of tubercular meningitis, first-line
drugs are Isoniazid (5mg/kg) along with
pyridoxine 50mg, Rifampin(10mg/kg) given
before breakfast, Pyrizinamide (25 mg/kg), and
Ethambutol (15 mg/kg).
Duration of treatment is upto 9 months to 1 year.
Steroids are given as Inj. Dexamethasone 4mg
three times a day for 3 weeks to be continued as
Tab Prednisolone 1mg/kg and tapered and
omitted over 1 and a half months duration.
4. Complications
Hydrocephalous.
Vasculitis induced stroke.
Drug induced hepatitis.
5. When to refer
Patient having any focal deficit.
Diminution of vision.
Patient not improving on treatment.
Page 60
 22. VIRAL MENINGITIS
1. Clinical features
Immuno compromised adult patients with viral
meningitis usually present with.
Headache, fever, and signs of meningeal
irritation coupled with an inflammatory CSF
profile.
Headache is almost invariably present and often
characterized as frontal or retroorbital and
frequently associated with photophobia and pain
on moving the eyes.
Constitutional signs can include malaise,
myalgia, anorexia, nausea and vomiting,
abdominal pain and/or diarrhea.
Patients often have mild lethargy or drowsiness;
however, profound alterations in consciousness,
such as stupor, coma, or marked confusion do
not occur in viral meningitis and suggest the
presence of encephalitis or other alternative
diagnoses.

2. Etiology
Acute Meningitis

Common Less Common

Enteroviruses (coxsackieviruses, echoviruses, and human Lymphocytic choriomeningitis virus

enteroviruses 6871)

Varicella zoster virus Cytomegalovirus

Epstein-Barr virus

Herpes simplex virus 2

Arthropod-borne viruses

HIV

Acute Encephalitis

Common Less Common

Herpesviruses Rabies

Herpes simplex virus 1 Powassan virus

Varicella zoster virus (VZV) Enteroviruses

Epstein-Barr virus (EBV) Mumps

Arthropod-borne viruses

Cytomegalovirus

Table No.1- Etiology

Page 61

3. Diagnosis
The most important laboratory test in the diagnosis of
viral meningitis is examination of the CSF. The
typical profile is a lymphocytic pleocytosis (25500
cells/L), a normal or slightly elevated protein
concentration [0.20.8 g/L (2080 mg/dL)], a normal
glucose concentration, and a normal or mildly
elevated opening pressure (100350 mmH2O).
4. Treatment: Acute Viral
Meningitis
Treatment of almost all cases of viral meningitis
is primarily symptomatic and includes use of
analgesics, antipyretics, and antiemetics.
Fluid and electrolyte status should be monitored.
IV fluids should be administered.
Oral or intravenous acyclovir may be of benefit
in patients with meningitis caused by Herpes
simplex virus -1 or -2 and in cases of severe
Epstein-Barr virus or Varicella zoster virus
infection. Seriously ill patients should receive
intravenous acyclovir (1530 mg/kg per day in
three divided doses for 7-10 days i.e. which can
be followed by an oral drug such as acyclovir
(800 mg, five times daily. Patients with HIV
meningitis should receive highly active
antiretroviral therapy).
Page 62
 23. VIRAL ENCEPHALITIS
1. Definition
In contrast to viral meningitis, where the infectious
process and associated inflammatory response are
limited largely to the meninges, in encephalitis the
brain parenchyma is also involved. Many patients
with encephalitis also have evidence of associated
meningitis (meningoencephalitis) and, in some cases,
involvement of the spinal cord or nerve roots
(encephalomyelitis, encephalomyeloradiculitis).
2. Clinical Manifestations
In addition to the acute febrile illness with evidence
of meningeal involvement characteristic of
meningitis, the patient with encephalitis commonly
has an altered level of consciousness (confusion,
behavioral abnormalities), or a depressed level of
consciousness ranging from mild lethargy to coma,
and evidence of either focal or diffuse neurologic
signs and symptoms.
Patients with encephalitis may have hallucinations,
agitation, personality change, behavioral disorders,
and, at times, a frankly psychotic state. Focal or
generalized seizures occur in many patients with
encephalitis.
Virtually every possible type of focal neurologic
disturbance has been reported in viral encephalitis;
the signs and symptoms reflect the sites of infection
and inflammation.
The most commonly encountered focal findings are
aphasia, ataxia, upper or lower motor neuron patterns
of weakness, involuntary movements (e.g.,
myoclonic jerks, tremor), and cranial nerve deficits
(e.g., ocular palsies, facial weakness).
3. Laboratory Diagnosis
3.1. CSF Examination
CSF examination should be performed in all
patients with suspected viral encephalitis unless
contraindicated by the presence of severely
3.2. MRI, CT, EEG
increased intracranial pressure (ICP).
The characteristic CSF profile is
indistinguishable from that of viral meningitis
and typically consists of a lymphocytic
pleocytosis, a mildly elevated protein
concentration, and a normal glucose
concentration. A CSF pleocytosis (>5 cells/L)
occurs in >95% of immunocompetent patients
with documented viral encephalitis.
In rare cases, a pleocytosis may be absent on the
initial LP but present on subsequent LPs.
Patients who are severely immunocompromised
by HIV infection, glucocorticoid or other
immunosuppressant drugs, chemotherapy, or
lymphoreticular malignancies may fail to mount
a CSF inflammatory response.
CSF cell counts exceed 500/L in only about 10%
of patients with encephalitis. Infections with
certain arboviruses (e.g., EEE virus or California
encephalitis virus), mumps, and LCMV may
occasionally result in cell counts >1000/L, but
this degree of pleocytosis should suggest the
possibility of nonviral infections or other
inflammatory processes.
Atypical lymphocytes in the CSF may be seen in
EBV infection and less commonly with other
viruses, including CMV, HSV, and
enteroviruses.
However, persisting CSF neutrophilia should
prompt consideration of bacterial infection,
leptospirosis, amoebic infection, and
noninfectious processes such as acute
hemorrhagic leukoencephalitis. About 20% of
patients with encephalitis will have a significant
number of red blood cells (>500/L) in the CSF in
a nontraumatic tap. The pathologic correlate of
this finding may be a hemorrhagic encephalitis
of the type seen with HSV; however, CSF red
blood cells occur with similar frequency and in
similar numbers in patients with nonherpetic
focal encephalitis.
A decreased CSF glucose concentration is
distinctly unusual in viral encephalitis and
should suggest the possibility of bacterial,
fungal, tuberculous, parasitic, leptospiral,
syphilitic, sarcoid, or neoplastic meningitis.
Patients with suspected encephalitis almost
invariably undergo neuroimaging studies and
often EEG. These tests help identify or exclude
alternative diagnoses and assist in the
differentiation between a focal, as opposed to a
diffuse, encephalitic process.
Focal findings on MRI in a patient with
encephalitis should always raise the possibility
of HSV encephalitis. Approximately 10% of
patients with PCR-documented HSV encephalitis
Page 63
 will have a normal MRI, although nearly 80%
will have abnormalities in the temporal lobe, and
an additional 10% in extratemporal regions.
4. Treatment
Vital functions, including respiration and blood
pressure, should be monitored continuously and
supported as required. In the initial stages of
encephalitis, many patients will require care in an
intensive care unit.
i. Intravenous fluids.
ii. IV mannitol 100cc 12 hourly for 3 days
Seizures should be treated with standard
anticonvulsant regimens (Inj. Diazepam 10 mg,
IV or Inj. Midazolam 2mg), and prophylactic
therapy should be considered in view of the high
frequency of seizures in severe cases of
encephalitis.
iii. Acyclovir is of benefit in the treatment of HSV
and should be started empirically in patients with
suspected viral encephalitis, especially if focal
features are present, while awaiting viral
diagnostic studies.
Adults should receive a dose of 10 mg/kg of
acyclovir intravenously every 8 h (30 mg/kg per
day total dose) for 1421 days.
CSF PCR can be repeated at the completion of this
course, with PCR-positive patients receiving
additional treatment, followed by a repeat CSF PCR
test.
Prior to intravenous administration, acyclovir should
be diluted to a concentration 7 mg/mL. (A 70-kg
person would receive a dose of 700 mg. which would
be diluted in a volume of 100 mL.) Each dose should
be infused slowly over 1 h, rather than by rapid or
bolus infusion, to minimize the risk of renal
dysfunction. Care should be taken to avoid
extravasation or intramuscular or subcutaneous
administration. The alkaline pH of acyclovir can
cause local inflammation and phlebitis (9%). Dose
adjustment is required in patients with impaired renal
glomerular filtration. Penetration into CSF is
excellent, with average drug levels 50% of serum
levels. Complications of therapy include elevations in
blood urea nitrogen and creatinine levels (5%),
thrombocytopenia (6%), gastrointestinal toxicity
(nausea, vomiting, diarrhea) (7%), and neurotoxicity
(lethargy or obtundation, disorientation, confusion,
agitation, hallucinations, tremors, seizures) (1%).
iv. Antipyretics for fever
5. Complications
Aspiration pneumonia, stasis ulcers and decubitus
ulcer, contractures, deep venous thrombosis and its
complications, and infections of indwelling lines and
catheters.
6. When to refer
Ideally all suspected patients of viral encephalitis
after starting therapy as mentioned above and patients
of viral meningitis not improving over or worsening
over 48 hours should be referred to a higher centre.
Page 64
 24. EPILEPSY

1. Definition
This is a condition characterized by recurrent
episodes of seizures which are paroxysmal abnormal
discharges at high frequency from an aggregate of
neurons in cerebral cortex.
2. Types of epilepsy
2.1 Grand mal epilepsy or Tonic-Clonic Seizures-
Aura, epileptic cry, sudden fall due to tonic
convulsions followed by clonic convulsions
and then prolonged sleep and depression. The
attack lasts for 1-2 min. Tongue bite, urinary
incontinence may occur.
2.2 Petit mal epilepsy or Absence seizures - No
aura, no loss of consciousness. Prevalent in
children and episode lasts for few seconds.
There is momentary loss of consciousness
hardly for 5 sec without loss of postural
control. Presence of freezing or staring in one
direction.
2.3 Partial seizures- Most common seizure types
occurring in 80% of epileptic patients. Seizure
activity is restricted to a discrete area
belonging to one cerebral hemisphere only.
2.4 Other types of seizures: Myoclonic seizures,
Atonic seizures, tonic seizures.
2.5 Febrile seizures- Young children develop
seizures during high fever.
3. Investigations
Apart patients of epilepsy can be further
investigated with an EEG and MRI. from routine
laboratory investigations.
4. Treatment
1. Correct any metabolic cause (hypo or
hyperglycaemia, hypo or hypernatremia).
2. Stop drugs like theophylline (CNS Stimulant)
which may cause seizures.
3. Look for any structural CNS lesions like Brain
tumour, vascular lesions, meningitis, CVST or
abscess and treat them.
4. Avoid precipitating factors like sleep
deprivation, Fasting, video games.
4.1 Antiepileptic should be started
when
1. A history suggestive of recurrent epileptic
seizure is established.
2. An abnormal neurological examination.
3. Presenting as status Epilepticus.
4. Abnormal EEG suggestive of general seizure.
5. Family history of epilepsy.
To start anti epileptics in single isolated seizure is not
yet established. Monotherapy should be the mantra of
treatment.

4.2 Anti epileptic drugs

Table No.1: Antiepileptic Drugs & their Doses with type of seizure

Seizure Drug Dose

Generalized onset tonic clonic Valproic acid 750-2000mg/day
convulsions
(20-60mg/kg/day)
In divided doses
Phenytoin 300-400mg/day
(3-6mg/kg/day for adult, 4-8mg/kg/day for
Children) BD doses
1 gm 3gm per day
Levetiracetam
1000-3000mg/day BD doses
Lamotrigine
150-500mg/day, BD doses
Topiramate

Page 65
Focal onset tonic clonic Carbamezapine 600-1800mg/day (15-35mg/kg, child) in BD
convulsions doses
Lamotrigine
Same as Above
Levetiracetam
Same as Above
Oxcarbazepine
900-2400mg/day (30-45mg/kg, child) BD
doses
Typical Absence Valproic acid Same as Above
Ethosuximide 750-1250mg/day in BD doses, 20 40 mg
per kg divided in BD doses
Atypical Absence, myoclonic, Valproic Acid, Same as Above
Atonic Seizures Lamotrigine, Topiramite
Same as Above

Phenytoin 15-20 mg/kg, at a rate not to exceed 50

5. Status Epilepticus mg/min (Never mix Phenytoin with a 5% dextrose
Status Epilepticus refers to continuous seizures or solution) put it in a normal saline solution to
repetitive discrete seizures with impaired minimize the risk of crystal precipitation or
consciousness in the interictal period for duration of fosphenytoin 20mg/kg iv to maximum
15-30 minutes traditionally but practically for 150mg/minute.
generalized convulsive status Epilepticus the duration Correct any metabolic imbalances. Control
is 5 minutes. hyperthermia.
It is a medical emergency and must be treated If seizures continue after 20 minutes, give maximum
immediately. rate 50mg/minute or Fosphenytoin 7 to 10 mg/kg to
Monitor vital signs. Maintain airway, breathing, and maximum rate of 150mg/minute.
circulation. Administer supplemental oxygen by If seizures continue after 20 minutes, give
mask. Phenobarbital (20 mg/kg IV at 60 mg/min)
Laboratory analysis-glucose, electrolytes, calcium, Other Antiepileptic Drugs which can be given IV are
magnesium, creatinine, CBC and urine analysis. - Valproate sodium 30mg/kg IV bolus or IV
Establish intravenous access. Levetiracetam 10-50mg/kg
Lorazepam (0.1 mg/kg) IV over 1-2 min, Repeat if no If seizures continue, consider administering general
response after 5 minutes. anesthesia with medications such as propofol,
midazolam, or pentobarbital.
Figure-1: Management of Status Epilepticus algorithm

Page 66
 Figure 2: Pharmacological treatment algorithm of non-convulsive status epileptics

Lorazepam (0.1, 0.15 mg/IV) (repeat once if no Admit to ICU and EEG monitoring
seizure supprenssion

Seizures continuing

Phenytoin (7-10 mg/kg Iv) or Fosphenytoin Consider valproate in absence SE (30

(Phenytoin equivalent dose) mg/kg IV)

Seizures continuing

Phenytoin (7-10 mg/kg Iv) or Fosphenytoin (Phenytoin equivalent Consider valproate in absence SE (30
dose) mg/kg IV)

Refractory NCSE

Intravenous anesthetic agents

Midazolam/propofol/pentobarbital

Seizures continuing

Newer AEDs - Topiramate/Ievetiracetam

or

Inhalational anesthestics - Isoflurance/desflurance

All the Patients after initial IV Antiepileptic Drug should be followed by maintenance doses with the oral
antiepileptic drugs regularly.

Page 67
 25. GUILLAIN-BARRE SYNDROME (GBS)
1. Definition
Guillain-Barre syndrome (GBS) is an acute,
frequently severe, and fulminant polyradiculopathy
that is autoimmune in nature.
2. Clinical Features
GBS manifests as rapidly evolving areflexic motor
paralysis with or without sensory disturbance. Usual
pattern is an ascending paralysis. Weakness typically
evolves over hours to a few days and frequently
accompany by tingling dysesthesias in extremities.
Legs are usually more affected than arms. Facial
diparesis is present in 50% of affected individuals.
The lower cranial nerves are also frequently
involved, causing bulbar weakness with difficulty
handling secretions and maintaining airway. Pain in
the neck, shoulder or back is also common in the
early stages.
Fever and constitutional symptoms are absent at the
onset, and if present cast a doubt on the diagnosis.
Deep tendon reflexes disappear within the first few
days of onset. Bladder dysfunction may occur in
severe cases but is usually transient. Autonomic
involvement is common, usually presenting as wide
fluctuation in blood pressure, postural hypotension &
cardiac dysrhythmias.
Approximately 70% of cases of GBS occur 1-3
weeks after an acute infectious process, usually
respiratory or gastro-intestinal.
3. Differential diagnosis
The diagnosis is made by recognizing the pattern of
rapidly evolving paralysis with areflexia, absence of
fever or other systemic symptoms, and characteristic
antecedent events. Other disorders that may enter into
the differential diagnosis include:
Acute myelopathies prolonged back pain and
sphincter disturbances.
Botulism pupillary reactivity lost early.
Poliomyelitisfever and meningismus is common.
4. Investigations
CSF analysis by lumbar puncture by the end of first
week Elevated CSF protein 100-1000mg/dl without
pleocytosis called as albumino cytological
dissociation.
Can refer for electrodiagnosis- Demyelination or
axonal involvement seen according to the variant
type
5. Treatment
Treatment should be initiated at the earliest. Each day
counts. >2 weeks after the first motor symptoms,
immunotherapy is no longer effective. Either high
dose intra-venous immune globulin (IVIg) or
plasmapheresis can be initiated, as they are equally
effective.
1. Intra-venous immune globulin (IVIg): Total dose
of 2g/kg body weight divided into 5 doses given
over 5 consecutive days.
2. Plasmapheresis: 40-50ml/kg plasma exchange
four times over a week.
In the worsening phase of GBS, most patients require
monitoring in a critical care setting, with particular
attention to vital capacity, heart rhythm, blood
pressure, nutrition, DVT prophylaxis and chest
physiotherapy. Nearly 30% of patients with GBS
require ventilator assistance.
6. When to refer: Any of the
following
Single breath count 12/min
Respiratory failure.
Fulminant quadriparesis.
Poor Gag reflex with risk of aspiration.
Autonomic dysfunction
Recurrent GBS.
Page 68
 26. APTHOUS ULCERS
1. Introduction
Recurrent aphthous stomatitis (RAS) is a common
condition, restricted to the mouth, that typically starts
in childhood or adolescence as recurrent small,
round, or ovoid ulcers with circumscribed margins,
erythematous haloes, and yellow or gray floors. A
positive family history of similar ulcers is common,
and the natural history is typically of resolution in the
third decade of life.
2. Causes
2.1. Some RAS cases involve a familial and genetic
basis; approximately 40% of patients with RAS
have a familial history, but inheritance may be
polygenic with penetrance dependent on other
factors.
2.2. Most relevant studies have found hematinic
(e.g. iron, folic acid, vitamin B-12) deficiencies
in as many as 20% of patients with recurrent
ulcers. In addition, deficiencies of vitamins B-1,
B-2, and B-6 have been noted in some patient
cohorts.
3. Symptoms
Significant pain while chewing food. Minor
apthae are recurrent, painful, single or multiple,
shallow surrounded by erythematous mucosa
anywhere in the oral cavity. Small ulcers heal
without scar, while larger and deep ulcers leave a
scar.
Fever, adenopathy, gastrointestinal sympyoms
are typically absent.
Important note Repeated ulcers at the same site or
slow healing ulcers with systemic symptoms eg,
uveitis, arthritis, fever adenopathy are
worrisome.Malignancy should be excluded.
4. Treatment
4.1 Topical and systemic
antibiotics
Tetracycline 250 mg dissolved in 180 ml of water
and used as swish andspit 4 times a day for several
days.Avoid in children and pregnancy.
4.2Probiotics in powder form
placed in oral cavity and
swallowed 3 -4 times a day
4.3 Antiinflammatory
Hydrocortisone pellets 5 mg kept at ulcer base and
swallowed every 4 hrs for 3-4 days.Triamcinolone
0.1 % applied to ulcers 2-4 times a day.
Betamethasone (Betnesol) mouthwash -0.5 mg tab
dissolved in 5-10 ml of water for mouth wash 6 hrly
during attack.
4.4 Immune modulators
Levamisole 50 mg twice a day
for three consecutive days for 4
weeks, no medication for 2
weeks; then levamisole 150 mg
tab, half tab twice daily for 3
days for 2 weeks.

Page 69
 27. OESOPHAGEAL CANDIDIASIS

1. Introduction
Oesophageal candidasis is an oppurtunistic infection AIDS, postchemotherapy, uncontrolled diabetes
of the oesophagus by Candida albicans. Occurs in mellitus, chronic steroid therapy.
immune compromised patients like

Figure 1: Endoscopic view of Oesophageal Candidiasis

2.Signs and symptoms 4. Treatment

Oral lesions are painless but oesophageal lesions
produce painful dysphagia.Discrete or confluent
curdy plaques on the oesophageal mucosa.
3. Investigations
Nysyatin suspension local application in mouth.
Clotrimazole oral lozenges 10 mg dissolve 1
lozenge 5 times a day.
Tab flucanozole 100 mg/day for 10-14 days.

Demonstration of pseudohyphae on wet smears and

culture.

Page 70
 28. DYSPEPSIA

1. Introduction 5. Treatment
Non specific group of symptoms related to upper Cap Omeperazole 20 mg once a day taken 45
GITract. Also reffered to as non-ulcer dyspepsia, min before breakfast for 4 weeks. or Tab
functional dyspepsia, GERD. Ranitidine 150mg twice a day before food 45
mins for 4-6 weeks.
2. Symptoms For those with dysmotility symptoms-tab
Domperidone 10 mg three times a day 30 mins
Upper abdominal symptoms simulating an ulcer
before food.
disease or heart burn with or without regurgitation,
heaviness, post-prandial fullness or early Antacids 2-3 teaspoon when symptomatic.
satiety.Symptoms of gas in abdomen is common.
Anti H.Pylori treatment is recommended for
those on long term NSAIDS, those with
3. Red flag signs duodenal/gastric ulcers.
Anorexia, weight loss, anemia, dysphagia and mass Treatment of H Pylori- Combination of
in abdomen.
Cap. Omeperazole 20 mg twice a day plus
4. Investigations Cap. Amoxicillin 1gm bd or Tab. Metronidazole
500mg bd for 14 days plus
History and upper GI scopy.
Tab clarithromycin 500mg bd for 14 days

Page 71
 29. GASTROOESOPHAGEAL REFLUX

1. Introduction 3. Treatment
GERD is a common disorder caused by retrograde Antacid with or without alginate acid liquid or
flow of gastric contents through an incompetentent tab 2-3 chewed- 4-6 times a day1/2-1 hr after a
gastroesophageal junction.There are two groups- meal.
erosive GERD and non erosive GERD. Untreated
may result in to oesophagitis, ulceration, stricture, Cap. Omeperazole 20 mg OD/BD OR
and rarely adenocarcinoma. Rabeprazole 20mg OD or Pantoprazole 40mg
OD.
2. Symptoms Esomeprazole 40mg OD, OR

Retrosternal pain, heart burn, regurgitation mostly Lansoprazole 30mg OD.

after meals. Rarely present with chronic cough, All taken 45 mins before meals for 4-6 weeks.
laryngitis, bronchospasm, recurrent
pulmonaryinfections, otitis media etc. Add prokinetic Domperidone10 mg thrice a day
30 mins before meals if regurgitation is
significant.

Page 72
 30. PEPTIC ULCER DISEASE

a posterior penetrating gastric ulcer

1. Introduction complicated by pancreatitis.
Peptic ulcer is an important organic gastrointestinal
disease.
4. Alarm features that warrant
prompt gastroenterology
2. Etiology
referral include the
Peptic ulcer disease (PUD) may be due to any of the
following: following
H pylori infection Bleeding or anemia
Drugs Early satiety
Lifestyle factors Unexplained weight loss
Severe physiologic stress Progressive dysphagia or odynophagia
Hypersecretory states (uncommon) Recurrent vomiting
Genetic factors Family history of GI cancer
There is ulceration of the gastric and duodenal
mucosa due to acid and pepsin. 5. Physical Examination
In uncomplicated PUD, the clinical findings are few
3. Clinical features and nonspecific and include the following:

3.1 Obtaining a medical history, especially for

Epigastric tenderness (usually mild)
peptic ulcer disease, H pylori infection,
ingestion of NSAIDs, or smoking, is essential Right upper quadrant tenderness may suggest a
in making the correct diagnosis. Gastric and biliary etiology or, less frequently, PUD.
duodenal ulcers usually cannot be
Guaiac-positive stool resulting from occult blood
differentiated based on history alone, although
loss
some findings may be suggestive.
Malena resulting from acute or subacute
3.2 Epigastric pain is the most common symptom gastrointestinal bleeding
of both gastric and duodenal ulcers. It is
characterized by a gnawing or burning 6. Differential Diagnosis
sensation and occurs after mealsclassically,
shortly after meals with gastric ulcer and 2-3
hours afterward with duodenal ulcer. Food or Acute Coronary Syndrome
antacids relieve the pain of duodenal ulcers but
Aneurysm, Abdominal
provide minimal relief of gastric ulcer pain.
Cholangitis
3.3 Duodenal ulcer pain often awakens the patient
at night. About 50-80% of patients with Cholecystitis
duodenal ulcers experience nightly pain, as Cholecystitis and Biliary Colic in Emergency
opposed to only 30-40% of patients with Medicine
gastric ulcers and 20-40% of patients with
nonulcer dyspepsia (NUD). Pain typically Cholelithiasis
follows a daily pattern specific to the patient.
Diverticular Disease
Pain with radiation to the back is suggestive of

Page 73
 Esophageal Perforation, Rupture and Tears
Esophagitis
Gastritis, Acute
Gastritis, Chronic
Gastroenteritis
Gastroesophageal Reflux Disease
Inflammatory Bowel Disease
Viral Hepatitis
7. Approach Considerations
Testing for H pylori infection is essential in all
patients with peptic ulcers. In most patients with
uncomplicated peptic ulcer disease (PUD),
routine laboratory tests usually are not helpful.
Documentation of PUD depends on radiographic
and endoscopic confirmation.
If the diagnosis of PUD is suspected, obtaining
CBC count, liver function tests (LFTs), amylase,
and lipase may be useful. CBC count and iron
studies can help detect anemia, which is an alarm
signal that mandates early endoscopy to rule out
other sources of chronic GI blood loss.
Figure-1: Endoscopic view of Peptic Ulcer
8. Treatment
Anti H pylori treatment is recommended for patients
on long term NSAIDS, bleeding peptic ulcer.
Drugs Dose(mg)
PPI Clarithromycin 20mg
Metronidazole 500 400
7.1 H pylori Testing
Testing for H pylori infection is essential in all
patients with peptic ulcers.
Endoscopic or invasive tests for H pylori include
a rapid urease test, histopathology, and culture.
Rapid urease tests are considered the endoscopic
diagnostic test of choice. The presence of H
pylori in gastric mucosal biopsy specimens is
detected by testing for the bacterial product
urease
7.2 Endoscopy
Upper GI endoscopy is the preferred diagnostic test
in the evaluation of patients with suspected PUD. It is
highly sensitive for the diagnosis of gastric and
duodenal ulcers, allows for biopsies and cytologic
brushings in the setting of a gastric ulcer to
differentiate a benign ulcer from a malignant lesion,
and allows for the detection of H pylori infection
with antral biopsies for a rapid urease test and/or
histopathology in patients with PUD. (See the images
below.)
Hpylori treatment
Frequency Duration
BD 14 days
BD BD
Page 74
PPI Amoxycillin Metronidazole 20mg BD 14 days
1gm bd TDS
400
PPI Amoxycillin Clarithrmycin 20mg BD 14 days
1gm 500 BD BD

Tab ranitidine (150mg)BD, 9. Dos and donts

Famotidine (40mg) OD equally efficacious, but
Avoid alcohol
takes longer time.
Stop smoking
Maintenance dose of PPI for patients on
NSAIDS, IHD patients. Avoid NSAIDs
Prefer paracetamol, avoid foods that aggravate
symptoms
No role of bland diet
Excess milkMeals at regular intervals.

Page 75
 31. VOMITING
1. Introduction
Vomiting is the forceful expulsion of the gastric
contents due to contraction of abdominal musculature
and simultaneous relaxation of gastric fundus and
lower oesophageal sphincter.
2. Causes
1. Central (stimulation of vomiting centre)
neurological disease raised intracranial pressure.
2. Vestibular system disorders
3. Drugs and toxins
4. Toxic and metabolic disorderssuch as
ketoacidosis
5. Systemic infections
6. Pregnancy
7. Psychogenic vomitting
8. Obstructive diseases of GIT
9. Acute gastritis, gastroenteritis
10. Radiation exposure.
3. Investigations
Evaluation should exclude CNS causes and upper GI
endoscopy to rule out upper GI pathology. Barium
meal is recommended if upper GI scopy is normal.
Psychogenic vomiting is considered after excluding
organic cause.
4. Treatment
Intravenous fluids if dehydrated. Start oral fluids
as soon as patient tolerates.
Rule out gastric outlet obstruction then
Inj Metoclopramide 10 mg IM repeat after 6 hrs
if needed or
Tab Mozapride 5 mg thrice a day, or
Tab Domperidone 10 mg thrice a day or
Tab Metoclopramide 10 mg thrice a day or
Tab Prochlorperazine 5 mg thrice a day repeat
after 4- 6 hrs if needed,or
Tab /inj Ondensetron 8 mg stat dose and
repeated 8 hrly.
In Pregnancy Tab /Inj Promethazine 25 mg is
safe in the first trimester.
For motion sickness Tab Cyclizine 50 mg thrice
a day.
If vomiting is part of suspected acute abdomen,
acute MI, refer for further evaluation.
Page 76
 32. CONSTIPATION
1. Introduction
Common causes of constipation are Diet deficient in
roughage Ignoring the urge to defaecate e.g. due to
immobility, lack of exercise.
Other causes are neurological, myxoedema, drugs
like Atropine, Codeine, and Malignancy
2. Symptoms
Constipation itself is a symptom. When associated
with inability to pass flatus, severe abdominal pain,
or vomiting there may be the need for urgent referral
to a surgeon.
3. Signs
Constipation, if associated with frequent high pitched
bowel sounds or absent bowel sounds
4. Investigations
Stool routine examination
Stool for occult blood
Sigmoidoscopy/Colonoscopy
A rectal examination with a short length colonoscopy
is a must for all patients with recent onset of
constipation irrespective of bleeding per
rectum.When acute, the constipation may be a part of
a serious illness such as acute bowel obstruction.
These patients present with abdominal pain, vomiting
and distension and non-passage of flatus. These
patients should be referred immediately to a higher
center after rectal examination, passage of rectal tube
(for passage of flatus) and a plain X-ray abdomen.
5. Treatment
Bisacodyl, oral, Adults10-20 mg at night
Or
Psyllium (ispaghula husk), oral, Adults5-10 ml once
or twice a day
Or
Liquid paraffin, oral,10-30 ml at night Or Glycerol
suppositories Adults 4mg at night ; 1 mg at night Or
Lactulose liquid, oral, Adults 15-30 ml orally daily
until response then 10-20 ml daily
Alternative treatment - Magnesium sulphate,
oral, Adults5-10 g in a glass of water, once or
twice daily
6. Dos and Donts
Advice patients to take plenty of fluids, high
fiber diet green leafy vegetables, fruits, avoid
caffeinated drinks.
Regular walk and exercise to 1 hr daily,
abdominal exercise.
To use Indian closet as far as possible (this will
straighten the anorectal angle).
Avoiding suppression of urge to defecate,
(making a regular habit).
Avoid purgative frequently to treat constipation,
as it may be habit forming.
Suppository or simple enema is preferred in IHD
Page 77
 33. IRRITABLE BOWEL SYNDROME
1. Definition
A constellation of gastrointestinal symptoms
associated with lower bowel symptoms that occur in
absence of an organic disease.
2. Symptoms
Clinically the diagnosis is made when continuous or
recurrent symptoms of abdominal pain are associated
with any of the three features viz. Relief by
defecation and / or onset with change in stool
frequency or consistency for at least 3 months.
Supportive symptoms of IBS include passage of
mucous, abnormal stool passage (straining, urgency,
and feeling of incomplete evacuation) and feeling of 4. Dos and Donts
abdominal fullness. Exclude IBS if individual has
alarm symptoms such as fever, weight loss, bleeding
per rectum or anaemia
3. Treatment
Stool bulking agents High fibre diet
Antispasmodics Anticholinergic drugs
(dicyclomine)
Antidiarrhoels Tab Loperamide 2 to 4 mg daily
for several days
Anti depressants IBD Diarrhoeal type TCA (
Imipramine)
IBD constipation type SSRI (paroxetine)
Calcium channel activators Lubiprostone
8microgm x 3 months
Any IBS patient with change in presentation e.g.
change in bowel habit requires re-evaluation.
Diet should contain high fibre and supplemented
with bulk forming agents such as isaphghul husk
Avoid caffeine and alcohol
Avoid milk and other dietary constituents, which
worsens the symptoms
Psychotherapy may be helpful in selected cases
Page 78
 34. ULCERATIVE COLITIS
1. Introduction
Ulcerative colitis is a chronic inflammatory bowel
disease of unknown aetiology.
2. Symptoms
During the first attack the patient often presents with
bloody diarrhoea, with systemic symptoms of low to
moderate fever, backache, arthralgia.The first attack
is a close mimicker of acute infective diarrhoea. A
stool examination followed by sigmoidoscopy is
mandatory, especially if the bloody diarrhoea persists
for more than a month. It is important to exclude
amoebic infection prior to institution of steroids.
Rectum is uniformly involved in these patients.
Frequency of stool can provide information on
severity of the disease: mild (2 - 4 stools/day),
moderate (4 6 stools/day) or severe (> 6
stools/day). During remission, patient may be
asymptomatic or may have extra-intestinal
symptoms.
3. Treatment
These patients require a referral to a tertiary unit.
Aim is induction of remission in acute stage and then
maintenance of remission.
Therapeutic decisions depend on disease activity and
extent. Patients with severe disease require hospital
admission, whereas those with mild/moderate disease
can generally be managed as outpatients.
Disease extent can broadly be divided into
distal and more extensive disease.
Distal disease (proctitis/procto-sigmoiditis): Topical
management is appropriate.
Extensive disease: Oral or parenteral therapy is the
mainstay of treatment.
3.1 Choice of drugs
Mesalamine preparations and Steroid preparations
Treatment of active left sided, or extensive UC:
Mesalazine 2 4 g daily or Balsalazide 6.75 g
daily are effective first line therapy for mild to
moderate active disease.
Sulpha-salazine has a higher incidence of side
effects compared with newer 5-ASA drugs.
Selected patients, such as those with a reactive
arthropathy, may benefit.
Prednisolone 40 mg daily is appropriate for
patients in whom a prompt response is required,
or those with mild to moderate active disease, in
whom Mesalazine in appropriate dose has been
unsuccessful. It should be reduced gradually
according to severity of the patient.
Long-term treatment with steroids is undesirable.
Patients with chronic active steroid dependent
disease should be treated with Azathioprine 1.5
2.5 mg/kg/day
Topical agents (either steroids or Mesalazine)
may be added to the above agents. Although they
are unlikely to be effective alone, they may
benefit some patients with troublesome rectal
symptoms.
Severe UC: close monitoring at a tertiary centre.
3.2 Maintenance of remission
Lifelong maintenance therapy is generally
recommended for all patients, especially those
with leftsided or extensive disease, and those
with distal disease who relapse more than once a
year.
Discontinuation of medication may be
reasonable for those with distal disease who have
been in remission for 2 years and are averse to
such medication. However, there is some
evidence that maintenance therapy reduces the
risk of colo-rectal cancer.
For the maintenance of remission in UC:
Most patients require lifelong therapy, although
some patients with very infrequent relapses
(especially if with limited extent of disease) may
remain in remission without maintenance
therapy.
Oral Mesalazine 1 2 g daily or Balsalazide 2.5
g daily should be considered as first line therapy.
Page 79
 Sulpha-salazine 24 g daily has a higher
incidence of side effects compared with newer 5-
ASA drugs.
Topical Mesalazine 1 g daily may be used
Steroids are ineffective at maintaining remission.
Azathioprine 1.5 2.5 mg/kg/day or
mercaptopurine 0.75 1.5 mg/kg/day are
effective at maintaining remission in UC.
However, in view of toxicity they should be
reserved for patients who frequently relapse
despite adequate doses of amino-salicylates, or
are intolerant of 5-ASA therapy. It is a common
practice to continue amino-salicylates with
azathioprine, but limited evidences that this is
necessary.
Important Note
Regular surveillance is necessary for UC lasting
for more than 10 years.
Explain to the patient the chronic nature of the
disease and continuation of maintenance
Treatment for life with regular follow-up. Risk
of colonic cancer after 10 years of disease onset
must be explained
3.3 Dos and Donts
Milk is preferably avoided during the acute phase of
illness.
Page 80
 35. AMOEBIC LIVER ABSCESS
1. Introduction
Liver abscess is the commonest extra-intestinal form
of amoebiasis, caused by E. histolytica infection but
occurs in only less than 1% of E. histolytica
infections. The disease usually affects young males,
particularly chronic alcoholics, in endemic areas.
Patients commonly affected are between 20 to 40
years of age with residence in or recent travel to or
emigration from an endemic region.
2. Clinical Manifestations
2.1. History
The signs and symptoms of amebic liver abscess
often are nonspecific, resembling those of pyogenic
liver abscess or other febrile diseases.
Abdominal pain
Weight loss
Fever with rigors
Diarrhoea/Dysentry
2.2. Physical
Fever is the most common sign and is found in
as many as 99% of cases.
Hepatomegaly is present in some cases.
Signs of complications
Signs of peritoneal irritation, such as rebound
tenderness, guarding, and absence of bowel
sounds, are present when the abscess ruptures in
the peritoneal cavity. Peritonitis occurs in 2-7%
of cases.
Pericardial friction rub can be audible when the
abscess extends into the pericardium. This sign is
associated with very high mortality.
Signs of pleural effusion are present when the
abscess ruptures in the pleural cavity
3. Investigations
3.1. Laboratory Studies
Examination of the stool for hematophagous
trophozoites of E histolytica must be made on at least
3 fresh specimens because the trophozoites are very
sensitive and may be excreted intermittently
3.2. Imaging Studies
Ultrasonography is the preferable initial
diagnostic test. It is rapid, inexpensive, and is
only slightly less sensitive than CT scan (75-
80% sensitivity vs 88-95% for CT scan).
4. Treatment
4.1 Medical Management
1. Tab. Metronidazole 800 mg three times orally
(or IV, if necessary) daily for 5-10 days or Tab.
Tinidazole 600 mg 2 times a day for 7-10 days
2. If the patient is very toxic, Inj. Metronidazole
500 mg given 8 hourly until patient improves.
Switch over to oral therapy whenever
possible.Followed by Diloxanidefuroate (luminal
agent for cysts) 500 mg three times a day for 10
days
3. Chloroquine 600 mg orally daily 2 days,
followed by 300 mg daily for 2 weeks; dose is
calculated as chloroquine base. Drug is active
against E.histolyticatrophozoites
4.2 Indications for drainage of an
abscess
1. If pyogenic abscess cannot be excluded
2. No improvement with medical therapy in 72
hours
3. Impending rupture of abscess (severe pain,
pleuritic pain, hiccups) - one very close to the
surface of the liver
4. Large left lobe abscess, to prevent rupture in to
the pericardium
4.3 Follow-up
1. Monitor the patient for resolution of symptoms
with medical treatment and aspirate if there is
any indication.
2. Abscess cavity may persist for several weeks
even after cure of infection. Frequent US scan is
unnecessary unless patient develops fever etc.
Scan may be repeated after 4 - 6 weeks, after
thepatient becomes asymptomatic.
Page 81
 4. Maintain good hygiene during food intake to
5. Dos and Donts prevent enteric infections
1. Avoid taking alcohol, specifically if on treatment
with Metronidazole 6. Refer
2. Avoid contaminated food and drinking water.
Vegetables should be cooked or washed well. Patients with abscesses that are large or not
3. Use boiled water (kills the cyst) or bottled water responding to treatment will need to be referred to a
from a known source. physician or surgical specialist.

Page 82
 36. PYOGENIC LIVER ABSCESS
1. Introduction
Liver abscess constitutes about 48% of all visceral
abscesses. Pyogenic liver abscess is usually caused
by spread of infection from peritoneum, abdominal
viscera such as appendicitis/ diverticulitis/portal
pyemia or diseases of biliary tract. It is most
commonly caused by coliform organisms.
2. Clinical Manifestation
Fever, abdominal pain, toxaemia, features of
associated problems such as appendicular pain/
massetc. Mostly abscesses are small and multiple.
3. Investigations
Diagnostic investigations include total counts, USG
scan of the abdomen, blood culture, and pus culture.
CECT and MRI is seldom indicated.
4. Treatment
4.1. Drainage
Percutaneous catheter or open surgical- remains the
mainstay of treatment for a large abscess
Patient should be kept nil by mouth and given IV
fluids if toxic and sick.
4.2 Recommended antibiotics
Metronidazole plus ampicillin and gentamicin,
ciprofloxacin, or a third-generation cephalosporin
Standard dosage
Ceftriaxone 2 g intravenously every 24 hours, or
cefotaxime 2 g intravenously every 8 hours.
Initial empirical treatment should include broad
spectrum antibiotics.
Various combinations recommended are:
Metronidazole: 500 mg I/V three times daily
Ampicillin: 2 g I/V 6 hourly
Gentamicin: 2 mg/kg load, then adjust for renal
function
Ciprofloxacin: 400 mg I/V 12 hourly for 10 days
or
Inj. Ceftriaxone 1-2 g IV every 12 hours 2 times a
day
or
Inj. Cefotaxmine 2 g 8-hrly for 10 days
Combination of Amoxycillin +Ciprofloxacin
+Metronidazole is also a recommended schedule
In the elderly or those with renal impairment: a
Penicillin (such as amoxicillin) plus an injectable
Cephalosporin (such as cefotaxime or
cefuroxime) plus metronidazole is recommended
Inj penicillin allergic patients: ciprofloxacin
plus clindamycin
Once the sensitivity is known, antibiotic therapy
is amended accordingly. Duration of therapy is
usually from 24 weeks or longer depending on
number of abscesses and the clinical response.
5. Follow-up
1. Monitor for clinical improvement and modify the
therapy based on culture sensitivity report.
2. Abscess should always be drained.
3. Surgery is considered if no improvement with
medical treatment and percutaneous drainage
in4-7 days.
Important Note
1. Avoid taking alcohol, specifically if on treatment
with Metronidazole.
2. Maintain good hygiene regarding food intake to
prevent enteric infections.
Page 83
Figure-1: Approch to Pyogenic Liver Abscess

Page 84
 37. INTESTINAL PROTOZOAL INFECTION
giardiasis may contribute to protein-energy
1. Amoebiasis malnutrition in children.
Entamoeba Histolytica is the most prevalent Protein-losing enteropathy has also been described.
intestinal protozoa in India.

1.1 Clinical Features 2.2. Investigations

Diagnosis is made by stool examination and looking
Intestinal Amoebiasis / Amoebic Dysentery: for cysts and trophozoites.
Patient with acute amoebic dysentry present with a 1-
2 weeks history of abdominal pain, tenesmus, and Parasites are best seen in fresh watery stools.
frequent loose stools containing blood and mucus.
Duodenal aspirate is better for isolation but invasive.
Fever may or may not be present.

1.2 Investigations 2.3. Treatment

Despite thepresence of ulcerations and occult blood
in stools, leucocytes may not be present in stools.
A definite diagnosis is made by the demonstration of
E. Histolytica cysts/ trophozoites in stools by a WET
MOUNT PREPARATION.
Treatment is Metronidazole 400mg TID for 5 days
orally or Tinidazole 2gm PO once is equally
effective.
Furazolidone 6 mg/kg q.i.d for 7-10 days is effective
and well tolerated in children.

1.3 Treatment 3. Spore forming protozoa

The drug of choice for amebic colitis is These include:
tinidazole/metronidazole Doses are:
Tinidazole: 2g/day with food for 3 days or Cryptosporidium parvum
Metronidazole: 750 mg tid orally /iv for 5-10 days. Isospora belli
Cyclospora cyatenensis
Treatment of intraluminal amoebiasis is Diloxanide Microsporidia
Furoate 500mg PO-TID for 20 days or paromomycin The spectrum of diseases caused by these is as
30 mg/kg qd in 3 divided doses for 5-10 days. follows:

2. Giardiasis 3.1 Asymptomatic infection

It is a parasitic infection caused by Giardia Lamblia a
single celled organism.
2.1 Clinical Features
Acute symptoms include:
Crampy abdominal pain
Watery diarrhoea, vomiting and fever which last for
few days.
In the chronic stage:
Patients have bloating, nausea, abdominal fullness,
epigastric or substernal burning, malaise and fatigue.
Although severe forms of chronic giardiasis may
occur in otherwise healthy individuals, they are
common in patients with hypoglobulinemia,
particularly IgA deficiency in association with
lymphoid hyperplasia of the bowel. Chronic
This can be seen in immunocompetant as well as
immunocompromised patients.
3.2 Acute infectious diarrhea in
immunocompetent hosts
Acute watery diarrhea with abdominal pain, with
malaise with or without fever can be seen in all
except microsporidia. (generally pathogenic only for
immunocompromised patients)
3.3 Infections in immune
compromised hosts
All spore-forming protozoa have a predisposition for
more frequent and prolonged infections in patients
who are immunodeficient.
Patients with HIV especially with low CD4 count
(<50-100) are more prone.

Page 85
Severe life-threatening watery diarrhea, dehydration
and chronic malabsorption leading to lethargy, failure
to thrive, and malnutrition may occur.
3.4. Investigations
Stool examination with a wet mount preparation is
required for isolation of the parasites.
Modified acid fast staining is used to identify
cryptosporidium, isospora and cyclospora as these are
acid fast.

3.5. Treatment

PATHOGEN TREATMENT
Cryptosporidim Nitazoxanide 500 mg b.d for 3 days
Paromomycin 30 mg/kg per day divided
Isospora Septran (TMP/SMX,160/800 MG) four times a day for 10 days and
then 3 times a day for 21 days
Microsporidia No definite drug but albendazole 400- 800 mg/day divided in b.d
can be given
Cyclospora Septran ( TMP/SMX , 160/800 MG)twice daily for 7 days

Supportive treatment with ORS or iv fluids for fluid Pulmonary consolidations

and electrolyte supplementation is necessary.
Eosinophilia

4. Intestinal helminthic Urticaria

(nematodes) infections Asthma

Nematodes are round worms infesting the intestines. Angioneurotic edema
The infective forms are the eggs/larvae transmitted
by the feco oral route. Intestinal invasion:
Generally seen in low socio economic states with
poor sanitation and hygiene. May be asymptomatic (small number).
Their life cycle is complex with stage of passage
through lungs in some worms (ascaris, hookworm, Abdominal pain (usually vague).
strongyloids) leading to various manifestations like Abdominal cramps/colic.
LOEFFLERS SYNDROME.
Diarrhea.
Several clinical signs and symptoms can occur as
Vomiting (rarely).
follows:
Constipation (occasionally).
Lung invasion - Leffler or Leffler like Intestinal obstruction due to worm mass.
syndrome (ascariasis, hookworm infections, The common nematode infections are described
strongyloidiasis) below:

Fever 4.1 Ascariasis

Ascaris Lumbricoides is the largest of the intestinal
Cough nematodes. Symptoms can be divided into 2
Blood-tinged sputum categories: early larvae migration and late
mechanical effects.
Wheezing
In the early phase (4-16 hours after eggs ingestion),
Rales respiratory symptoms occur because of migration of
larvae through the lungs with symptoms of
Dyspnea eosinophilic pneumonia (Loffler Syndrome). Patient
Substernal pain may have fever, non-productive cough, dyspnoea or
wheezing.

Page 86
In the late phase (6-8 weeks after egg ingestion)
gastrointestinal symptoms may occur. Patient may
vomit out worms from mouth, nose.
Diffuse abdominal pain, nausea, vomiting, billiary
and intestinal obstruction, appendicitis and
pancreatitis.
Ascarisworms invade the biliary duct and cause
pancreatic-biliary ascariasis. The most common
presenting feature is abdominal pain, observed in
98% of patients. Less common features include
ascending cholangitis, acute pancreatitis, and, rarely,
obstructive jaundice.
Diagnosis
i. In early infection (larval migration):
CBC may show peripheral eosinophilia
Sputum may show charcot layden crystals.
Chest X Ray may show patchy infiltrates of
eosinophilic pneumonia.
ii. In the late stage(adult worm):
Stool microscopic examination shows eggs.
USG may be used for ascariasis related biliary
disease.
CT abdomen may show adult worms or
obstruction due to worm mass.
Treatment:
Albendazole 400mg one dose orally is the drug of
choice OR Mebendazole 100 mg twice daily for 3
days. It is contraindicated in pregnancy.
4.2 Anclostoma Duodenale:
(Hookworm)
Many patients may be asymptomatic carriers.
Clinical features -
The symptoms are classified into 2 phases:
In the migratory phase:
Pruritus and erythema and vesiculation will occur
once the falciform larvae have penetrated the skin of
the feet and hands. This is called as ground/dermal
itch in people who goes barefeet.
The pulmonary symptoms may develop with A.
Duodenale during the phase of lung migration like
mild transient pneumonitis.
In the intestinal phase:
Patients may present with abdominal pain (often
epigastric).
Inflammatory diarrhea, with eosinophilia.
Chronic hookworm infection:
Generally presents with Iron deficiency anemia,
Hypoproteinemia.
Diagnosis:
Demonstration of eggs in stool examination.
Sensitivity improved with stool concentration.
Microcytic hypochromic anemia with proteinemia
may be seen in chronic cases. Eosinophilia may be
present.
Treatment:
Albendazole 400 mg once/ Mebendazole 500 mg
once/ pyrantel pamoate 11 mg/kg for 3 days.
Treat anemia with iron supplements.
4.3 Enterobiosis
Enterobius vermicularis / pinworm is prevalent in
most tropical countries.
The adult worms migrate to perianal area at night and
release upto 10,000 eggs which after hatching are
transmitted by hand to mouth passage.
Clinical features-
The infection is generally asymptomatic.
The primary symptoms of pinworm infestation occur
at night which include pruritus in the perianal region.
Heavy infection can cause abdominal pain and
weight loss.
Diagnosis:
Since pinworm eggs are not released in feces stool
examination is not informative.
Detection of worms/ eggs in perianal cellophone
swab/ cellophane tape applied in the early morning
establishes diagnosis.
Treatment:
Single dose Mebendazole 100 mg once /Albendazole
400 mg once.
4.4 Strongyloidosis
S. stercoralis is the only intestinal nematode with the
ability to replicate inside humans, thus leading to
repeated auto infection.
In immunocompramised hosts it can lead to invasive
and disseminated infection which can be fatal.
Clinical features:
Page 87
 Many patients are asymptomatic.
Cutaneous manifestations include recurrent
urticaria involving buttocks and wrists.
Larva currens: cutaneous migration of larvae the duration for 5 to 7 days or upto clearance of
results in serpiginous eruption which is pruritic,
erythematous.
Burning or colicky abdominal pain, often
epigastric, occurs and is associated with
diarrhea and the passage of mucus. Pain is
aggravated by food.
Some patients with strongyloidosis report
nausea, vomiting, and weight loss, with evidence
of malabsorption or of protein-losing
enteropathy.
Massive larval invasion of the lungs and other
tissues may occur with hyperinfection, usually in
immunocompromised hosts.
Disseminated infection in immunocompramised
hosts severe generalized abdominal pain, diffuse
pulmonary infiltrates, ileus, shock, and
meningitis or sepsis due to gram-negative bacilli
may occur.
Diagnosis:
Stool examination for rhabditiform larvae is
diagnostic.
Doudenal aspirate may reveal the larvae if stool is
persistently negative.
In disseminated infections filariform larvae should be
sought in stool, sputum, broncho alveolar lavage etc.
Treatment:
Ivermectin (200 mcg/kg daily for 2 days) is most
effective. In cases with disseminated infection extend
parasites. Albendazole (400 mg daily for 3 days.) is
also effective.
4.5 Trichuris Trichura
Also called as whip worm.
Most infections are asymptomatic. Heavy infections
can cause gastro intestinal symptoms.
Common in low socio economic status with children
especially affected.
Clinical features:
Usually mild symptoms with abdominal pain,
anorexia, diarrhea which can be bloody/mucoid.
Rectal prolapse may occur in massive infections in
children.
Diagnosis:
Stool examination for eggs.
Proctoscopy for adult worms.
Treatment:
Mebendazole 500 mg once/ albendazole 400 mg
daily for 3 days.
Page 88
 38. ASCITES
1. Causes
Cirrhosis is the common cause of ascites. Other
causes are malignancy, cardiac failure, tuberculous
ascites, pancreatitis, nephrotic syndrome, alcoholic
hepatitis, acute liver cell failure etc.
2. Physical Exam
Almost all patients with cirrhosis severe enough
to cause ascites will have stigmata of cirrhosis
spider angiomata, palmar erythema, and caput
medusiae.
Elevated JVP should raise suspicion of heart
failure or constrictive pericarditis as a cause,
although cirrhosis with tense ascites or
pulmonary HTN may cause this.
Sister Mary Joseph nodule with ascites may be
caused by gastric or colon CA, HCC, or
lymphoma. If found, FNAC can provide a rapid
tissue diagnosis.
3. Investigations
Ultra sonography of abdomen is useful to
confirm/refute presence of ascites, cirrhosis,
splenomegaly, biliary obstruction, vessel patency,
signs of portal hypertension, and cancer.
CT-abdomen, tumour markers, HBsAg Anti HCV,
serum amylase are other investigations.
Abdominal paracentesis
Along with history and physical exam, ascitic
fluid analysis helps in the diagnosis of etiology.
It is a safe procedure Ascitic fluid analysis.
Appearance.
Turbid/cloudy 98% sensitive but only 23%
specific for SBP.
Milky chylous ascites, TG level usually greater
than serum TG level and >200mg/dl.
Bloody/pink usually a traumatic tap, but seen
in 50% of patients with HCC and 22% with
malignancy overall.
Dark brown if bilirubin level is higher than in
serum, worry about ruptured gallbladder or
perforated duodenal ulcer.
Lab tests
In general, start with cell count and differential,
TP and albumin when uncomplicated ascites due
to cirrhosis is suspected. Culture is also usually
sent.
In patients with PMN >250, only 50% of cultures
grow bacteria if sent down to lab in a syringe or
plain tube. 80% grow bacteria if inoculated into
blood culture vials at bedside (prior to
antibiotics).
Glucose < 50, LDH > upper limit of normal for
serum, TP >1, and culture results can help
differentiate secondary from spontaneous
peritonitis.
SAAG (serum albumin and ascitic albumin
gradient) > or = 1.1 has ~97% accuracy for
portal hypertension.
TP > or = 2.5 can help differentiate cardiac from
cirrhosis ascites.
When PMN > or = 250, but less than 50% of
WBC, consider peritoneal carcinomatosis and
tuberculous ascites.
4. Management
Goal is to minimize ascitic fluid volume and
peripheral edema without intravascular volume
depletion.
First line treatment includes 2 gram per day
sodium restricted diet and oral diuretics
(spironolactone / lasix).
The usual diuretic regimen is single morning
doses of 100mg spironolactone and 40mg
frusemide (lasix).
The 100:40 ratio generally maintains
normokalemia. Usual max dose is 400mg and
160mg per day.
Other specific management as per the cause of
ascites.
5. When to Refer
Acute ascites, bleeding tendency, refractory ascites,
hepatic encephalopathy.
Page 89
 39. HEPATITIS
1. Introduction
Onset is gradual or sometimes rapid.
There is fever, fatigue and nausea for a few days
followed by jaundice accompanied by dark urine
and sometimes clay- coloured stools.
The severity of jaundice varies.
On examination liver may be mildly enlarged
with mild tenderness.
This being the most common cause one must
always make this clinical diagnosis after the
exclusion of obstructive or haemolytic jaundice.
In most cases this can be done on clinical
grounds alone.
There are five viruses that are commonly
associated with hepatitis called Hepatitis A, B,
C, D and E virus. Of these two, hepatitis A and E
spread through faecal contamination of water.
When there is an outbreak of jaundice in a
village it is probably this virus. Almost always
this jaundice becomes alright on its own. Except
in pregnant women where it can be life
threatening. Three other types of viruses spread
through the blood and through unprotected
sexual contact (hepatitis B, C, D). These types
are more severe, tend to worsen and have more
long term complications.
2. Acute fulminant hepatitis
Sometimes, especially with hepatitis B and D
hepatitis turns severe due to cell necrosis.
Patient develops confusion, stupor and then
coma and it is difficult to save the life.
Pregnant women are prone to develop this
picture with all viruses but commonly with
hepatitis E.
3. Chronic hepatitis
Sometimes the liver disease goes on for years
without becoming well.
Such patients have frequent intermittent episodes
of jaundice.
Elevated liver enzymes over 6 months is enough
to make this diagnosis.
Eventually it can become well but more often
leads to cirrhosis of the liver and portal
hypertension and end stage liver disease
develops.
4. Obstructive jaundice
Sometimes jaundice is due to obstruction to flow
of bile and not due to a virus.
On such cases the yellowing of eyes is very
marked and may even be greenish.
There is much itching and the stools are always
whitish in colour.
Usually the liver is enlarged.
Ultrasound of the liver confirms obstruction best
and the patients should be referred to a centre
with ultrasonography facilities.
Refer to higher centre as these cases need
surgery.
5. Haemolytic jaundice
Sometimes jaundice is due to increased
breakdown of haemoglobin secondary to
destruction of RBCs in a haemolytic anaemia.
Jaundice is invariable light coloured, and urine is
also normal in colour.
Diagnosis needs to be established by blood
smear examination, by ruling out hepatitis by
liver function tests and by specific tests for
haemolytic anaemia.
6. Alcoholic hepatitis
Excessive alcohol consumption is a significant cause
of hepatitis and liver damage (cirrhosis). Alcoholic
hepatitis usually develops over years-long exposure
to alcohol. Alcohol intake in excess of 80 grams of
alcohol a day in men and 40 grams a day in women is
associated with development of alcoholic hepatitis.
Alcoholic hepatitis can vary from mild asymptomatic
disease to severe liver inflammation and liver failure.
Symptoms and physical exam findings are similar to
other causes of hepatitis. Laboratory findings are
significant for elevated transaminases, usually with
elevation of aspartate transaminase (AST) in a 2:1
ratio to alanine transaminase (ALT).
Alcoholic hepatitis may lead to cirrhosis and is more
common in patients with long-term alcohol
consumption and those infected with hepatitis C.
Page 90
Patients who drink alcohol to excess are also more
often than others found to have hepatitis C. The
combination of hepatitis C and alcohol consumption
accelerates the development of cirrhosis.
7. Investigations for jaundice
These tests are needed to establish diagnosis &
monitor improvement.
Urine examination for bile salts & pigments.
Serum bilirubin & Serum liver enzymes level.
8. Treatment for hepatitis
Only supportive: rest, hydration, correct but not
specific diet.
Avoid oily spicy foods that are ill tolerated.
Avoid corticotherapy. NEVER give steroids.
There are no specific drugs to cure jaundice.
Fortunately most persons become well on their
own.
Remember many drugs commonly used are harmful
when given to a person with jaundice.
8.1. Treatment for Acute fulminant
hepatitis
Patient needs hospitalization.
Treatment is supportive & consists of
maintaining parenteral fluids.
Care is taken to treat infections or other
precipitating factors like haematemesis.
Gut sterilization with capsule amoxicillin and/or
metronidazole may help.
8.2. Treatment for obstructive
jaundice
Refer for Surgery.
8.3. Treatment for Haemolytic
anaemia
Referral for further work up in higher centre with
tests for type of haemolysis.
9. Vaccine
Vaccine against hepatitis B is available.
Hepatitis-B Vaccine is included in National
Immunization Schedule.
Page 91
 40. HEPATIC COMA
coma. Asterixis / flapping tremors is also commonly
1. Introduction seen.
Hepatic Encephalopathy is a term used to describe a Search for precipitating factors every advanced
spectrum of neuropsychiatric abnormalities occurring cirrhotic patient displaying a change in mental status
in patients with significant liver disease and/or porto is septic until proven otherwise. Common
systemic shunting of blood. precipitating are GI bleeding, sepsis, hypokalemia,
high protein load, constipation, hyponatriemia, Other
2. Diagnosis causes include sedative
drugs, superimposed liver injury.
There are 2 major components of HE, altered mental
status and generalized motor disturbance. 3.Grade / Stage the severity of
Disturbunces in awareness and mentation from
forgetfulness and confusion to stupor and finally disease
Table-1: West-Haven Criteria for Hepatic Encephalopathy (HE)

Stage Consciousness Intellect and Behavior Neurologic Findings

0 Normal Normal Normal examination; if impaired psychomotor
testing, consider MHE*
1 Mild lack of awareness Shortened attention span Impaired addition or subtraction; mild asterixis or
tremor

2 Lethargic Disoriented; Inappropriate Obvious asterixis; Slurred speech

behavior
3 Somnolent but arousable Gross disorientation; Muscular rigidity and clonus;
Bizarre behavior Hyperreflexia
4 Coma Coma Decerebrate posturing
*MHE, minimal hepatic encephalopathy.

ii. Rifaximin 400mg PO tid marginally better

4. Treatment than lower doses(400mg-550mg bid) or
A. 4-pronged approach to treatment Neomycin 1gm PO q6 hourly for up to 6 days
Supportive care. (if used chronically, 1-2gm/day).
Search for and correct precipitating factors iii. Dietary protein restriction no longer
Exclude and treat other causes of altered mental recommended.
status. iv. L-ornithine-aspartate promotes waste nitrogen
Start empiric therapy for HE excretion.
i. Lactulose : 30cc bid-qid titrated to goal 2-4 v. Antibioics if sepsis suspected.
soft BMs/day or retention enema 300cc
lactulose + 700cc tap water retained for 1 hour
reduces the ammonia production and 5. When to refer
absorption. Deteriorating sensorium, hematemesis, malena,
bleeding tendencies.

Page 92
 41. NEPHROTIC SYNDROME
6. Renal Function Test: Blood Urea Level and
1. Definition Serum Creatinine Level
Nephrotic Syndrome is a clinical complex 7. Renal Biopsy: In Adult patients for a)
characterized by a number of renal and extrarenal Establishing a Definitive Diagnosis b) Guiding
features, the most prominent of which are Therapy & c) Assessing Prognosis.
Proteinuria of 3-3.5gm / 24 hour,
Hypoalbuminemia,
Edema, 5. Treatment
Hyperlipidemia, Lipiduria i. Steroid: Minimal change disease accounts for
about 80% of Nephrotic Syndrome in children
younger than 16 year and 20% of adult.
2. Symptoms and Signs Adult: Tab Prednisolone 1-1.5 mg/kg body
Puffiness of face, increase in morning weight per day for 4 week followed by
Ankle pitting edema with increasing severity to 1mg/kg/day on alternate day for 4 week.
generalised anasarca Ascites, Pleural Effusion Check for urine protein after four weeks if nil
no treatment needed and if present start with
Prednisolone 1.5 mg for 2 weeks
3. Complications ii. HMG Co A Reductase Inhibitor: Tab
Recurrent Infections, hypocalcemia, Anemia,
Atorvastatin 10 Mg Od
Thrombotic Tendencies
iii. Loop Diuretic
iv. Salt Restriction 1-2 Gram per Day.
4. Investigation v. High Protein Diet
1. Urine Analysis for Proteinuria, Protein / vi. Vitamin D Supplementation.
Creatinine ratio
2. Urine Microscopy for Deposit 6. When to Refer
3. 24 Hour Urinary Protein
i. For Renal Biopsy
4. Serum albumin
ii. When Dialysis is required.
5. Ultra sonography abdomen and pelvis

Page 93
 42. ACUTE NEPHRITIC SYNDROME
It is Clinical Correlate of Acute Glomerular Blood Urea and Serum Creatinine elevations.
Inflammation Which May Be a Primary Disease OR
Decrease C3 Level, Normal C4 Level
Secondary to Systemic Process.
ASO Titer
1. Definition Ultra sonography renal
It is characterized by sudden onset (over days to
Renal Biospy
weeks) of acute renal failure and Oliguria (400ml/day
of urine) and renal blood flow and GFR fall as a
result of obstruction of the glomerular capillary
4. Treatment
lumen. 4.1 General Management
2. Clinical Features Bed Rest
Tetrad of
Adequate Fluid Intake to ensure 400 ml Urine per
Edema Day
Hypertension mild Salt restriction especially if edema present
Hematuria [macroscopic]
4.2 Managementof Renal Failure
Proteinuria (Subnephrotic Range < 3g/24 Hr)
Tab Frusemide if volume overload hypertension
Symptom:
Not to be given if no evidence of fluid excess
Puffiness of Face
Rarely require Dialysis
Edema of Feet
Cola Coloured Urine
4.3 Antihypertensive Drug
Dyspnea If Pulmonary Edema 4.4 Controlof Infection
Hypertension
Generalized Symptoms- Anorexia, Nausea, 4.5 Renal Biopsy
Vomiting, Malaise, Flank OR Back Pain. If features not suggestive of Post Streptococcal
Glomerulonephritis.
3. Investigation
Urine Microscopy: Dysmorphic RBCs and RBC 5. When to Refer
Cast, Leucocytes
i. For Renal Biopsy
Urine- Gross Hematuria (Red or Smoky Urine) ii. When Dialysis is required.
Subnephrotic range Proteinuria

Page 94
43. ACUTE RENAL FAILURE / ACUTE KIDNEY
INJURY

1. Definition 3. Acute tubular necrosis

AKI is a syndrome characterized by rapid decline in Ischemia, Exogenous toxins: radiocontrast,
glomerular filtration rate (hours to days), retention of chemotherapy, acetaminophen, Endogenous toxins:
nitrogenous waste products and perturbation of rhabdomyolysis, hemolysis, myeloma.
extracellular fluid volume and electrolyte and acid
base homeostasis. 4. Interstitial nephritis
AKI is defined as any of the following (Not Graded): Antibiotic, NSAID, Sulfonamide, eta lactam
Increase in Sr.Creatinine by X0.3 mg/dl (X26.5
Post renal:
lmol/l) within 48 hours; or
Increase in Sr.Creatinine to X1.5 times baseline, Ureter: calculi, blood clot, carcinoma
which is known or presumed to have occurred
Bladder neck: prostatic hypertrophy, calculi,
within the prior 7 days; or
carcinoma
Urine volume 0.5 ml/kg/h for 6 hours
Urethra: stricture, phimosis.
2. Classification
3. Symptoms
Prerenal:
a. Hypovolemia: 3.1. Prerenal
Haemorrhage, burns, dehydration, vomiting, diarrhea, Evidence of true volume depletion- thirst,
pancreatitis, peritonitis. postural or absolute hypotension and
b. Low cardiac output: tachycardia, dry mucous membrane.
Urine- low volume, low sodium and high
CCF, Disease of myocardium, valves and osmolality.
pericardium,
Pulmonary hypertension, pulmonary emboli. 3.2. Renal
c. Altered renal systemic vascular resistence ratio; Symptom and sign of underlying disease affecting
glomeruli or tubule.
Systemic vasodilatation- sepsis, antihypertensive
drug 3.3. Postrenal
Renal vasoconstriction: hypercalcemia
Abdominal or flank pain, palpable bladder.
Cirrhosis with ascitis- hepatorenal syndrome.
Intrinsic renal: 3.4. Symptoms of uremia
1. Renovascular obstruction: Anorexia, nausea, vomiting, Mental status changes,
Pruritus, shortness of breath
Renal artery obstruction: atherosclerosis, thrombi,
emboli, Renal vein obstruction: thrombi, compression
4. Signs
2. Disease of glomeruli: Asterixis, Pericardial rub, Pedal edema, pulmonary
Glomerulonephritis and vasculitis, Hemolytic uremic edema, Raised JVP
syndrome, DIC, toxemia of pregnancy, Accelerated
hypertension. 5. Investigation
Urine analysis: routine microscopy

Page 95
Routine blood chemistry: BUN, creatinine, Serology: ANA, ANCA, anti GBM, complement,
electrolyte, ca, po4 ASO
Complete hemogram Imaging: Renal ultrasound, Plain radiograph of
abdomen.
Special test: bence jones protein
Renal biopsy.

6. Staging of aki

STAGE Serum creatinin criteria Urine output criteria

I 1.5 to 2 fold increase <0.5 ml/kg/hr for > 6 hr
II 2 to 3 fold increase <0.5 ml/kg/hr for >12 hr
III >3 fold increase , absolute value > 4 mg/dl < 0.3 ml/kg/hr for 24 hr or anuria
for 24 hr.

IV.Calcium gluconate (10ml 10% solution)

7. Treatment Inhaled 2 agonist- Salbutamol
IV glucose insulin infusion (100ml 25% dextrose
7.1. Prerenal with 10 unit of human actrapid in 1 hour)
Restore blood volume (with isotonic saline 0.9%, or Dialysis.
blood, plasma)
Treat underlying cause.
7.5. Treatment of metabolic
7.2 Renal acidosis
Inj Na bicarbonate iv
Eliminate toxins, Nephrology consultation

7.3. Postrenal 7.6. Dialysis: indication

Metabolic acidosis, Hyperkalemia, Encephalopathy,
Relieve obstruction, Urology consultation Volume overload, Pericarditis

7.4. Hyperkalemia

8. Complication
COMPLICATION MANIFESTATION
1.Metabolic Hyperkalemia, hypocalcemia, hyperphosphatemia, hypermagnesaemia,
hyperuricemia, metabolic acidosis.
2.Cardiovascular Cardiac arrhythmia, pulmonary edema, pericardial effusion, pericarditis
3.Gastrointestinal Gastrointestinal hemorrhage
4.Neurological Altered sensorium, seizures
5.Hematological Anaemia, bleeding.

9. Prevention
Nephrotoxic drug should be stopped if patient is at
Apropriate and adequate fluid management
Optimization of hemodynamic risk of developing AKI.
Management and prevention of sepsis

Page 96
 44. CHRONIC KIDNEY DISEASE
3. Nondiabetic glomerular disease- Nephritic and
1. Definition nephrotic presentation
4. Cystic kidney disease
A. Presence of marker of kidney damage more than 5. Tubulo interstitial disease.
3 month as defined by structural or functional
abnormality of the kidney with or without decrease 3. Staging
GFR manifested by either pathological abnormality According to GFR (glomerular filtration rate)
or other marker of kidney damage. Cockcroft-Gault equation for calculation of
B. GFR < 60 ml/min/1.73m2 for more than 3 month creatinine clearance:
with or without sign of kidney damage.
(140- Age) Body weight (kg)
2. Causes 72 plasma creatinine (mg/dl)
1. Diabetes Multiply by 0.85 for women.
2. Hypertension

Table-1: Staging of CKD

STAGE DESCRIPTION GFR(ml/min/1.73m2

1 At increased risk of kidney damage with normal or raised 90
GFR
2 Kidney damage with mildly Decreased GFR 60-89
3 Moderately decreased GFR 30-59
4 Severelydecreased GFR 15-29
5 Renal failure <15

4. Symptoms and signs 6. Evaluation and

Hypertension, proteinuria, anemia, deep
respiration(Kussmauls respiration), tiredness,
management of patient of
breathlessness, pruritus, anorexia, nausea, vomiting. ckd
5. Risk factors 6.1. History and physical
Age> 65yr examination
Diabetes
H/O HTN, DM, use of analgesic Measure blood
Family h/o renal disease pressure

Autoimmune disease 6.2. Laboratory investigation

Systemic infection
Haemoglobin level.

Urine for proteinuria and hematuria

UTI, stone, urinary tract obstruction,
Blood urea,serum creatinine
HTN

Page 97
 Blood sugar level 6.3. Imaging study
Serum electrolyte
USG abdomen for the renal size and
Serum calcium,phosphorus level Corticomedullary differentiation.

Table-2: To Delay Progression to Next Stage:

MEASURES GOAL
1.ACE inhibitors/ARB Proteinuria <0.5 g/day and GFR decline<2ml/min/yr.
2.Additinoal antihypertensive drug as needed BP<130/80 if proteinuria<1 gm/day
BP<125/75 if proteinuria>1gm/day
3.Dietary protein restriction 0.6 to 0.8 gm/kg/day
4.Glycaemic control HbA1C <7 %
5.Anaemia correction Target Hb 10 to 12 gm/dl
6. Cholesterol lowering agent LDL <100 mg/dl
7. Dietary salt restriction 3 to 5 gm/day

6.4. Treatment diseases, Anaemia: target Hb 11 gm/dl, Use of iron

and erythropoietin injection, Renal osteodystrophy:
1. Slowing the progression of CRF:
target Ca 8.8 9.7, phosphorus 3.5 5.5, Use of
Protein restriction 0.6gm/kg/day calcium carbonate, phosphorus restriction avoid

2. Slowing diabetic renal disease: dairy product,meat,colas Oral calcitriol.

Glucose control target HbA1c <7.2 4. Renal replacement therapy:

3. Managing complications of CRF:Cardiovascular Dialysis: refer to higher center, A-V fistula; if GFR
complication-yearly screening of cardiovascular <25ml/min Serum creatinine> 4 mEq/L.

Page 98
 45. MALARIA
1. Introduction
Malaria is a protozoal disease caused by infection
with parasites of the genus plasmodium and
transmitted to man by female anopheles mosquito. It
is a very important public health problem in India
particularly due to Plasmodium falciparum which is
prone to various complications.
2. Agent
Malaria in man is caused by Plasmodium vivax,
Plasmodium falciparum, Plasmodium ovale and
Plasmodium malaria. Out of these, Plasmodium
vivax and Plasmodium falciparum are very common
in India including Maharashtra.
3. Mode of transmission
Direct through blood or plasma.
Vectors bite of female anopheles mosquito.
4. Incubation Period
The duration varies with species of parasite.
12(9-14) days for falciparum malaria.
14(8-17) days for vivax malaria.
5. When to suspect
The typical attack comprises three distinct stages viz.
cold stage, hot stage and sweating stage.
Cold Stage:
The onset is with lassitude, headache, nausea and
chilly sensation followed in an hour or so by rigors.
The temperature rises rapidly to 39-41C. Headache
is often severe and commonly there is vomiting. In
early part of this stage, skin feels cold; later it
becomes hot. Parasites are usually demonstrable in
the blood. The pulse is rapid and may be weak. This
stage lasts for -1 hour.
Hot Stage:
The patient feels burning hot and casts off his
clothes. The skin is hot and dry to touch. Headache is
intense but nausea commonly diminishes. The pulse
is full and respiration rapid. This stage lasts for 2 to 6
hours.
Sweating Stage:
Fever comes down with profuse sweating. The
temperature drops rapidly to normal and skin is cool
and moist. The pulse rate becomes slower; patient
feels relieved and often falls asleep. This stage lasts
for 2-4 hours.
The febrile paroxysms occur with definite
intermittent periodicity repeating every third or
fourth day depending upon the species of the parasite
involved. The classical 3 stages (cold, hot and
sweating) may not always be observed due to
maturation of generations of parasite at different
times. The disease has a tendency to relapse and is
characterized by enlargement of the spleen and
secondary anaemia.
In patients with P.falciparum infection the primary
fever in its first few days is usually irregular or even
continuous and then the classical 48 hour periodicity
becomes established or the fever may continue to be
irregular and the hot and cold stages, so typical of
other malarial infections are less clearly separated
from one another, in persons with poor immunity.
The paroxysms are associated with marked
prostration. Headache, nausea and vomiting are
usually more severe, and there is greater tendency
towards the development of delirium, haemolytic
jaundice and anaemia. The mortality is much greater
than in other forms of malaria.
With P. vivax infection, symptoms are same but are
usually milder and more regularly divided into hot
and cold stages than in P.falciparum infections.
6. Complications
The complications of P. falciparum malaria are
cerebral malaria, acute renal failure, liver damage,
gastro-intestinal symptoms, dehydration, collapse,
anaemia, black water fever etc. The complications of
P. vivax, infection are anaemia, splenomegaly,
enlargement of liver, herpes, renal complications,
ARDS etc.
7. Investigations
Diagnosis of Malaria: One of the above clinical
features, supported by blood smear examination
for malarial parasites.
Fever with splenomegaly in a patient with the
above mentioned clinical features make
diagnosis of malaria more likely.
Page 99
 Confirmation of diagnosis always depends on
seeing the parasite in the blood. In all cases,
thick and thin smears should be examined.
Blood smears may be negative in severe and
chronic forms and this would need repeated
smears.
8. Diagnosis of Malaria
It is stressed that all fever cases should be suspected
of malaria after ruling out other common causes and
should be investigated for confirmation of malaria by
Microscopy or Rapid Diagnostic Kit (RDK) so as to
ensure treatment with full therapeutic dose with
appropriate drug to all confirmed cases. Presumptive
treatment of malaria with a single dose of
chloroquine has been stopped.
All fever cases diagnosed as malaria by either RDT
or microscopy should be promptly given effective
treatment. The medicine chosen will depend upon
whether the patient has vivax malaria or falciparum
malaria as diagnosed by the blood test. The flow
charts in different settings for diagnosis and drug
selection for the treatment of malaria are mentioned
below.

Where microscopy result available within 24 hours

Suspected malaria case

Take slide and send for microscopic examination

Result?

Positive for Positive for Positive for Negative

P. vivax P. falciparum Mixed infection No anti-malarial
Treat with: Treat with: SP-ACT 3 days Treatment.
CQ 3 days + ACT-SP + Treat as per
PQ 0.25 mg for 3 days + PQ 0.75mg Primaquine clinical
per kg body per kg body 0.25 mg per kg diagnosis
weight daily for weight body weight
14 days Single dose on daily for
second day 14 days.

Figure-1: Management chart for suspected Malaria case

Page 100
 ACT-SP- Artemisinin-based Combination Where microscopy result is not available within 24
Therapy(Artesunate+Sulfadoxine-Pyrimethamine)CQ hours and Monovalent RDT is used
Chloroquine PQ Primaquine
TfR= Test falciparum rate

Suspected malaria case

Where TfR>=1%, and In other areas, if

Pf %> 30% in any of Patient not
last at high risk of Pf*
3 years

Do RDT for detection Wait for slide result. Give

of CQ 25mg/kg over 3 days
Malaria & only if high suspicion of
Prepare slide malaria

Positive for Positive for

Positive for RDT Negative:
P. vivax P. falciparum
P. falciparum Wait
CQ if not In other states:
Treat with: ACTSP for slide result.
already Treat with: ACTSP
for 3 days + Give CQ 25mg/kg
given + for 3 days
PQ Single dose over 3 days, if
PQ 0.25 + PQ Single
on second day high suspicion of
mg/kg single dose onPQ 0.75mg
dose for 14 per kg body
If confirmed as days over weight
Pv 3days, if high Single dose on
CQ if not already suspicion of second day
Given PQ 0.25 malaria
mg/kg/day over
14 days

Figure-2: Management of suspected Malaria

Note: if a patient has severe symptoms at any ACT-SP- Artemisinin-based Combination

stage, then immediately refer to a facility with
indoor patient management.
Note: PQ is contra-indicated in pregnancy
and in children under 1 year (Infant).
Therapy (Artesunate+Sulfadoxine-
Pyrimethamine) CQ Chloroquine PQ
Primaquine.
Where microscopy result is not available
within 24 hours and Bivalent RDT is used

Page 101
 Suspected malaria case

Do blood test with RDT

Positive for Positive for Positive for Negative

P. falciparum P. vivax Mixed infecion No anti-
Treat with: ACTSP Treat with: SP-ACT 3 days + malarial
for 3 days + CQ 3 days Primaquine 0.25 mg per Treatment
PQ Single dose on second + PQ 14 days kg body weight daily for
day malaria case 14 days.

Figure-3: Suspected Malaria management based on RDT results

ACT-SP- Artemisinin-based Combination Therapy
(Artesunate+Sulfadoxine-Pyrimethamine).
CQ Chloroquine PQ - Primaquine
Differential Diagnosis:
Other causes of fever like Dengue, UTI, URTI. All
D/D can be excluded by using lab investigation
(microscopy/RDT).
9. Treatment
9.1. Treatment of Vivax Malaria
Diagnosis of vivax malaria may be made by the use
of RDT (Bivalent) or microscopic examination of the
blood smear. On confirmation following treatment is
to be given:
Drug schedule for treatment of P vivax malaria:
i. Chloroquine:
25 mg/kg body weight divided over three days i.e.
10 mg/kg on day 1,
10 mg/kg on day 2 and
5 mg/kg on day 3.
ii. Primaquine:
0.25 mg/kg body weight daily for 14 days.
Primaquine is contraindicated in infants, pregnant
women and individuals with G6PD deficiency.
14 day regimen of Primaquine should be given under
supervision.

Table-1: Dosage Chart for Treatment of Vivax Malaria

Day 4 to 14
Day 1 Day 2 Day 3
Age
CQ (150 PQ CQ (150mg PQ (2.5 CQ (150mg PQ (2.5mg) PQ (0.25
mg base) (2.5mg) base) mg) base) mg)
Less than
0 0 0 0
1 yr
1-4 years 1 1 1 1 1 1
5-8 years 2 2 2 2 1 2 2
9-14 years 3 4 3 4 1 4 4

Page 102
15 yrs or
4 6 4 6 2 6 6
more*
Pregnancy 4 0 4 0 2 0 0

Note: Chloroquine250mg tablet is having 150 mg base

9.2. Treatment of Falciparum Treatment of uncomplicated P.falciparum cases in

Malaria
Diagnosis of falciparum malaria may be made by the
use of RDT (Monovalent or Bivalent) or microscopic
examination of the blood smear. It is imperative to
start the treatment forfalciparum malaria immediately
on diagnosis. The treatment for falciparum malaria is
as follows:
Dose schedule for Treatment of uncomplicated
P.falciparum cases:
i. Artemisinin based Combination Therapy (ACT-
SP)*
Artesunate 4 mg/kg body weight daily for 3 days Plus
Sulfadoxine (25 mg/kg body weight)
Pyrimethamine (1.25 mg/kg body weight) on first
day.
* ACT is not to be given in 1st trimester of
pregnancy.
ii. Primaquine: 0.75 mg/kg body weight on day 2.
pregnancy:
1st Trimester: Quinine salt 10mg/kg 3 times
daily for 7 days.Quinine may induce
hypoglycemia; pregnant women should not start
taking quinine on empty stomach and should eat
regularly, while on quinine treatment.
2nd and 3rd trimester: ACT as per dosage
schedule given above.
9.3. Treatment of mixed infections
(P.vivax + P.falciparum) cases
All mixed infections should be treated with full
course of ACT and Primaquine 0.25 mg per kgbody
weight daily for 14 days.
SP-ACT 3 days + Primaquine 0.25 mg per kg body
wt. daily for 14 days.

Table-2: Treatment of mixed infections

Day 4to
Day 1 Day 2 Day 3
14
Age As tablet SP tablet PQ (2.5 As tablet PQ (2.5 As tablet PQ PQ (0.25
(50 mg) mg) (50mg) mg) (50 mg) (2.5mg) mg)
Less than
1 yr 0 0 0 0

1-4 years 1 1 1 1 1 1 1 1
5-8 years 2 1 2 2 2 2 2 2
9-14 years 3 2 4 3 4 3 4 4
15 yrs or
more 4 3 6 4 6 4 6 6

All cases of mixed infection are to be treated as Pf treatment and is still having symptoms after 72 hours,
plus primaquine for 14 days. treatment failure may be suspected.

When a patient fails to respond to treatment
(symptoms fail to disappear, or they reappear), one
should think of the possibility of drug resistance in
such case refer patient to FRU. In the absence of any
of these conditions, if a patient has completed full
The course of action when a patient has persistent
symptoms is:
Ask the patient and the family a series of
questions to help rule out some of the causes
(Did the patient get the drug from an authentic,
designated provider? Did the patient get the right

Page 103
 amount of the drug? Was all of it swallowed as
prescribed? Was the drug vomited out? How
many days has it been since drug treatment was
begun (if it is not yet72 hours, one can wait)?
Can you see the packing to check the expiry
date? Are there symptoms of other obvious
causes of fever? If the symptoms had
disappeared and then reappeared, how long was
the interval (if more than 15 days, it could be a
fresh infection)?)
If it appears that the drug was not adequately
taken or retained, a fresh course may be given
unless the patient has symptoms of severe
malaria. Take a fresh blood11smear (take two,
for checking in different laboratories, if need be),
and ask the nearest health care provider to keep
an eye on the patient.
Refer any patient who has symptoms despite
taking and retaining a full course of treatment, or
who has developed symptoms of severe malaria.
10. Severe and complicated
malaria
10.1. Clinical Features
Severe manifestations can develop in P. falciparum
infection over a span of time as short as 12-24 hours
and may lead to death, if not treated promptly and
adequately. Severe malaria is clinically characterized
by confusion or
Drowsiness with extreme weakness (prostration)
along with one or more of the following features:
Impaired consciousness/coma
Repeated generalized convulsions
Renal failure (Serum Creatinine>3 mg/dl)
Jaundice (Serum Bilirubin >3 mg/dl)
Severe anaemia (Hb<5 mg/dl)
Pulmonary oedema/acute respiratory distress
syndrome
Hypoglycaemia (Plasma glucose <40 mg/dl)
Metabolic acidosis
Circulatory collapse/shock (Systolic BP<80 mm
Hg, <50 mm Hg in children).
Abnormal bleeding and disseminated
intravascular coagulation.
Haemogolobinuria.
Hyperthermia (Temperature >106F or 42C).
Hyperparasitaemia (<5% parasitized RBCs in
low endemic and >10% in hyperendemic areas).
Metabolic acidosis.
Circulatory collapse/shock.
Spontaneous bleeding and laboratory evidence of
DIC.
Macroscopic haemoglobinuria.
Hyperthermia.
Hyperparasitaemia.
Foetal and maternal complications are more common
in pregnancy with severe malaria; therefore, they
need prompt attention.
10.2 In children, febrile convulsions, repeated
vomiting and dehydration are common if the
temperature is high due to any cause.
Therefore, these symptoms are not
necessarily indicative of severe malaria.
However, children with such symptoms
should be managed as severe malariain
routine program situations, and a diagnosis
of malaria should be confirmed at the
earliest.
10.3 In pregnancy, malaria, especially
P.falciparum is a serious disease because
with each bout of malaria, there is a
reduction in haemoglobin and profound
anaemia may develop rapidly. They are also
at high risk of abortions or intrauterine
growth retardation because sequestration of
parasites in placenta restricts oxygen and
nutrients flow to the fetus. The management
of severe malaria is possible in health
facilities which are equipped with the
following:
Parenteral Antimalarials, antibiotics,
anticonvulsants, antipyretics.
Intravenous infusion equipment and fluids.
Special nursing for patients in coma.
Facilities for blood transfusion.
Well-equipped laboratory.
Oxygen respirator.
Often these items are not available at the PHC level.
Under such circumstances, the MedicalOfficer, PHC
and paramedical staff should be able to administer
emergency treatment and refer the case without delay
to other institutions where such facilities are
available.
10.4. Treatment of severe malaria
cases
Severe malaria is an emergency and treatment should
be given as per severity and associated complications
which can be best decided by the treating physicians.
The guidelines for specific antimalarial therapy is as
follows:
Parenteral artemisinin derivatives or quinine should
be used irrespective of chloroquine resistance status
of the area with one of the following options:
Page 104
 Table 3: Chemotherapy of severe and complicated malaria

Initial parenteral treatment for at least48hours:CHOOSE
ONE of following four options
Artesunate: 2.4 mg/kg i.v. or i.m. given on admission
(time=0), then at 12 h and24 h, then once a day.
Quinine: 20mg quinine salt/kg body weight on
admission (IV infusion or
divided IM injection) followed by maintenance dose
of10 mg/kg 8 hourly;
Infusion rate should not exceed 5 mg/kg per hourin
normal saline. Loading dose of 20mg/kg should not be
given, if the patient has already received quinine.
Follow-up treatment, when patient can takeoral
medication following parenteral treatment
Full oral course of Area-specific ACT:
In other states: Treat with: ACT-SP for 3days + PQ
Single dose on second day
Quinine 10 mg/kg three times a day
with:
doxycycline 100 mg once a day or
Clindamycin in pregnant women and children under 8
years of age,- to
Complete 7 days of treatment.

Note: The parenteral treatment in severe malaria cases should be given for minimum of 24 hours once started
(irrespective of the patients ability to tolerate oral medication earlier than24 hours).

Note:
The parenteral treatment should be given for minimum of 48 hours.
Once the patient can take oral therapy, give:
Quinine 10 mg/kg three times a day with doxycycline 100 mg once a day orclindamycin in pregnant women and
children under 8 years of age, to complete 7days of treatment, in patients started on parenteral quinine.
Full course of ACT to patients started on artemisinin derivatives.
Use of mefloquine should be avoided in cerebral malaria due to neuro psychiatric complications associated with
it.

Supplementary treatment
In unconscious patient, monitor blood glucose level every 4 to 6 hours and treat hypoglycemia with IV dextrose. If
blood sugar estimation is not available one can presume hypoglycemia in all cases of severe and complicated
malaria especially cerebral malaria and treat with intravenous glucose 100 ml of 25% glucose before giving
quinine.
All unconscious patients on quinine should receive a continuous infusion of 5 to10%dextrose.
Parasite count and hematocrit level should be measured every 6 to 12 hourly.
Transfuse whole blood or packed cell concentrate when hematocrit drops to <20%.
Renal function should be checked daily, institute early hemodialysis if necessary.
Fluid management should be carefully done.
Treat convulsions with IV diazepam and shift the patient to an Intensive Care Unit with facilities for ventilator
support.

10.5. Some donts in severe malaria case management

Do not use corticosteroids, give intravenous mannitol, use heparin as anticoagulant, administer adrenaline or
overhydrate.

In recent years, increased attention has been drawn to severe malaria caused by P.vivax, especially in Indonesia and
Papua New Guinea, where this parasite has become chloroquine resistant. Some cases have been found in India, and
there is reason to fear that this problem will become more common in the coming years. Historically, P.vivax has
been an important cause of death in India and in Europe, and this parasite can no longer be considered as benign.

Page 105
 10.6. When to refer: Any of the following
i. Platelet count 20,000/cmm.
ii. Pregnancy with malaria.
iii. Any feature of complicated malaria.
iv. Renal failure.
v. ARDS.
vi. Malaria with sepsis.
vii. Malaria with shock.

Page 106
 46. DENGUE
1. Introduction
In Maharashtra State, cases of Dengue Fever /
Dengue Hemorrhagic Fever occur eitherin post-
monsoon period when breeding of mosquitoes is
highest due to accumulation of rainwater in discarded
materials or during scarcity season due to Aedes
breeding in stored waterin cement tanks and earthen
pots which are not emptied regularly.
2. Etiologic agent
Table-1: Recommended diagnostic tool according to laboratory service level
DF/DHF is caused by a group B arbovirus
(Flavivirus) and includes serotypes 1, 2, 3 and 4
(Den-1, Den-2, Den-3 and Den-4). Infectionwith any
one serotype confers lifelong immunity to thevirus
serotype, but no cross protection for other serotypes.
It is caused due to bite of an infected female Aedes
aegypti mosquito.
Mode of Transmission It is transmitted through
bite of Ades aegypti mosquito.
Incubation period: Varies from 5-10 days.
3. Diagnosis

Primary health District health Reference

care centres centres centres
Genome Detection Yes
NS1 Ag detection Rapid tests Yes Yes Yes
ELISA Yes Yes
IgM detection Rapid tests Yes Yes Yes
ELISA Yes Yes
IgG detection ELISA Yes
IHA Yes
Neutralization assay Yes

ELISA = enzyme-linked immunosorbent assay; IgG = immunoglobulin G; IgM = immunoglobulin M; IHA = indirct
haemagglutination; NS1 Ag =non- structural protein 1 antigen.

4. Clinical spectrum
Following is the spectrum of dengue viral
infection.

Figure-1: Dengue Clinical Spectrum

Dengue Viral infection

Asymptomatic Symptomatic

MILD MODERATE SEVERE

Undifferentiated fever Dengue fever Dengue Hemorrhagic fever

Without Bleeding With bleeding DHF DSS

Page 107

5. Clinical management
Depending upon severity of infection, management
of the cases differs. Early diagnosis & admission of
DHF patients is important in order to reduce case
fatality rates.
5.1. Dengue fever
Management of Dengue fever is symptomatic and
supportive.
Bed rest is advisable during acute febrile phase.
Antipyretics and sponging is essential to keep
body temperature of patient below 370C. Do
not prescribe Salicylates (Aspirin) to suspected
DF patient. Paracetamol is preferred.
Analgesic or a mild sedative may be prescribed
for severe pain.
ORS solution is recommended for patients with
excessive sweating, nausea, vomiting or
diarrhoea to prevent dehydration.
Patients should be monitored in DHF area until
they become afebrile & after platelet &
hematocrit determinations are normal.
5.2 Dengue Hemorrhagic Fever
Management of Grade I DF/DHF
Management during febrile phase is similar to
that of DF.
Patient should be monitored closely. Critical
period for monitoring is transition from febrile
to afebrile stage, which usually occurs after
third day of illeness.
Platelet count & hematocrit estimation is
essential.
Drop in platelet count to <1,00,000/cumm i.e.
1-2 platelets per oil immersion field usually
precedes rise in hematocrit. A rise of more than
20% indicates need for intravenous fluid
therapy.
If hematocrit determination is not possible,
hemoglobin estimation may be carried out as an
alternative.
Hematocrit should be determined daily from
the third day until the temperature remains
normal for one or two days.
Paracetamol is recommended to keep
temperature below 400c. Dosages of
paracetamol recommended are: 1 - 2 years: 60-
120 mg/dose, 3 - 6 years: 120 mg/dose & 7 - 12
years: 240 mg/dose.
Plenty of fluids like ORS & or fruit juices
should be given orally, to the extent patient
tolerates.
Management of Grade II DF/DHF
Any person who has DF with
thrombocytopenia & hemoconcentration &
presents with abdominal pain, black tarry
stools, epistaxis, bleeding from gums etc. needs
to be hospitalized. Such patient should be
observed for signs of shock.
The critical period for development of shock is
transition from febrile to afebrile. phase of
illness, which usually occurs after third day of
illness.
A rise of hematocrit of 20% or more reflects
need for IV fluid therapy.
If despite of treatment, patient develops features
of shock, management of grade III & IV should
be started.
Blood transfusion may be indicated in patients
with severe shock, massive bleeding and DIC.
Page 108
 5.3. Figure-2: Management of grade I & II DHF - Volume replacement flow chart

Hemorrhagic tendencies, Thrombocytopenia, hematocrit rise, pulse

pressure low

Initiate IV therapy 6ml/kg/hr with crystalloid solution for 1 - 2 hours

Improvement No Improvement

Reduce IV 3ml/kg/hr Increase IV 10ml/kg/hr

crystalloid solution, 6-12 hrs crystalloid solution, 2 hrs

Further Improvement

No Improvement
Improvement
Unstable vital signs
Discontinue IV after
24 hrs

Hematocrit rises Hematocrit falls

Reduce IV 6ml/kg/hr
cry. solution, with
further reduction to IV colloid Dextran Blood transfusion
3ml/kg/hr, discontinue (40) 10ml/kg/hr, 10ml/kg/hr,
after 24-48 hrs duration 1 hr duration 1 hr

Improvement

IV therapy by crystalloid. Successively reduce the flow from 10 to 6 & 6

to 3ml/kg/hr. Discontinue after 24 - 48 hours

Improvement: Hematocrit falls, pulse rate & BP stable, urine output rises
No improvement: Hematocrit, pulse rate rises, pulse pressure falls below 20 mm Hg, urine
output falls
Unstable vital signs: Urine output falls, signs of shock

Page 109
 Figure-3: Management of grade III & IV DHF - Volume replacement flow chart

Unstable vital signs

Urine output falls, signs of shock

Immediate, rapid volume replacement: Initiate IV

therapy 10-20 ml/kg/hr crystalloid solution for 1 hr

Improvement No improvement

IV therapy by crystalloid. Oxygen

Successively reduce the flow from 20

to 10, 10 to 6 & 6 to 3ml/kg/hr.

Hematocrit Hematocrit falls

Further RISESRISESNBN
Improvement

IV colloid (Dextran 40) or plasma Blood transfusion 10

Discontinue IV 10 ml/kg/hr as IV bolus (repeat if ml/kg/hr if, hematocrit is
after 24 hrs necessary) still more than 35%

Improvement

IV therapy by crystalloid.

Successively reduce the flow from 10 to 6 & 6 to

3ml/kg/hr. Discontinue after 24 - 48 hours

Page 110
 47. LEPTOSPIROSIS
1. Introduction
Leptospira is an infectious disease caused by
spirochetes leptospire interrogans
Leptospires enter the host through abrasions in the
skin or through intact mucosa, especially the
conjunctiva and the lining of oro- and nasopharynx
when they come in contact with water contaminated
with leptospira.
2. High risk group
Agricultural workers.
Fisherman,sewer workers.
Lorry drivers and masons.
Usually starts at the onset of rainy season and
declines as the rains recede.
3. Anicteric leptospirosis
Acconts for 90% cases, usually recover completely
with proper treatment.
Fever - with chills. Moderate to severe.
Myalgia very characteristic finding. Calf,
abdominal& lumbosacral muscles are very
painful & severely tender. Increase in serum
Creatinine Phosphokinase.
Conjunctival Suffusion reddish colouration.
Headache commonly in frontal region.
Renal involvement is invariable.Asymptomatic
in the form of mild proteinuria with few casts in
urine.
Cough chest pain & few cases hemoptysis.
Bleeding tendency in few cases.
All cases of fever with myalgia & conjunctival
suffusion should be considered as a suspect case
of leptospirosis.
4. Icteric leptospirosis
Weils disease.
Fever, Myalgia, Headache, Conjunctival
suffusion.
Oliguria, anuria, proteinuria.
Nausea, vomitting,diarrhoea, abominal pain.
Hypotension & circulatory collapse.
Jaundice Important clinical feature.
Mild to severe.
Starts after 4 to 7 days of illness.
Hepatomegaly liver tenderness usually present.
Almost invariably present is renal involvement.
ATN and interstitial nephritis are pathologic
features.
Hematuria and cola coloured urine with RBC
casts.
Oliguria and anuria.
Edema, facial puffiness, breathlessness,
convulsions.
Renal impairment worsens in 1st to 2nd week,
recovers by the end of 4th week with treatment.
Lung-Hemorrhagic pneumonitis with interstitial
and alveolar hemorrhages.
High mortality.
Death occurs within few hrs to 2 days.
Mild cases- cough, chest pain and hemoptysis.
Severe cases- breathlessness increases and
patient goes into respiratory failure.
Pancreatitis and acalculous cholecystitis can
occur.
Cardiac involvement
Hypotension shock- cold clammy skin,
tachycardia and hypotension due to dehydration
and peripheral vasodilation.
Arrhythmias- palpitations, syncope and irregular
pulse, AV blocks and ST and T wave changes.
CNS Meningitis usually present. Headache,
irritability, restlessness, seizures and late stage is
coma.
Maculopapular erythematous skin lesions over
face, trunk and extrimities.
Bleeding in leptospira not directly related to the
level of thrombocytopenia.
Page 111

5. Investigations
CBC Thrombocytopenia is characteristic.
LFT direct hyperbilirubinemia., raised
Alk.PO4 ,rise in bilirubin is very fast & reaches
high level.
Rise in enzyme level is not very high as
compared to that in viral or alcohalic hepetitis.
Raised CPK helps to differentiate from viral and
alcoholic hepatitis.
Raised serum creatinine levels.
Urine albuminuria.

Table 1: Lab Investigations for Leptospirosis

CULTURE MICROSCOPY IMMUNOLOGICAL MOLECULAR

Blood (10 days) Dark Field MAT PCR

Urine (10-30 days) Silver impregnation ELISA
CSF (5-10 days) Latex agglutination tests

Labotratory diagnosis for current leptospirosis
Culture positive
MAT- seroconversion/four fold rise in the titre
High titre
ELISA/Latex agglutination positive.
6. Treatment
6.1 Mild Case
Tab. Doxy 100 mg BD for 7 days
Cap. Ampi and Cap. Amox 30-50 mg/kg 5-7
days.
Inj. CP 20 lac units 6 hrly AST for 5-7 days or
Inj ampicillin 500mg-1 gm 6 hrly 5-7 days
6.2 Severe case
Inj. Ceftriaxone/ Cefotaxime or Erythromycin
AVOID NEPHROTOXIC DRUGS in cases with
renal involvement
Severe cases- meticulous correction of
hypovolumia and electrolyte imbalance, fluid
management as per CVP.
Patient with renal failure may require
hemodialysis.
7. Complications
Fluid overload, hyperkalemia, acidosis
LUNG INVOLVEMENT-Continue O2 therapy
In patients with alveolar hemorrhages with
ARDS, they require mechanical ventilation with
low tidal volume and high PEEP.
Mortality is very high.
Supportive treatment with Platelet conc, FFP, Vit
K.

Page 112
 48. INFLUENZA A- H1N1 (SWINE FLU)
We have faced pandemic of this Communicable air
borne disease in 2009. This is commonly known as
swine flu.
1. Epidemiological factors
Pandemic Influenza A (H1N1) 2009, currently the
most common circulating strain of influenza virus
globally, first caused illness in Mexico and the
United States in March and April, 2009.
2. Agent factors
The causative agent is Influenza virus. It is an
enveloped RNA virus and belongs to the family
orthomyxoviridae. The size of the virus is 80-200 nm
/.08 -0.12 micron in diameter. There are three types
of influenza viruses, namely A, B & C which are
characteristically distinct and bear no cross
immunity. The virus contains two surface antigens H
(hemagluttinin) and N (neuraminidase).
3. Host factors
The disease can occur in all ages and both sexes.
4. High Risk Groups
These risk groups include:
Children younger than 5 years old;
Adults 65 years of age and older;
Chronic pulmonary condition (including
asthma), cardiovascular (except hypertension),
renal, hepatic, hematological (including sickle
cell disease), neurologic, neuromuscular, or
metabolic disorders (including diabetes
mellitus);
Immunosuppression, including that caused by
medications or by HIV;
Pregnant women;
Residents of nursing homes and other chronic-
care facilities;
Obesity.
5. Mode of transmission
Influenza spreads form person to person by droplet
infection created by sneezing, coughing or talking.
The portal of entry is the respiratory tract.
6. Incubation period
It could range from one to seven days, and most
likely from one to four days.
7. Signs and symptoms
An acute Respiratory Tract Infection (RTI), caused
by Influenza virus, characterised by sudden onset of:
Fever/chills, Headache, myalgia, Sore throat, Cough,
Coryza, and Prostration.
Range of symptoms differs by age. Vomiting &
diarrhea in children/elderly. Fever alone in infants
may be atypical in elderly. Serious complications can
occur among high risk groups.
8. Diagnosis
The recommended test to confirm the diagnosis of
H1N1 influenza A virus is real-time Polymerase
Chain Reaction (RT-PCR) in designated laboratories.
Also viral culture and four-fold rise in new influenza
A (H1N1) virus-specific eutralizing antibodies can be
done.
8.1. What sample to be collected?
Nasopharyngeal/oropharyngeal swabs.
Brochoalveolar lavage.
Tracheal aspirates.
Nasopharyngeal/oropharyngeal aspirates as
washes.
Samples should be collected in VTM.
8.2. Transportation of samples:
All samples should be kept at 2-8 degree Celsius
until they can be placed at -70 C.
Samples transported on dry ice in triple
packaging.
Clear labels with patients complete information.
Samples should be sent to within 24 hrs.
Page 113
9. Treatment
Treatment with oseltamivir or zanamivir is
recommended for all people with suspected or
confirmed influenza who require hospitalization. It is
given in a dose of 75 mg Bid in adults.
All individuals seeking consultations for flu like
symptoms should be screened at healthcare facilities
both Government and private or examined by a
doctor and these will be categorized as under:
9.1. Category- A
Patients on long term cortisone therapy.
Obese persons.
No tests for H1N1 is required for Category-B
(1) and (2).
All patients of Category-B (1) & (2) should
confine themselves at home and avoid mixing
with public and high risk members in the family.
Broad Spectrum antibiotics as per the Guideline
for Community-acquired pneumonia (CAP) may
be prescribed.

Patients with mild fever plus cough / sore

throat with or without bodyache, headache,
diarrhoea and vomiting will be categorized as
Category-A. They do not require Oseltamivir
and should be treated for the symptoms
mentioned above. The patients should be
monitored for their progress and reassessed at 24
to 48 hours by the doctor.
No testing of the patient for H1N1 is required.
Patients should confine themselves at home and
avoid mixing up with public and high risk
members in the family.
9.2. Category-B
9.3. Category-C
In addition to the above signs and symptoms of
Category-A and B, if the patient has one or more of
the following:
Breathlessness, chest pain, drowsiness, fall in
blood pressure, sputum mixed with blood, bluish
discolouration of nails;
Children with influenza like illness who had a
severe disease as manifested by the red flag signs
(Somnolence, high and persistent fever, inability
to feed well, convulsions, shortness of breath,
difficulty in breathing, etc).
Worsening of underlying chronic conditions.

1. In addition to all the signs and symptoms

All these patients mentioned above in Category-C
mentioned under Category-A, if the patient has
require testing, immediate hospitalization and
high grade fever and severe sore throat, may
treatment.
require home isolation and Oseltamivir;
2. In addition to all the signs and symptoms
mentioned under Category-A, individuals having 9.4. Oseltamivir Medication -Doses
one or more of the following high risk conditions Details
shall be treated with Oseltamivir:
Children with mild illness but with predisposing Oseltamivir is the recommended drug for treatment.
risk factors.
In the current phase, if a person confirms to the case
Pregnant women;
definition of suspect case, should be provided
Persons aged 65 years or older;
Patients with lung diseases, heart disease, liver Oseltamivir.
disease,kidney disease, blood disorders, diabetes,
neurological disorders, cancer and HIV/AIDS;

Page 114
 Dose for treatment is as follows:
By Weight:
For weight <15kg 30 mg BD for 5 days
15 -23kg 45 mg BD for 5 days
24 -<40kg 60 mg BD for 5 days
>40 kg 75 mg BD for 5 days

risk persons (DM, HT, Obese, Respiratory diseases,

10. Vaccine Immuno comproised).
A Vaccine is available for swine flu. It gives imunity
for one year. It is given to pregnant mothers, high

Page 115
 49. DIARRHOEAL DISEASES
Diarrhoeal diseases include acute diarrhoea,
persistent diarrhoea (diarrhoea duration two weeks
or more) and dysentery (blood stained stools with
fever). Diarrhoeal diseases are one of the most
common causes of epidemic in our State. Most of
the deaths in diarrhoeal diseases are due to
dehydration which is preventable by timely and
adequate replacement of fluids.
1. Following are important
causes of diarrhoeal
diseases in rural areas
Acute diarrhoea Cholera, Rota virus, Food
poisoning, gastrointestinal disorders and
medications (rare).
Persistent diarrhoea Chronic bacterial
infections, inflammatory bowel disorders,
malabsorption syndrome.
Dysentery Amoebiasis, Giardiasis,
Shigellosis.

Table-1: Diagnosis of diarrhoea

Sign/symptom Acute diarrhoea Persistent diarrhoea Dysentery
Frequency of stools/day Three or more Three or more Three or more
Consistency of stools Watery Variable Variable
Duration of diarrhea Less than 2 weeks Two or more weeks Less than 2 weeks
H/o fever No Variable Yes
H/o blood stained mucus No Variable Yes
Effect on appetite No Loss of appetite Loss of appetite
Dehydration Important, may lead to Patient may have Patient may have
severe dehydration if not some dehydration. some dehydration
treated in time.
Treatment principle Management of Start management of Start management of
dehydration is priority dehydration. dehydration.
Simultaneously find Simultaneously start
cause of persistent appropriate
diarrhoea and treat antibiotics.
accordingly.
Long term effects No long term effect for If not treated Repeated attacks may
occasional episodes. correctly, child may lead to Protein
Repeated attacks may get severe Protein Energy Malnutrition
lead to PEM. Energy Malnutrition

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 Table-2: Dehydration Diagnosis Chart
Severity of symptoms and signs (Encircle the finding)
Sign/Symptom
No dehydration Some dehydration Severe dehydration
General condition of Patient well alert Restless and irritable Lethargic, unconscious,
Patient floppy
Presence of thirst Normal/not thirsty Thirsty, drinks water Not able to drink
immediately when
offered
Dryness of mouth and Moist mouth and tongue Mouth and tongue dry Mouth and tongue very
tongue dry
Condition of eyes Normal Sunken Very sunken, patients
face looks like old
man's face.
Condition of tears Tears appear while Tears appear while No tears, dry eyes even
crying crying in crying child
Skin turgor Normal. Pinch to skin Pinch slowly goes back Pinch remains as it is
immediately goes back and takes some time to for 2-3 seconds and then
to normal. become flat. slowly goes back.
Classification of No dehydration Some dehydration Severe dehydration
dehydration
Treatment of Plan A Plan B Plan C
dehydration

Symptoms and signs of cholera are entirely due to

2. Important diseases causing loss of large volume of isotonic fluid and resultant
diarrhoea or dysentery in depletion of intravascular and extra vascular fluid
leading to severe dehydration, metabolic acidosis
adults and hypokalemia. Patient develops thirst, cramps,
Cholera and anxiety due to depleting isotonic fluid.

Cholera is the most important diarrhoeal disease Diagnosis

which leads to rapid dehydration. Suspect cholera when patient has severe watery
Etiologic agent diarrhoea and vomiting. Collect stool sample of
suspected cases in Cary Blair media and transport to
Cholera is caused by bacteria Vibrio cholerae which District Public Health Laboratory. However,
exists in two biotypes, Classical and El tor. Each treatment and control measures should be started
biotype is further divided into two subgroups Inaba immediately on the basis of clinical
and Ogawa. symptomatology without waiting for laboratory
Clinical manifestations confirmation.

Cholera is an acute infection of small intestine Treatment

manifested as watery diarrhoea and vomiting.
Clinical spectrum of cholera is broad, ranging from
in-apparent infection to cholera gravis, which may
be fatal in few hours. Incubation period of 24 to 48
hours is followed by abrupt onset of painless,
profuse and watery diarrhoea associated with
vomiting.
Carefully examine patient for signs of dehydration
and treat as per dehydration status. Most important
treatment of cholera is rehydration of patient with
ORS and Ringers Lactate. In addition to this, start
one of the following antibiotics to patient -
Cap. Doxycycline 6 mg/kg/ day as a single
dose for 3 days OR

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 Cap. Tetracycline 50mg/kg/day in 4 divided
doses for 3 days OR
Tab. Erythromycin 30mg/kg/day in 3 divided
doses for 3 days.
3. Diagnosis of dehydration
Although number of organisms are responsible for
causing diarrhoea, clinical presentation is same i.e.
passage of watery stools leading to dehydration in
all these cases. Therefore assessment of
dehydration status and correct management of
dehydration by ORT is mainstay of diarrhoeal
disease control programme.
4. Management of
dehydration
Most important aspect in management of diarrhoeal
diseases is correction of dehydration.
Treatment of dehydration is divided into three plans
as follows -
Plan-A: For patients with no dehydration
principle is to prevent dehydration.
Plan-B: For patients with some dehydration
principle is treatment of some dehydration and
preventing patient from going into severe
dehydration.
Plan-C: For patients with severe dehydration -
This is life saving plan. Rehydrate patient as
early as possible and prevent from going again
into severe dehydration.
Description of treatment plans in details is as
follows.
4.1. Plan-A
Plan-A is for patients who are having diarrhoea but
no signs of dehydration.
Dissolve the packet in one litre of water to prepare
ORS.
Show caretaker how to prepare ORS.
Following steps should be carried out for
preparation of ORS -
Take clean pot of one and half litre capacity
and one clean spoon.
Pour 1 litre of clean drinking water in the pot.
(No need to boil water).
Principle of treatment
As diarrhoea is continuing, there is continuous loss
of water and electrolytes from body of patient
which may lead to dehydration. Therefore principle
of Plan-A schedule is correction of whatever loss of
water and electrolytes before the patient develops
signs of dehydration. Plan-A can be advised at
home to caretaker of patient. However make sure
that care taker has understood danger signs of
dehydration (like thirst). Following steps are
recommended in Plan-A.
a. Home available fluids
Advise to give Home Available Fluids (HAF)
e.g. sarbat, lassi, vegetable soup, khir,
buttermilk, tea, coconut water, etc. i.e. any
liquid available at home to patient as much
he/she can drink.
Continue breast feeding and feeding If child
is being breastfed, then breast-feeding should
be continued. Regular feeding of non-breast fed
child should also be continued.
b. ORS to prevent dehydration
If frequency and amount of diarrhoea is not
declining or amount of stool is large, then start
ORS.
Contents of WHO ORS are as follows (New
low osmolarity ORS).
Sodium chloride - 2.6 grams
Potassium Chloride - 1.5 grams
Trisodium Citrate - 2.9 grams
Glucose - 13.5 grams
Add whole packet of ORS into one-litre of
water and stir till all powder is dissolved. Now
ORS is ready for use.
Give ORS by cup or spoon to small children
and by glass to bigger children and to adults as
per indicated dose.
If patient has vomiting, wait for 5 minutes and
start again.
Keep ORS covered. Once prepared ORS should
be used within 24 hours. Do not use ORS
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 beyond 24 hours, as there are chances of Less than 6 months - 50ml
contamination.
6 months to 2 years - 50 - 100 ml
If child develops swelling on eyelids, stop ORS
2 to 5 years - 100 - 200 ml
as it indicates overdose.
Ask her to give ORS in following doses after
passage of each liquid stool.
4.2. Plan -B Principle of treatment

Start Plan-B treatment to patients showing signs and Patient with some dehydration should be given ORS
symptoms of some dehydration as per dehydration for correction of dehydration.
diagnosis chart. Aim of this plan is to correct Dose of ORS: Dose of ORS is calculated preferably
dehydration and prevent patient from going into according to weight of patient. Give ORS in a dose
severe dehydration. of 100ml/kg in 4 hrs. If weighing is not possible,
calculate age wise ORS requirement for four hours
as follows
Table -3: Age wise ORS requirement for four hours
Age < 4 months 411 months 1223 months 2 4 years 5 14 years 15 + years
Dose 200-400 ml 400 600 ml 600 800 ml 800 1200 ml 1200 2200 ml 2200-4000 ml

Continue breast feeding and feeding If child is Re-examination of patient

being breastfed, then breast-feeding should be Re-examine patient after every four hours for status
continued. Regular feeding of non-breast fed child of dehydration with the help of Dehydration.
should also be continued.

Table-4: Management advice based on re-examination findings

Condition of patient on re-examination
Patient improves, no signs of dehydration on
examination and diarrhoea stops
Patient improves, no signs of dehydration on
examination but diarrhoea continues
Dehydration status same
Signs of severe dehydration appear
Management advise
Keep patient under observation for 24 hours. Continue
HAF. Observe if diarrhoea and/or vomiting start again.
Continue giving ORS in doses suggested in Plan-A, re-
examine after four hours.
Continue with Plan-B. Check whether ORS is being
given in correct dose. Re-examine after four hours.
Switch on to Plan - C (start IV fluids). Continue to give
ORS as much as possible.

4.3. Plan C
If signs and symptoms of patient are suggestive of
severe dehydration, start Plan C. This is
emergency plan. Incorrect or incomplete
management of severely dehydrated patient may
lead to death of patient. Medical Officer must
personally examine patient and treat for severe
dehydration.
Principles of management
Principle of management of severe dehydration is
replacing fluid loss by giving rapid IV infusion.
Only Ringer's lactate should be used as IV fluid and
the dose is 100ml/kg body weight.

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 Table -4: Details of Ringers Lactate administration
Duration of
Age group Intensive phase Maintenance phase Remarks
treatment
Infants (0-1 30-ml/kg body wt. 70ml/kg body wt in Assess patient after
6 hrs
year) during first 1 hour. next 5 hours. every 6 hours
Older children 30-ml/kg body wt. 70ml/kg body wt in Assess patient after
3 hrs
and adults in first half hour. next 21/2 hrs. every 3 hours
Re-examination of patient dehydration with the help of dehydration diagnosis
chart and decide management plan as follows -
Re-examine patient after every six hours in infants
and three hours in adults for status of
Table-5: Treatment advice based on condition of patient
Condition of patient Treatment advise
Patient improves, no signs of dehydration on Keep patient under observation for 24 hours as patient
examination and diarrhoea stops may start diarrhoea/vomiting again
Patient improves, no signs of dehydration on Continue giving ORS (Plan-A)
examination but diarrhoea continues
Patient improves, signs of some dehydration Stop IV fluids after required dose is administered.
on examination. Continue giving ORS (Plan-B)
Dehydration status same Continue with Plan-C. Check for any complications
like anuria. If yes carefully examine the patient and
decide for referral. Continue giving IV during
transportation of patient.

ORS or Oral rehydration therapy (in case ORS is

5. Use of antibiotics and not available), irrespective of type of dehydration.
other drugs Zinc administration as per age of child:

Antibiotics are recommended only to suspected a) Children from 2-6 months:

patients of cholera and dysentery. Other drugs like
anti motility drugs, binding agents, anti secretary
agents and steroids are not of any use in
management of diarrhea. They are harmful to
patients and therefore not at all recommended for
treatment. Judicious use of antibiotics is appropriate
in selected patients. Severely ill patients with febrile
dysentery can be treated with ciprofloxacin 500mg
bd for 3-5 days.
Use of Zinc Tablets
Zinc Dosage Recommendation:
Zinc is very safe drug and has a very large window
of safety. Zinc dispersible tablets are to be given in
each diarrhoeal episode along with low osmolality
Children aged between 2-6 months should be given
10 mg of elemental zinc per day for a total period of
14 days from the day of onset of diarrhoea. A tablet
of zinc contains 20 mg of elemental zinc. Therefore
half tablet should be given to the children in this age
group. Zinc when supplied in the form of
dispersible tablets, easily dissolves in breast milk or
water. Therefore, in infants below 6 months of age,
the tablet should be given by dissolving in breast
milk and in infants above 6 months of age, it should
be given by dissolving in breast milk or water.
b) Children above 6 months:
One full tablet (20mg) should be given to all
children with diarrhoea above 6 months of age. It
should start from the day of onset of diarrhoea and
continued for a total period of 14 days.

Page 120
 50. RHEUMATOID ARTHRITIS
1.Introduction
Rheumatoid arthritis (RA) is a chronic inflammatory
disease of unknown etiology marked by a symmetric,
peripheral polyarthritis. It is the most common form
of chronic inflammatory arthritis and often results in
joint damage and physical disability.
2. When to suspect
The incidence of RA peaks between 25 and 55
years of age.
Figure-1: Hand changes in RA
Extra-articular features
i. Neurologic-atlanto-axial dislocation, cervical
myelopathy.
ii. Hematological-anemia of chronic disease,
neutropenia, splenomegaly, feltys syndrome.
iii. GI-vasculitis.
iv. Skeletal- osteoporosis.
v. Ocular-episcleritis, scleritis,
keratoconjunctivitis sicca.
vi. Oral -xerostomia, periodontitis.
vii. Pulmonary pleural effusion, pulmonary
nodules, interstitial lung disese, pulmonary
vasculitis, organizing pneumonia.
viii. Cardiac- pericarditis, IHD, myocarditis,
cardiomyopathy, mitral regurgitation.
ix. Renal membranous nephropathy.
x. Skin rheumatoid nodules, pyoderma
gangrenosum.
Early morning joint stiffness lasting more than 1
hour and easing with physical activity.
Earliest involved joints typically the small joints
of the hands and feet.
The wrists, metacarpophalangeal (MCP), and
proximal interphalangeal (PIP) joints stand out
as the most frequently involved joints.
Flexor tendon tenosynovitis is a frequent
hallmark of RA.
Deformities are swan-neck deformity,
boutonnire deformity, Z-line deformity.
3. Investigations
The clinical diagnosis of RA is largely based on signs
and symptoms of a chronic inflammatory arthritis,
with laboratory and radiographic results providing
important supplemental information.
3.1 Rheumatoid factor
Serum IgM RF found in 75-80% of RA patients;
therefore the negative result does not exclude RA.
Found in other connective diseases as well.
3.2 Anti CCP antibodies
Highly specific 95%
So, useful for distinguishing RA from other forms of
arthritis.
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3.3 Synovial fluid analysis-
Inflammatory state.
Synovial fluid WBC count ranges from 5000 to
50000 WBC/u3.
Useful for confirming inflammatory arthritis,
excluding infection or crystal induced arthritis.
Other findings include soft tissue swelling,
symmetric joint space loss, subcondral erosions.
3.5 MRI
Offers greatest sensitivity for detecting synovitis,
joint effusions as well as early bone and bone marrow
changes.

3.4 X ray hands

Juxta articular osteopenia, 4. Treatment
Table-1: Treatment of RA

Non pharmacologic treatment Pharmacologic treatment

Counselling, physical therapy, diet NSAIDS
Stress reduction, exercise Glucocorticoids
DMARDS

4.1 NSAIDs 4.3 DMARDS

Tab. Ibuprofen (200 mg BD or TDS) / Tab.
Diclofenac (50 mg BD) - Now considered to be
adjunctive therapy for management of symptoms
uncontrolled by other measures.
4.2 Glucocorticoids
May be administered in low-to-moderate doses to
achieve rapid disease Control before the onset of
fully effective DMARD therapy, which often takes
several weeks or even months.
Hydroxycloroquine, Methotrexate, Leflunomide,
Sulfasalazine, Biologicals, anti TNF agents,
Rituximab.
5. When to refer
Severe case of rheumatoid arthritis not responding to
first line therapy (Hydroxycloroquine, Methotrexate,
NSAIDS), with extra articular manifestations should
be referred to Higher institute for further work up.

Page 122
 51. SNAKE BITE
Immobilisation of the part, Getting to Hospital
1. Introduction without delay and Telling the doctor of any
Envenoming by poisonous animals (Snakes, symptoms that develops.
Scorpions, Wasps, Ants and Spiders) is an
occupational hazard often faced by farmers, farm
laborers. Poisoning by venomous snakebite is a 2. Common Poisonous snakes
common acute life-threatening time-limiting medical
emergency.The majority of current first aid methods in India
adopted by the victims such as tourniquet, cutting and
suction and herbal remedies are completely (1) Cobra (2) Krait (3) Russells Viper (4) Saw
ineffective and dangerous. It is now recommended to Scaled Viper (5) Indian Pit Viper
adopt what has been called the Do it R.I.G.H.T. (6) Sea snake
approach, stressing the need for Reassurance,

HISTORY OF SNAKE BITE

ABSENT LOCAL EDEMA PRESENT

Floor bed BLEED

Neuroparalysis DIC Bleeding
SHOCK
Abdominal colic l RF

Pain Pain

Neuro-paralysis

RUSSELLS ECHIS
KRAIT COBRA VIPER CARINATUS

ASV, Ventilator ASV, N + A, ASV, Dialysis, ASV, Dialysis,

N+A Ventilator Blood transfusion Blood transfusion

Snake Bite: Diagnostic Algorithm and Treatment

(ASV- Antisnake venom, N- Neostigmine, A- Atropine, RF- renal failure, DIC- Disseminated intravascular
coagulation)

(Bungarus Caeruleus)
3. Clinical manifestations
Local Names- Kala gandait, Kala taro, Kandar,
3.1. Common Indian Krait Manyar chitti, kattu viriyan and valla pamboo.The

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common krait is regarded as the most dangerous AChEI or not can be confirmed by putting ice-filled
species of venomous snakes in the Indian glove finger over eyelid. Hypothermia sensitizes the
subcontinent. Majority of krait bite cases are reported Ach receptors of acetyl choline. If there is slight
between 11pm 5 am. improvement in ptosis, you can try AChEI.
Neostigmine 50ug/kg over first hr. & then 25 ug/kg
Symptoms
in the next hour preceded by Atropine
Mild pain at the site
Parasthesia or numbness 3.2. Cobra Bite
Abdominal pain/vomiting/chest pain Cobra bite tends to occur during day time.
Difficulty in bringing tongue beyond teeth
margin Symptoms
Slurred speech Pain at site
Difficulty in breathing Progressive swelling /ecchhymosis
Signs Blurred vision

Bradycardia, hypotension Signs

Bilateral ptosis, external ophthalmoplagia, Sinus bradycardia, hypotension
dysphagia Ptosis, bulbar palsy
Paralysis, coma Respiratory depression
Management Management
(a) First aid at home or place where bite happens: Victim should not be allowed to walk or run and the
If one succeeds in locating the bite site on the bitten part should be kept below heart level.
victims body, clean the surface where venom is On arrival 100ml (10 vial) ASV to be added to 200
deposited by clean cloth or cotton. Keep the bitten c.c. of normal saline run over 30-50 minutes.
part below heart level.
Maximum dose 200-250ml (20-25 vials).
Neostigmine 50ug/kg over first hr. & then 25 ug/kg
(b) At hospital: in the next hr preceded by Atropine
Thorough clinical examination including If patient develop respiratory paralysis intubate the
neurological exam patient and refer to higher centre
Haemogram, urine exam, ECG, serum electrolytes, Local wound care is done by intravenous antibiotic,
renal profile sterile dressing and skin grafting of all victims with
Anti-snake venom (ASV): non-healing wound.

- On arrival 100ml (10 vials) ASV to be added to 3.3. Sea snakes

200 cc of normal saline run over 30-50 minutes. Sea snake bite cases are reported from coastal region.
- Repeat dose of 100ml (10 vials) after 30 min if Fishermen accidentally handle sea snake resulting in
no improvement in neurological manifestation. envenoming. Its venom is neurotoxin, myotoxic and
haematotoxic.
- Maximum dose 200ml (20vials).
Symptoms
Ventilation
Indicated if victim has pooling of saliva, unable to lift Headache
the neck from pillow, reduction in oxygen saturation, Nausea
respiratory failure, abdominal-thoracic respiration, Vomiting
suffocation and signs of cerebral hypoxia. Tinglingnumbness
Refer the patient to higher centre with intubation and Foreign body sensation in throat
Ambu bag ventilation Swelling of tongue
Severe muscle pain
Anticholine esterase inhibitor (AChEI): Brown coloured urine
Indian common krait venom contains both pre and Signs
post synaptic blocker. Whether victim responds to

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 Trismus
Muscular paralysis
Respiratory arrest
Myoglobinuria
Management
On arrival 100ml (10 vial) ASV to be added to 200 cc
of normal saline run over 30-50 minutes.
Ventilator for respiratory failure. Refer to higher
centre with intubation.
Correction of hyperkalemia- Calcium gluconate,
insulin glucose drip (10% dextrose 100ml add 12
units insulin for 6hrs), salbutamol nebulization or
dialysis.
3.4. Russells viper
It is found in South Asian Countries. In Pakistan,
India, Sri Lanka, Bangladesh, Burma and Thailand it
ranks amongst the most important causes of snakebite
mortality. With protecting the paddy, wheat by
containing rodents (rats), the Russells viper kills
many farmers unlucky enough to treat on it during
harvesting.
Symptoms
Severe local pain at the site of bite.
Rapid swelling progresses to whole limb
within six to eight hours.
Signs
Regional lymphagntis with ecchymosed
skin.
Development of compartment syndrome
characterized by swelling, hypotension and
shock.
Renal dysfunction
20-40% cases subsequently develop anuria, oliguria,
acute renal failure. Renal angle tenderness is most
important clinical sign for early diagnosis of renal
failure. There is serial rise in blood urea and serum
creatinine with acidosis and hyperkalaemia.
Generalized anasarca, renal failure is due to tubular
damage by venom itself.
Hemoglobinuria, hypotension and micro thrombi in
the kidney contribute to the acute tubular necrosis
which is the most common cause of death. Ptosis,
bulbar palsy, internuclear opthlamoplegia and
respiratory paralysis due to presynaptic
neuromuscular block in a Russells viper bite
poisoning are often seen and reported from kerala
(South India) and Sri Lanka.
Management
- No tourniquet
- Bitten part should be kept below heart level
- No intramuscular injection unless 20MWBCT is
done and blood clots within 20 minutes.
20 minutes whole blood clotting test (20 MWBCT)
Before injection of ASV take 2-3 ml of blood in a
new dry glass test tube which is not irrigated by any
detergents. Keep the tube undisturbed for 20 minutes
and then tip it off. If blood does not clot, it confirms
hypofibrinogemia. ASV 100 ml (10 Vials) ASV
diluted in 200 ml of 5% dextrose run over 30 minute
by intravenous route. If external bleeding does not
stop within 20-30 minutes one can repeat 50 ml of
ASV. Thrombocytopenic, abnormal fragmented
RBCs are a diagnosis of DIC. In addition, if victim
is too late in such situation in addition to ASV one
has to try plasma products and whole blood
transfusion which is rarely required if ASV is
administered in time with adequate dose.
Hypotension is to be managed with fluid and
inotropic agents. Severe hypotension due to bleed in
adrenal and pituitary glands and abdominal bleed and
endothelial dysfunction with capillary leak needs
heavy doses of intravenous methyl-prednisolone and
correction of electrolytes.
Renal failure
One should keep in mind and look for renal failure
from the time of admission. Risk factors such as
hypotension, hypovolumia can be corrected.
Intravenous frusemide 80-100 mg and oral acetyl
cysteine 600mg three times a day may help to arrest
the renal damage.
Refer to higher centres for haemo-dialysis, if needed.
3.5. Saw scaled viper or Carpet
viper or Echis-cariniatus
Farmers, hunters, labourers and persons walking bare
foot or in jungle and rocky areas are often bitten by
this snake.
Clinical manifestations
Soon after the bite within one hour there is
development of swelling over the bitten part.
Swelling progresses in more than one segment. The
victim experiences a painful lymphadenopathy at the
drainage area of the bitten part.
At times if the patient remains untreated, bleeding
persists for 1-2 weeks in the form of blood stain
sputum, haematuria and disappears on its own. Such
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patients are markedly anemic and report to hospital
for weakness or non-healing cellulites with
uncontrolled bleeding from cellulites.
Management
Local wound care
ASV required is 30-50 ml
3.6. Green pit viper and bamboo
pit (Trimeresurus)
Pit viper victims report during the monsoon season.
Clinical manifestation
It shows up in sudden rapid development of massive
edema without regional involvement. Rarely the
victim manifests external bleeding or renal failure.
Management
Antivenom should be administered as soon as signs
of systemic or severe local swelling are noted.
The mean times between envenoming and death are
8 hours (12 minutes to 120 hours) in cobras,
18 minutes (3-63 hours) in bungarus caeruleus,
3 days (15 minutes to 264 hours in Russells viper
5 days (25 to 41 days) for echis carinatus.
The approximate serum half life of antivenom in
envenomed victims ranges from 26 to 95 hours.
Before discharge envenomed victims should be
closely observed daily for minimum 3 to 4 days.
ASV doses and repeat doses
The recommended initial dose of ASV is 8 to 10 vials
administered over 1 hr.
Repeat doses for neurotoxic species is based on 1-2
hr rule.
Repeat doses for haematotoxic species is based on
the 6 hr rule.
The maximum recommended dose for neurotoxic bite
is 20 vials of ASV.
The maximum recommended dose for haematotoxic
bite is 30 vials of ASV.
ASV Reactions
No ASV test doses are to be administered.
At the first sign of an adverse reaction the ASV is
halted
Adrenaline 0.5 ml is given SC
Steroid and antihistamine perform a secondary
supportive function to Adrenaline.
(National Snakebite Management Protocol 2008)
Page 126
 52. SCORPION STING
1. Introduction
Scorpion envenomation is an occupational
hazard for farmers, farm labourers, migrating
population and hunters.
The endemic areas are western Maharashtra,
Karnataka and Konkan Region.
Severe Scorpion stings are due to
MesobuthusTamulus species of scorpion.
2. Clinical features
2.1. The venoms of genera Hadrurus,Vejovis and
Uroctonus has local effects only including sharp
burning, swelling and discoloration at the bite site.
2.2. The second type of venom produced by the
genera of the poisonous varieties of Centruroides and
Mesobuthus contain neurotoxins which block sodium
channels. This leads to spontaneous depolarization of
parasympathetic and sympathetic nerves which
results in stimulation.
In adults, the first time is rarely dangerous. But if the
second time, the person may die if not treated soon.
The body becomes allergic after the first sting. So it
is important to find out if he had an earlier scorpion
sting.
2.3. Severe pain, redness and swelling at the site of
the sting.
2.4. Clinically autonomic storm evoked due to
venomous envenoming is characterized by transient
parasympathetic stimulation- vomiting, profuse
sweating, ropy salivation bradycardia, ventricular pre
mature contraction, priapism in male, hypotension
and prolonged sympathetic stimulation - cold
extremities, hypertension, tachycardia, pulmonary
edema and shock.
3. Gradation
On basis of clinical manifestations at the time of
arrival to hospital and according to severity they are
graded in 4 grades.
Grade 1: Severe excruciating local pain at the
sting site radiating along with corresponding
dermatomes, mild local oedema with sweating at the
sting site, without systemic involvement.
Grade 2: Pain, paresthesias remote from the site
of sting, in addition to local findings.
Grade 3: Either cranial nerve / autonomic
dysfunction.
Cold extremities, tachycardia, hypotension
(Respiratory rate > 24 perminute, basal rales or
crackles in lungs).
Grade 4: Combined cranial nerve / autonomic
dysfunction and somatic nerve dysfunction.
4. Investigations
ECG- Tall T waves is a common finding. Others are
atrial arrhythmias, non sustained ventricular
tachycardia, and various conduction defects seen.
Chest Xray- shows pulmonary edema.
5. Management
If it is for the first time in adult, do the following:
Give Paracetamol if possible, put ice on sting.
Infiltration of site with local anaesthetic may
relieve pain and anxiety.
Anti histaminic tablets can be given
If the sting is for the second time in adult, or is
in children under 5, do the following
- IV Fluid management
- Inj. Scorpion antivenom 30ml in 200ml of
normal saline neutralises circulating venom.
- If evidence of myocarditis and pulmonary
oedema, strict bed rest and management of
heart failure is indicated.
- Prazosin 0.5mg 3hrly orally for first 2 days
(or 0.25mg in children and for adults) is
acceptable therapy
- Injection Frusemide 20 to 60mg I.V. to
control Pulmonary edema
- Inj.Dobutamine 5-20 microgram/kg/min I.V.
given in heart failure, tachycardia ,
pulmonary edema with warm extremities
- Patients in Pulmonary edema may need inj
NTG drip 5 microgram/kg
Page 127
 - At times with severe respiratory distresss mechanical ventilation.
may need non invasive ventilation or

Stage- 1 - Stage- 2 Stage-3 - Stage-4 - Stage-5 -

(0-4hrs) (4-6hrs) (6-10hrs) (10-12hrs) (>12hrs)

- - - - - - - - - -
Sweating Hypertension - Tachycardia - Massive - Warm -
Salivation Tachycardia Hypotension pulmonary extremities
Mydriasis Cold extremiries Pulmonary edema edema Tachycardia
Priapism Cold extremities Hypotension
Hypertension Pulmonary
Hypotension edema
Cold Gray
extremities pallor(warm
shock)

- - - - - - - - - -
ASV + Prazosin ASV + - ASV +Prazosin - ASV - Dobutamine -
Prazosin + +
Dobutamine SNP or NTG
+
NIV/MV

Scorpion sting: stages, clinical presentation and treatment.ASV Anti Scorpion Venom, SNP- Sodium Nitro
Prusside, NTG- Nitroglycerine, NIV-Non inavasive ventilation, MV Mechanical Ventilatioin

Page 128
 53. DOG BITE (RABIES)
Rabies can be transmitted by dog bites or licks of
rabid animals on abraded skin and intact mucosa.
Other animals which can transmit rabies are cat,
monkey, horse, sheep, goat, mongoose, jackal, fox,
hyena and bat. Exposure to rodents, rabbits and hares
seldom, if requires specific anti-rabies treatment.
1. Clinical features
Prodromal symptoms- such as headache, malaise,
sore throat and fever last about 3-4 days. Pain and
tingling at the bitten site.
Stage of excitation- Patient is intolerant to noise;
bright light or a cold draught. Aerophobia may be
present. Hydrophobia is a characteristic symptom of
rabies. Examination shows increased reflexes,
dilatation of pupils, increased sweating, lacrimation
and salivation. Mental changes include fear of death,
anger, irritability and depression. Convulsions may
occur resulting in death.The last stage is that of
paralysis and coma. The total duration of illness lasts
for 2-3 days.
Table-1: WHO Guide for post-exposure treatment against rabies
Category
Type of contact with a suspect or confirmed rabid
domestic or wild animal or animal unavailable for
observation
I. Touching or feeding of animals Licks on
intact skin
II. Nibbling of uncovered skin Minor scratches
or abrasions without bleeding Licks on
broken skin
III. Single or multiple transdermal bites or
scratches Contamination of mucous
membrane with saliva (i.e. licks)
A. Exposure to rodents, rabbits and hares seldom, if ever, requires specific anti-rabies treatment
B. If an apparently healthy dog or cat in or from a low-risk area is placed under observation, The situation
may warrant delaying initiation of treatment.
Treatment (post-exposure prophylaxis)
2. Categories of dog bite
Category I Touching or feeding animals, licks
on the intact skin
Category II Nibbling of uncovered skin, minor
scratches or abrasions without bleeding, licks on
broken skin
Category III Single or multiple transdermal
bites or scratches, contamination of mucous
membrane with saliva from licks; exposure to
bat bites or scratches
The WHO recommended classification of animal bite
for post-exposure treatment should be followed.
Every instance of human exposure to a suspected
rabid or wild animal must be treated as a category III.
The post-exposure treatment is a three-pronged
approach. All three carry equal importance and
should be done simultaneously:
Recommended treatment.
None, if reliable case history is available
Administer vaccine immediately. Stop treatment if
animal remains healthy throughout an observation
period of 10 days or if animal is killed humanely and
found to be negative for rabies by appropriate
laboratory techniques
Administer rabies immunoglobulin and vaccine
immediately. Stop treatment if animal remains healthy
throughout an observation period of 10 days or if
animal is killed humanely and found to be negative
for rabies by appropriate laboratory techniques.
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 C. This observation period applies only to dogs and cats. Except in the case of threatened or endangered
species, other domestic and wild animals suspected as rabid should be killed humanely and their tissues
examined using appropriate laboratory techniques.
3. Treatment of dog bite
3.1. Management of wound
Immediate washing of the wound is a priority.
Wound toilet must be done even if several hours or
days have elapsed. The wound is immediately
flushed and washed with plenty of soap and water
(avoid direct touching of wounds with bare hands).
Punctured wounds should be irrigated with the help
of catheters followed by 70% alcohol or povidone
iodine application.The application of irritants (like
chillies, oil, turmeric, lime, salt etc.) is unnecessary
and damaging.
Do not suture bite wounds immediately. If suturing is
required, hold it for 24-48 hours, applying minimum
number of stitches under the cover of antirabies
Immunoglobulin locally. Anti tetanus treatment can
be given after local wound treatment.
3.2. Passive immunization with
rabies immunoglobulin RIG)
Local infiltration of RIG in category III rabies-RIG
should be infiltered in the depth and around the
wound even if the lesion has begun to heal followed
by administration of antirabies vaccine.
(Caution: RIG should never be administered in the
same syringe or at the same anatomical site as
vaccine).
Doses of rabies immunoglobulin (IG)
Human rabies immunoglobulin (HRIG) 20 IU/kg
(max 1500 IU), available in concentration of 150
IU/ml, it does not require any prior sensitivity testing.
SHOULD NEVER BE INJECTED
INTRAVENOUSLY. The antirabies sera should
always be brought to room temperature (20-25C)
before use.
Or
Equine antirabies serum (ERIG) 40 IU/kg (max 3000
IU), available in concentration of 300 IU/ml, given
after prior skin sensitivity testing, single dose on day
0. Half the dose is infi ltrated around the bitten
wound and the rest is given I.M.
(Caution: A negative skin test must never reassure
the physician that no anaphylactic reaction will
occur. Avoid alcohol, glucocorticoids and
chloroquine during vaccination; avoid multiple
needle injections into the wound. Must not exceed the
total recommended dose of IG as it may reduce the
efficacy of the vaccine).
If the calculated dose of IG is insufficient to cover
infiltration in all wounds, sterile saline can be used to
dilute 2 or 3 fold to permit thorough infiltration.
RIG is notindicated beyond the seventh day after
administration of the first dose of vaccine.
3.3. Active immunization with
antirabies vaccine:
Antirabies vaccine (ARV)
Intramuscular schedule.
The course for post-exposure prophylaxis consists of
five injections (days 0, 3, 7, 14 and 28) irrespective
of severity of exposure. The 6th injection (day 90) is
optional for immunologically deficient and extremes
of age and on steroid therapy. The dose of vaccine
per injection is 2.5 IU/dose/ml for HDCV. Preferable
site is deltoid; anterolateral thigh in children
(Caution: Must NOT be given into gluteal muscle).
Intradermal (ID) schedule.
(i) The 2 site ID TRC schedule (2-2-2-0-1-1) to be
administered: One ID injection of 0.1 ml per ID site
over each right and left deltoid on days 0, 3, 7 and 0.1
ml at a single site on days 28 and 90 or as per
updated TRC schedule (2-2-2-0-2) on days 0, 3, 7
and 28.
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Note: Correct ID injection should result in a raised
papule with an orange peel appearance. If a papule is
not observed, the needle should be withdrawn and
vaccine re-administered correctly nearby.
(ii) The 8-site ID method (8-0-4-0-1-1) for use with
HDC/PCECV in emergency, when no RIG is
available.
The intradermal route is preferred as it reduces cost
but must not be used in case of immunocompromised
patients, individuals receiving long-term
corticosteroids or other immunosuppressive therapy
or chloroquine.
Antirabies vaccine should be kept and transported at
a temperature range of +2C to 8C. The
reconstituted vaccine should be used immediately or
within 6-8 hours of reconstitution.
3.4. Post-exposure treatment of
persons previously vaccinated
Managing re-exposure following post-exposure
treatment with tissue culture vaccine (TCV)
If re-exposed, persons who have previously received
full post-exposure treatment with a potent cell-culture
vaccine should be given only two booster doses,
intramuscularly (0.5 ml/1 ml)/intradermally (0.1 ml
at 1 site) on days 0 and 3, but no rabies
immunoglobulin. Proper wound toilet should be
done.
4. Pre-exposure prophylaxis
Indications: Laboratory staff working with rabies
virus, veterinarians, animal handlers and wildlife
officers. Three full IM or ID doses of tissue culture
vaccine given on days 0, 7, and 28. Laboratory staff
and others at high continuing risk of exposure should
have their neutralizing antibody titer checked every 6
months. If it is less than 0.5 IU/ml, a booster dose of
vaccine should be given. Such individuals on getting
exposed to rabies virus after successful pre-exposure
immunization require only two booster injections of
vaccine given on days 0 and 3 without any antirabies
serum/RIGs.
5. Patient education
Dog bite (category II and III) is an emergency and as
a general rule rabies postexposure treatment should
not be delayed or deferred.
Immediate washing with plenty of water and
disinfecting with alcohol/iodine.
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 54. POISONING

Anilides
1. Introduction
Poisoning due to the pesticides is increased due to the 3. Stepwise Case Approach
accessibility to the pesticides used in agriculture. Of
the total burden of acute pesticide poisoning the Diagnosis - Suspect and identify poison, if
majority of deaths are from self-poisoning with possible.
organophosphorus pesticides, aluminium phosphides Management includes basic principles,
and paraquat. antidotes, symptomatic and supportive
treatment.
2. Classification of Pesticides Anticipate complications, preserve evidence and
prevent sequelae as well as recurrence
2.1. Insecticides
Acetylcholinesterase inhibitors 4. Organophosphorus
Organophosphates
Carbamates
Compounds
Organochlorines Broadly OP compounds can be divided in to
Pyrethrins 1] Dimethyl compounds - Dichlorvos, Fenthion,
Pyrethroids Malathion, Methamidophos, Dimethoate
2.2. Herbicides 2] Diethyl compounds Chlorpyrifos, Diazinon,
Parathion-ethyl, quinalph
Dipyridyl pesticides
Paraquat and diquat 4.1. Mechanism of toxicity
Chlorphenoxyacetate weed killers
Bromoxynil, 2,4-D 1] Organophosphosphorus compounds inactivate
acetylcholinesterase by phosphorylation leading to
2.3. Fungicides accumulation of acetylcholine at cholinergic
synapses.
Substituted benzene
Chloroneb The rate of spontaneous reactivation of AChE is very
Chlorothalonil slow with diethyl OPs while it is relatively fast with
Thiocarbamates dimethyl OPs. Further, there is ageing of the
Organomercurials phosphorylated enzyme after which the enzyme
Methylmercury cannot be reactivated by oximes. The half-life of
Phenylmercuric acetate ageing of dimethlyphosphorylated and
diethylphosphorylated AChE in vitro is 3.7 hours and
Molluscicides Metaldehyde
33 hours, respectively, and the therapeutic windows
2.4. Rodenticides therefore are 13 and 132 hours, respectively (4 times
the half-life).
Aluminium phosphide
Zinc phosphide 4.2. Organophosphorus intoxication
Warfarin and superwarfarin compounds
Yellow phosphorus results in triphasic illness
Heavy metal : Thallium containing pesticides including
2.5. Insect repellants (a) Acute cholinergic syndrome
Diethyl toluamide (DEET) (b) Intermediate syndrome
2.6. Miscellaneous (c) Organophophate-induced delayed polyneuropath

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(a) Acute cholinergic syndrome
Acute cholinergic syndrome may occur within
minutes
Pathognomonic features via muscarinic and
nicotinic receptors-
Muscuranic effects Include miosis, bronchorrhoea,
salivation, lacrimation, pain in abdomen, bradycardia,
urination, defecation
Nicotinic effects Muscle fasciculation, muscle
cramps, flaccid muscle weakness with reduced
tendon reflexes, tachycardia, hypertension
Central nervous systemeffects Headache, dizziness,
confusion, convulsions, central respiratory
depression, coma
(b) Intermediate syndrome
This begins 48 hours after poisoning in
approximately 20% of patients but may be
delayed for 72-96 hours.
The onset is often rapid with progression of muscular
weakness from ocular muscles to neck and proximal
limbs to respiratory muscles over 24 hours.
Endotracheal intubation and ventilation are to be
done, if not instituted early, cyanosis, coma and
death may follow rapidly.
(c) Organophosphate induced delayed
polyneuropathy
This occurs 1-3 weeks after acute exposure and
uncertain period following chronic exposure due
to degeneration of long myelinated nerve fibres.
Cramping muscle pain in the legs are followed
by numbness and parasthesia in distal upper and
lower limbs.
Symmetrical flaccid paralysis in distal muscles
especially in the legs. The dominant hand may
be more affected.
4.3. Investigations
Plasma cholinesterase (pseudocholinesterase) is less
reliable. Red cell cholinesterase level falls to 20% of
normal when symptoms appear.
4.4. Treatment of
Organophosphorus Poisoning
1. Airway, breathing and circulation should be
ensured and monitored.
2. Further contamination is prevented by removal
from the site of exposure and of contaminated
clothing. Skin should be cleaned thoroughly with
water.
3. The airway is cleared and high-flow oxygen is
administered.
4. Direct mouth to mouth and nose resuscitation
must be avoided.
5. Following ingestion, gastric lavage must be done
within an hour of intake, followed by activated
charcoal via nasogastric tube after establishing
intravenous and airway protection.
Sample should be collected from the gastric lavage,
sealed and handed over to the police registering the
medicolegal case.
6. Convulsions are treated with intravenous
diazepam 10mg or midazolam 2mg.
7. Monitoring of ECG, blood gases, temperature,
blood urea and serum electrolytes, amylase and
glucose is mandatory.
For muscuranic effects
Injection Atropine 1.8-3mg bolus immediately
double the dose every 5minutes until atropinized.
Once patient is atropinized give 20%- 30% dose
required for atropinization as infusion/hour
[5mg/hour]. The best guide to adequate atropinisation
is to monitor features of cholinergic poisoning
(Bradycardia, Sweating, miosis, bronchorroea and
hypotension). A confused, agitated, febrile patient
with no bowel sounds and a full bladder with urinary
retention certainly has atropine toxicity, indicating
the need to reduce or stop atropine temporarily.
For nicotinic effects
Pralidoxime chloride- Cholinesterase reactivator
which reverses the nicotinic effects and some CNS
effects. It is given 1gm bolus in 30minutes then
infusion at 0.5gm/hour. (Loading dose of 30mg/kg
and 10mg/kg/hour infusion).
Treatment of the intermediate syndrome
Early institution of ventilatory support, which may be
required for a prolonged duration, is essential for
management. Close monitoring of respiratory
function such as chest expansion, arterial blood gas
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monitoring and oxygen saturation is essential to
identify the onset and monitor the progress of the
intermediate syndrome. Some patients develop an
offensive and profuse diarrhoea and it is important to
maintain a close watch and a positive fluid balance.
Recovery usually occurs without residual deficit.
5. Organochloride
Compounds (OC)
5.1. The commonly used OC insecticides are Endrin,
Aldrin, Benzene Hexachloride (BHC), Endosulphan,
Dieldrin, Toxaphene, DDT, Heptachlor, Kepone,
Dicofol, Methoxychlor, etc. DDT, the most toxic OC,
is available in dry powder form or as a mixture with
other pesticides in powder or liquid form.
5.2. Mechanism of toxicity
OC compounds impair nervous system function by
depolarization of the nerve membranes they also
cause sensitization of the myocardium to both
endogenous as well as exogenous catecholamines and
predispose to arrhythmias.
5.3. Clinical effects within minutes
to hours
Nausea
Vomiting
Agitation
Fasciculations
Parasthesia of face and extremities
Seizures dizziness
Tremors
Myoclonus
Coma
Respiratory depression and death
5.4. Complications
Hyperthermia, Rhabdomyolysis, Pulmonary oedema
and Disseminated intravascular coagulation. Lindane
is particularly toxic to the central nervous system. It
can also produce alterations in the ECG including
rhythm abnormalities and changes in STT waves
suggesting hyperkalaemia. Besides the features
related to OCs, associated solvents may produce
aspiration pneumonitis.
5.5. Management
Nasogastric aspirate may be useful if liquid
preparation has been taken and should be kept and
handed over to medical official for medicolegal
purposes.
Activated charcoal is given within 1hour of
ingestion.
Seizures should be treated with Benzodizapenes.
(Diazepam 10mg or Midazolam 2mg I.V.)
Patients should be kept on cardiac monitor. Use
Dopamine instead of Epinephrine if patient has
hypotension, as OC compounds sensitise the
myocardium.
6. Carbamate Poisoning
Carbamate insecticides- Aldicarb,
Carbofuranmethomyl inhibit a number of tissue
esterases-AchE. Aldicarb, Benomyl, Carbaryl,
Carbendazim, Carbofuran, Propuxur, Triallate, etc.
are the commonly used carbamates.
6.1. Clinical features
Clinical featuresare similar and less severe compared
to organophosphorus poisoning.
6.2.Complications
Pancreatitis and death.
6.3. Treatment
Nasogastric aspirate may be useful if liquid
preparation has been taken and should be kept and
handed over to medical official for medico-legal
purposes.
Injection Atropine 0.5-1mg I.V. in small doses for an
adult till atropinization occurs.
Role of PAM is unclear.
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 55. ALCOHOL INTOXICATION /ALCOHOL
WITHDRAWL
7.1. When to Suspect
Alcohol has CNS depressant effect; hence person
intoxicated with alcohol will present with depressed
level of consciousness, sometimes with respiratory
depression, cardiac arrhythmia, or blood pressure
instability.
If the patient agrees to stop drinking, sudden
decreases in alcohol intake can produce withdrawal
symptoms, many of which are the opposite of those
produced by intoxication. Features include tremor of
the hands (shakes); agitation and anxiety; autonomic
nervous system overactivity including an increase in
pulse, respiratory rate, and body temperature; and
insomnia. These symptoms usually begin within 510
hrs of decreasing ethanol intake, peak on day 2 or 3,
and improve by day 4 or 5. About 25% of alcoholics
experience a withdrawal seizure.
7.2. Investigation
i. History of Alcoholism
ii. Blood ethanol level (Avoid cleaning with spirit
while collecting Sample)
iii. CBC, LFT, obtaining toxicology screens for
opioids or other CNS depressants
iv. Neuroimaging
7.3. Treatment
i. Adequate nutrition and oral or I.V. Vitamin B
complex, including 50100 mg of Thiamine daily for
a week
ii. Inj Dextrose 25% in patients of altered sensorium
(dose 100 cc 25% dextrose)
iii. Administering any depressant in doses that
decrease the agitation- 2550mg of Chlordiazepoxide
or 10mg of Diazepam given PO every 46 hr on the
first day, with doses then decreased to zero over the
next 5 days.
iv. Rehabilitation
7.4. When to Refer
i. Those with poor Glasgow coma scale, Recurrent
Seizure, Focal neurological deficits or with delirium
tremens / korsakoff psychosis.
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 56. ANAEMIA
vii. H/O chronic diarrhea, malabsorption
1. Introduction viii. H/O chronic illness e.g. chronic renal failure,
Anemia is one of the most common disease a TB or any other causing anemia of chronic
physician can come across in the community. It can disease
be defined as HB < 13 g/dLfor male and < 12 g/dL ix. H/O blood transfusion in the past
for females as per WHO. x. H/O similar complaints in the past
xi. H/O pure vegetarian diet causing Vit. B12
Anemia can be due to nutritional deficiency, blood
deficiency causing Megaloblastic Anemia
loss, and increase in destruction of RBCs or due to
disturbance in formation of RBCs in bone marrow.
Detailed history and clinical examination is must to
4. Signs
reach the diagnosis. Patients especially females dont i. Pallor Conjunctiva, mucous membranes, skin
report to clinics until they have severe anemia. ii. Nails platynychia (flat) or koilonychias
Chronic anemia patients are usually well adjusted to (spoon shaped) nails in iron deficiency anemia
HB as low as 5 g/dL. (IDA)
iii. Severe anemia signs of hyper dynamic
2. When to suspect circulation eg. tachycardia, flow murmurs
(ejection systolic loudest at apex),
Symptoms cardiomegaly
i. Easy fatigability iv. Congestive Heart failure with edema feet,
ii. Breathlessness right hypochondriac tenderness, raised JVP
iii. Swelling of feet and basal crepitation
iv. Hypomenorrhea, amenorrhea v. Other signs of etiology may be found eg.
v. Stunted growth in adolescent icterus, Lymphadenopathy, stigmata of TB

3. History to be inquired for

etiology of anemia 5. How to Investigate
3.1. Acute 5.1. Complete blood count
The most important investigation gives maximum
i. H/O blood loss hematemesis, hemoptysis or information regarding diagnosis.
any other Mean Cell Volume (MCV) -Normal 76 -96
ii. H/O Fever or jaundice acute blood loss due
to either hemolysis or blood loss due to Low MCV (microcytic anemia)
coagulopathy
Iron deficiency anemia (IDA) most common
iii. H/O petaeche, ecchymosis or
Hereditary hemolytic anemia eg Thalassemia
lymphadenopathy with fever Acute
Leukemia Normal MCV (normocytic anemia)
iv. Recovering from recent surgery
Acute blood loss
Hemolysis
3.2. Chronic Anemia of chronic disease
i. Antenatal or postnatal female Chronic renal failure
ii. H/O passage of worms in stool causing Pregnancy
chronic blood loss
Bone marrow failure e.g Aplastic anemia
iii. H/O Chronic blood loss Hemorrhoids,
Hypothyroidism
Malena, Menorrhagia
iv. H/O Chronic Alcoholism leading to Vit. B12 High MCV (Macrocytic anemia)
deficiency
v. H/O Anorexia or any GI complaints leading Vit. B12 or folate deficiency (strict vegetarian
to malnutrition diet, Pernicious anemia)
vi. Poor socioeconomic status leading to Alcoholism
malnutrition Mylodysplastic syndromes(MDS)

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 Drug induced e.g Phenytoin - Elemental Iron 100mg once daily can be
5.2. Stool examination increase up to 300mg OD
Parasites, occult blood, malabsorption Repeat HB at the end of 1 month to confirm
response to treatment, if HB is increasing then
5.3. Other Baseline investigations repeat after 3months.
FBS, Creatinine, Liver enzymes, reticuolyte count, ii. Megaloblastic anemia-
LDH Oral supplementsVit. B12 (7.5mcg) +Folate
(0.75mg) BD for 1 month.
5.4. Iron studies, serum folic / Vit. iii. Deworming - All patients Tab Albendazole
(400mg) 1 stat, can be repeated after 2 weeks
B 12 levels iv. Treat etiology if possible
v. Packed cell transfusion if hemoglobin is less
5.5. Bone marrow biopsy if than 7
malignancy suspected 7. When to refer
Severe anemia (HB < 4g /dL) requiring blood
transfusion
6. Treatment Signs of Heart failure
i. IDA No response to oral supplements of Iron or B12
and folate at the end of 2 months
Oral iron Ferrous Sulphate (200mg) thrice a
Any suspicion of leukemia, lymphoma, MDS or
day for 3 months.
Aplastic anemia
Or (300mg) BD No apparent cause found
- Ferrous fumarate, Ferrous ascorbate can also
be used

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 57. HEAT STROKE
1. Definition
Heat Stroke is a syndrome of acute thermoregulatory
failure in warm environments characterized by
central nervous system (CNS) depression, core
temperatures usually above 40C (1050F), and typical
biochemical and physiologic abnormalities.

Figure 1: Effects of Heat Exhaustion and Stroke

Hyperthermia: Hypothalamic set point is Heat Exhaustion

unchanged; does not respond to antipyretics.
Distinct from fever (pyrogens change Heat Stroke
Hypothalamic temperature set point).

Uncontrolled increase in body temperature

3. When to Suspect Heat
that exceeds the body's ability to lose heat
due to failed thermoregulation.
Life-threatening medical emergency.
Core temperature >40 C (105 F) & CNS
disturbances in patients with a history of
heat exposure.
2. Clinical spectrum of heat
illness
Heat Edema
Heat Rash (miliaria)
Stroke
i. In any patient exercising in hot weather or in
susceptible individuals; mainly elderly
population.
ii. Coma or profound stupor is nearly always
present.
iii. Diagnostic criteria for Heat Stroke should
include
a. A core temperature above 40C
b. Severely depressed mental status or
Coma on Central Nervous System examination
c. Elevated Serum Creatinine and Serum
Electrolyte levels (Hyperkalemia)
d. Compatible historical setting.

Heat Cramps 4. Causes

1) Increased Heat production- Exercise,
Heat Tetany Fever, Thyrotoxicosis, Amphetamines, Atropine
toxicity.

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2) Impaired Heat loss- High ambient temperature or Exertional: Typically seen in healthy young
humidity, Ineffective voluntary control, Lack of adults who over exert themselves in high
acclimatization, Dehydration, Cardiovascular ambient (Surrounding) temperatures or in a hot
diseases. environment to which they are not acclimatized
(To adapt). Sudden inability to dissipate / Lose
3) Drugs- Anticholinergics, Phenothiazines,
body heat through perspiration (evaporation) or
Butyrophenones, Thiothixenes, Barbiturates,
cutaneous vasodilatation (convection),
Anti-Parkinson's agent, Alcohol.
especially after strenuous physical activity in hot
4) Debilitating conditions- Skin diseases, Cystic weather. (Increased heat production).
fibrosis, Central nervous system lesion, older
age. Non-exertional (classic): Usually affects elderly
and debilitated patients with chronic underlying
5. Clinical examination of disease. Result of impaired thermoregulation
combined with high ambient temperatures. Often
patient with Heat Stroke due to impaired sweating.

Anhidrosis often present (but is no longer a 7. Management

criteria for diagnosis)
Primary therapy includes cooling and decreasing
(hot, dry skin) thermogenesis.
Altered mental State. i. Evaporative cooling methods involve placing a
Often missed in physically inactive patients. nude patient in a cool room, wetting the skin
with water and encouraging evaporation by the
Baseline body temperature increased (core use of fans.
temperature).
ii. Direct external cooling involves immersing the
Non-glass medical thermometer. patient in water. Close monitoring of
Rectum preferred site haemodynamics i.e Pulse, Blood pressure,
respiration and urine output is mandatory.
Axillary and inguinal sites are unreliable

6. Types

Figure: Primary therapy of hyperthermia

Seek medical attention immediately-continue It is not advisable to give the victim anything by
first aid to lower temprature until medical help mouth (even water) until the condition has been
takes over. stabilized.
Do NOT give any medication to lower fever- It Body cooling methods
will not be effective and may cause further harm.
Body immersion in iced water
Do NOT use an alcohol rub

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 Evaporative cooling: Spraying water and the use - Avoid alcohol and caffeine, which dehydrate the
of fans over the patient facilitates evaporation body.
and convection
- Avoid foods that are high in protein, which
Gastric lavage with cold water / ice, bladder, or increase metabolic heat.
peritoneal lavage - Stay indoors when possible.
Immersion method of body cooling - Take regular breaks when engaged in physical
Aggressive ice water immersion is gold standard activity on warm days.
for life threatening heat stroke - Take time out to find a cool place.
Advantages: Cools patients faster; cooling rate of
0.20C/min for iced water 9. Complications
Disadvantages Acute renal failure
Rhabdomyolysis
- May cause peripheral vasoconstriction (not Liver failure
clinically relevant in RCT) Disseminated intravascular coagulation(DIC)
Acute respiratory distress syndrome (ARDS)

- Difficult in patients with reduced level of

CNS: Altered Mental state, confusion, delirium
Seizure, decorticate posture
consciousness
Coma and Death
Dehydration
- For alert - It is uncomfortable and often Caution - Overhydration
intolerable
Electrolyte Imbalance
Hypernatremia
- Shivering leads to worsening Hyperkalemia
Other cooling methods Hypokalemia
Localized muscle pain on active/passive flexion
(a) Placement of ice packs in the axillae, groin, of limbs
and neck Urine- Hemoglobinuria, Myoglobinuria
- Easy method, slower cooling
(b) Gastric, peritoneal, and bladder lavage with 10. Management of
cold water
complications
- Used in resistant cases i. Benzodiazepines- Lorazepam (2 to 4mg I.V.
(c) Cooling gloves slowly) or Midazolam (2 to 5mg I.V. slowly)
Indicated in patients with agitation & shivering to
Supportive treatment prevent heat production. Also given in patients with
convulsions.
- Treated in ICU settings
- IV Fluids, treat electrolyte disturbance ii. Rhabdomyolysis- Common in Exertional heat
stroke & in patients with hypotension.
- Mechanical Ventilation
Signs& symptom
8. Preventing heat- related - Dark urine
illness - Acute renal failure
- Treatment
- Wear loose, lightweight, light-coloured clothing. - I.V. fluids
Light colours will reflect away some of the suns - Alkalinisation of urine sodium Bicarbonate
energy.
iii. Metabolic support- Correcting the electrolyte
- Wear hats or to use an umbrella. disturbances like hyponatremia, hypercalcemia,
- Drink water- Carry water or juice with you and hypocalcemia, hyperphosphatemia
drink continuously even if you do not feel iv. Hepatic injury- Monitor liver function tests
thirsty. - Avoid hypoglycemia

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 - Early recognisation & treatment of DIC
- Respiratory support
11. When to Refer
v. Pulmonary injury- Pulmonary edema is ii. Evaporative and direct external cooling
common complication. methods fail to reduce the temperature.
ARDS- Patient should be referred for iii. Arrhythmias, metabolic acidosis and
mechanical Ventilation. cardiogenic failure complicate the early
management of hyperthermic crises.
iv. Those with evidence of renal failure,
vi. Renal injury- ARF may develop due to many disseminated intravascular coagulation or
reasons. These patients may need hemodialysis superadded infections.
& so referred to higher centre.

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 58. TUBERCULOSIS (RNTCP)
1. Introduction
Tuberculosis is an infectious disease caused
predominantly by Mycobacterium tuberculosis.
Pulmonary tuberculosis is the most common form of
TB (more than 85% of all TB cases), while extra
pulmonary tuberculosis can affect almost any organ
in the body. Transmission occurs by the airborne
spread of infectious droplets and droplet nuclei
containing the tubercle bacilli. The source of
infection is a person with sputum smear-positive
pulmonary TB. Transmission often occurs indoors,
where droplets and droplet nuclei can stay in the air
for a long time.
2. Epidemiology of
Tuberculosis
TB is a bacterial disease caused by
Mycobacterium tuberculosis. These organisms
are also known as tubercle bacilli or as acid-fast
bacilli.
Transmission of tuberculosis occurs by airborne
spread of infectious droplets and droplet nuclei.
Source of infection is patient of tuberculosis who
spreads tuberculosis bacilli during coughing,
sneezing, etc.
Most common symptom of pulmonary TB is
persistent cough for two weeks or more, usually
with expectoration. Persistent cough for 2 weeks
or more may be accompanied by one or more
symptoms such as weight loss, loss of appetite,
tiredness, evening rise fever, chest pain,
shortness of breath and hemoptysis.
Incidence of tuberculosis is usually similar in
both sexes below 15 years of age, thereafter
incidence is higher in males than females and
difference is greatest in old people.
Early detection of sputum positive tuberculosis
case and conversion into sputum negative by
effective treatment are most important measures
for tuberculosis control.
3. Diagnosis of TB
Identification of Tuberculosis Suspects
The most common symptom of pulmonary TB is
persistent cough, usually with expectoration.
Persistent cough may be accompanied by other
symptoms such as weight loss, tiredness, fever with
evening rise, night sweats, chest pain, shortness of
breath, anorexia and haemoptysis.
a. Pulmonary TB Suspects
A pulmonary TB suspect is defined as:
An individual having cough of 2 weeks or more.
Contacts of smear-positive TB patients having
cough of any duration.
Suspected/confirmed extra-pulmonary TB
having cough of any duration.
HIV positive client having cough of any
duration.
b. Extra-Pulmonary TB Suspects
A patient with extra-pulmonary TB (EP TB) may
have general symptoms like weight loss, fever with
evening rise and night sweats. Other symptoms
depend on the organ affected.
Examples of these symptoms are, swelling of a
lymph node in TB lymphadenitis, pain and swelling
of a joint in TB arthritis, neck stiffness and
disorientation in a case of TB meningitis. Patients
with EP TB, who also have cough of any duration,
should have sputum samples examined. If the smear
result is positive, the patient is classified as
pulmonary TB and his/her treatment regimen will be
that of a case of smear-positive pulmonary TB.
4. Screening for TB among
high risk groups
a) Contact investigation among the diagnosed
smear-positive cases is to be systematically
implemented and monitored, and it offers a
major opportunity for early case detection.
b) HIV care centres: Intensified TB case finding
should be implemented in all facilities providing
HIV care, like ICTCs, ART Centres, Care and
support centres etc.Involve NGOs working with
HIV programmes in TB case finding activities.
c) Diabetic patient: regularly screening for TB in all
diabetic patients at each visit.
d) Elderly patients.
e) Smokers.
f) Other High risk groups: Malnutrition, patients
with silicosis, patients on corticosteroids and
other chronic diseases need to be screened for
TB regularly.
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5. Tools for diagnosis of TB
Following are RNTCP recommended diagnostics
tests for TB
Sputum smear microscopy.
Histopathology/cytology/radiology.
Solid/liquid culture and DST for diagnosis TB
and Drug Resistant TB.
PCR based newer rapid diagnostic tools for
diagnosis of TB/drug resistant TB eg.
Line probe assay (LPA), CBNAAT.
6. Guidelines for collecting
sputum
The patient is given the sputum container with
Laboratory Serial Number written onits side. The
patient is instructed to inhale deeply 23times
with mouth open, cough out deeply from the
chest, open the container and spitout the sputum
into it. Sample should be at least 2 ml. If the
quantity is less, then the procedure can be
repeated. Once adequate quantity of sample is
collected, the container should be closed. This is
the first spot specimen (A).
The patient is given a labelled container with
instructions to cough out sputum intothe
container early in the morning after rinsing the
mouth, before breakfast. This is the early
morning specimen (B).
The person collecting the sputum specimens should
follow the guidelines specified below:
If the sputum specimens are to be sent
immediately to the laboratory, the person should
put the container into a special box meant for
transport.
If the sputum specimens are not being sent
immediately to the laboratory, these should be
stored in a cool and shady place in the referring
health facility.
The person should wash hands thoroughly with
soap and water every time when the material is
handled.
Patients should be told to come back to receive
the results of sputum examination.
Alternatively, sputum results may be sent to the
referring health facility by hand. Laboratory
serial number (and/or specimen identification
number) should be clearly written on the side of
the sputum container.
7. Management of Patient
after receiving the sputum
results
7.1 Smear positive pulmonary TB.
Patients with at least one sputum positive smear
resultout of two samples are diagnosed by the
physician as having smear-positive pulmonary TB.
They are further classified as a new or re-treatment
case based on their previous treatment history and
appropriate regimen is prescribed.
7.2 Follow up of the sputum
negative symptomatic
Patients, who are negative for AFB in both the
samples, will be prescribed a course of antibiotics for
duration of 10-14 days. In such cases antibiotics such
as fluoroquinolones (Ciprofloxacin, Ofloxacin,
Levofloxacin, and Moxifloxacin etc.),
clavulunatemacrolides, rifampicin or streptomycin,
which are active against tuberculosis, are not to be
used. Antibiotics of choice include Cotrimoxazole,
Amoxycillin, & doxycycline. Most patients are likely
to improve with antibiotics if they are not suffering
from TB. If the symptoms persist after a course of
broad spectrum antibiotics, repeat sputum smear
examination (2 samples) must be done for such
patients.
However, if repeat sputum examination turns to be
negative, they are subjected for chest x-ray
examination. If chest x-ray is suggestive of
pulmonary TB, they will be diagnosed as smear
negative pulmonary TB and treated accordingly. If
chest x-ray is not suggestive of TB, then they should
be evaluated for other respiratory diseases.
For patients infected with HIV, antibiotic trial is not
indicated and Chest X-ray needs to be taken to avoid
delay in diagnosis of smear negative TB.
Patients with suspected EP TB should be referred to a
competent medical practitioner / doctor / specialist
for expert opinion. Diagnosis of such patients may be
made using appropriate diagnostic procedures (such
as FNAC/Biopsy/Radiology) as well as clinical
methods.
Diagnosis of TB by chest X-ray alone is unreliable
because no radiological pattern is pathognomic of
pulmonary TB. Unless the prescribed algorithm is
followed, a large number of patients who do not have
TB will be falsely diagnosed and treated.
Page 143
 its duration, and the need for prompt evaluation of
8. Diagnostic Algorithm children under six years or contacts with cough of
any duration living in the household. The patient
When the referring doctor receives the results of
should also be informed that his address would be
sputum examination, and it is decided to put the
verified by a competent person prior to the start of
patient on chemotherapy, health education must be
treatment.
imparted to the patient. The patient is told about TB,
how it spreads, precautions to be taken to prevent the
spread, importance of directly observed treatment and

Figure-1: Diagnostic Algorithms for Pulmonary Tb

9. Treatment of TB
MO must undertake detailed clinical examination and V. Culture / Drug Susceptibility Test (DST)
history before starting the TB treatment. report from RNTCP certified laboratory (if
available).
The following is required before starting treatment:
I. History of patient, including history of any 9.1. Directly Observed
previous treatment for TB.
II. Sputum smear examination results from an Treatment (DOT)
approved DMC.
RNTCP Definitions: Case Definitions, Types of
III. Chest X-ray report if the case warrants
Cases and Treatment outcomes
radiographic examination.
IV. Other supporting investigation reports, if any.

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 Table-1: Definitions under RNTCP
9.2.Treatment Regimens
For the purpose of treatment regimen to be used, TB
patients are classified into two groups, namely,
New or Previously Treated, based on the history
of previous treatment.
i. Regimen for New cases
This regimen is prescribed to all new pulmonary
(smear-positive and negative), new extra pulmonary
and new others TB patients.
The regimen is 2H3R3Z3 E3 / 4 H3R3.
Treatment is given in two phases. For New
patients, the intensive phase consists of isoniazid (H),
rifampicin (R), pyrazinamide (Z) and ethambutol (E)
given under direct observation thrice a week on
alternate days and lasts for 2 months (8 weeks, 24
doses).
This is followed by the continuation phase, which
consists of 4 months (18 weeks; 54 doses) of
isoniazid and rifampicin given thrice a week on
alternate days with at least the first dose of every
week being directly observed. If the sputum smear is
positive after 2 months of treatment, the intensive
phase of four drugs (H, R, Z and E) are continued for
another one month (12 doses), and sputa sent for
culture and drug susceptibility testing (C&DST) to an
accredited RNTCP C&DST laboratory. Treatment
remains continued as per regimen if C&DST report is
Rifampicin-sensitive. Sputum is examined after the
completion of the extension of intensive phase.
Irrespective of the sputum results after this extension
of the intensive phase, the 4 months (18 weeks) of the
continuation phase is started.
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If the sputum smear is positive after 5 or more
months of treatment, the patient is declared as a
Failure and is placed on the Previously Treated
treatment regimen afresh. If patient remains smear
positive in any follow-up sputum examination, then
sputum samples are sent for culture and drug
susceptibility testing (C&DST) to an certified
RNTCP C&DST laboratory. If the report indicates
Rifampicin resistant, then the Cat I regimen is
stopped and patient is counselled and referred to
District / Drug Resistance TB centre for pre-
treatment evaluation and treatment initiation.While
treating TB meningitis(TBM) in New patients,
streptomycin is to be used in place of ethambutol
during the intensive phase (H3R3Z3S3 instead of
H3R3Z3E3). The continuation phase of treatment for
patients with TBM or spinal TB is for 7 months.
Hence, the total duration of treatment will be for 9
months.
ii. Regimen for Previously Treated
cases
This regimen is prescribed for TB patients who have
had more than one month anti-tuberculosis treatment
previously. These patients are at a higher risk of
having drug resistance. Hence all such patients are
also subjected to C&DST for identification of
MDRTB. If C&DST report is expected beyond 7
days, then patients are initiated on Cat II regimen
with 5 drugs in the intensive phase, and the total
Table-2: Treatment regimine under RNTCP
Treatment groups
Type of patient
(category)
New Sputum smear-positive
(Cat I: Red Box) Sputum smear-negative
Extra-pulmonary
Others
Previously Smear-positive relapse
Treated** Smear-positive failure
/Retreatment case Smear-positive treatment after
(Cat II: Blue Box) default
Others2
1. The number before the letters refers to the number
of months of treatment. The subscript after the letters
refers to the number of dosesper week.
The dosage strengths are as follows: Isoniazid (H)
600 mg, Rifampicin (R) 450 mg, Pyrazinamide (Z)
duration of treatment is 8 months. Relapses,
Treatment after Default, Failures and Others are
treated with this regimen.
The regimen is IP: 2S3H3R3Z3 E3+ 1H3R3Z3 E3
CP: 5 H3R3 E3.
Treatment is given in two phases. For Previously
Treated cases, the intensive phaseconsists of two
months (24 doses, 8 weeks) of isoniazid (H),
rifampicin (R), pyrazinamide(Z), ethambutol (E) and
streptomycin (S), followed by one month (12 doses, 4
weeks) ofisoniazid, rifampicin, pyrazinamide and
ethambutol, all given under direct observation thricea
week on alternate days. Patient is subjected for
follow-up sputum examination at theend of three
months. If the sputum smear is positive at the end of
3 months of treatment, the intensive phase drugs (H,
R, Z and E) are extended for another one month (12
doses,4 weeks). Irrespective of the sputum results at
the end extended intensive phase, 5 months(22
weeks) of continuation phase is started. If the sputum
remains positive at the end ofthe extended intensive
phase, sputum is sent to an accredited RNTCP
C&DST laboratory for culture and drug susceptibility
testing. The continuation phase consists of 5 months
(22 weeks; 66 doses) of isoniazid, rifampicin and
ethambutol given thrice a week on alternatedays,
with at least the first dose of every week being
directly observed.
Regimen1
Intensive phase (IP) Continuation phase
(CP)
2H3R3Z3E3 4H3R3
2H3R3Z3E3S3 5H3R3E3
/ 1H3R3Z3E3
1500 mg, Ethambutol (E) 1200 mg, Streptomycin (S)
750 mg.
Patients who weigh 60 kg or more receive
additional rifampicin 150 mg.
Patients who are more than 50 years old receive
streptomycin 500 mg. Patients who weigh less
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 than 30 kg, receive drugs as perPaediatric weight
band boxes according to body weight.
2.In rare and exceptional cases, patients who are
sputum smear-negative or who have extra-pulmonary
disease can have recurrence or nonresponse.This
diagnosis in all such cases should always be made by
an MO and should be supported by culture or
histological evidence ofcurrent, active TB. In these
cases, the patient should be typed as Others and
given treatment regimen for previously treated.
Note: - All doses in Intensive phase and at least first
dose in Continuation phase should be directly
observed by DOT provider.
Table-3: Pediatric patient wise boxes for new cases according to weight band
9.3. Pediatric TB
Pediatric cases are to be treated under RNTCP with
the same thrice weekly short course chemotherapy
regimens (New or Previously Treated) given
under DOT as for adult patients. They are to be
registered in the respective RNTCP TB Register.
Pediatric patient-wise boxes are available with
different dosages as two product codes to be used
under four weight bands for children weighing 6 to
10 kgs, 11 to 17 kgs, 18 to 25 kgs and 26 to 30 kgs.

INH Chemoprophylaxis
9.4. Monitoring of Treatment
All children aged < 6 years in contact with smear- Follow up of patient
positive pulmonary TB case are screened by MO to
rule out TB. If suffering from TB, should be treated
appropriately. Children not having TB are to be
administered preventive chemotherapy with INH,
10mg/kg body weight for 6 months.

Table-4: Follow up of DOTS patients

CAT Follow up sputum If smear + at the end of IP Remarks
Action Follow up
sputum
CAT-I At 2,4,6 months of Extend IP for another one 3,5,7 months If sputum +ve at 5 months,
treatment month of treatment declare patient as failure and
put on CAT-II
CAT-II At 3,5,8 months of If +ve at 3 months then 4,6,9 months -
treatment extend IP, 4 drugs for one of treatment
more month

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Default retrieval action
In spite of counseling and health education at the
time of diagnosis and follow up by health workers,
some patients remain irregular for treatment.
Defaulter retrieval action is action taken to bring
back patients for treatments who do not take
medicines regularly. DOT provider should take
defaulter action. Following actions are suggested
under RNTCP for defaulter patients-
If patient does not come as scheduled during
Intensive Phase (IP) then health worker / DOT
provider makes home visit immediately same
day or next day and brings patient for regular
treatment.
If patient is in Continuation Phase (CP) home
visit should be made and patient should be
retrieved within a period of a week after missed
dose.
In case of community DOT provider / ASHA/
Anganwadi, the respective ANM/MPW of that areas
should supervise the DOT provider fortnightly for
ensuring DOT implementation and assist in ensuring
patient adherence, timely follow-up.
9.5. Programmatic
Management of Drug
Resistant TB (PMDT)
MDR-TB Suspects
The following are the criteria to label a patient as
MDR-TB suspect.
All previously treated pulmonary TB cases at
diagnosis.
Any smear positive follow up result in new or
previously TB cases.
HIV TB co-infected cases at diagnosis.
All pulmonary TB caseswho are contacts of
known MDR TB case
Once the districts will have adequate laboratory
capacity for DST, all TB patients will be
provided DST at the time of diagnosis.Two fresh
sputum samples (Spot and early morning) are to
be collected from MDR TB suspects and
transported from DMC/PHIto the RNTCP
certified C & DST laboratory in cold chain by
using transport mechanism (courier/post/human
carrier) within 72 hrs.
Definitions
MDR-TB case: A TB patient whose sputum is
culture positive for Mycobacteriumtuberculosis and
is resistant in-vitro to isoniazid and rifampicin with
or without otheranti-tubercular drugs based on DST
results from an RNTCP-certified Culture &
DSTLaboratory.
XDR TB case: An MDR TB case whose recovered
M. tuberculosis isolate is resistant toat least isoniazid,
rifampicin, a fluoroquinolones (Ofloxacin,
Levofloxacin, orMoxifloxacin) and a second-line
injectable anti-TB drug (Kanamycin, Amikacin,
orCapreomycin) at a RNTCP-certified Culture &
DST Laboratory.
Diagnosis of MDR-TB
Presently, 3 technologies are available for diagnosis
of MDR TB viz. the conventional solidEgg-based
Lowenstein-Jensen (LJ) media, the liquid culture
(MGIT), and the rapid molecular assays such as Line
Probe Assay (LPA) and similar Nucleic Acid
Amplification Tests likeXpert MTB/Rif (CBNAAT).
Molecular/genotypic tests are much faster than
phenotypic tests, as molecular tests dont require
growth of the organism, and M. tuberculosis is
notoriously slow growing. The turnaround time for
C-DST results by Solid LJ media is around 84 days,
by Liquid Culture (MGIT) is around 42 days, by LPA
is around 72 hours and by CBNAAT is around 2
hours. Currently LPA does the DST of INH and
Rifampicin and CBNAAT gives the DST of
Rifampicin. Liquid culture DST is used to do the
DST of second line drugs Oflox/Kanamycin.
RNTCP MDR/XDR-TB Treatment
As per PMDT guidelines, a specializedcenters named
Drug Resistant TB Centres are been established at
tertiary care hospitals like medical college/ TB
hospitals/civil hospital for admission of MDR TB
patients for pre-treatment evaluation and to initiate
treatment.Patients should receive counselling at every
level on 1) the nature and duration of treatment, 2)
need forregular treatment, 3) possible side effects of
these drugs and 4) the consequences of irregular
treatment or pre-mature cessation of treatment.
Regimen for MDR-TB
This regimen comprises of 6 drugs - Kanamycin,
Levofloxacin, Ethionamide, Pyrazinamide,
Ethambutol and Cycloserine during 6-9 months of the
Intensive Phase and 4 drugs-Levofloxacin,
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Ethionamide, Ethambutol and Cycloserine during the
18 months of theContinuation Phase.
All drugs should be given in a single daily dosage
under directly observed treatment (DOT) by a DOT
Provider. All patients will receive drugs under direct
observation on 6 days of the week. On Sunday, the
oral drugs will be administered unsupervised whereas
injection Kanamycin will be omitted. If intolerance
occurs to the drugs, Ethionamide, Cycloserine and,
PAS may be split into two dosages and the morning
dose administered under DOT. The evening dose will
be self-administered. The empty blister packs of the
self-administered doses will be checked the next
morning during DOT. Pyridoxine should be
administered toall patients on Regimen for MDR TB.
Drugs are provided to the DOT provider in monthly
patient wise boxes (PWB). PWBs are prepared at
State Drug store as per the five weight bands- <16kg,
16-25Kg, 26-45kg, 46 -70kg and > 70kg.
If patient gains or loses >5 kg weight during
treatment and crosses the weight band range,
Committee may consider moving the patient in higher
or lower weight band in next supply of drugs.
Follow-up investigations during MDR TB
treatment
One specimen for follow up culture at the end of
3,4,5,6,7,9,12,15,18,21,24 months of treatment.
Monthly weight.
Chest X-ray during pretreatment evaluation, end
of IP, end of treatment and whenever indicated.
Physician evaluation every month for 6 months
and then every 3months for 2 years.
Serum Creatinine monthly for first 3 months and
then every 3 months till inj. Kanamycin is given.
TSH during pretreatment evaluation and when
indicated.
Patients will be considered culture converted
after having two consecutive negative cultures
taken at least one month apart. Based on culture
conversion patient is shifted from IP to CP.
Regimen for XDR TB
The Intensive Phase will consist of 7 drugs
Capreomycin (Cm), PAS, Moxifloxacin (Mfx), High
dose-INH, Clofazimine, Linezolid, and Amoxyclav.
The Continuation Phase will consist of 6 drugs
PAS, Moxifloxacin (Mfx), High dose-INH,
Clofazimine, Linezolid, and Amoxyclav.
Follow-up monitoring in XDR TB
XDR TB requires more intensive monitoring during
follow-up.
Complete Blood Count with Platelets Count:
weekly in first month, then monthly torule out
bone marrow suppression and anaemia as a side
effect of Linezolid.
Kidney Function Test- monthly creatinine and
addition of monthly serum electrolytesto the
monthly creatinine during the period that Inj
Capreomycin is being administered.
Liver Function Tests: monthly in IP and 3
monthly during CP.
CXR every 6 months.
No difference to follow-up Culture for patients on
regimen for MDR TB and XDR TB.
M/XDR TB Treatment Outcome definitions
Standardised treatment outcome definitions are to be
used following treatment of an MDRTBcase. These
definitions apply to patients with rifampicin
resistance (who are taken to beMDR TB for
management purposes), and XDR TB cases as well:
Cure: A patient who has completed treatment
and has been consistently culture negative (with
at least 5 consecutive negative results in the last
12 to 15 months). If one follow-up positive
culture is reported during the last three quarters,
patient will still be considered cured provided
this positive culture is followed by at least 3
consecutive negative cultures, taken at least 30
days apart, provided that there is clinical
evidence ofimprovement.
Treatment completed: A patient who has
completed treatment according to guidelinesbut
does not meet the definition for cure or treatment
failure due to lack of bacteriological results.
Treatment failure: Treatment will be
considered to have failed if two or more of the
fivecultures recorded in the final 12-15 months
are positive, or if any of the final threecultures
are positive.
Death: A patient who dies for any reason during
the course of M/XDR-TB treatment.
Treatment default: A patient whose treatment
was interrupted for two or more
Consecutive months for any reasons.
Transfer out: A patient who has been
transferred to another reporting unit (DR-TB
Centre in this case) and for whom the treatment
outcome is not known.
Page 149
 Switched to Regimen for XDR TB: A By an RNTCP certified C-DST laboratory,
MDR-TB patient who is found to have who subsequently switched to a regimen
XDR-TB. forXDR TB treatment initiated.

Page 150
 59. LEPROSY (NLEP)
2) Thick and/or Tender nerve
1. Cardinal signs of leprosy Selection of Leprosy case on clinical sign &
1) Hypopigmented / Erythematousanesthetic symptoms.
patch/s.

Figure-1: Algorithm for Confirmation

Treatment for 6
PB case month (6 BCP in
Confirmation of
9 Month)
Suspect Case cases at
PHC/RH
MB case Treatment for 12
month (12 BCP
in 18 Month)

Table-1: Cardinal signs for classification of Leprosy Case

Clinical aspects PB (Paucibacillary) MB (Multibacillary)

Skin lesions 1 to 5 skin Patches with definite sensory 6 & 6 + skin Patches with
deficit definite sensory deficit
Nerve involvement And/or one definite thicken or tender And/or More than one definite
peripheral nerve involvement thicken or tender peripheral nerve

If any one or both signs present in suspected case then it is diagnosed as leprosy.

2. Management
Table-2: Management of Leprosy case as per classification2
Multi Drug Treatment for PB leprosy
Drug Adult Children 10- Children below 10 years Frequency
14 yrs
Rifampicin 600 mg 450 mg 300 mg
Once a month
Dapsone 100 mg 50 mg 25 mg
25 mg daily or 50 mg alternate day Daily/ alternate
Dapsone 100 mg 50 mg
day

Page 151
 Multi Drug Treatment for MB leprosy.

Drug Adult Children 10-14 yrs Children below 10 years Frequency

Rifampicin 600 mg 450 mg 300 mg
Dapsone 100 mg 50 mg 25 mg Once a month
Clofazimine 300 mg 150 mg 100 mg
Dapsone 100 mg 50 mg 25 mg Daily
50 mg 50 mg 50 mg
Clofazimine weekly twice
(Daily) (Alternate day)

The appropriate dose for children under 10 Dapsone: 2 mg per kilogram body weight daily.
years of age can be decided on the basis of
MDT Multi drug Treatment is safe and well tolerated
body weight. by most of the patients.
Rifampicin: 10 mg per kilogram. 3. Management of Reaction
Clofazimine:6mgperkilogrammonthlyand1mgper
kilogramperbody weight daily.

Table-3: Features of Lepra Reaction

Features Type I Type-II
Skin Existing lesions suddenly become red, Red, painful, tender, subcutaneous (deep)
swollen, warn and tender. New lesions nodules (ENL) appear commonly on face,
may appear arms and legs. They appear in groups and
subside within a few days.
Lesions when subsiding, may show scales
on surface
Nerves Nerves close to skin become enlarged, Nerves may be affected but not as common as
tender and painful with loss of nerve in Type-I reaction
function.
Other organs Not common Fever, joint pains fatigue

Treatment of Lepra Reaction (Type-I and Type 15 mg OD for first7-8 weeks.

II) 10 mg OD for first 9-10 weeks.
5 mg OD for first 11-12 weeks.
Assurance to the patient & family (The total duration should not exceed 12 weeks even
in type 2).
Early diagnosis & prompt treatment to prevent
Cap Clofazimine 100mg T.D.S. in type 2 reaction for
deformity.
12 weeks,followed by 100 mg od for 12 weeks &
Removal of precipitating factor wherever 100 mg od for 12-24 weeks.
possible. Rest: Adequate rest to the affected nerve until
symptoms clear, by applying a padded splint or
Tab.Prednisolone
any other suitable material to immobilize the
40 mg OD for first 2 weeks.
joints near the affected nerve.
30 mg OD for first 3-4 weeks.
20 mg OD for first 5-6 weeks.

Page 152
 Continuation of Anti Leprosy Treatment only if the appearance of reactions with new
not completed. development of the disease.
It has been observed that many medical officers
become panicky and start MDT again equating

Figure-2: MDT Blister Packs

Page 153
PEDIATRICS

Page 154
 1. Emergency Management in Paeditrics

In children under five years of age Pneumonia, Keepthebabyunderaradiantwarmerandre-

diarrhoea, Birth asphyxia, Low birth weight and
neonatal infections were the most important causes
of death. Many children suffer from more than one
illness at a time and also many different diseases
presents with similar symptoms. It describes a
sequential process for managing sick young infants
and children as soon as they arrive in the facility.
Only the key protocols from Integrated Management
of Childhood Illness (IMNCI) and Facility Based
IMNCI (F IMNCI) are re-emphasized.
1. Emergency Management
process of the sick child (0-
5 years)
The firststep in assessing children referred to a
hospital should be triage The process of rapid
screening to decide to which of the following
group(s) a sick child belongs:
Firstassesseverychildforemergencysigns.Thos
ewithemergency signs require immediate
emergency treatment.
Ifemergencysignsarenotpresent,lookforpriorit
ysigns.Thosewithpriority signs should alert
you to a patient who is seriously ill and needs
immediate assessment and treatment.
Childrenwithnoemergencyorprioritysig
nsaretreatedasnon-urgent cases.
warmsoastobringthechildstemperatureto36.5
C.Payspecialattentiontoavoidchillingtheinfantdur
ingexaminationorinvestigation.
Monitortemperature everyhalfhourly
forfirst2hrsandthenevery2hourly.
4. How to Treat Hypoglycemia
Check for blood glucose in all children presenting
with emergency sign, those with severe acute
malnutrition and all sick young infants (0-2
months):
i. Ifhypoglycemiadetecteddefinedas
ii. a) <45mg/dlforyounginfants andb)
<54mg/dlinoldersickchildrenbeyond2 months.
iii. GiveI.V.
bolusdoseof10%dextrose,inthedoseof2ml/kgfory
ounginfants,and5ml/kgforolderchildren.
iv. Ifyoucannotmeasurebloodglucose,givebolusdose
asabove. Refer the case to higher center.
5. Airway and Breathing :

2. Triage
All sick children are assessed for Airway,
Breathing, Circulation, Coma, Convulsions and
Severe Dehydration (ABCD). Table 1
Efforts should be made to maintain euglycemia and
euthermia while managing ABCD. Thus Blood
sugars should be done for every sick
Newborn,Infant and older children.

3. How to keep baby warm

Keeptheinfantdryandwellwrapped.
Cap,glovesandstockingsarehelpfultoreduceheatl
oss.
Keeptheroomwarm(atleast25C)makingsurethatt
hereisnoheatsourcedirectedstraightatthenewbor
n.

Page 155
 Table-1: Assessment of Airway and Breathing

Table-1: Assessment of Airway andBreathing

No Manageairway
ASSESS AIRWAY
breathingorgaspingor Providebasiclifesupport
AND BREATHING
Centralcyanosis (No breathing/gasping)
ANY SIGN POSITIVE
Or Giveoxygen
Severerespiratorydistre Makesurechildiswarm
ss

Severe lower chest in-drawing

5.1. Signs of severe respiratory Head nodding
distress Grunting
Apnoeic spells
Respiratory rate Unable to feed due to respiratory distress
0 -2 months > 60,
Stridor in a calm child
2 months 1 year > 50 &
>1 year 5 years > 40.

5.2. Management of airway in a child with gasping or who has just stopped
breathing.
Table-2: Positioning to Improve the Airway when no neck trauma suspected.

Child Conscious Child Unconscious

Inspectmouthandremoveforeignbody,ifpresent.
Clearsecretionsfromthroatusingsuctioncatheter.
Letchildassumepositionofmaximalcomfort.
GiveOxygen.
Continuewith furtherassessment.
Opentheairwayby Head tilt andChinliftmethod.
Inspectmouthandremoveforeignbody,ifpresent.
Clearsecretionsfromthroat.
Checktheairwaybylookingforchestmovements,
listening for breath sounds and feeling for breath.

5.2.1. Head tilt-chin lift maneuver (Fig 1)

Theneckisslightlyextendedandtheheadistiltedbyplacin
gonehandontothechildsforehead.Liftthemandibleup
and outward by placing the fingertips of other hand
under the chin.
a) Positioning to improve the Airway when
neck trauma suspected
To limit the risk of aggravating a potential cervical
spine injury, open the airway with a jaw thrust while
you immobilize the cervical spine. It is safe to use in
cases of trauma for
Figure-1: Position for opening airway
Children of all age.
b) Neck trauma suspected (possible cervical
spine injury)
Stabilizetheneck,asshowninfigure2.
Inspectmouthandremoveforeignbody,
ifpresent.
Clearsecretionsfromthroatbysuctioncatheter.
Checktheairwaybylookingforchestmovements,li
steningforbreathsoundsandfeelingforbreath.
5.2.2 Jaw thrust maneuver
The jaw thrust is achieved by placing two or
three fingersunder the angle of the jaw on
both sides, and lifting the jaw upwards and
outward. The jaw thrust maneuver is
alsoused to open the airway when bag-mask
ventilation is performed.

Page 156
 Figure-2: Using Jaw thrust without head tilt
If after any of these maneuvers the child starts
breathing, an oropharyngeal airway should be put
and start oxygen.
If the child is not breathing even after the above Figure-3: Difference in padding for an infant and
maneuvers or spontaneous ventilation is older child
inadequate (as judged by insufficient chest Bags and masks should be available in sizes for
movements and inadequate breath sounds), the entire pediatric range (size 0, 1 and 2).
ventilate with a self-inflating bag and mask
It is important for the mask to be the correct
5.3. Ventilation with Bag and mask size for the child;it must completely cover
the
Positioning (Fig 3)
Mouth and nose without covering the eyes
A sniffing position (padding under
or overlapping the chin.
theshouldertopreventexcessiveflexionofthenec
kthatoccurswhentheirprominentocciputrestsont
hesurface onwhich the child lies without
hyper-extension of the neck) is usually
appropriate for children less then 2 years old. .
In correct sniffingposition, the opening of the
external ear canal should be in line with or in
front of (anterior to) the anterior aspect of the
shoulder. Extreme hyperextension of the infant
neck can produce airway obstruction.
In children older than 2 years you may need to Figure-4: Bag and mask ventilation
give padding under the occiput to
The correct size and position are shown in
Obtain optimal airway position. the figure4 & 5

Figure 5: Choosing the correct mask size

Page 157
 Self-inflating bags of minimum volume 450-
500ml should be used. Use force and tidal
volume just enough to cause the chest to rise
visibly.
Reservoir and oxygen (5-6 L/min)
should be connected to the self inflating
bag during resuscitation.
After two effective ventilations, check
the pulse (femoral, brachial or carotid)
for no more than ten seconds. If pulse is
absent, the second person should start
chest compression.
5.3. Chest compressions:
The techniques for chest compression vary
for a child under 1 year and those between
1-8 years and are detailed below:
5.3.1 Chest compression in the infant (less
than 1 year of age)
There are two techniques for performing chest
compression. These techniques are:
Thumb technique, where the 2 thumbs are
used to depress the sternum, while the
hands encircle the torso and the
fingerssupport the spine
Figure-6: Thumb technique
2-fingertechnique, where the tips of the middle
fingerand either the index fingeror ring
fingerof one hand are
usedtocompressthesternum,whiletheotherhandi
susedtosupportthebabysback(unlessthebabyiso
naveryfirmsurface).
Using either method to give chest
compressions, compress the lower half of the
sternum but do not compress over the xiphoid.
After each compression allows the chest to
recoil fully because complete chest re-
expansion improves blood flow into the heart.
Push hard: push with sufficient force to
depress the chest approximately one third to
one half the anterior- posterior diameterof the
chest.
Push fast: push at a rate of approximately 100
compressions per minute.
Release completely to allow complete recoil of
the chest by completely releasing the pressure
but maintaining contact with the compression
site.
Minimize interruptions in chest compressions.
During cardiopulmonary resuscitation, chest
compressions must always be accompanied by
positive-pressure ventilation.
Avoid giving a compression and ventilation
simultaneously, because one will decrease the
efficacy of the other.
Therefore, the 2 activities must be coordinated,
with one ventilation interposed after every third
compression (3 compressions followed by one
ventilation), for a total of 30 breaths and 90
compressions per minute
5.3.2 Chest compressions for the child (1 to 8
years of age)
Place the heel of one hand over the lower half of the
sternum. Lift your fingers to avoid pressing on the
ribs.
Figure-7: Chest compression for the child (1 to 8
years of age)
Depress the sternum 1/3 to 1/2 of the depth of
the chest. This corresponds to a 1 to 1- inches.
Compress at the rate of approximately 100
times per minute.
Theratioofchestcompressionsandventilationshou
ldbe 15:2(Fifteen compressions followed by
two ventilation).
Bag and mask ventilation is a very effective
way of ventilation if done correctly.
Setup an intravenous or an intraosseous line for
use of any drugs, whereneeded.
6. Use of Adrenaline
Adrenaline 0.1 ml /kg (1:10,000) intravenous can be
used in a child who does not respond toinitial
ventilation and chest compressions and his pulses
are absent. Two such doses can be used 3-5 minutes
apart.
Page 158
7. Giving Oxygen to a child
with respiratory distress
With a Head box (8-10 L/min) or a Face mask
(5-6 L/min).
Should be allowed to take a comfortable
position of his choice and should be given
oxygen.
Continue giving oxygen continuously until the
child is able to maintain a SaO2 > 92% in
room air. When the child is stable and
improving, take the child off oxygen for a few
minutes. If the SaO2 remains above 92%,
discontinue oxygen, but check again hour
later, and 3 hourly thereafter on the first day
off oxygen to ensure the child is stable. Where
pulse oximetry is not available, the duration of
oxygen therapy is guided by clinical signs,
which are less reliable. Figure-8: Capillary refill time

Any child who has been successfully

resuscitated or any unconscious child who is
breathing and keeping the airway open should
be placed in the recovery position. This
position helps to reduce the risk of vomit
entering the childs lungs. It should only be
used in children who have not been subjected
to trauma. A child with cyanosis or severe
respiratory distress should be allowed to take a
comfortable position of his choice.
8.1.1 Checking capillary refill
Weak & Fast Pulse: Evaluation of pulses is critical
to the assessment of systemic perfusion. The radial
pulse should be felt. If it is strong and not obviously
fast the pulse is adequate; no further assessment is
needed.
Weak and fast pulse is defined:
In Infants : >160 per min.

Organize Urgent Transfer to higher centers in In children - > 140 per min.
Ambulance and ensure doctor accompanies the Thus if the child has cold extremities, a capillary
sick child. refill time more than 3 seconds, and a fast weak
pulse, then he or she is in shock.

8. Circulation: 9. Treatment of Shock:

After the Airway has opened, assess if a child has a
circulation problem you need to know:
The letter Cin ABCD stands for Circulation,
Coma and Convulsions.
Assess the circulation for signs of shock
Themostcommoncauseofshockinchildrenisduetoloss
offluidfromcirculation,eitherthroughlossfromthebody
as in severe diarrhoea or when the child is bleeding,
or through capillary leak in a disease such as severe
Dengue fever.
Inallcases,itisimportanttoreplacethisfluidquickly.Anin
travenouslinemustbeinsertedandfluidsgivenrapidlyins
hocked children without severe malnutrition.
Capillary Refill Time: To assess the
circulation, take the childs hand and feet in your
own. If it feels warm, the child has no circulation
problem and you do not need to assess capillary
refill or pulse. If the childs hands and feet feel cold,
you need to assess the capillary refill.
If the child has any bleeding, apply pressure
to stop the bleeding. Do not use a tourniquet.
Give oxygen.
Give fluids and other treatment for shock.
9.1 Young Infants:
Fluid bolus of 20ml/kg of normal saline over
20-30 minutes.e.g. in a baby weighing 3 kg,
60 ml of normal saline should be infused over
20-30 minutes. If no or partial improvement
(i.e. tachycardia and CRT still prolonged),
repeat a bolus of 20 ml/kg of normal saline.
If the signs of poor perfusion persist despite 2
fluid boluses, start vasopressor support,
except in infants with severe dehydration
who should be treated as per Plan C of
diarrhea management.
9.2 Children above 2 months of

Page 159
 age:The recommended volumes of fluids to
treat shock depending on the age/weight of
child.If the child has severe malnutrition, you
must use of different fluid and a different rate
of administration and monitor the child very
closely. Therefore a different regime is used
for these children.
10. Coma and Convulsion
Calso represents Coma and Convulsion.
Assess the child for coma and convulsion
10.1 Coma
Table-3: For assessment of the conscious level of a
child is, a simple scale (AVPU) is used.
A isthechildAlert?Ifnot,
V isthechildrespondingtoVoice? Ifnot,
P isthechildrespondingtoPain?
U the child who is Unresponsive to voice (or being
shaken) AND to pain is Unconscious.
A child who is not alert, but responds to voice, is
lethargic.
An unconscious child may or may not respond to
pain.
A child with a coma scale of P or U will
receive emergency treatment for coma as described
below.
10.2 Convulsions
The child must be seen to have a
convulsion during the triage process for
emergency treatment for convulsion.
Convulsion ARE RECOGNIZED by the
sudden loss of consciousness associated
withuncontrolledjerkymovementsoftheli
mbsand
ortheface.Thereisstiffeningofthechildsarm
sandlegsanduncontrolled movements of
the limbs. The child may lose control of
the bladder, and is unconscious during
and after the convulsion.
Sometimes, in infants, the jerky
movements may be absent, but there may
be twitching (abnormal facial
movements) and abnormal movements of
the eyes, hands or feet.
10.3 Treatment of Coma
&Convulsions is similar and is
as follows:
Managethe Airway
a) Coma
Managing the airway is done in the same way
as treating any child with an airway or
breathing problem. This has been discussed
earlier. Give oxygen for the emergency
setting.
b) Convulsion
To manage the airway of a convulsing child
gentle suction of oropharyngeal secretions
should be done & child put in recovery
position and oxygen started.
Do not try to insert anything in the mouth to
keep it open.
10.3.2 Put the child in Recovery Position
Any unconscious child who is breathing and
keeping the airway open should be placed in
the recovery position.
T hispositionhelpstoreducetherisk
ofvomitenteringthechildslungs.
Ifneck trauma is not suspected
Turnthechildonthesidetoreducerisk
ofaspiration
Keeptheneckslightlyextendedandstabilizebypl
acingthecheekononehand
Bendonelegtostabilizethebodyposition
Position of unconscious child (trauma
Position of unconscious child (no trauma)
Figure-9: Position of Unconsious child
If trauma is suspected
- Stabilize the child while lying on the back.
- When the patient is not being moved, a
sandbag placed on each side or a cervical
collar can splint the neck.
- Use bottles or rolled towels in case
sandbag
LogareRoll
not available as shown in the
figure10 belo
Page 160
 Figure 12
10.3.4 Inserting an oropharyngeal airway in
an infant: convex side up
Selectanappropriatesizedairway
Positionthechildtoopentheairwayasdescribeda
bove, taking
carenottomovetheneckiftraumasuspected.

Figure 10 Usingatonguedepressor,inserttheoropharyngea
lairwaytheconvexsideup.
Use the log roll technique to turn the child
on the side if the child is Re-checkairwayopening.

Vomiting. Useadifferentsizedairwayorrepositionifnecess
ary.
Giveoxygen.
Management of Convulsions in
infantup to 2 weeks of age :
SecureIVaccess.
Ifbloodsugar<45mg/dl,give2ml/kg10%dextros
e.
Ifseizurescontinue:IV10%Calciumgluconate2ml
/kg to be diluted in distilled water in proportion
1:1over10minutes to be diluted in
whilemonitoringheartrate(in younginfants).
Ifseizurescontinue:IVphenobarbitone20mg/kg
Figure 11 in 20ml of 5% dextrose or saline
Insertionof an oropharyngeal (Guedel) over20min(Table1).
airway Ifnocontrol:Repeatphenobarbitone10mg/kgtill
atotalof40mg/kg.
The oropharyngeal or Guedel airway can be
used in an unconscious patient to improve Ifseizurescontinue:Givephenytoin20mg/kg in
airway opening. 20 ml of normal saline over20min.
It may not be tolerated in a patient who is Inj. Phenobarbitone intravenous dose
awake and may induce choking or vomiting. (200mg/ml)

Guedel airways come in different sizes

(Guedel size 000 to 4). An appropriate sized Weight Initial Repeat dose
airway goes from the centre of the teeth of Infant dose
(incisors) to the angle of the jaw when laid
on the face with the convex side up.
2 kg or 0.2 0.1 ml
less ml

2 to 4 kg 0.3 0.15 ml
ml

Page 161
 Dose of Phenobarbitone for young
infants (Table 4)
Caution:
DonotuseDiazepamforcontrolofconvulsionsin
Neonates<2weeks.
Managingconvulsions more than 2
weeks of age:
Diazepam is the firstdrug used to stop
convulsions (anticonvulsant), if the child is
Intravenous dose is 0.25mg/kg (0.05 ml/kg)
over 1 minute.Diazepamcan
affectthechildsbreathing,soitisimportanttore
assesstheairwayandbreathingregularly.
convulsing in front of you. No drug should
be given if the convulsion has stopped.
Diazepam can be given by the rectal or
intravenous route.
Rectal diazepam dose is 0.5mg/kg (0.1ml/kg)
by tuberculin syringe or a catheter acts within
2 to 4 minutes. Hold the buttocks together for
a few minutes

Per rectal dose of Diazepam (Table 5)

Diazepam given rectally 10 mg / Diazepam given IV
2 ml solution 10 mg / 2 ml solution
Age / weight
Dose 0.1 ml/kg Dose 0.05 ml/kg
2weeksto2months(<4kg) 0.3 ml 0.15 ml
2-<4months(4-<6kg) 0.5 ml 0.25 ml
4-<12months(6-<10kg) 1.0 ml 0.5 ml
1-<3years(10-<14kg) 1.25 ml 0.6ml
3-<5years(1419kg) 1.5 ml 0.7ml

12. Dehydration
If convulsions do not stop after 10 minutes The letter D in the ABCD formula stands for
of second dose of diazepam. Dehydration. Assess for severe

Inj Phenytoin can be given intravenously if Dehydration:To assess if the child is severely
access has been achieved. 15 - 20 mg/kg dehydrated ask for:
Phenytoin is diluted in about 20 ml of saline Lethargic
and given slowly (not more than 1 mg/kg
Phenytoin per minute). Childhavesunkeneyes

Alternatively phenobarbitone can be used in Skinpinchtakelongerthan2secondstogo back

a dose of 15- 20mg/kg IV (in 20 ml 5%
dextrose or saline) or IM.
At this stage, seek help of a senior or more
experienced person, if available If child has diarrhea with any two of the above signs
he is classified to have severe dehydration.
11. If there is high fever: 12.1 Treatment of severe
Spongethechildwithroom- dehydration in an emergency
temperaturewatertoreducethefever.
setting
Donotgiveoralmedicationuntiltheconvulsionhas
beencontrolled(dangerofaspiration).
Page 162
12.1.1 Severe dehydration (without severe IV fluidsfor severe dehydration (Table 6)
acute malnutrition)
StartIVfluidimmediately.Ifthechildcan AGE First give 30 Then give 70
drink,giveORSbymouthwhilethedripissetup.Gi ml/kg in ml/kg in
ve100ml/kgRingerslactatesolution (or
ifnotavailable,normalsaline)dividedasfollows:
*Repeatonceifradialpulseisstillveryweakornot
detectable.
Reassessthechildevery15-
30minutes.Ifhydrationstatusisnotimproving,giv Infants (Under 12 1hour* 5 hours
etheIVdripmorerapidly. months)

AlsogiveORS(about5ml/kg/hour)assoonasthechi
ldcandrink:usuallyafter3-4hours(infants)or1-
2hours(children).

Volume of ORS (Table 7) Children (12 months 30minutes* 2 hours

up to 5 years)

Weight Volume of ORS solution per hour

<4kg 15 ml

4-<6kg 25 ml

6-<10kg 40 ml

10-<14kg 60 ml

14 19 kg 85 ml

Themothercanmaintainhydration by giving the

If IV treatment not possible, give ORS 20 child ORS solution by mouth.
ml/kg/hour for 6 hours (120 ml/kg/day) by NG tube 12.1.2 Severe dehydration with severe acute
Reassessaninfantafter6hoursandachildafter3h malnutrition
ours.Classifydehydration.Thenchoosetheappr It is difficult to determine dehydration status in a
opriateplan(A,B, or C) to continue treatment severely malnourished child, as the usual signs
as you have learned in IMNCI / F-IMNCI. of dehydration (Such as lethargy, Sunken eyes)
may be present in these children all of the time
Giveoralantibioticforcholeraifchild2is whether or not they are dehydrated.
yearsorolder.
Signs of Dehydration
Lethargy
Restless, irritable:
Ifpossible,observethechildforatleast6hoursaft
errehydrationtobesurethat Sunken eyes
Thirsty
Page 163
 Skin pinch goes back slowly RECORD the respiration rate.
Treatment of dehydration in the children In addition the following should be recorded:
with SAM without shock Pulse rate.

If the child has had watery diarrhea or vomiting,
assume dehydration and give ORS. WHO
recommends use of ReSoMal, which is not available
commercially. Use either WHO-low Osmolarity
ORS with potassium supplements (15 ml
ofpotassium chloride syrup added to one litre ORS)
as mentioned in step 4 or ReSoMal prepared from
WHO-low Osmolarity ORS
Calculate amount of ORS to give
Table-8: Give ORS as follows in amounts based on
the childs weight
The capillary refill time
The malnourished child is managed preferably by:
Clinical signs of improvement and
Clinical signs of over-hydration.
13. MANAGEMENT OF
SHOCK IN CHILDREN
WITH SAM
Give this treatment only if the child has signs of
shock and is lethargic or has lost consciousness

How often to give ORS Amount to give 13.1 Weigh the child Estimate the
Every 30 minutes for the 5 ml/kg body weight weight if child cannot be
first 2 hours
Alternate hours for up to 5-10 ml/kg weighed or weight not
10 hours known
The amount offered in this range should be based on
the childs willingness to drink and the amount of
13.2 Give oxygen
ongoing losses in the stool. Starter (diet is given in 13.3 Make sure child is warm
alternate hours during this period until the child is 13.4 Insert an IV line and draw
rehydrated.
blood for emergency
BEFORE starting any rehydration treatment:
laboratory
WEIGH the child (The weight should be taken on
admission)
MARK the edge of the liver and the costal margin
on the skin

Page 164
 Investigations

Give IV 10% Glucose (5ml/kg)

Give IV fluid 15 ml/kg over 1 hour of either ringers lactate in 5%

Dextrose or half-normal saline with 5% glucose

Measure the pulse and breathing rate at the start and every 5-10 minutes

If the child fails to

Improve after the first
15ml/kg IV
Repeat same fluid IV
15ml/kg over 1 hour
more; then
If the child deteriorates
During the IV
(RR increases by 5/min or
PR by 15 beats per min)
Stop the infusion and reassess

Give maintenance IV
fluid (4 ml/kg/hr) Assume
The child has septic shock
Start dopamine
Sign of improvement
(PR and RR fall)
Rehydration
Review antibiotic treatment

Switch to oral or nasogastric rehydration

With ORS 10ml/kg/hr up to 10hours Initiate re-feeding as soon as
Initiate feeding with starter formula Possible

Figure-13:Treatment of shock

Page 165
The management of shock in child with severe acute
malnutrition is given is char3
13.5 Broad spectrum antibiotic
should be administered
Immediately to all SAM with septic shock (table2)
packed RBCs 10ml/kg should be given over
4-6 Hours if HB is less than 4 gm/dl or active
bleeding. If there is no improvement with fluid
Bolus start dopamine at 10pg/kg/min if there is no
improvement in next 24-48 hours upgradesan
ntibiotics.
13.6 How to give Dopamine (By
infusion pump)
Amount of dopamine (mcg) to be added =
weight in kgX6
To convert this dose into amount to ml of
dopamine dived by 40 (1 ml of dopamine=
40mg of doplamine
Add this amount of dopamine (ml) to make 10
ml of total fluid.
0.1 ml/hour of this fluid gives 1 mcg/kg/minute
To give 10 mcg/kg/minute gives infusion at the
rate on 1ml /hr
Amount of dopamine to be added = 5X6=
30mcg
Page 166
2. NEONATAL RESUSCITATION GUIDELINES
Stabilization (warm, position, clear airway, dry,
1. What is Neonatal stimulation, reposition )
Resuscitation? Ventilation
Neonatal resuscitation means to revive orrestore life Chest compression
to a baby from the state of asphyxia. Intubation
The following guidelines are intended to neonates Drug administration
undergoing transition from intrauterine to extra (The decision to progress from one category to
uterine life. another should be assessed by vital signs;
respiration, heart rate, colour. Approximately 30
seconds is allotted to complete each step)
2. A rapid assessment of the
following 4 characteristics: 3. Preparing for Birth
Was the infant born full-term gestation? Essential:
Is the amniotic fluid clear of meconium and i. A draught free, warm room with
evidence of infection? temperature >25 degree Centigrade
Is the infant crying or breathing, colour of ii. A clean, dry and warm delivery surface
baby? iii. A radiant warmer / overhead lamp with
Does the infant have good muscle tone? 200 watt bulb if available
iv. A newborn size self inflating bag
If the answer is to all 4 of these question is yes, the v. Infant masks in two sizes: size 1 for
infant does not need resuscitation and should not be normal weight baby and 0 for small baby.
separated from mother. vi. A suction device, feeding tube 6F/8F/9F
Observation of breathing, activity, and colour vii. Oxygen (if available)
should be ongoing. viii. Endotracheal Tube size 2.5/3/3.5

If answer is no then the infant should receive 1 or

more of the following 4 categories in sequence.
ix. Laryngoscope 0/1

Page 167
 Table-1: Immediate Newborne Care

Immediate Newborn Care

Assess by checking
Is the baby term gestation?
Is the amniotic fluid clear?
Is the baby Breathing or crying?
Does the baby have Good muscle tone?

If yes, provide Routine careRoutine If no

Place the baby on the mother's abdomen. Dry the baby

with a warm clean sheet. Do not wipe off vernix. Proceed for
Wipe the, mouth and nose with a clean cloth. resuscitation
Clamp the cord after 1-3 min and cut with a sterile instrument. Tie the cord with a sterile tie.
Examine the baby quickly for malformations/birth injury.
Leave the baby between the mother's breasts to start skin-to skin care.
Support initiation of breastfeeding.
Cover the baby's head with a cloth. Cover the mother and baby with a warm cloth.
Place an identity label on the baby.
Give Inj Vit K 1 mg IM (0.5mg for preterm).
Record the baby's weight
Refer if birth weight <1500g. has major congenital malformations or has severe respiratory
distress

Page 168
 3. GUIDELINES FOR MANAGEMENT OF
NORMAL NEWBORN

- Endotracheal tubes (3, 3.5 mm)

1. Care at Birth:
The four basic needs of ALL newborns at the time - IV cannula (24G)
of birth and for the firstfew weeks of life are:
- Drugs (Inj. Epinephrine , Normal saline,
1. To be warm Inj.Vitamin K)
2. To breathe normally
3. Immediate Newborn Care
3. To be protected (prevent infection)
of a NormalNewborn at
4. To be fed
the time ofBirth:
Most babies would require routine care; 5-10%
Module I : Care ofthe normal baby atbirth

2. Newborn Care Corner may need assistance to establish adequate

breathing and therefore will need resuscitation.
2.1 This is a space within the Deliverthebabyontoawarm,cleananddrytowell
delivery room for facilitating orclothandkeeponmother's
immediate care of the abdomenorchest(betweenthebreasts).
Dry the Baby with a warm clean sheet. Do not
newborn. This area is wipe off vernix
mandatory for all health Wipeboththeeyesseparatelywithsterileswab.
facilities where deliveries take Clampandcuttheumbilicalcordafter1to
place. 3minute,ifbabyisbeathing.

2.2 Equipment and supplies that Well.

should be available in the Assessthebaby'sbreathingwhiledrying.
corner: Examine the baby quickly for Malformation and
birth injury.
2.2.1 Equipment: - Radiant warmer with
bassinet Leavethebabybetweenthemother'sbreaststostartskin
- Suction equipment -to-skincareforatleastan hour.

- Weighing machine Coverthebaby'sheadwithacap.Coverthemotherandb

abywithawarmcloth.
- Self inflatingresuscitation bag (500 ml) with masks
(size 0, 1) Placeanidentitylabel/band/tag onthebaby and mother

- Oxygen source Encouragemothertoinitiatebreastfeeding(withinhalf

anhourofbirth).
- Laryngoscope (straight blade, size 0,1)
- Wall Clock
- Room thermometer
4. Ensuring WARM
CHAIN'
2.2.2 Supplies: - Clean baby sheets
4.1. At delivery
- Sterile cord ties Ensurethedeliveryroomiswarm(25-
- Sterile Gloves 28C),withnodraughtsofair
Drythebabyimmediately; removethewetcloth.
- Sterile blade/scissors Put the baby on the mothers abdomen.
- Mucus extractors Coverthebaby and mother withcleandrycloth
Keep the baby in skin to skin contact with mother
- Suction catheters (10F, 12F) on chest or abdomen
- Feeding tube (6F, 8F) Postpone bathing/sponging for at least 12 hours or
next day
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4.2. After delivery
Keep the baby clothed and wrapped with the head
covered.
Avoid bathing especially in cool weather or for
small babies.
Keep the baby close to the mother
Use kangaroo care for stable LBW babies and
for re-warming stable bigger babies
Show the mother how to avoid hypothermia,
how to recognize it, and how to re-warm a cold
baby.
The mother should aim to ensure that the
baby's feet are warm to touch
4.3 If mother and babys
separation is necessary, do the
following.
Wrap the baby in a clean dry warm cloth and place
under a radiant warmer. If warmer is not available
ensure warmth by wrapping the baby in a clean dry
warm cloth and cover with a blanket. Ensure babys
head, hands and feet are covered.
Re-start Skin-to-skin contact as soon as mother and
baby can be roomed-in
5. Prevention of infections:
CLEAN CHAIN'
5.1. Clean delivery (WHOs six
cleans)
Clean attendant's hands (washed with soap)
Clean delivery surface
Clean cord- cutting instrument (i.e. razor, blade)
Clean string to tie cord
Clean cloth to cover the baby
Clean cloth to cover the mother
5.2. After delivery
All caregivers should wash hands before handling
the baby
Feed only breast milk
Keep the cord clean and dry; do not apply anything
Use a clean absorbent cloth as a diaper/napkin
Wash your hands after changing diaper/napkin.
Keep the baby clothed and wrapped with the head
covered
5.3. Immediate Cord Care
Clamp the cord after 1-3 min of delivery and cut
with a sterile instrument
Tie the cord between 2 to 3 cms from the base and
cut the remaining cord.
Observe for oozing blood. If blood oozes, place a
second tie between the skin and first tie.
Do not apply any medication/substance on the
stump.
Leave stump uncovered and dry.
5.4. Care of the eyes
No routine eye care is required
Do not instill any medicine in the eyes
6. Weighing the baby
Weigh all babies before transfer from the delivery
room
Initiate breastfeeding within 1 hour
Support mother to initiate breast feeding within
the first hour.
The babys first feed of colostrum is very
important because it helps to protect against
infections.
The baby can feed from its mother whether she is
lying down or sitting; baby and mother must be
comfortable
Do not give artificial teats or pre-lacteal feeds to the
newborn e.g. sugar water or local foods or even
water.
7. Examine the baby
7.1 A complete examination should
be performed within about 60
minutes after birth
Count the number of breaths during one minute.
Observe the movement of the limbs when
awake, their position when not moving and
their tone.
Observe the skin color.
Inspect the following body areas for
abnormalities: head, face, mouth and palate,
chest, abdomen, genitalia, anus, limbs and skin
7.2 A well baby should have
Normal temperature , warm to touch, pink with
Weight > 2.5 kg
Breathe easily at 40-60 breathes/minute
Move arms and legs equally when active and
rest with limbs flexed
Explain to mother the examination findings to
allay her concern.
Document in case record and ask her to inform
you , in case any other concerns develop
subsequently.
8. Give Vitamin K
Vitamin K will protect babies from serious
bleeding.
Give Vitamin K by intramuscular (IM)
injection 1.0 mg for every newborn (0.5 mg
for <1000 gms).
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 Encourage mothers to breastfeed their baby
during the injection for comfort.
9. Monitoring the Baby
Table-1: Monitoring the baby in the first hour after
birth
Parameter Whattolookfor?
Breathing Listenforgrunting;Lookforchestin-
drawingandfastbreathing
Warmth Check to see if baby's feet are
cold to touch (by using dorsum of
your hands)
Color Evaluatethecolorofthetrunkandextremitie
s llypreparedtotakecareoftheirbabies afterbirth.
10. Special Situations
10.1 Caesareansection,instrumentaldelivery:
Skin-to-skin contact and breastfeeding in
difficult deliveries (caesarean section,
instrumentalandbreechdelivery):
Breastfeedingcanbegivnassoonasthemotherisco
mfortableandabletorespondto
herbaby.Itdoesnothavetobedelayed
Amotherwhowasgivenageneralanaestheticagent
shouldbegivenskin-to-skincontact
assoonassheisabletorespondtoherbaby.Thismayb
einitiatedwithinonehourof birth.
Amotherwhohashadanepidural
(spinal)anaesthetiamaybeabletostartskin-to-
skincontactverysoonaftersurgery
Thesemotherswill
needadditionalassistanceinpositioningandattachi
ngthebaby
comfortably.Breastfeedinginlyingdownposition
maybemorecomfortableinthefirst days
10.2 HIV and newborn care at birthCare of a baby
born to HIV+ve mother
Care of the baby at delivery should be no different
from the care already described.
Standardsafetyprecautionsmustbefollowedaswithany
otherdelivery.
Babycanhaveimmediateskin-to-
skincontactasanyothermotherandbaby.
Exclusivebreastfeedingistherecommendedfeedingch
oiceintheir first6
months,irrespectiveofthefactthatthemotherisonARTe
arly(or)infantis
providedwithprophylaxisfor6weeks.(preferably)*
If mother chooses replacement feeding,
prepare formula for the first few
feeds.Ensureitissafe,affordableandsustaina
bleforfamily.
Allothercare(includingcordcareandeyecare)remainst
hesame.
Giveoralnevarapineforsixweekstotheneonateaspernat
ionalpolicy.
Mothershouldbecounseledregardingthemodeoff
eedingbeforedelivery
anddangersofmixedfeeding.
11. Postnatal Care of
Normal Baby
Ideally, allpregnant women should be counseled
regarding the care of the baby during the
antenatalperioditself.Thiswouldhelpthemtobementa
11.1. Postnatal environment
Ensure that the room is warm without air currents.
Keep mother and baby close together in same room
and same bed.
Provide bed nets to sleep.
11.2 The key areas of every day
care of a newborn baby
include:
11.2.1. Breastfeeding
Supportexclusivebreastfeedingondemanddayan
dnight.
Askthemothertogethelpifthereisabreastfeedingdi
fficulty.
Assessbreastfeedingineverybabybeforeplanning
fordischarge.
If
themotherreportsabreastfeedingdifficulty,assess
breastfeeding
andhelpherwithattachmentandpositioning.
DONOTdischargethebabyifbreastfeedingisnotes
tablished.
11.2.2Keeping the cord healthy
Washhandsbeforeandaftercordcare.
PutNOTHINGonthestump.
Foldnappy(diaper)belowthelevelofthestump.
Keepcordstumplooselycoveredwithcleanclothes.
If stump is soiled, wash it with clean water and
soap.
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 Dry it thoroughly with clean cloth.
Lookforsignsof infection (daily).
- Pusdischargefromthecordstump.
-
Rednessaroundthecordespeciallyifthereissw
elling.
- High temperature (more than 37.5C) or other
signs of infection
Explain to the mother that she should seek care
if the umbilicus is red or draining pus or blood.
It is important to teach the mothers that the
umbilical stump should be left dry; they SHOULD
NOT APPLY ANYTHING on the stump.
11.2.3 Ensuring hygiene
Wash the face, neck, and underarms of the baby
daily.
Do not bathe the baby before 24 hours of age or
if the baby is cold.
In case of small babies, bathe only
after the baby reaches a weight of
2000g.
If bath is given
Ensureroom is warm and there is no draught
while changing clothes, washing and bathing
Use warm water for bathing
Thoroughly dry the baby, dress and cover after
bath
Take extra precautions if the baby is small
Wash the buttocks when soiled. Dry thoroughly.
Use cloth diaper on baby's bottom
to collect stool. Dispose off the
stool as for woman's pads. Wash
hands after disposing.
Do not apply Kajal on eyes
11.2.4 Looking for danger signs and giving
treatment
Itisimportantthatmothers,caregiversandhealthwork
ersareableto recognize thesigns
andsymptomswhichindicatethatthebabyisnot well
('DANGERSIGNS').
Earlyrecognition of the danger signs will help in
identifying those babies who need urgent care and
treatment.
Danger Signs are -
Not feeding well
No movement
Fast breathing (more than 60 breaths per
minute)
Moderate or severe chest in-drawing
Jaundice on day 1 or palms or sole stained
yellow any age abnormal movements.
Fever (temperature >37.5C)
Temperature <35.5C or not rising after re-
warming
Normal neonate: Preparing for discharge
12. Ensure immunization
Allbabiesshouldreceivethefollowingvaccinesim
mediately after birth
beforedischargefromthehealthfacility:
- BCG,
- OPV-0,
- Hepatitis B(HB-0)
13. Criteria for discharge
from a health facility
Feeding well (suckling effectively) at least 8
times in 24 hours
No danger signs
Mother is confident to take care of baby
Understands the need for follow up and danger
signs when to report early
For small baby below 2500gms: feeding well
and gaining weight adequately
14. Advise on essential care
for neonate at discharge
14.1. Feed breast milk
Breast milk is the best and is the only food
baby needs for first six months Mother needs
to breastfeed day and night, at least eight
times in 24 hours Mothers need to take
nutritious meals and should drink lots of
clean water.
For a smallbaby who finds difficult to
suckle,express breast milk and collect in a
clean cup to feed the baby with a paladai, cup
or spoon.
14.2. Keep clean
Wash your hands with clean water and soap
before every feed and after visiting toilet and
handling baby's faeces / urine.
Keep the surroundings clean
Keep the cord stump clean; do not apply
anything on cord
14.3. Keep warm
Keep the baby well wrapped in a clean dry
cloth or blanket (in cold season) Cover baby's
head with part of cloth / blanket or put a cap
on the head Keep the room warm avoid direct
draught of air
Keep next to mother for warmth; it promotes
lactation and mother-baby bonding
Encourage KMC for Low birth weight babies
14.4 Counsel and educate the
mother and family
Build confidence of the family intaking care
of baby at home
Ensure that the family understands
importance of administering prescribed
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 medicines for the whole duration.
Educate mother when to reportfor follow up
after discharge
Educate mother when to reportearly if
thereisworsening of condition at any time
after discharge
Educate mother for signs of well babyfeeds
on breast, active behavior,pink extremities
and trunk &extremities are warm to touch.
Ensure baby is
gaining weight on
follow up.
Advicefor timely immunization
15. Management of Common
Clinical Conditions in
New Borns
There are several phenomena after birth that are
normal and mothers only need reassurance. These
include:
Developmental variations & Physiological
conditions
Knowledge of developmental variations,
physiological conditions and their evolution
innewborns is important for advising and assuring
the mother. Mothers observe their babies very
carefully and are often worried by minor physical
peculiarities, which may be of noconsequence and
do not warrant any therapy.
15.1. Mastitis neonatorum
Engorgement of breasts occurs in term babies
of both sexes on the third or fourth day and
may last for days or even weeks which is due
to persistence of maternal hormones for some
time.
Local massage, fomentation and expression
of milk should not be done as it may lead to
infection. Mother should be reassured that
this regresses on its own.
15.2. Vaginal bleeding
Vaginal bleeding may occur in female babies
about three to five days after birth which is
because of withdrawal of maternal hormones.
The bleeding is mild and lasts for two to four
days.
Additional vitamin K is unnecessary.
15.3. Mucoid vaginal secretions
Most female babies have a thin, grayish,
mucoid, vaginal secretion, which should not
be mistaken for purulent discharge.
15.4. Toxic erythema or Erythema
neonatorum
This is an erythematous rash with a central
pallor appearing on the second or third day in
term neonates which begins on the face and
spreads down to the trunk and extremities in
about 24 hours. This should be differentiated
from pustules which need treatment.
It disappears spontaneously after two to three
days without any specific treatment. The
exact cause is not known.
Weight loss of 6-8% (10-12% in preterm
infants) in the first few days of life is normal
and most infants regain their birth weight by
10-14 days.
15.5. Bowel disorders.
No medication should be prescribed for passage of
stools after each feed (exaggerated gastrocolic
reflex) as this is normal in some babies. From 3rd to
14 days many exclusively breasfed babies pass
loose stools (10-15 times/day) without
illness/dehydration. These are transitional stools and
require no medication.
15.6. Delayed passage of urine.
Non-passage of urine by 48 hours after birth may
suggest urinary tract anomalies. Such babies need to
be investigated. Crying before passing urine is
normal.
Jitteriness is abnormal only when it is excessive or
persists even during feeding and then it may suggest
hypoglycaemia or hypocalcaemia.
15.7. Dehydration fever.
Transitory moderate fever (up to 38.50C) usually
during the second or third day of life in summer
months in an active baby, who sucks well, is normal
and responds to lowering the environmental
temperature.
15.8. Excessive crying.
Most baby cry when either they are hungry or are
having discomfort such as due to full bladder before
passing urine, wet napkin, nose block, etc.
Excessive inconsolable crying or high-pitched
crying is indicative of meningitis or any other
painful inflammatory conditions.
15.9. Umbilical granuloma.
A red flesh-like nodule at the base of umbilical cord
can be managed by cautery with Silver Nitrate or
application of common salt for 3 to 4 days.
16. Normal phenomena in
new born
Peeling skin: Dry skin with peeling and
exaggerated transverse sole creases is seen in
all postterm and some term babies.
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Milia: Yellow white spots on the nose or face
due to retention of sebum, are present in
practically all babies and disappear
spontaneously.
Storkbites (Salmon patches or nevus simplex):
These are discrete, pinkish- gray, sparse,
capillary hemangiomata commonly seen at the
nape of neck, upper eyelids, forehead and root
of the nose.. They invariably disappear after a
few months.
Mongolian blue spots: In babies of Asiatic
origin irregular blue areas of skin pigmentation
are often present over the sacral area and
buttocks, though extremities and rest of the
trunk may also be affected. These spots
disappear by the age of six months.
Subconjunctival hemorrhage: A semilunar arc
of sub-conjuctival hemorrhage is a common
finding in normal babies. The blood gets
reabsorbed after a few days without leaving any
pigmentation.
Epstein Pearls: These are white spots, usually
one on either side of the median raphe of the
hard palate. Similar lesions may be seen on the
prepuce. They are of no significance.
Sucking callosities: The presence of these
buttons like, cornified plaques over the centre
of upper lip has no significance.
Tongue Tie: It may be in the form of a fibrous
frenulum with a notch at the tip of the tongue.
This does not interfere with sucking or later
speech development.
Non retractable prepuce: The prepuce is
normally nonretractable in all male newborn
babies and should not be diagnosed as
phimosis. The urethral opening is often pinpoint
and is visualized with difficulty. The mother
should be advised against forcibly retracting the
foreskin.
Hymenaltags: Mucosal tags at the margin of
hymen are seen in two-third of female infants.
Umbilical hernia: Umbilical hernia may
manifest after the age of two weeks or later.
Most of these disappear spontaneously by one
or two years of age.
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 4. CARE OF AT-RISK NEONATES

The care of 'at-risk' neonate should be initiated at

1. An 'at-risk' neonate has the health facility itself under direct supervision.
one or more of the After initial improvement, further care can be
provided at home
following features:
Weight 1500-2499g 2. The care of at-risk babies
Temperature (axillary) 36.0C-36.4C
Babies with moderate or severe hypothermia
is outlined below:
who respond to warming 2.1. Warmth:
Cried late (>1min) but within 5 minutes of Grading of hypothermia
birth
Sucking poor, but not absent sucking reflex Normal temperature: 35.5-36.5C
Depressed sensorium, but is arousable Cold stress : 36.4-36.0C
Respiratory rate of over 60 per minute, but no Moderate hypothermia : 35.5-
chest retractions 32C
Jaundice present, but no staining of Severe hypothermia : <32C
Module 8:Care ofAt-risk and Sick Neonates

palms/soles
Presence of any one of the following:
- Diarrhea or vomiting or abdominal distension
- Umbilicus draining pus or pustules on skin
- Fever

The steps are dependent up on the current temperature of the baby (see below). (Table 1)

Temperature Management
Normal -Prevent hypothermia
temperature - Wrap the baby in layers of clothing
- Cover the head and limbs
- Place the baby in direct contact with mother
- In winter months, the room may have to be warmed with heater,
etc

Cold stress -Treat hypothermia

(temperature - Wrap the baby with extra layers of clothing
36.0C and 36.4C) - Cover the head and limbs
-Place the baby in close contact with the mother, preferably skin-to skin
In winter months, heat the room with a heater , etc.

Hypothermia - Requires immediate exposure to a radiant

(Temperature heat source (such as radiant warmer) or heater
2.2. Stabilization Most of these babies do not require stabilization

Page 175
other than prevention for hypothermia as above. If
there is occasional apnea, physical stimulation may
be provide
2.3. Feeds
The baby is started on direct breast feeding. If not
sucking well, she is provided expressed breast milk
by spoon or paladai. Occasionally, expressed
breast milk may have to be given by gavage
feeding.
2.4. Specific therapy

Some simple conditions can be readily treated at the health facility and later at home. (Table 2)
Condition Treatment
Umbilical redness - Local application of 1% gentian violet
And Discharge -Syrup Amoxycillin 1.25ml TDSx7days
Skin pustules Local application of 1% gentian violet.
Syrup Amoxycillin 1.25ml TDSx7days

Module 8:Care ofAt-risk and Sick Neonates

Pneumonia (Respiratory
rate >60/min, no chest syrup Amoxycillin 1.25ml TDSx7days) retractions)

2.5. Monitoring 2.7. Communication

The following signs should be monitored everytwo Communication with the family, especially the
hours: mother is very important during the management of
at-risk and sick neonates.
Signs to be monitored
Communication with the family
Temperature
1. Reassure the mother and family.
Convulsion
Sucking
2. Prepare a note regarding baby's condition and
care.
Bleeding
3. If baby improves and is to be sent home,
Sensorium explain care of the baby at home.
Diarrhea 4. If baby does not improve or worsens,
explain the need for referral and care
Respiration
during transport.
Vomiting
Apnea
3. FOLLOW - UP
Advice about follow-up visits
Abdominal distension
Keep the baby warm
Cyanosis
Provide exclusive breast milk feeding
2.6. Re-evaluation Continue the prescribed treatment
Observe progress of baby
After stabilization and/or specific therapy, the baby
Counsel and educate the mother and family
has to be re-evaluated for improvement.The two
Follow-up:
cardinal signs of improvement are:
A home visit by the health worker one day after
i. The temperature will become normal evaluation at hospital is desirable. Thereafter
(36.5C -37.5C) and the baby should be seen again after 2 and 7
ii. The baby will accept feeds well. days by health worker.

Page 176
 5. CARE OF SICK NEONATES
1. A sick neonate is the one
who has any of the
following features:
Weight <1500 g
Temperature <36C despite warming for one
hour
Cried after 5 minutes of birth
Absent sucking
Not arousable
Respiratory rate more than 60/min with chest
retractions
Apnea or gasping respiration
Central cyanosis
Jaundice staining palms/soles
Convulsions
Bleeding
Major malformation
Presence of two of the following
- Diarrhea or vomiting or abdominal distension
- Umbilicus draining pus
- Multiple skin pustules
- Fever
Alsorememberthatifan'at-
risk'neonatedoesnotimprovewhilebeing
observedunderyourcare,heisalsoconsideredasickneo
nate.
2. Grading and management
of hypothermia
Baby who is cold to touch both centrally and
peripherally or temperature is less than 35.5C
2.1. Management of hypothermia
Record the actual body temperature
Re-warm a hypothermic baby as quickly as
possible:
Severe hypothermia Radiant warmer
Mild to moderate hypothermia- Kangaroo
mother care or Radiant warmer
If hypothermia still persists despite taking above
measures, infection should be suspected
2.2. Management of severe
hypothermia
Keep under radiant warmer
Reduce further heat loss
Infuse IV 10% Dextrose @ 60ml/kg/day
Inject Vitamin K 1.0 mg intramuscular
Provide oxygen
Consider and assess for sepsis
3. Prevent hypothermia: warm
chain
Baby must be kept warm at all times right from
birth. The "warm chain" is a set of 10 interlinked
procedures carried out at birth and later
Warm delivery room (>25C)
Warm resuscitation
Immediate drying
Skin-to-skin contact between baby and the
mother
Breast feeding
Bathing and weighing postponed
Appropriate clothing and bedding
Mother and baby together
Warm transportation
Training/awareness-raising of healthcare
provider
4. Expression of breast milk
Breast milk expression is required for optimal
feeding of newborns for preterm, low birth weight
and sick newborns that cannot breastfeed but can
tolerate assisted feeding.
Expressing breast milk
4.1. Teach the mother to:
Wash hands with soap and water before
expression. Hold, handle or cuddle the baby
Sit comfortably and hold the clean container
near the breast
Put thumb and index finger on the breast at the
rim of the areola opposite each other. Support
the breast with other three fingers.
Press thumb and index finger slightly inward
towards the chest wall
Press the breast between the fore-finger and
thumb. Press and release, press and release.
This should not hurt
Press the areola in the same way from the sides,
this ensures that milk is expressed from all
segments of the breast
Avoid rubbing or sliding fingers along the skin
Express one breast for at least 3-5 minutes until
the flow slows; then expresses the other side;
and then repeats on both sides
Page 177
 To express breast milk adequately it may take Feed with cup or spoon or paladai, never feed
20-30 minutes with bottle

4.2. Storing expressed breast milk 5. Assisted feeding of low

(EBM) birth weight neonates
Cover the container of EBM with a clean cloth
or a lid 5.1. Newborns that require
EBM can be kept at room temperature for 8 assisted feeding:
hours and in the refrigerator for 24 hours Preterm <34 weeks or birth <1800 g
EBM stays in good condition longer than Babies having mild respiratory distress
animal milk. Do not boil the EBM. For Babies with inability to feed at breast or by
warming place the container in a bowl of warm katorispoon/paladai
water Oro-facial defects/malformation (Cleft lip or
Before feeding gently shake the container or palate)
use a stirrer to recombine the separated fat
globules with the rest of the milk

Table 1
Guidelines for the modes of providing fluids and feeding

Birth weight (grams) < 1200 1200-1800 >1800

Gestation (weeks) < 30 30-34 >34
Initial feeding Intravenous fluids try Gavage, try katori- Breastfeeding, if
gavage feeds, if not spoon if not sick unsactisfactory, give
sick katori-spoon feeds
After 1-3 days Gavage Katori-spoon Breastfeeding
Later (1-3 weeks) Katori-spoon Breastfeeding Breastfeeding
After some more time Breastfeeding Breastfeeding Breastfeeding
(4-6 weeks)

5.2. Mode for providing fluids and
feeds
Breast milk is the ideal feed for low birth weight
babies.
Those unable to feed directly on the breast can be
fed expressed breast milk (EBM) by gavage OR
katori-spoon or paladai.
Leave oro-gastric tube in situ
Pinch the oro-gastric tube during withdrawal
Measure pre-feed abdominal girth just above
the umbilical stump. Do not attempt pre-feed
aspirates
Evaluate baby for ileus, if abdominal girth
increases by >2cm from baswline

5.3. Techiques of assisted feeding: 5.4. ROUTINE RE-FEED

Gavage feeds
Place an oro-gastric feeding catheter of size 5-6
Fr after measuring the correct insertion length
from ala of nose to tragus and from tragus to
midway between xiphisternum and umbilicus
Check correct placement by pushing in air with
10 ml syringe and listening with stethoscope
over upper abdomen
Attach 10 ml syringe (without plunger) at the
outer end of the tube, pour measured amountof
milk and allow milk to trickle by gravity. Close
outer end of tube after feeding
Place baby in left lateral position for 15 to 20
minutes to avoid regurgitation
GASTRIC ASPIRATES ARE
NOT RECOMMENDED
Katori-spoon/paladai feeds
Place the baby in a semi-upright posture
Place the milk filled spoon at the corner of
mouth
Allow milk flow into baby's mouth slowly,
allowing him to actively swallow, avoiding
the spill
Reapeat process till required amount has been
fed
Try gently stimulation if baby does not
actively accept and swallow the feed
If unsuccessful, switch back to gavage feeds.

Page 178
 Change the IV infusion set and fluid bag
6. Intravenous fluid therapy every 24 hours
for newborn: Before infusing IV fluid, carefully check:
Expiry date of the fluid
6.1. Criteria for starting Seal of the infusion bottler or bag
intravenous fluids Fluid is clear and free from any visible
Among newborns particles
Neonates with lethargy and refusal to feed
Moderate to severe breathing difficulty 6.4. Monitoring of babies receiving
Babies with shock
Babies with severe asphyxia
IV fluid:
Inspect infusion site every hour for redness
Abdominal distension with bilious or blood
and swelling
stained vomiting
If redness and/or swelling is present, stop
6.2. Choice of intravenous fluids infusion, remove cannula, and establish a
Determine required volume of fluid as per new IV line in a different vein
birth weight and age (Table 2) Check the volume of fluid infused, compare
Use 10% Dextrose for initial 48 hours of life to the prescribed volume and record all
After 48 hours, if baby is passing urine, use findings
commercially available IV fluids such as Measure blood glucose every nursing shift,
lsolyte P i.e. 6-8 hours
If the premixed solution is not available or If the blood glucose is less than 45 mg/dl,
baby requires higher GIR (Glucose infusion treat for low blood glucose
rates) If the blood glucose is more than 150 mg/dl
Take normal saline (NS) 20 ml/kg body on two consecutive reading: Change to 5%
weight Dextrose solution-measure blood glucose
Add remaining fluide volume as 10% again in three hours
Dextrose Weigh the baby daily. If the daily weight loss
Add 1 ml KCL/100 ml of prepared fluide is more than 5% increase the total volume of
fluid by 10 ml/kg body weight for one day
6.3. Administration of IV fluid If there is no weight loss in the initial 3 days
Use micro-drip infusion set (where 1 ml=60 of life, do not give the daily increment
microdrops) If there is excessive weight gain (3-5%)
In this device, ml of fluid per hour is equal to decrease t he fluid intake by 15-20 ml/kg/day
number of micro-drops per minute Check urine output: Normally a baby passes
e.g. 6ml/hr = 6 micro-drops/minute urine 5-6 ml/kg/day
Calculate rate of administration, monitor to Check urine output: Normally a baby passes
ensure that micro-dropper deliver requires urine 5-6 times everyday
rate Fluid requirements of newborns
Establish an IV line. Infuse a bolus of 2 ml/kg
Table 2 body weight of 10% dextrose slowly over 5 min
If baby had convulsions, give bolus of 4-5 ml/kg of
Day of life Amount of fluids required 10% dextrose
(ml/kg/day)
Birth weight > Birth weight
7. Management of
1500 g <1500 g hypoglycaemi
1 60 80 Hypoglycemia in newborns is defined as blood
2 75 95 glucose levels less than 45 mg/dl
3 90 110 Management of hypoglycaemia
4 105 125 Establish an IV line. Infuse a bolus of 2 ml/kg
5 120 140 body weight of 10% dextrose slowly over 5 min
6 135 150 If baby had convulsions, give bolus of 4-5
ml/kg of 10% dextrose
Day 7 150 150
If an IV line is not available, administer 2 ml/kg
onwards body weight of 10% dextrose by gastric tube
Hypoglycemia in newborns is defined as blood Start infusion of dextrose at the daily
glucose levels less than 45 mg/dl maintenance volume to provide at the rate of 6
Management of hypoglycaemia mg/kg/min

Page 179
Measure blood glucose after 30 min and then Repeat bolus of dextrose as above
every four to 6 hrs Increase to infusion rate of 8 mg/kg/min
If blood glucose < 25 mg/dl:

Page 180
 6. Management of Low Birth Weight Babies

Nearly 75 percent neonatal deaths and 50 percent
infant deaths occur among the low birth weight
neonates. Even after recovering from neonatal
complications, some LBW babies may remain more
prone to malnutrition, recurrent infections, and
neurodevelopment handicaps. Low birth weight,
therefore, is a key risk factor of adverse outcome in
early life.
1. Low birth weight
Low birth weight (LBW) baby is the one who
weighs less than 2500 g at birth.
Low birth, weight may result from either
prematurity (gestational age <37 weeks) or
intrauterine growth retardation (IUGR), which is
also called small for date baby (SFD).
Preterm babies have distinct physical features
that help in their recognition These are:
1.2.1 Skin:The skin of preterm neonate is thin,
transparent and gelatinous whereas that of aterm
neonate is thick gelatinous and keratinized.
Hair: The back of the preterm babies has abundant
growth of fine hair called lanugo.

1.2.2 Ear Cartilage:The external ear or the pinna is soft and devoid of
cartilage in preterm neonates and hence, it does not recoil back promptly
on being folded. In a term baby there is instant recoil.

Figure 1

1.2.3 Breast Nodule:Breast nodule measures less than 5mm in

preterm neonates and 5 mm or more in term babies.

Figure 2

1.2.4 Sole Creases:Anterior one third of the sole reveals a deep

transverse skin crease in preterm neonates and in term neonates they are
present over the anterior two-thirds.

Figure 3

1.2.5 External Genitalia:In males, the scrotum does not have rugae
and testes are not descended into the scrotum. In female infants, the labia
are widely separated, not covering the labia minora, resulting in the
prominent appearance of the clitoris.

Page 181
 Figure 4
1.3 Pre-Term Full-Term
Small-for-dates neonates have an emaciated look
and loose folds of skin because of lack of
subcutaneous tissue. These are particularly
prominent over the buttocks and the thighs. They
look alert and often plethoric.
2. Problems of preterm
neonates
The basic underlying feature of the preterm LBW
infant is immaturity of its organ system. They are
prone to develop
Asphyxia necessitating resuscitation.
Hypothermia
Feeding problems - Preterm neonates less than
34 weeks of gestation cannot coordinate
sucking and swallowing. Therefore, they are
unable to feed from the breast.
Respiratory distress syndrome (RDS): Preterm
babies especially those less than 34 weeks have
immature lungs, hence they develop RDS
characterized by rapid and labored respiration,
indrawing of the chest, grunting and cyanosis.
Apneic spells: Because of the immature
respiratory control mechanisms these babies
also have a tendency for apneic
4. Treatment:
Indication for hospitalization are :
Birth weight of less than 1800g; Gestational age
of less than 34 weeks;
Neonate who is not able to take feeds from the
breast or by cup (Katori) and
A sick neonate (irrespective of birth weight and
gestation).
4.1. Keeping LBW Babies warm:
Room temperature should be kept between
28to300C.
Baby should be provided skin to skin contact
care (KMC) in the following ways :
Provide privacy to the mother. If mother is not
available, skin to skin contact may be
spells. In an apneic spell the baby stops
breathing; develops slow heart rate and turns
blue.
Intra-ventricular hemorrhage (IVH): Preterm
infants also have immature vascular bed around
the brain ventricles. These delicate vessels may
rupture and cause intra-ventricular hemorrhage.
Hypoglycemia - Immature metabolic pathways
of preterm infants predispose them to develop
hypoglycemia.
Hyperblirubinemia
Infection is another major problem among
preterm babies and indeed an important killer
because they are immuno-compromised hosts.
Retinopathy of Prematurity (ROP):Preterm
infants given excess oxygen may develop
blindness because of damage to the immature
retina.
3. Problem of SGA neonates
The basic underlying problem amongst them is in-
utero undernutrition and hypoxia. They are prone to:
Fetal distress,meconium passage in utero and
birth asphyxia.
Hypothermia.
Hypoglycemia
Congenital malformations.
provided by the father or any other adult.
Request the mother to sit or recline comfortably.
Undress the baby gently, except for cap, nappy
and socks.
Place the baby prone on mother's chest in an
upright and extended posture, between her
breasts, in Skin to Skin contact; turn baby's head
to one side to keep airways clear.
Cover the baby with mother's blouse, 'pallu' or
gown; wrap the baby-mother duo with an added
blanket or shawl.
Breastfeed the baby frequently.
If possible, warm the room (>250C) with a
heating device.
Skin to Skin contact is the most practical,
preferred method of warming a hypothermic
infant in a primary health care facility. If not
possible:
Cloth the baby in 3-4 layers, cover head with a
cap and body with a blanket or a shawl; hold
Page 182
 baby close to caregiver's body, OR
Place the baby under overhead radiant warmer,
if available.
Keep the young infant warm on the way to the
hospital
By Skin to Skin contact OR
Clothe the baby in 3-4 layers, cover head with a
cap and body with a blanket or a shawl; hold
baby close to caregiver's body.
4.2. Nutrition & Fluids
Neonates weighing less than 1200 g. or those
having sickness should receive intravenous fluid
initially.
Enteral feeds should be introduced gradually by
gavage as the baby's acute problem begins to
settle.
Infants weighing 1200-1800 g and not having
significant illness should be put on gavage feeds
initially.
In order to promote lactation and enable the
baby to learn sucking, all babies on gavage or
katori-spoon feds should be put on the breasts
before each feed for 5 to 10 minutes. This will
promote lactational and enable the baby to learn
how to suck.
When shifting a baby from one mode of feeding
to another, be very careful. Introduce in new
mode for only some of the feeds to begin with.
The feeding of every baby should be
individualized. The above recommendations
should only serve as broad guidelines.
Ensure use of expressed breast milk & start with
small volume, and gradually build up.
Most LBW babies weighing more than 1800 g
are able to feed directly from the breast. In a
stable, growing LBW baby daily intake of feeds
should be gradually built upto 180-200ml/kg.
LBW babies should be fed every 2-3 hours
starting at 2 hours of age.

Table 1

Guidelines for the modes of providing fluids and feeding

Age Categories of neonates
Birth weight (gm) < 1200 1200-1800 > 1800
Gestation (weeks) < 30 30-34 > 34
Initial - IV fluids Gavage feeds - Breast feeds
- Triage - If unsatisfactory, give
- Gavage feeds if not cup-spoon feeds
sick
After 1-3 days Gavage feeds Cup-spoon feeds Breast feeds
Later (1-3 wks) Cup-spoon feeds Breast feeds Breast feeds
After some time Breast feeds Breast feeds Breast feeds
(4-6 wks)

Note: 4 weeks (to ascertain a weight gain of at least

i. On the first day the fluid requirements range 200-300g) and then every month. Hospitalized
from 60 to 80 ml/kg. LBW babies should be weighed every day on
ii. The daily increment in all the groups is the same weighing machine.
around 15 ml per kg till 150 ml/kg is reached. Excessive weight loss, or inadequate weight gain
iii. Adequacy of therapy is indicated by weight indicates inadequate feeding, cold stress, excessive
pattern in the expected range. insensible water loss or systemic illness (like
4.2.1 Judging adequacy of nutrition anemia, sepsis, late metabolic acidosis etc).
The key measure of optimal feeding is the
weight pattern of the baby. A pretermLBW
baby loses upto 1 to 2 percent weight every day 4.3 LBW babies require dose
amounting to 10 percentcumulative weight loss
during the first week of life. Birth weight is
monitoring and follow up of
regained bythe14th day. Growth monitoring- head circumference and
SGA-LBW babies who are otherwise healthy weight
should not have any appreciable weight loss at Developmental assessment and early
all and they should start gaining weight early. stimulation
It is desirable to weigh all LBW babies at 2
weeks (to check regaining of the birth weight),

Page 183
 Intraventricularhaemorrhage screening by
ultrasound cranium on day 1, 3,7& at 4-6
weeks.
Screening tests for hearing at discharge
Retinopathy of pre maturityscreening at 1
month of age
Screening for osteopenia of prematurity
4.4. Vitamin Supplements:
All LBW Babies should receive intramuscular
Vitamin K at birth. Every new born should
Calcium 80-100 mg/kg/day.
Phosphorous 40-50 mg/kg/day
4.4.3 All these supplements to be given till at
least 6 months of age.
Iron should be started at a dose of age.
1mg/kg/day at 4 weeks of age and provided till
12 months of
Vaccination in LBW Babies
If the LBW baby is not sick, the vaccination
schedule is the same for as the normal babies. A
sick LBW babies however, should receive these
vaccines only on recovery.
Vitamin A 1000 IU orally daily from 1 week
age onwards
5.. Immunization in special
circumstances
5.1Immunization in preterm
infants:
In general, all vaccines may be administered as
per schedule according to the chronological age
irrespective of birth weight or period of
gestation. Very low birth weight / preterm
babies can be given or period of gestation. Very
low birth weight / preterm babies can be given
immunization, if they are stable otherwise.
5.2Children receiving
corticosteroids:
Children receiving oral conticosteroids in high
doses (Prednisolone 1-2 mg/kg/day) for more
than 14 days should not receive live virus
vaccines until the steroid has been discontinued
for at least one month. Killed vaccines are safe
but may not be completely effective in such
situations. Patients on topical or inhaled
steroids should not be denied their age
appropriate vaccine.
receive Injection Vitamin K 1 mg and 0.5 mg,
Intramuscular, as per the birth weight > = 1000
gm and < 1000 gm respectively.
All pre-terms < 2000gms should receive oral
Vitamin and mineral supplement in doses shown
below:
Multivitamin preparation 0.3-0.6 ml (5-10
drops) / day (which usually provides vitamin A
of 1000 IU/day and vitamin D 400 IU/day)
5.3 Children awaiting splenectomy
Immunization with pneumococcal, Hib, and
meningococcal vaccine should be initiated a
few weeks prior to splenectomy.
5.4Vaccination in children with
HIV infection:
Immune response may be suboptimal as it
depends on the degree of immunodeficiency at
that point of time. Re-administration of
childhood immunization may be considered
when their immune status has improved
following anti-retroviral therapy.
5.5Lapsed immunization:
There is no need to restart a vaccine series
regardless of the time that has elapsed between
individuals doses. In case of unknown or
uncertain immunization status, however, it is
appropriate to start the schedule as for an
unimmunized child.
5.6Minor illnesses,
e.g. fever, diarrhea, respiratory infections and
malnutrition should not be construed as
contraindications to immunization.
6. Prognosis
Mortality of LBW babies is inversely
related to gestation and birth weight and directly
tothe severity of complication.
In general, over 90% Low birth weight
babies who survivethe newborn period have no
neurodevelopment handicaps.
Therefore, essential care of theLBW
neonates is a highly rewarding exper
Page 184
 7.Assessment of Neonatal Sepsis
Neonatal sepsis is one of the three major causes of 1.5 CNS:
neonatal mortality. Sepsis is largely preventable.
Fever, seizures, blank look, high pitched cry,
1. Clinical manifestations of excessive crying/irritability, neck retraction, bulging
fontanel
neonatal sepsis
2. Laboratory diagnosis of a
1.1 Non-specific:
newborn with sepsis
Lethargy, refusal to suckle, poor cry, not arousable,
comatose Sepsis Screening: Any of two tests that come
positive out of the following five tests strongly
1.2 Gastrointestianal: indicate presence of sepsis:
Abdominal distension, diarrhea, vomiting, poor 1. Leukopenia (TLC/ Total leucocyte count
weight gain <5000/cmm)

1.3 Cardiovascular: 2. Neutropenia (ANC/ Absolute neutrophil count

<1800/cmm)
Hypothermia, poor perfusion, shock, bleeding and
sclerema 3. Immature neutrophil to total neutrophil (I/T) ratio
(>0.2)
1.4 Respiratory: 4. Micro ESR/Erythrocyte sedimentation rate
Cyanosis, tachypnea, chest retractions, grunt, (>15mm 1st hour)
apnea/gasping 5. Positive CRP/ C-reactive protein

Page 185
 3. Figure-1: Approach to newborns at- risk of sepsis

Neonate at risk of sepsis

Symptomatic Asymptomatic

High suspicion Low suspicion Do sepsis screen

Blood culture

Blood culture Sepsis Screen Negative Positive

Blood Culture Take blood
culture
And start antibiotics

Start antibiotic Negative screen Repeat sepsis screen

After 12 hr after 12 hr
Positive screen

Negative screen Duration - acc

to
Clinical
Course& culture*

Duration according Monitor clinically Monitor clinically

To clinical course

Culture sterile - 7-10 days Culture Positive - 10-14 days

Escherichia coli, Staphylococcus aureus and

4. Antibiotic therapy for a Klebsiella pneunoniae
newborn with sepsis A combination of Ampicillin and Gentamicin is
recommended for treatment of sepsis and
4.1 Choice of antibiotics pneumonia
Antibiotic therapy should cover the In suspected or confirmed meningitis, add
Cefotaxime with an aminoglycoside
common causative bacteria, namely
Page 186
 Following table provides the antibiotics and
dosages of antibiotics for newborn sepsis

4.2 Antibiotic therapy of

neonatal sepsis
4.2.1 Septicemia of Pneumonia

Table-1: Antibiotic Management for Septicemia of Pneumonia

Antibiotic Each dose Frequency Route Duration

<7 days age >7 days age
Inj Ampicillin or 50 mg/kg/kg/dose 12 hourly 8 hourly IV 7-10 days
Inj Cloxacillin 50 mg/kg/kg/dose 12 hourly 8 hourly IV 7-10 days
and
Inj Gentamicin or 5 mg/kg/kg/dose 24 hourly 24 hourly IV 7-10 days

Inj Amikacin 15 mg/kg/kg/dose 24 hourly 24 hourly IV 7-10 days

4.2.2 Meningitis

Table-2: Antibiotic management of Meningitis

Antibiotic Each dose Frequency Route Duration

<7 days age >7 days age
Inj Ampicillin or 100 mg/kg/kg/dose 12 hourly 8 hourly IV 3 weeks
and
Inj Gentamicin 2.5 mg/kg/kg/dose 12 hourly 8 hourly IV 3 weeks
OR
Inj Gentamicin or 50 mg/kg/kg/dose 12 hourly 8 hourly IV 3 weeks

and
Inj Amikacin 2.5 mg/kg/kg/dose 12 hourly 8 hourly IV 3 weeks
Infuse 10% dextrose 2 ml/kg stat
Inject Vitamin K1 mg intramuscularlyStart
5. Supportive care of a oxygen by hood or mask, if cyanosed or
grunting
newborn with sepsis Provide gentle physical stimulation, if apneic.
Provide warmth, ensure consistently normal Provide bag and mask ventilation with oxygen
if breathing inadequate
temperature
Avoid enteral feed if hemodynamically
compromised, give maintenance IV fluids
Consider use of dopamine if perfusion is
Start intravenous line persistently poor

If CFT >3 seconds, infuse normal saline 10

ml/kg over 20-30 minutes, repeat the same 1-2
times, if perfusion continues to be poor

6. Summery of commonly used doszge in neonates

Page 187
 Table-3: Administration of commonly used drugs

Drug Dose Route

Ampicillin Age <7 days: 50 mg/kg/dose, q 12 hour IV

Age <7 days: 50 mg/kg/dose, q 8 hour

Gentamycin Sepsis/ pneumonia IV

5 mg/kg/dose, q 24 hour

Meningitis

Age <7 days: 2.5 mg/kg/dose, q 12 hour

Age <7 days: 2.5 mg/kg/dose, q 8 hour

Amikacin <7 days: 15 mg/kg/dose, q 24 hour IV
Cefotaxime <7 days: 50 mg/kg/dose, q 12 hour IV

<7 days: 50 mg/kg/dose, q 8 hour

Chloramphenicol 12 mg/kg/dose, q 12 hour IV
Aminophylline 5 mg/kg loading, IV

then 2 mg/kg/dose q 8-12 hour

Vitamin K 1 mg IM
Phenobarbitone 20 mg/kg loading over 10-15 minutes Loading IV Then
IV, IM or oral
then 3-4 mg/kg q 24 hour
Phenytoin 15-20 mg/kg loading over 10-15 minutes IV

then 5 mg/kg q 24 hour

Dopamine/ Dobutamine 5-20 micro g/kg/minute IV continuous

Page 188
 8. Treatment of Respiratory Distress
In Newborn
im od for
1. Incidence:Increases as 2 days
Gestation age decreases OR
28 weeks => 60 %
Dexamethasone => 6mg im bd 2 Days
28-34 weeks => 30%
(NOTE: validity of this injection is for one week
34 weeks => 5-10%
And have to repeat after that if more delay in
delivery
2. Prevention: Can be
prevented by giving steroid 3. Assessment after delivery:
gestational age
to mother
Temperature
Antenatally
Indicated for those who are at risk for Heart rate
preterm
Sao2
delivery in next 8 days
Treatment for Prevention Capillary refill time
Betamethas
one 12 mg

Silverman anderson score

Figure 1

4. Scoring Chart
Table 1: Scoring Chart

Page 189
Interpretation: Start CPAP
SA score=> 3 Oxygen by hood CPAP Begin With 4-6 cm of waterpressure
3 -7 => CPAP ventilation And use Fio2 10
% more than required
>7Mechanical ventilation
Monitor ABG
4.2 Investigation : W/F Apnea
X ray chest: PA view Increase CPAP BY 1-2cm up to 8cm water pressure

Septic screening And Fio2 up to 100%

Blood culture Start Mechanical ventilator: if with Fio2 of 100% and

CPAP of 8cm
Serum electrolyte
ABG
Blood glucose

SA score is > 7
5. Management:
In general: OR
Maintain temperature = Baby with persistent Apnea
36.5 -37.5 c
Other
Restrict fluid to 2/3 maintenance Watch for diuresis
Maintain Sao2 88-95% Watch for clinical improvement
Give maintenance of fluid
Antibiotics if septic screen +ve
Main management 5.4 Fluid management
If fio2 requirement is < 30% & SA score <3 If CRT is more than 3
Oxygen by hood
Watch for diuresis Give 10ml/kg NS bolus
If improvement noticed give maintenance Monitor liver size
Fluid and start feed
If require give Dopamine 5-10 microgr/kg/min
If fio2 Requirement is > 30% & SA score >3
OR Dobutamine 10 microgr/kg/min

Page 190
 9. MECONIUM ASPIRATION SYNDROME

1. Management in delivery
Vertex or breech presentation
room
1.1 If MAS watch for Colour Birth Asphyxia

/consistency of meconium Perineal suction With Dee Lee mucus Aspirator at

delivery of Head of baby

Figure-1: Indication of Endotracheal intubation

MAS -----------------> IF babys cry is vigorous

If cry is not vigorous No Intubation

ROUTINE CARE

Intubation ------------------ Meconium not retrieved

Under cord suction No suction

Meconium retrieved

Continue suction HR < 100/min

HR > 100 /min IPPR

Continue suction

Page 191
2. Management in NICU
2.1 Assessment of baby: 2.2 Interpretation
Gestational age score
r/o IUGR 1 -3 => mild respiratory distress => Oxygen by
r/oU.cord /nail/skin hood
staining
4-6 => moderate respiratory distress=> CPAP
Downe ventilation
score >6 => severe respiratory distress => Ventilator
0 1 2 3. Investigation: CBC, ABG, x
Respiratory rate <60 ray chest, blood culture
60-80 >80
Grunting NO Audible with
4. Supportive management
Audible without Pass infant feeding tube=> gastric lavage
Stethoscope Stethoscope Iv fluid initially if require
Antibiotic if respiratory distress OR
Cyanosis NO In room air If septic screen is positive
with 40% oxygen Treat complication
Ventilator if required along with surfactant
Air entry good decrease
markedly decrease
5. Complication
Retraction NO mild
severe Atelectasis
Hypoxic Ischaemic encephalopathy
Pneumothorax
PPHN (Persistant primary pulmonary hyper
tension) requiring nitrousoxide and sildenafil

Page 192
 10. BLEEDING NEONATE
Slipped ligature
1. Common causes Vit k deficiency
G I BLEEDING Skin: petechiae
Swallowed maternal blood Sepsis
Hemorrhagic disease of New Born Platelet disorder
Sepsis Ecchymosis
Stress ulcer
Platelet defect Sepsis
Clotting factor deficiency Clotting factor deficiency
Umblical cord

1.4 Occult blood Cephalehematoma Preterm

Intra VentricularHaemorrhage Vit.k deficiency
Subdural Heaemrrahe sick neonate

2. APPROCH
Maternal History INCREASE RISK OF
2.1.1 Antenatal infection
eg. TORCH Thrombocytopenia

2.1.2 Drugs given to mother

Phenytoin
Phenobarbitone Heamorrhagic disease of NB
Aspirin/Anticoagulant
2.1.3 Bleeding in mother = Thrombocytopenia
eg.ITP /SLE
Birth Asphyxia
Trauma DIC

Time of Bleeding
2.2.1< 24hrs = Swallowed maternal blood
Hemorrhagic disease of NB
2.2.2> 24 hrs = Classical hemorrhagic disease
of NB
Sepsis /DIC
Platelet abnormality
Trauma
Liver dysfunction
2.1.3 Other clinical features
Petechiae Jaundice
Echymosis Hepatosplenomegaly
Pallor Bulging Ant .fontannel

3. Investigation

Page 193
 Figutre-1: Apt .test:

1 ml gastric aspirate + 5ml distilled water

Centrifuge to formSupernatant

4 ml of Supernatant + 1ml NAOH 1%

Change of colour to colour remains to pink

Yellow /brown

Maternal blood fetal blood

Figure-2: Differential Diagnosis

Platelet PT PTT

Thromobocytopenia N N

Haemohagic disease N
Of newborn

Clotting factor N N
Deficiany

Dic

Page 194
4. Management
A) If APT test showns Maternal =>parental counseling
B) If APT test shows fetal blood
a) Injvit k 1 mg IV stat
b) if PT/PTT increases OR in sick neonate

10-15ml /kg FFP (IF required repeat after 12hrs)

c) If Hb<10 gm% = Give fresh blood transfusion
d) If platelet <50000 in sick Neonate
OR <25000 in Healthy Neonate

Platelet transfusion 10-20ml/kg

C) Treat for sepsis / DIC / primary disease

Antibiotics: Ampicilline 50 to 100 mg/kg in divided doses IV.
Gentamycin 7.5 mg/kg in divided doses IV. If not responding to these then start higher antibiotics such
as ceftriaxone, merupenum etc.
Treatment of DIC.
Treatment of primary disease.

Page 195
 11. JAUNDICE IN THE NEWBORN
1. Introduction:
Hyperbilirubinemia is the commonest morbidity in
the neonatal period and 5-10% of all newborns
require intervention for pathological
jaundice.Nearly 60% of term newborn becomes
visibly jaundiced in the firstweek of life. In most
cases, it is benign and no intervention is required.
2. Physiological jaundice:
Jaundice attribute to physiological immaturity of
neonates to handle increased bilirubin production.
Visible jaundice usually appears between 24-72
hours of age. Total serum bilirubin (TSB) level
usually rises in full-term infants to a peak of 6 to 8
mg/dL by 3 days of age and then falls. A rise to
12mg/dL is in the physiologic range. In premature
infants, the peak may be 10 to 12 mg/dL on the fifth
day of life, possibly rising over 15 mg/dL without
any specific abnormality of bilirubin metabolism.
Fig. 1: Levels of Jaundice
4.2 Clinical determination of jaundice by Kramers criteria
Area of body
Head and neck
Upper trunk
Lower trunk and thigh
Arms and lower limbs
Palms and soles
3. Pathological jaundice:
A TSB concentration exceeds 5 mg/dl on first
day of life in term neonate, 10 mg/dl on second
day, or 12-13 thereafter.
Any TSB elevation exceeding 17 mg/dl.
Appearance of jaundice within 24 hours, peak
TSB levels above the expected normal range,
Presence of clinical jaundice beyond 3 weeks
and conjugated bilirubin (dark urine staining
the clothes and light colored stool)
4. Signs &Symptons:
4.1 Clinical examination of
jaundice:
The newborn should be examined in good
daylight.
The skin should be blanched with digital
pressure and the underlying color of skin and
subcutaneous tissue should be noted.
Dermal staining in newborn progress in a
cephalo-caudal direction. Newborns detected to
have yellow discoloration of the skin beyond the
legs should have an urgent laboratory confirmation
for levels of TSB.
Range of serum bilirubin (mg%)
4-8
5-12
8-16
11-18
>15
5.
Page 196

Investigations:
Following investigations must be done in a
case of neonatal jaundice
Serum bilirubin direct and indirect.
Blood grouping of mother and child ABO and
Rh.
Direct coombs test in infant.
Haematocrit and peripheral smear for RBC
morphology and reticulocyte count.
Indirect coombs test in mother if she is Rh
negative
6. Complication:
Transient encephagopathic: Early bilirubin induced
neurologic dysfunction is transient and reversible.
Clinically, kernicterus is described in phases, which
may progress over 24 hour to 7 days:
FIGURE-1: DIAGNOSTIC WORKUP FOR HYPERBILIRUBINEMIA
This is suspected by increasing lethargy with
risingbilirubin levels but recovery following or
prompt exchange transfusion.
6.2 Kernicterus.:
This term has been traditionally used to describe the
pathological findings of bilirubin toxcity within the
brain. This includes staining and necrosis of neurons
in the basal ganglia, hippocampal cortex,
subthalamic nuclei and cerebellum followed by
gliosis of these areas, should the baby survive. The
cerebral cortex is generally spared, but 50 % of
babies have extraneuronal lesions with necrosis of
renal tubular cells, intestinal mucosa and pancreatic
cells. They may manifest as gastrointestinal
hemorrhage or hematuria
Page 197
 IN NEWBORN

Clinical jaundice

Measure bilirubin( total serum bilirubin-TSB)

Bilirubin >12mg/dl bilirubin <12mg/dl

Age <24hrs old age >24hrs old
(pathological) (physiological)

Coombs test observe

POSITIVE NEGATIVE Follow

bilirubin
Rh
ABO Direct bilirubin
Kell
Less than 2mg%

Hct

NORMAL OR LOW HIGH POYCYTHEMIA

RBC morphology
Reticulocyte count

ABNORMAL NORMAL
Spherocytosis Enclosed hemorrhage
ABO incompatibility Brestmilk jaundice
Red cell enzyme defect Hypothyroidism
Alpha thalassemia Crigler-najjar syndrome
Gilbert syndrome
7.
Page 198
TREATMENT HYPERBILIRUBINEMIA
MODALITIES OF
Hydration 7.2. Phototherapy (table 1 and 2)
Phototherapy (Do not keep in sunlight).
Exchange transfusion Special blue lights to be used

Drugs to increase conjugation. 45cm distance between baby and phototherapy

unit
7.1. HYDRATION Eys and genitelia shuld be covered
Double surface phototherapy is preferred
Countinued and frequent breast feeding 8-10
Watch for side effects(diarrhoea, skin rash,
times/day
hyper/hypothermia)

TABLE 1- Guidelines for Phototherapy according to APP

Healthy, term newborn (>37 weeks)

Age (hours) ConsiderPhototherapy TBS (mg/dl) Phototherapy

TSB (mg/dl)
< 24
25-48 >12 >15
49-72 >15 >18
>72 >17 >20

NOTE: TSB-Total serum bilirubin

TABLE 2- Phototherapy indications

7.2.2 Based on birth weight and health of the newborn

Borth weight(grms) Healthy; TSB Sick ; TSB

(mg/dl) (mg/dl)
<1000 5-7 4-6
1001-1500 7-10 6-8
1501-2000 10-12 8-10
2001-2500 12-15 10-12
TERM
>2500 15-18 12-15

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 Fig. 2 : Namogram for age & serum bilirubin level

7.3 Points to remember 7.4 Exchange transfusion.

Try to establish diagnosis before instituting Choice of blood
phototherapy by carrying out necessary
7.4.1 Choice of blood
investigations.
If baby and mother is Rhve use only Rh-ve
Check blue light functioning; life of these light
blood.
is 1500-2000hrs(appox 3 months). Keep lights
Always cross match donors blood with both
at distance of 18 from the baby.
mothers and babys blood.
When blue lights are not available four pairs of
white tube light may be usedinstead. 7.4.2Criteria for Exchange Transfusion
Change the position of baby after every 2 hrs. Cord bilirubin more than or equal to 4.5mg%
Babies can be taken out of phototherapy for and Hb < 11g%
breast feeding Rate of rise of bilirubin >1mg/dl despite
Monitor babys temperature 2 hourly. phototherapy
Monitor fluid balance daily weight and urine In LBW babies indirect bilirubin> (weight in
output. Increase fluid as necessary. g)/100
Shield the eyes in both sexes to prevent the Exchange earlier at level of 2 mg% less for
retinal damage and genitals in male to prevent following criteria-
mutation defect in adulthood. Sepsis
Monitor rise or fall of bilirubin every 12 hourly. RDS
Do not give phototherapy for direct Asphyxia
hyperbilirubinemia. Acidosis
Hypoglycemia.

Page 200
12. MANAGEMENT OF SURGICAL NEONATE
Neonatal surgical problems 1.2.2 Gastrointestinal

1.1 Major: Esophageal Atresia

Cong. Hyperpyloric stenosis (CHPS)
Tracheoesophagial fistula Gastrochiasis
Diaphragmatic hernia Abdominal wall defect
Intestinal Obstruction
Neural tube defect Omphalocele
Omphalitis
Other:
Chest Deformities
1.2.1 Orofacial
Congenital Lobar emphysema
Cleft lip Vascular Ring
Cleft palate Orthopedic
ChoanalArtesia CTEV (Cong Talipus Equine Varus)
Pierre robin sequel Developmental dysplasia of hip
Laryngeal web Other
Clavicle fracture
Humerus fracture
Femur fracture

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 13. VITAMIN A DEFICIENCY

1. Introductions 3.2 Importatant aspects of Vit A

Vit A deficiency Symptons If the child more than 1 year of age and weighing
Delayed dark adaptation less than 8 kg., then Vit A dose is 1,00,000 IU to
More prone for intestinal , respiratory and avoid hypervitaminosis A
urogenital infections Give oil based preparation
Bottles have solution strength of 100000IU Vitamin
2. Classification A/ml
XN------Night Blindness Cold chain is not required.
X1A----ConjunctivalXerosis Shelf life of unopened opaque container is 2 years.
X1B-----Bitot Spots Opened liquid is to be used in 6to 8 weeks.
X2-----Corneal Xerosis Capsules are partially protected against loss of
X3A---Corneal Ulceration <1/3 potency.
X3B---Corneal Ulceration >1/3 3.3 Treat Night blindness
XS----Corneal Scarring Conjunctivalxerosis, Bitotspots, Cornealxerosis,
XF---Xeropthalmic Fundus Cornealulceration, Keratomalacia in all except
3 Treatment immediately women of reproductive age group.
In acute corneal lesion, patient should be referred to
after diagnosis hospital on emergency basis.
3.1 Age wise doses of Vit A High dosages of Vit A can causes pseudotumar
<6 months-----------50,000IU VitaminA orally cerebri which will manifest as vomiting headache
6 to 12 months------100000IU Vitamin A orally and bulging anterior fontenelle
>12 months----------200000IU Vitamin A orally
Next day-------------------------Same age specific 3.4 Corneal Xeropthalmia
dose i. Topical Antibiotic ointment (Tetracycllin 1%, eye
At least 2 weeks later-------Same age specific dose oitment, Tobramycin eye ointment 3% bd)
ii. Eye protection

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 14. RICKETS
1. Metabolic disease of childhood in which the Malabsorption
osteoid, the organic matrix of bone fails to Renal disease
mineralise, due to interference with calcium Celiac disease
metabolism. Hepatic osteodystrophy
Anti - epileptic drugs
Vitamin D deficiency

Fig. 1 : Clinical features in Rickets

Investigations Loss of transverse trabeculae

3.1 Seriology No sub-periosteal resorption of bone

Serum calcium - normal or decreased, 4. Treatment:

Serum phosphorus - decreased, Single oral dose of 6 lakh IU of vitamin D
Alkaline phosphotase - increased 2nd dose after 3 to 4 weeks (if no sclerotic
change is seen in x-ray)
3.2Urine Exam If the child responds to above treatment
maintenance dose of 400 IU of vitamin D is
Urinary calcium - decreased given once Serum alkaline phosphotase is
nomal, consider corrective surgery, If any.
3. X- ray: Calcium - 0.5 to 3 gm/day for 3 months
Generalized demineralization Vitamin D - 10,000 IU/day once a month
High protein diet

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 15. MANAGEMENT OF CHILDREN WITH
ANAEMIA

Mild to moderate anaemia is a common co- mayhavehyperpigmentationofknucklesandocca

morbidity in children attending health facility
for various conditions. Hence, anaemia/pallor
should be looked for in each patient attending
the health facility.
Severe anemia in a child is suggested by the
presence
ofseverepalmarpallorandmaybeassociatedwitha
fastpulserate,difficultyinbreathing,orconfusionor
restlessness.
Nutritionalanaemiaisthemostcommoncauseofan
aemiainchildren.
Nutritionalanaemiaresultsfromdeficiency
ofiron,folicacidandvitaminB12.
Childrenhavinganaemiaduetofolicacidand/orB1
2deficiency (megaloblasticanaemia)
sionally bleeding manifestations due to
thrombocytopenia.
The onset of anaemia in young children is
generally after 6 months of age. Before this,
iron in breast milk is sufficient to meet the
needs of a breastfed child.
In India, diets for children in the age group 6
23 months are predominantly plant-based and
provide insufficient amounts of micronutrients
to meet the recommended nutrient intakes.

Table 1
Clinicalassessmentofanaemiainchildrenlessthan5years

Findings on anaemia in children

History Examination
Durationofsymptoms Severepalmarpallor
Usualdiet(beforethecurrentillness) Skinbleeds(petechialand/orpurpuricspots)
Familycircumstances(tounderstandthechildssocialbackgr Lymphadenopathy
ound)
Hepato-Splenomegaly
Prolongedfever
Signsofheartfailure(galloprhythm,raisedJVP,
Worminfestation
respiratory distress, basal crepitations)
Bleedingfromanysite
Lymphnodeenlargement
Previousbloodtransfusions
Similarillnessinthefamily(siblings)

Facility level management All children referred from field to health

Any child reporting to any facility (PHC level
and above) with any illness will be assessed
clinically by the attending Medical Officer for
anaemia routinely and should undergo Hb
estimation if found to be anaemic clinically
facility due to palmar pallor will undergo Hb
level estimation before initiating treatment
Children will be categorised as having mild,
moderate and severe anaemia on the basis of
Hb levels and will be managed as per Table
below.

Page 204
 Table 2
Treatment of Anaemia

Level of HB Treatment Follow-up Referral

No Anaemia (>11 20 mg of elemental iron and 100 mcg of folic acid in biweekly regimen
gm/dl)
Mild Anaemia (10 3 mg of iron/ Kg/ day for Follow-up every 14 In case the child has not
10.9 gm/dl) 2 months days by ANM responded to the treatment of
anaemia with daily dose of
And Hb estimation after
iron
completing 2 months
Moderate Anaemia
of treatment to for 2 months, refer the child to
(79.9 gm/dl) document Hb>11 the FRU/DH with F-IMNCI
gm/dl trained MO/ Paediatrician /
Physician for further
investigation

Severe Anaemia Refer urgently to DH/FRU

(<7 gm/dl)

Note: malnutrition and in a known case of

After completion of treatment of anaemia and
attaining Hb level >11.5 gm/dl, the
IFAsupplementation to be resumed
Treatment of anaemia with iron should be
withheld in case of acute illness, severe acute
haemoglobinopathy and anaemia in these cases
should be treated as per the standard treatment
guidelines, by the attending physician, as per
the merit of the individual case.

3.1 Dose of IFA surup

Table 3
Dose of IFA syrup for anaemic children 6 months5 years
Age of Child Dose and Frequency
6 months12 months (610 kg) 1 ml of IFA syrup Once a day

1 year3 years (1014 kg) 1.5 ml of IFA syrup Once a day

3 years5 years (1419 kg) 2 ml of IFA syrup Once a day

Page 205
 Table 4
Management of severe anaemia at FRU/DH (as per F-IMNCI) in children 6 months5 years and 5-10 years

3.2.1 History of Examination

History to be taken for Examination for

Duration of symptoms Severe palmar pallor
Usual diet (before the current illness) Skin bleeds (petechial and/or purpuric spots)
Family circumstances (to understand the Lymphadenopathy
childssocial background) Hepato-splenomegaly
Prolonged fever Signs of heart failure (gallop rhythm, raised
Worm infestation JVP, respiratory distress, basal crepitations)
Bleeding from any site
Any lumps in the body
Previous blood transfusions
Similar illness in the family (siblings)

3.2.1 Investigation & blood transfusion indication

Table 5: Investigation & Management

Investigations Indication for Blood Transfusion Blood Transfusion

Full blood count and
examination of a thin film
forcell morphology
Blood films for
malariaparasites
Stool examination for ova,
cystand occult blood
All children with Hb 4 gm/dl If packed cells are available, give
Children with Hb 46 gm/dl with any 10 ml/kg over 34 hours
of the following: preferably. If not, give whole
Dehydration blood 20 ml/kg over 34 hours.
Shock
Impaired consciousness
Heart failure
Deep and laboured breathing
Very high parasitaemia
(>10% of RBC)

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 16. MUMPS
1. Introduction:
Mumps is swelling of parotid glands due to
infection of the parotids by mumps virus. Apart
from parotids, it affects some other vital organs and
systems in the body and can have serious
complications with risk of morbidity and mortality.
Therefore it is important to know the course of
illness, various complications, early detection for
prompt management, and preventive measures.
2. Signs &Symptons:
Fig. 1: Mumps : Paritid Swelling
3. Investigation:
Diagnosis: is mainly clinical more suggestive with
the history of contact. Typical painful tender
bilateral parotid swelling with systemic symptoms is
diagnostic.
4. Complication:
4.1 CNS-Aseptic meningitis-meningoencepnalitis
along with parotitis or 10 days later. Meningitis
indistinguishable from other meningitis.
Orchitis,Epididymitis - Occurs in older pts.
Occurs one week following parotitis with
painful swelling of testes. Illness lasts for about
4 days. Testicular atrophy may follow in l/3
patients with rare affection of fertility.
Oopharitis in females may rarely occur.
Pancreatitis -Epigastric pain, tenderness,
vomiting, fever are suggestive. Laboratory
evidence of raised amylase confirms the
diagnosis.
Thyroiditis - May follow after one week in
adults with development of antithyroid anti
bodies.
Myocarditis - Mild- moderate myocarditis with
ST changes on ECG is found in some older
patients. Chest pain, bradycardia and fatigue
Un-immunized host gets infected from a case.
Patient is infective l-2 days before appearance
to 2-3 days after disappearance of parotid
swelling. Incubation period ranges between 2-3
weeks. 30-40% infections are sub clinical. After
entry through air, the virus multiplies in
respiratory tract and reaches all organs via
blood. Prodromal symptoms are in the form of
fever, muscle pains, neck pain, and malaise.
are presenting symptoms in a patient with
mumps
Deafness - transient or permanent unilateral or
bilateral nerve deafness may follow mumps.
Arthritis - Migratory ploy arthralgia or even
arthritis may be seen. These complications
should be treated symptomatically.
5. Management:
Treatment:
Mainly symptomatic with paracetamol and
frequent gargling with warm saline.
Watch for evidence of complications. If orchitis
or arthritis occurs, prednisolone can be used to
reduce pain.
6. Prevention:
MMR vaccine - combination of mumps,
measles, and rubella offers above 95%
protection. Primary immunization at the age of
15 months, followed by revaccination at l0
years,
Since it is a live viral vaccine, immuno-
compromised hosts should not be vaccinated.
Isolation of the affected child is not useful to
prevent spread to other children in usual
contact. However, fresh contacts like guest
Page 207
children can be protected if the affected child is always gives lifelong protection against
isolated from them. another, therefore, such children do not benefit
Children usually recover from mumps in about from any immunization later.
10-12 days- First arrack of mumps almost

Page 208
 17. SEVER ACUTEMALNUTRITION (SAM)
Standardsor

1. Introduction Bipedaledema.

Malnutritionremainsoneofthemostcommoncauses If weight-for-height or weight-for-length cannot be

ofmorbidityandmortalityamongchildren.Thehighc measured, use the clinical signs for visible severe
asefatalityratesamongseverelymalnourishedchildr wasting
encan
bereducedbyusingstandardizedandeasilyimplemen 3. Assessment of severely
tableprotocols. malnourished child
2. Criteria for hospital A good history and physical examination is
required for deciding the treatment but always start
admission the emergency
Weightforheight/length<-3z Treatment
scoreofmedianofWHOchildgrowth first.Thedetailsofhistoryandexaminationcan
berecorded later.

Table 1:

History Examination

Recentintakeoffoodandfluids Anthropometry-weight,height/length,midarm
Usualdiet(beforethecurrentillness) circumference
Breastfeeding Oedema
Durationandfrequencyofdiarrhoeaandvomiting Pulse,respiratoryrate
Typeofdiarrhoea(watery/bloody) Signsofdehydration
Lossofappetite Shock(coldhands,slowcapillaryrefill,weakandrapid
Familycircumstances(tounderstandthechildssocial pulse)
backgronnd) Severepalmarpallor
Chroniccough EyesignsofvitaminAdeficiency:
Contactwithtuberculosis - dry conjunctiva or cornea,
Recentcontactwithmeasles -Bitotsspots
Known orsuspectedHIVinfection. -Cornealulceration
Immunizations -Keratomalacia
Localizingsignsofinfection,includingearandthroatinfection
s, skin infection or pneumonia
Fever(temperature37.5Cor99.5F)or
hypothermia(axillarytemperature <35.0 Cor<95.0 F)
Mouthulcers
Skinchangesofkwashiorkor:
- Hypo or hyperpigmentation
-Desquamation
-Ulceration(spreadingoverlimbs,thighs,genitalia,groin,and
behind the ears)
-Exudativelesions(resemblingsevereburns)oftenwith
secondaryinfection(includingCandida)

Serum electrolytes (sodium, potassium)

3. Laboratory Tests
Screeningforinfections:

Haemoglobinorpackedcellvolumeinchildrenwit - Total and differential leukocyte count,

hseverepalmarpallor. blood culture (If possible)
Bloodsugar. - Urineroutineexamination
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- Urineculture preparationofappropriatefeeds,andtocarryoutreg
ular feeding during the day and night. Accurate
- Chestx-ray
weighing machines are needed, and records
should be kept of the
4. Organization of care feedsgivenandthechildsweightsothatprogresscan
On admission, the child with severe malnutrition bemonitored.
should be separated from infectious children and
kept in a warm area (2530C, withnodraughts), 5. Providing general
and
constantlymonitored.Washingshouldbekepttoamini
treatment for malnutrition
mum, after whichthechildshould be dried Thereare10essentialstepsintwophases: an
immediately. initialstabilizationphaseandalongerrehabilitationphase
.
Facilitiesandsufficientstaffshouldbeavailabletoensu
recorrect

Table-2: Treatment for Malnutrition

Stabilization Rehabilitation
Days1-2 Days3-7 Weeks2-6
1. Hypoglycaemia
2.
3.
4. Electrolytes
5. Infection
6.Micronutrient Noiron withiron
7. Initiate
8. Catch-
9. Sensory stimulation
10. Prepareforfollow-up

rferewiththebodysimmunemechanismsagainstprolife
5.1 Important things not to do and ratingbacteria.
why?
5.1.1Do not give I/V fluids
routinely.I/Vfluidscaneasilycausefluidoverloadandhea 5.2 Treat hypoglycaemia
rtfailure.OnlygiveI/Vfluidstochildren with signs of
shock. Ifthechildislethargic,unconscious,orconvulsing,
giveIV10%glucose5ml/kgfollowedby50mlof10%gluc
5.1.2Do not gives diuretics to treat oedema. The oseorsucrosebyNGtube.IfIVdosecannotbegivenimme
oedema will go away withproper feeding. Giving diately, givetheNGdosefirst.Give appropriate
diuretics will antibioticsandstart feeding as soon as possible.
worsenchildselectrolyteimbalanceandmaycausedeat
h. Ifnotlethargic,unconscious,orconvulsing,givethefirstf
eedofstarterformula(75cals/100ml),ifitisquicklyavaila
5.1.3Do not gives high protein formula. Almost all
severely malnourished children have infections, bleandthencontinuewith2hourly feeds.
impaired liver and intestinal function. Because of Ifthefirstfeedisnotquicklyavailablegive50mlof10%gluc
these problems, they are unable to tolerate the usual oseorsugarsolution(4roundedteaspoonofsugarin200
amount of dietary protein.
mloronecupofwater)orallyorbynasogastrictube,follo
5.1.4 Do not give iron during the initial feeding wedbythefirstfeedassoonaspossible.
phase.
Give2-
Add iron only after the child has been on catch-up hourlyfeeds,dayandnight,atleastforthefirstday.
formula for2days Giveappropriateantibiotics.
(usuallyduringweek2).Givingironearlyintreatmenthas
beenassociatedwithfreeradicalgenerationandmayinte Keepthebabywarmandchecktemperature.

Page 210
Prevent hypoglycaemia/Begin Starter Formula
Feed2hrly,startingimmediatelyor,ifnecessary,rehydra
tefirst.Continuefeedingthroughoutthenight.
5.3 Infection
5.3.1 Presume and treat infection
Assume all children with severe malnutrition
admitted in a hospital have an infection and give
broad spectrum
antibiotics.Ifaspecificinfectionisidentified(suchasShige
lla),givespecificappropriateantibioticsaccordingtocond
ition
identified.Hypoglycaemiaandhypothermiaareoftensign
sofsevereinfection.
5.3.2 Select antibiotics and prescribe regimen
Select antibiotics as shown in the chart below.

Table 3: Antibiotic Treatment

Status Antibiotic
All Inj.Ampicillin50mg/kg/dose6hrlyandInj.Gentamicin7.5mg/kgoncea
admitte day for 7 days
d cases AddInj.Cloxacillin50mg/kg/dose6hrlyif staphylococcalinfectionis
suspected
Revisetherapybasedonsensitivityreport
For septic IVCefotaxime50mg/kg/dose6hrlyorInj.Cerftriaxone50mg/kg/dose12hrlyplusInj.A
shock or mikacin15mg/kg/onceaday
worsening/ no
improve
ment in
initial
ho urs
Meningi IVCefotaxime50mg/kg/dose6hrlyorInj.Ceftriaxone50mg/kg/dose12
tis hrlyplusInj.Amikacin15mg/kg/onceaday

Dysente Inj.Ceftriaxone100mg/kgonceadayfor5days
ry

5.3.3 Duration of antibiotic therapy depends on the InvestigateandfollowHIVguidelines.

diagnosis i.e.: 5.4.5
Suspicion of clinical sepsis: at least 7 days Severeanaemia:Givewholebloodorpackedcelltransfus
Culturepositivesepsis: 10-14days Meningitis: ionifHbis<4g/dlorHbis4-
atleast14-21days 6g/dlandchildhasrespiratorydistress.Give10ml/kgslo
Deepseatedinfectionslikearthritisandosteomyelitis: wlyover4-
atleast4weeks 6hoursandgiveInj.Frusemide1mg/kgatthestartofthetra
nsfusion.Donotrepeatbloodtransfusionwithin4days.
5.4.5 Ifeyeproblems(keratomalacia) due
tovitaminAdeficiency,inadditiontovitaminAdosesinsti
5.4 Treat Associated Conditions llciprofloxacineyedrops2-3hourly
5.4.1 Giveantimalarials andatropineeyedrops3timesadayfor7-
ifbloodsmearpositiveformalariaparasites. 10days.Alsocovertheeyeswithpadandbandage.

5.4.2 5.4.6Skinlesions:Batheorsoaktheaffectedareasfor10
StartATTiftuberculosisisdiagnosedorstronglysuspect minin1%potassium
ed(Mountaux TestandXraychest). permanganatesolutionandapplygentianvioletornystati
ncreamifavailable
5.4.3 toskinsoresandanybarriercream(zinccream)totheraw
SuspectHIVifhehasalsootherproblemslikepersistentd areas.
iarrhoea,oral
5.4.7
Thrush, Persistentdiarrhoea:Diarrhoeaiscommoninseveremal
pneumonia,parotidswellingorgeneralizedlymphaden nutritionbutwithcautiousrefeeding,itshouldsubsidedu
opathys. ringthefirstweek.Intherehabilitationphase,
Page 211
thepoorlyformedloosestoolsarenotacauseforconcern,
providedthechildsweightgainissatisfactory.Ifthechild
has persistentdiarrhoea,screenfornon-
intestinalinfectionsandtreatappropriately.Continuebr
eastfeedingandtrytogivefeedswithlowlactoseinitiallya
ndsubsequently change to lactose free options if
diarrhoea persists.
5.4 Micronutrients
5.4.1 Give oral vitamin A in a single dose.
Vitamin A orally in single dose as given below:
<6months :50000IU (if
clinicalsignsofdeficiencyarepresent).
6-12months:1lakhIU.
Olderchildren: 2lakhIU.
Children<8kgirrespectiveofageshouldreceive1la
khIUorally.
Givehalfoftheabovedoseifinjectable
(intramuscular)vitaminAneedstobegiven.
GivesamedoseonDay0, 1and14
ifthereisclinicalevidenceofvitaminAdeficiency.
5.5.2 Other micronutrients should be given
daily for at least 2 weeks:
Multivitaminsupplement(shouldcontainvitaminA,
C,D,EandB12&
NotjustvitaminB-complex):
2RecommendedDailyAllowance.
Folicacid:5mgonday1,then1mg/day.
Zinc: 2mg/kg/day.
Copper:0.3mg/kg/day
(ifseparatepreparationnotavailableuse
Commercialpreparationcontainingcopper).
Whenweightgaincommencesandthereisno
diarrhea add3mgofiron/kg/day.
5.6Initiate feeding
Essentialfeaturesofinitial feedingare:
Startfeedingasearlyaspossible.
Feedthechildifalertanddrinkingevenduringrehydratio
n.
Givefrequentandsmallnutrientrichfeedsoflowosmolar
ityandlowlactose.
Offer130ml/kg/dayofliquids(100ml/kg/dayifchildhas
severeoedema),80-
100Kcal/kg/dayand1-1.5g/kg/dayofproteins.
Usenasogastricfeedingtillchildtakesorally75%ofallfee
ds.
Ifchildbreastfed,continuebreastfeedingbutgivethefeed
first.
Ensurenightfeeds.
5.6.1 Starter Formula
Starterformulaistobeusedduringinitialmanagement.Iti
sstartedassoonaspossibleandcontinuedfor2-7days
untilthechildisstabilized.Severelymalnourishedchildr
encannottolerateusualamountsofproteinsandsodium
atthisstage, or high amounts of fat. They may die if
given too much protein or sodium. Starter formula is
specially made to
meetthechildsneedswithoutoverwhelmingthebodys
systemsintheinitialstageoftreatmentwhichprovides75
calories/100mland0.9gmofprotein/100ml.
5.6.2 Feed the child Starter formula orally, or by NG
tube if
Necessary: Oral feeding
Itisbesttofeedthechildwithacupandspoon.Encourag
ethechildtofinishthefeed.Ittakesskilltofeedaverywea
kchild,sonursingstaffshoulddothistaskfirstandmothe
rmayhelpwithfeedinglaterwhenchildbecomesstrong
er.Encouragebreastfeedingondemandbetweenstarte
r formulafeeds.
Nasogastric feeding
ItmaybenecessarytouseaNGtubeifchildisveryweak.U
seanNGtubeifthechilddoesnottake75%ofthefeedfor2
-3consecutivefeeds.
Remove the NG tube when the child takes:
75%ofthedaysamountorally;or
Twoconsecutivefeedsfullybymouth.
5.6.3 Record intake and output on a 24-Hour
food intake chart.
Criteriaforincreasingvolume/decreasingfrequencyoff
eeds
1. Ifthereisvomiting,significant
diarrhoea,orpoorapetite,continue2-hrlyfeeds.
Page 212
2.
Ifthereislittleornovomiting,diarrhoeaislessthanbefore,and 5.6.4 Monitoring
mostfeedsareconsumed,changeto3-hrlyfeeds. Monitorandrecord(seeAppendixformonitoringcharts
3. Afteradayon3- )
hrlyfeeds:Ifthereisnovomiting,occasionaldiarrhoea,andm Amountsoffeedofferedandleftover
ostfeedsareconsumed,changeto4-hrly.
Stoolfrequencyandconsistency
Recommended schedule with gradual increase in Vomiting
feed volume is as follows
Canreplacefreshmilk30mlwith3.5gmwholedriedmilk Dailybodyweight

Page 213
 18. FEVER WITH RASHES
1. Introduction :
Fevers associated with generalized skin eruptions/
rashes (exanthematous fevers) are common in
childhood. These are often seen as epidemics in the
periods of 'season change' like March-April and
October-November when adenoviruses become
active.
Differential Diagnosis of Exanthema
Macular and/or papular rash
a) Measles, rubella, erythema infectiosum, roseola,
coxackievirus, echovirus, CMV, hepatitis B
infections.
b) Erythema multiforme due to herpesvirus, Epstein
barr
virus,adenovirus,chlamydiae,Salmonella,Mycobacte
ria,histoplasma or coccidioses.
2. Nodular
a)Fungal diseases, atypical mycobacterial and
pseudomonas infections.
b) Erythema nodosum. Due toStreptococcus,
Mycobacterium tuberculosisand leprae, Yersinia,
hepatitis C, sarcoidosis, drugs and inflammatory
bowel diseases.
Diffuse erythematous with peeling or desquamation
Scarlet fever, toxic shock syndrome, Kawasaki
disease, staphylococcal scalded skin syndrome,
Stevens Johnson syndrome.
3. Vesiculobullous
Figure 1 : Various types of Rashes
1.2. Investigation:
HB,TLC, DLC, X-RAY Chest, measle
antibody test.
Varicella, herpesvirus, coxackievirus, enterovirus,
meningococcal, group A streptococcal and
Pseudomonas infections.
4. Petechial/purpuric
Epstein barr virus, echovirus 9, cytomegalovirus,
rickettsial, malaria, pneumococcal, meningococcal
and Listeria infections.
1. Measles
Measles is a communicable disease manifesting
with fever, cough, coryza, lacrimation and Koplik
spots in the pre-eruptive phase and a maculopapular
rash starting on 4th or 5th day of illness. The rash
heals leaving brawny pigmentation.It is caused by a
RNA virus classified as Morbillivirus, belonging to
paramyxovirus family.Clinical Features: Incubation
period is 8-12 days.
Prodromal Phase: The onset is acute with moderate
elevation of temperature, dry hacking cough,
running of nose, sneezing, redness of the eyes and
excessive lacrimation.
1.1. Signs &Symptons:
Typical measly look in young babies is due to
conjunctivitis, stomatitis and rhinitis due to viral
rash. The first place for the rash to be seen is around
opening of parotid ducts in the mouth/inner cheeks
(Koplik's spots). Rash appears on face and
progresses to appear on trunk and limbs over the
following three to four days. Drying of rash and
peeling of skin appears in the same sequence in
next4- 5 days.
1.3. Complication:
Acute precipitation of Vitamin A deficiency in a
child with measles can occur and hence corneal
ulceration is a complication to watch out for and to
prevent. All children with measles should routinely
receive vitamin A orally 2 lakh units each on day
l, 2 and 14 (for infants the dose is half)
Due to depressed immunity due to measles, child
can catch infections like diarrhoea, otitis media,
pneumonia and TB. If the child continues to get
fever even after the rash is dry, bacterial pneumonia
should be suspected. Continued low fever and lack
of appetite should make one suspect TB infection.
Extra-feeding during convalescence and when
the child gets well is important to prevent
malnutrition after measles.
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1.4. Management:
Symptomatic treatment should be given
Paracetamol 10 to 15 mg per kg for fever and
Antihistaminics (Cetrizine) 0.5 to 1mg per kg for
itching and rhinitis. Advice continued feeding. Keep
baby clean by sponging or quick clean bath.
Treatment with antibiotics (Amoxycilline 30
mg per kg per day in 2 to 3 divided doses for 5
days) for superadded bacterial infections when
detected.
1.5. Prevention:
Figure 2: Chicken Pox Rash
Due to multiple 'trops" appearing over a week or so,
one can observe all types of lesions simultaneously
on a patient's body. The rash is more on covered
areas like trunk of body, and can appear inside
mouth. conjunctivae. Vagina leading to irritation
o
Figure 3: Vescicles & umbilication in chicken pox
2.2. Investigation:
Clinically Diagnosed
2.3. Complication:
Aspirin given to a child with chicken-pox infection
may precipitate acute fatty infiltration of liver. Liver
failure and encephalopathy (Reye's syndrome).
Reyes' syndrome is to be suspected if there is
disproportionate vomiting, rapid breathing (in the
absence of chest signs suggestive of pneumonia)
and altered sensorium. The patient should be
referred for specialist care, where respirator is
Measles immunization as routine immunization
should be promoted.
Immunization given early to contact of measles
case can prevent severe disease in the contact.
2. Chicken-pox:
2.1. Signs &Symptons:
Symptom of chicken-pox is characteristic rash.
The rash is often more severe in older children and
adolescents. The rash appears in several "crops" of
macules (red spots) quickly turning into watery
vesicles and pustules over the next 2 to 3 days and
then drying after scab formation over next 5 days.
symptoms. Chicken-pox patient is infective till all
scabs are formed. Itching is prominent and
scratching can lead to super added staphylococcal
infection.
available; as this is a very serious condition with
high mortality rate.
2.4. Management:
Sympromatic treatment with Paracetamol 10
to 15 mg per kg per day for 5 days and anti-
histaminics (Cetrizine) 0.5 to 1mg per kg per day for
5 days is advised. Daily bath is also advised.
Acyclovir in the dose of 20mg/kglday in 4 divided
doses for 5 days can be given to immuno-
compromized patients and patients with
encephalopathy.
Page 215
 19 ENTERIC FEVER / TYPHOID

1. Introduction: 2. Clinical Manifestations :

Although Enteric fever is still a common infection
its presentation has changed partly due to
vaccination and partly due to institution of
antibiotics early in the course of illness.
Diagnosis is problematic since blood
cultures may not reveal much and Widal test is
positive only after 1 week and has many false
positive and false negative results. Bone marrow
culture is more informative, but not practical.
Hence possibility of enteric fever must be
borne in mind while treating any pyrexia, which
shows toxicity, and signs suggestive of enteric like
confused sensorium, (no meningeal focal
neurological signs).
Classical presentations are becoming rare. Common
specific manifestations are -
Relative bradycardia compared to fever.
Tumid tender abdomen (abdomen feels like balloon
filled with water)
Cloudy sensorium.
Maculopapular erythematous rash on abdomen
blanching on pressure (Rose. spots)
Centrally coated tongue.
Soft spleen - 1-2 cm tender.
Continuous fever, not touching the baseline. (If
antipyretics are not given)
Pea soup diarrhea, nausea, vomiting.
Headache, myalgia, anorexia, malaise.
Enteric fever in children.is more severe as compared
to adults.

Fig. 1: Rose spot in typhoid
Chloramplenicol -75 mg/kg/dayOr
3. Investigation: Amoxiycillin 100mg/kg/day (with clavulinic acid)
HB, TLC, DLC, WIDAL TEST (RISING
Or
TITERS),BLOOD CULTURE.
Trimethoprim Sulphamethaxazole 10& 50
Complication: Shock, enteric perforation, mg/kg/day are also used with some success.
haemorrhagemeningits, myocarditis. can complicate
the illness. 4.3 Early institution of steroids
Management: Dexamethasone 3 mg / Kg
stat dose followed by:
4.2 Drug Treatment 1 mg/kg 6 hourly for 48 hours improves the survival
Multi-drug resistant typhoid fever has emerged and of patients in shock, myocarditis' CNS
is difficult to treat. Following drugs are found to be complication.
useful:
Third generation cephalosporins
Cefixime 20 mg /kg 1 day in 2 divided doses 4.4 Intestinal perforation
Or Ceftriaxone 50 mg/Kg per day requires broader spectrum
OrCiprofloxacin 20 mgl Kg per day,
Or Ofloxacin15 mg/Kg 1 day. antibiotics,
Platelet transfusions for severe thrombocytopenia
with haemorrhages' This treatment demands
referral to higher level'
The antibiotics should be continued at least 5-7
days after effervescence.

Page 216
 20.ACUTE MENINGOENCEPHALITIS

1. Introduction 2. Clinical Manestations

Acute meningoencephalitis is an acute infl
ammatory process involving meninges andbrain
tissue, due to infectious causes. The common
aetiological agents are viruses and bacteria.
Children of any age may be affected.
Fever, headache, vomiting, irritability altered state
of consciousness signs of meningeal irritation and
seizures.
3. Investigations
CSF examination differentiates the viral from
bacterial cause of acute meningoencephalitis
CSF findings in meningoencephalitis

Table 1: CSF Findings

Pressure Glucose
(mmH2O) Leucocytosis Protein (mg/dl)
(mg/dl)
(mm3)
Normal 50-80 <5, >75% 20-45 >50 or
lymphocytes
75% serum
glucose

Acute bacterial Meningitis Usually 100-10,000 100-500 Decreased

Elevated PMNs*
(<40)
(100-300) predominate

Acute viral Normal or r Rarely 50-200 Normal

Meningoencepha litis elevated >1000 PMNs early
rarely decreased
but
lymphocytes
predominate in
the most of the
course
Tubercular Usually elevated 100-500 PMNs 100-3000 <50
Meningoencephalitis early but later
lymphocytes
predominate
*PMNs = Polymorphonuclear leucocytes

Treatment
Supportive treatment is the mainstay of therapy and is started immediately.
a. Maintain airway, breathing and circulation.
b. Control of seizures with IV injection of Diazepam 0.2 to 0.4 mg/kg stat followed by Inj. Phenytoin 10-20
mg/kg stat followed by 5 mg/kg/day in divided doses.
c. Increased intracranial tension is treated by proper positioning of patient with headelevated at 15-30 position,
fluid restriction to 2/3rd of maintenance, 20% Mannitol5 ml/kg over 10-15 min followed by 3 ml/kg every 6
hourly for 48 hours and thenSOS. Or Acetazolamide 50-75 mg/kg/day in 3 divided doses through feeding tube Or
Glycerine 1 ml/kg/day through feeding tube may be added, if increased intracranial tension persists.
d. Fever is controlled as given in section on fever.
(Caution: Never give aspirin).
e. The intravenous fluid at two-thirds of the maintenance requirement initially. The electrolyte concentration of
the blood is monitored very closely. Any imbalance is treated promptly. Fluid restriction is not done, if patient is
dehydrated or is inshock.

Page 217
f. Feeding: Initially the patient is kept nil orally for first 24-48 hours. Later on the feeding is guided by the level of
sensorium. A tube feeding is helpful for feeding as well as for giving medicines.

4.2 Specific treatment

Until a bacterial cause is excluded, parenteral antibiotic therapy should be administered.The choice of antibiotics
depends upon age of the patient and prevalence of organismin the area.

4.2.1 Age 0-3 months

1. Inj Cefotaxime 200 mg/kg/day IV in 4 divided doses for 14 days.
2. Inj Ampicillin 300 mg/kg/day IV in 4 divided doses for 14 days.

4.2.2 Age 3 months-12 years

1. Inj Ceftriaxone 100 mg/kg/day IV over 30-60 minutes in 2 divided doses for 10 days Or Inj Cefotaxime 200
mg/kg/day IV in 3 divided doses for 10 days
Or Inj Ampicillin 300 mg/kg/day IV in 4 divided doses for 10 days
2. Inj Chloramphenicol 100 mg/kg/day in 4 divided doses for 10 days
If Meningococci is suspected/isolated, Inj Penicillin G 300,000-400,000 IU/kg/day in 4 divided doses for 7-10
days.

4.2.3 Treatment of Viral meningoencephalitis

Herpes simplex virus (generally diagnosed by focal encephalitis or CT scan):
Inj Acyclovir 30 mg/kg/day in 3 divided doses for 14-21 days. Non-HSV viral
Encephalitis is treated by supportive therapy only.
Lumbar puncture is repeated at 48 hours to see the response. However, if the patient is improving well, a repeat
lumbar puncture may not be necessary.

5. Advice at discharge
Regular follow-up for neurological assessment including deafness is advised.
Anticonvulsant therapy to be continued, if seizures are recurrent during course of meningitis. Children with
sequalae would require assessment of handicap and multidisciplinary management.
Occupational/physiotherapy may be taught during hospital stay itself.

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 21. TUBERCULOUS MENINGITIS
1. Introduction
Tuberculous meningitis is the inflammation of
meninges due to lymphohaematogenous spread of
the primary infection of tuberculosis to the
meninges, found in about 0.3% of untreated primary
infection in children. It is the most dangerous form
of extrapulmonary tuberculosis. 70% of the cases
are found in children less than 5 years of age.
2. Clinical Manifestations
The clinical progression of tubercular
meningitis (TBM) may be rapid or gradual.The
signs and symptoms progress slowly over
several weeks and can be divided into three
stages.
2.1 Stages
2.1.1 The 1st stage, which typically lasts 1-2
weeks, is characterized by non-specific symptoms,
such as fever, headache, irritability, drowsiness and
malaise. Focalneurologic signs are absent.
3.1.1 The 2nd stage usually begins more
abruptly. The most common featuresare lethargy,
neck-rigidity, seizures, positive Kernig or
Brudzinski signs, Hypertonia, vomiting, cranial
nerve palsies and other focal neurologic signs.
3.1.2 The 3rd stage is marked by coma,
hemiplegia or paraplegia, hypertension,
Decerebrate posturing, deterioration of vital signs,
and eventually, death.
4 Complications:
Survivors may have motor deficits, cranial
nerve deficits, mental retardation, learning
disabilities, seizures, hydrocephalus, blindness,
deafness and diabetes insipidus.
5 Investigations
The diagnosis is made by analysis of CSF on
lumbar puncture, which shows lymphocytic
leucocytosis with elevated protein and a low
sugar (for details see Table 19.21 in section on
Meningoencephalitis).
Demonstration of AFB in CSF confirms the
diagnosis, but the yield is very poor.
Culture of CSF shows growth of M.
tuberculosis, takes too much time.
Positivetuberculin skin test corroborates the
diagnosis but may be negative in
severelymalnourished/disseminated disease. 20-
50% of children have a normal chestradiograph
others may show primary disease. CT scan or
MRI of brain maybe normal during early stages
of the disease. Later, it can show exudates in
thebasal cisterns of brain, periventricular ooze
and hydrocephalus. Some may
showtuberculomas even.
6 Treatment
Treatment consists of proper supportive care,
including nonpharmacological treatment, specific
antitubercular therapy, treatment of increased
intracranial tension and, if required, surgical
treatment.
6.1 Nonpharmacological
Nutrition: After initial stabilization, nutritional
rehabilitation should be done as given in section on
protein energy malnutrition.
Skin care and prevention of bedsores.
Care of bowel and bladder.
Physiotherapy and occupational therapy should be
instituted early to preventdeformities and
contractures.
6.2 Pharmacological
1. Appropriate fluid therapy to correct dehydration
due to frequent vomiting anddecreased oral intake.
2. Treatment of SIADH. Fluid restriction to three
fouth or two third of maintenance. Treatment of
raised intracranial tension
3. Inj. Dexamethasone: 0.15 mg/kg IV 6 hourly for
2 weeks followed by Tab.Prednisolone 1.5
mg/kg/day orally through feeding tube for 4 week
this should be tapered over another 2 weeks. A total
of 6-8 weeks therapy with steroid is recommended.
4. Mannitol (20% solution) 1.5 to 2 g/kg or 8-10
ml/kg over 30-60 minutes. Repeat every 6-8 hours
for 7 days. Lower doses (0.25 g/kg/dose) can also be
tried. Or Glycerol 1 ml/kg/dose every 6-8 hours,
diluted in orange juice or water, given through
feeding tube. Or Tab. Acetazolamide 50 mg/kg/day
in 3 divided doses for 2-3 weeks.
5. Presence of seizures necessitates treatment with
phenytoin or carbamazepine in appropriate doses
(for details see section on Epilepsy in Chapter).
6. Specific antitubercular therapyas given in
management of tuberculosis (seeSection on
Tuberculosis).
7. Surgical treatmentventriculoperitoneal shunt
(VP shunt): TBM shows somedegree of
hydrocephalus by 4 weeks. Obstructive
hydrocephalus should be shunted immediately. Non-
obstructive hydrocephalus with increased
intracranial pressure as shown by ventricular tap or
Page 219
CT scan will also be benefi ted by VP shunt. An
early shunt is preferable.
6.3 Follow-up
1. Patient should be kept under follow-up after
discharge from the hospital andassessed for
neurological deficit and features of increased
intracranial pressure(ICP). One of the common
causes of increased ICP is untreated hydrocephalus
or blocked shunt.
2. Check compliance to drugs and ensure that
occupational therapy/physiotherapy isbeing
continued.
3. Assess physical, mental, visual and auditory
handicap and take expert opinion for rehabilitation
from other specialists. Patient/parent education
Seriousness of disease must be explained.
Contact survey should be done and any other
member in the family found to have active TB
should be counselled to attend TB clinic for therapy.
Need for compliance should be emphasized.
Drug toxicity and side effects must be explained.
Neurological defi cits may appear even in a patient
on therapy.
Page 220
 22. ACUTE RESPIRATORY INFECTION
1. Introduction
Acute Respiratory Infection (ARI) is an important
cause of infant and child mortality and also the
commonest cause of morbidity among children
below five years. ARI is the infection of any part of
respiratory tract, which includes cough, common
cold, pharyngitis, pneumonia, laryngitis and ear
infection.
Acute respiratory infections in children can involve
upper respiratory tract (nose, throat) or lower
respiratory tract (bronchi, lung). Lower respiratory
tract infections (broadly termed as pneumonias) are
a major cause of death of infants and children in
India, accounting for about 30% under-five deaths.
Timely treatment, based on well-researched
algorithms can save most children with ARI.
Majority of the cases of ARI have non-severe
Table 1 : Cut of points for fast breathing
Sr. Age group
1 0 - 2 months
2 2 months to 1 year
3 1 year to 5 years
Chest in-drawing
In normal child, during respiration, chest expands
when the child breathes in and compresses when the
child breathes out. In children with severe
pneumonia, chest moves in when the child breathes
in. This is called chest in-drawing.
2.3 Pneumonia in 0-2 months age
group
Important aspects about pneumonia in age group 0-2
months are as below:
In these children, there are no usual features of
pneumonia like fever, cough, etc.
Child may have only fast breathing and/or chest
in-drawing.
Pneumonia in child less than 2 months age is
always severe & mortality is high
Such cases should be treated in the facility where
specialist & ICU are available.
Classification
disease and can be managed in the community with
oral co-trimaxazole. Severe ARI cases require
urgent referral to a facility where injectable
antibiotic therapy and supportive care are available.
2. Diagnosis & management
of ARI
Classification and management of ARI is based
upon three important factors. These are age of the
child, respiratory rate and danger sign like chest in-
drawing.
2.1Age of the child and respiratory
rate
Children are classified into three age groups for ARI
management. These age groups and criteria for fast
breathing are given in table below
Criteria for fast breathing
Respiratory rate more than 60 / minute
Respiratory rate more than 50 / minute
Respiratory rate more than 40 / minute
No pneumonia
Severe pneumonia/Very severe illness
2.3.1 No pneumonia
If respiratory rate of child is less than 60/minute
then the child is classified as 'No Pneumonia'.
Give Paracetamol tablet if there is fever and
demonstrate to the mother how to clean nose
with normal saline drops.
Advise mother to continue breast-feeding.
Inform mother about danger signs of
pneumonia, e.g. breathlessness (rapid
movement of abdomen), inability to drink,
excessive drowsiness, hypothermia, high fever
etc. Ask mother to immediately bring the child
back to health facility, if she observes any of
the signs mentioned above.
Severe pneumonia/Very severe illness
If child below 2 months presents with fast breathing
(RR > 60/minute) and/or chest in-drawing
Plus
Page 221
One or more of the following signs - - Cyanosis
- Inability to drink - Hypothermia
- Excessive drowsiness - Convulsions
- Stridor, wheeze Such child shouldbe referred to specialist.

In case referral can not be executed treat the child as below

Table 2: Treatment of Pneumonia

Antibiotic Dosage Frequency Route

Age < 7 days Age > 7 days - 2
months
Inj Benzyl penicillin 50,000 12 hrly 6 hrly IV/IM
OR IU/kg/dose
12 hrly 8 hrly IV/IM
Inj Ampicillin AND 50 mg/kg/dose
12 hrly 8 hrly IV/IM
Inj Gentamycin 2.5 mg/kg/dose
tohealth facility if she observes any of the
danger sign.
2.4 Pneumonia in 2 months to 5
years age group 2.4.2 Pneumonia
Children with ARI of 2 months to 5 years age are If child has fast breathing (RR: 2-12 mts > 50/ min.
classified into four groups as follows - & 1-5 yrs. > 40/ min.) and no chest in-drawing,
diagnose child as Pneumonia
- No pneumonia
a. Treatment of pneumonia
- Pneumonia
Give child Cotrimaxazole for 48 hrs. Treatment
- Severe pneumonia schedule for pediatric cotrimaxazole is -
- Very severe illness 2-12 months:
2.4.1 No pneumonia 2 tablets twice daily or syrup 5 ml. twice daily
When respiratory rate is normal and no sign of chest 1-5 yrs: 3 tablets twice daily or syrup 7.5 ml. twice
in-drawing is seen child is disgnosed as no daily.
pneumonia. These children should be treated at
home & observed for appearance of danger signs Pediatric tablet contains Sulphamethaxazole 100 mg
(increase in RR and chest in-drawing) by mother. & Trimethoprim 20 mg.
Following points should be advised to mother - Syrup 5 ml. contains Sulfamethaxazole 200 mg
Continue breast-feeding if child is breast-fed. and Trimethoprim 40 mg.

Give plenty of oral fluids including water or If fever is present, give Tab. Paracetamol. (5 to
ORS to child. 10 mg./kg)

If fever is present, give Tab. Paracetamol.
Teach mother how to clean nose with saline
water. This will clear airway of child and
improve breast-feeding.
In community, many home remedies are used
for ARI. One of the best among them
is honey & ginger. Advise mother to give honey
and ginger to child.
Inform mother about danger signs of
pneumonia, e.g. breathlessness, inability to
drink, excessive drowsiness, hypothermia, high
fever etc. Advise her to bring child back
Teach mother how to clean nose with normal
saline. This will clear airway of child and
improve breast-feeding.
Keep baby warm by covering with warm
clothes and keeping in lap.
Assess child after 48 hrs:
If improvement - Continue CTZ for 3 Days
Child has: - Chest in-drawing
And
RR may be fast complete 5 days course
If no improvement or child gets deteriorated
refer child to specialist.

Page 222
 Severe pneumonia: - Child with chest in- Treatment
drawing & having RR normal or fast is
a. Treat for first 48 hrs by
diagnosed as severe pneumonia should be
treated by specialist. Give oxygen if child has
cyanosis till the child is referred.
Table 3
Treatment of severe Pneumonia
Antibiotic Dosage Interval Route
Inj Benzyl penicillin OR 50,000 IU/kg/dose 6 hrly IM
Inj Ampicillin OR 50 mg/kg/dose 6 hrly IM
Inj Chloramphenicol 25 mg/kg/dose 6 hrly IM

b. Assess after 48 hrs

i. If improvement, continue for next 3 days as below
Table 4
Treatment of severe Pneumonia
Antibiotic Dosage Interval Route
Inj Procaine penicillin OR 50,000 IU/kg (Max 4 lac units) Once IM
Tab Ampicillin OR 50 mg/kg/dose 6 hrly Oral
Tab Chloramphenicol 25 mg/kg/dose 6 hrly Oral

ii. If no improvement, change antibiotic as below

If Ampicillin was given earlier then change 2.4.4 Very severe illness
to Inj Chloramphenicol a) Child has:
If Chloramphenicol was given earlier change Chest in-drawing and RR may be fast or normal
to Inj Cloxacillin 25 mg/kg/dose 6 hrly IM + plus
Gentamycin 2.5 mg/kg/dose 8 hrly IM.
One or more of following signs -
iii. Important aspects of antibiotic treatment
Inability to drink
Treatment with antibiotics should be
continued for at least five days. Excessive drowsiness
Stridor, wheeze
Cyanosis
Hypothermia
Convulsions
Continue treatment for at least 3 days after child
recovers. Diagnose the child as suffering from very severe
illness & refer the child to specialist having facility
If cloxacillin & gentamycin are started continue for of intensive care unit.
three weeks.
In addition to this give following 3. Treatment of childhood
Administer Oxygen if required community-acquired
Continue breast feeding during illness pneumonia
If fever, give tablet or syrup Paracetamol Themanagementofpneumoniaisguidedbytheseverity
ofthediseaseaslistedinTable below:

Table 5: Signs & symptems

Page 223
 Sign or symptom Classification Treatment

Centralcyanosis Very severe pneumonia Admittohospital

Severerespiratorydistress Managetheairway
Not abletodrinkduetorespiratory Giveoxygen
Distress. Giverecommendedantibiotic
Treathighfeverifpresent

Chestindrawing Severe pneumonia Admittohospital

Giverecommendedantibiotic

Fastbreathing Pneumonia Giveappropriateantibioticfor5

days
2monthsupto12months:50breaths/
Soothethethroatandrelievecough
min
with a safe remedy

(a) There is a rapid progression of the disease, or

3.2 Treatment of very severe
illness
3.2.1 Admit the child in hospital
3.2.2 Obtain a radiograph
ofthechestiffacilities
areavailableforthesame.Radiographyinverysever
epneumoniaisrequired at admission to assess
the extent of disease and to rule out presence of
puemothorax or effusion In case
ofseveredistress,stabilizeandoxygenatethechildb
eforesendingforradiograph.
3.2.3 Give antibiotics
- pyfor4-6weeks.
GiveInjectableAmpicillin(50mg/kgIM/IVevery6hours
)andGentamicin(7.5mg/kgIM/IVonceaday).Ifthechild
respondswell,dischargeafter5daystocontinuetreatm
ent
athomewithoralAmoxicillin(15mg/kgperdosethreeti
mesaday)plusIMGentamicinoncedailyforafurther5da
ys.
-Alternatively,
giveInjectableChloramphenicol(25mg/kgIMorIVever
y8hours)untilthechildhas
improved.Thencontinuethesamedrugorallyinthesa
medosefor3timesadayforatotalcourseof10days.
- lfluidsoncethedistresssettlesandthechildisabletofeed.
Ifthechilddoesnotimproveby48hourstoanyoneofthe
setreatments,reassessforcomplicationsandswitchto
InjectionCeftriaxone(80mg/kgIMorI/Voncedaily )
for10days.
- Staphylococcal pneumonia is suspected if:
(b) There is pneumatocoele, or pneumothorax, or
effusion on chest X-ray, or
(c) Child has large skin boils or abscess or infected
scabies, or
(d) post-
measlespneumoniawhichisnotrespondingwithin48ho
urstotheinitialtherapy.Ifstaphylococcalpneumoniaissu
spected,addInjCloxacilin(50mg/kg/dose,every6hourl
y)toanyoftheabovechoice of antibiotics.
Whenthechildimproves,continueCloxacillinorally4ti
mesadayforatotalcourseof3weeksatleast.Childrenwit
hcomplicatedpneumonia(Empyema)needlongerthera
3.2.4 Give Oxygen
-
Wherepulseoxymeterisavailable,useoxygensaturatio
noftheblood(SaO2)toguideoxygentherapy.Maintain
SaO292%.Continuewithoxygenuntilthesignsofhyp
oxia(suchasseverelowerchestwallin-drawing or
breathing rate of 70/min)arenolongerpresent.
3.2.5 Give supportive care
-
Ensurethatthechildreceivesdailymaintenancefluidsap
propriatetochildsage.Encouragebreastfeedingandora
- If the child has fever
(38.5C)whichappearstobecausingdistress,gi
veoralParacetamol(15mg/kg/dose).
-Ifwheezeispresent,givearapid-
Page 224
actingbronchodilator(asdescribedinthenextsection). - Improved ability to eat and drink.
- 3.2.7 Watch for complications
Removeanythicksecretionsinthenose/throat,whichth -
echildcannotclear,bygentlesuction. Ifthechildhasnotimprovedaftertwodays,orifthechild
3.2.6 Monitor the child sconditionhasworsened,lookforcomplicationsoroth
erdiagnoses.Ifpossible,obtainarepeatchestX-
- ray.Considertransfertoahigherfacilityincaseofpoor
Thechildshouldbecheckedbynursesatleastevery3hou response or deterioration despite second-line
rsandbyadoctoratleasttwiceaday.Monitorfor signs of therapy.
improvement. A patient who is improving on
treatment should have: 3.2.8 Monitoring
Thechildshouldbecheckedbynursesatleastevery6ho
- An improvement in the respiratory rate.
ursandbyadoctoratleastonceaday.Monitorforsignso
- Less indrawing of the lower chest wall. f improvement as discussed above.
- Less fever, and /or Table 5

Table 6 : summary of management of ARI cases.

No. Type Who can manage Where can be managed
Age group 2 months to five years
1 No pneumonia ASHA Anganwadi Worker, MPW Home management
2 Pneumonia MPW/HA, MO Management at home or PHC
3 Severe pneumonia PHC MO / specialist PHC/ referral center
4 Very severe illness Specialist Specialist with ICU facility
Age group below 2 months
Child should be referred immediately after giving one dose of CTZ

Page 225
 23. BRONCHIAL ASTHAMA

Less Preferred treatment: Monteleukast

1. Introduction: Theophylline Chromoglycate and treatment of mild
Bronchial asthma is a disease characterized by an intermittent asthama
increased responsiveness of the trachea and bronchi
to various stimuli. It manifests by widespread 3.2 Moderate persistent
narrowing of the airways causing paroxysmal Symptoms > 2 times/ week
dyspnea, wheezing or cough. The diffuse
obstruction to the airflow is reversible in a large Nocturnal symptoms >1/week
majority of cases, either spontaneously or in PEFR 60-80%
response to treatment. Bronchial reactivity is a
necessary component of asthma. Asthma is a result 3.2.1 Treatment
of multifactorial inheritance. Inhaled steroid med dose

2. Signs &Symptons: If response not satisfactory

Recurrent cough Add inhaled LABA
Breathlessness Salmederol/ Formeterol/Monteleukast/ long acting
Wheezing theophylline

3. Clinical classification
1) Mild Intermittent 3.3 Severe Persistent
2) Persistant Daily symptoms often severe
a) Mild Activity limited
b) Moderate Growth affected
c) Severe Frequent Nocturnal symptoms

3.1 Mild Intermittent Frequent hospitalization

Symptoms < 2times a week and asymptomatic in
between
Nocturnal symptoms < 2 times /month
3.1.1 Treatment
Salbutamol inhaled (100 MCG/puff)
1-2 puffs as per requirement
For children less than 2 years use face mask with
spacer
OR
Salbutamolsyrup/tablet
0.1-0.2 mg/kg/dose three times a day till symptoms
subside
Mild Persistent
Symptoms > 2times/week but, 1time/day
Nocturnal symptoms > 2 times / month
Asymptomatic in between exacerbations peak flow
rate( PEFR) > 80%
3.1.2 Preferrence of Treatment
Preferred treatment: Inhaled steroids (low dose) 2
puffs twice / day
PEFR<60%
3.3.1 Treatment
Inhaled steroids high dose
Inhaled LABA / Monteleukast / long acting
theophylline
If response not satisfactory
Oral Prednisolone2mg/kg/day in three divided doses
& inhaled salbutamol as required
1) Pulmonary function test
2) Absolute Eosinophili count
3) Chest X-ray
4) Skin test & Allergy test
3.4 Treatment Guidelines for acute
exacerbation of Asthama
O2 by mask (4-6 liters /min)
Salbutamol MDI (100MCG/puff)with spacer and
mask for < 2 years 4-8 puffs every 20 min x 3 OR
Salbutamol nebulization 0.15mg/kg(min 2-5mg)

Page 226
diluted in 3 ml saline can be repeated 3 times every Good response
20 min
Send home: salbutamol MDI+ Tab Pednisolone
InjAdrenaline (1:1000) or Terbutaline (0.01mg/kg) 2mg/kg/Day x 5-7 days
s/c may be repeated thrice every20 min if both
above are not available
AND Inj Hydrocortisone hemisuccinate 4. Investigation:
10mg/kg/dose 4 times a day OR Inj
1) Pulmonary function test
Dexamethasone0.2 mg /kg/dose
This must be converted to oral prednisolone once 2) Absolute Eosinophili count
patient is stable 3) Chest X-ray
If response not satisfactoryRefer to higher center
4) Skin test & Allergy test
statIMP: Evaluate after 1 hour

Medication Dosage form Dosage

Formoterol DPI: 12 ug per single-use capsule 1. Capsule every 12

years
Salmeterol MDI: 25 ug per puff 1-2 puff every 12 hours
Fluticasone/salmeterol DPI:100, 250, or 500 ug of fluticasone 1 inhalation twice daily;
with 50 ug of salmeterol dosage depends on
severity of asthma

Cromolyn MDI: 1 mg per puff 1-2 puffs 3 to 4 times

daily
Nebulizer solution :
1 ampule 3 to 4 times
20 mg per ampule
daily

Nedocromil MDI: 1.75 mg per puff 1-2 puffs 2 to 4 times

daily
Montetelukast 4 or 5 mg chewable tablets, Age 12-23 months: 4 mg
oral
4 mg packet of oral granules,
granules at bedtime
10 mg tablets
Age 2-5 years: 4 mg at
bedtime

Zafirlukast 10 & 20 mg tablets Age 7-11 years: 20

mg daily in

Theophylline Liquids, sustained- release Starting dosage is 10 mg /kg

per day
Tablets and capsules.
< 1 years : ( 0.2 [age in
weeks] ) + 5
= mg per kg day 1 years :
16 mg
per kg per day

Table1. Drugs used in the long-term control of asthma in children

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 24. BREATH HOLDING SPEL

1. Introduction: 3. Complication:Local trauma,

Aspiration pneumonia.
A baby with crying followed by loss of
consciousness, tonic posturing (features of cerebral
anoxia). Cyanotic Breath holding spell more
4. Management:
common form: Usual age of onset is 6 months, peak Examination to rule out other seizure mimicking
by 2 years, abate by 5 years. After a shrill cry, conditions.
forced expiration followed by apnea and cyanosis
leading to loss of consciousness associated with i. Reassurance of parent that these are not
clinical jerks or posturing. seizures, EEG not required, inter-ictal EEG is
normal.
2. Signs &Symptons: ii. Should not reinforce this behavior, put the
child in safe place and avoid cuddling.
Baby may be cyanosed (blue)\ Baby may be pale iii. Iron supplements if anemia, delayed weaning
etc.(3 mg/kg for 3 months.)
History of a predictable stubborn behavior,
iv. Syrup Piracetam( 40-100 mg /kg in BD) may
precipitating event like upsetting the infant
be used for few months if the breath holding
History of painful stimulus or hit on head cyanosis spells are very frequent,
leading to loss of consciousness associated with v. Parental counseling to prevent reinforcement
clinical jerks or posturing Less common, Apnoea of this behavior.
followed by pallor, hypotonia and tonic seizure.

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 25. BRONCHIOLITIS

Supportive measures such as oxygen by hood (10

1. Introduction: litres / mt) or by mask (5 lits / mt); IV fluids if child
is not able to feed orally.
Viral in aetiology (Respiratory syncitial virus) most
frequently in children < 12 months of age
IV fluids if child is not able to feed orally.
2. Signs &Symptoms:
An antibiotic has no role.
Initial URI symptoms followed by Increasing
cough, Respiratory distress, Wheeze and feeding
difficulty
4.2 Monitoring
(RR, Respiratory distress, pulse oximetry) - A trial
3. Investigations: dose of Nebulised salbutamol / epinephrine if
wheezing is marked as child improves wean off
CXR: Hyperinflated lungs with patchy infiltrates oxygen and increase oral feeds if child develops
severe respiratory distress, increasing hypoxemia,
4. Management: cyanosis or fatigue ventilatory support may be
4.1 Treament of bronchiolitis is essentially required.
symptomatic.Child should be treated in a humid
atmosphere preferably in sitting position with head
and neck elevated.

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 26. EMPYEMA
USG chest: size, site of effusion, adhesions or
1. Introduction: loculations can be made out.
Characterised by presence of pus or microorganisms Diagnostic thoracocentesis: usually in fifth
in the pleural fluid occurs as a complication of intercostal space over mid-axillary line using a
Pneumonia, Influenza. Streptococcus Pyogenes, large bore needle Pleural fluid for Gram stain,
Staph aureus, Streptococcus Pneumoniae, culture and sensitivity, Pleural fluid pH, sugar
Hemophilus are the common organisms. are reduced and protein is elevated.

2. Signs &Symptoms: 5. Management:

Common symptoms are 5.1 Treatment comprises of chest drain and
Fever antibiotics.

Chills Chest drainage using an intercostal drainage tube

inserted in the region of maximal dullness (usually
Toxaemia V or VI intercostal space in axillary region) and
connecting to a sterile under water drainage bottle
Respiratory distress
Chest drainage is kept till the drainage decreases to
Grunt and < 25 ml/day and there is good lung expansion. If
there is no chest expansion by clinical or
Chest pain (pleuritic pain)
radiological methods, surgical opinion is sought
3. on examination 5.2 Antibiotics
Decreased chest expansion Cloxacillin with cefotaxime or ceftrioxone is the
Diminished breath sounds first line antibiotic; switch over to oral antibiotics
after child becomes afebrile and chest tube is
Dullness on percussion on affected side and removed. Total duration of 4 - 6 weeks of antibiotic
Mediastinal shift to opposite side therapy or
Cloxacillin: 100 - 200 mg/kg/day in 4 div. doses
4. Investigations:
Cefotaxime: 150 - 200 mg/kg/day in 3 or 4 div.
Chest X-Ray: obliteration of costophrenic doses
angle; diffuse homogenous opacity.
Supportive care: oxygen, good nutrition

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 27. APPROACH TO FEVER

1. History: 3. Basic investigations

Type of fever
Associated symptoms chills / rigor, cough, sore
In high risk group and
throat, ear pain, urinary symptoms, bleeds etc. fever beyond 5 days in low
Previous illness and treatment. if any Feeding
difficulty, respiratory distress. risk:
Total count, differential count, peripheral smear,
2. Clinical Examination Platelet count
Check Temperature, Blood pressure, Pulse,
Perfusion Urine analysis, urine c/s

Skin: Rashes, Bleed, Cyanosis Blood culture and sensitivity

Eyes: Pallor, Icterus Chest x-ray

Mouth: Ulcer, Thrush C-reactive protein

Ear: Discharge, Redness, Tenderness Mantoux test

Throat: Congestion, Tonsillitis CSF analysis if required

CNS: Meningeal irritation, altered sensorium Other investigations

Abdominal examination: Hepatomegaly, Liver function test

Splenomegaly Renal function test
Respiratory System: Tachypnoea, Retraction, Creps, USG abdomen
Wheeze
Blood for leptospirosis
Serology for dengue
Widal
Bone marrow

4. Refer if,
Fever with unconsciousness
Fever with shock
Severe respiratory diseases
Bleeding diathesis
Refractory seizures

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 28. ACUTE FLACCID PARALYSIS (AFP)

1. Defination :
A case of AFP is defined as any child aged <15
years, with acute onset of Flaccid paralysis without
any obvious cause (e.g. severe trauma or electrolyte
imbalance like (hypokalaemia). AFP is a notifiable
disease and all cases must be reported immediately
to Nodal Officer and District Surveillance Officer,
NPSP Unit, Directorate of Family Welfare. India
has shifted to the virological system of case
classification, i.e. within 90 days of paralysis onset;
all cases should undergo final classification as
confirmed polio, non-polio AFP or compatible with
poliomyelitis. India has been declared polio free
since 3 years.
1. SALIENT FEATURES
The paralysis is of acute onset (<4 weeks) and the
affected limb(s) are flaccid (floppy or limp). If the
AFP is due to polio, then sensation is never affected.
Other important differentials to be considered in
cases with AFP are detailed in Table-1. This
includes possible illness due to Guillian-Barre
syndrome, transversemyelitis, traumatic neuritis;
viral infections caused by other enteroviruses,
toxinsand tumours. Isolated facial paralysis is also
included.Pseudoparalysis due to pain in congenital
syphilis, osteomyelitis, abscess, scurvy,
unrecognized trauma leading to contusions, slipped
epiphysis or fractures, etc. can also mimicAFP.

2. Differential Diagnosis:
Table 1- Important differential diagnosis of AFP (adapted from Field Guide, MOHFW, GOI)

Signs and Polio GBS Transverse Traumatic

symptoms myelitis or injection
neuritis
Age Most cases occur Usually above 2 Mostly above 4 No age limit
under 3 years of years of age years of age
age

Progression of 24-48 h onset to Hours to days Hours to 4 days Hours to 4 days

paralysis full paralysis

Fever onset High always Not common Rare Commonly

present at onset of present before,
flaccid paralysis during and after
disappears the paralysis
following day

Flaccidity Acute, Acute, Acute Acute,

asymmetrical, symmetrical, lower limbs asymmetrical
Proximal Distal symmetrical Limb

Muscle tone Diminished Diminished Diminished in Diminished in

lower limbs affected limb

Deep Decreased or Absent Absent in lower Decreased or

tendon absent extremities, later absent
refl exes hyper-refl exia

Sensation Severe myalgia but Cramps, tingling Pain in gluteal

no sensory defi cit hypoanaesthesia of Anaesthesia of region
palms and soles the lower limbs
with sensory loss

Cranial nerve Only in bulbar or Often present Absent Absent

bulbospinal cases. affecting VII, IX,

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 Loss of gag reflex X, XI, XII
most common Only
in bulbar or
bulbospinal cases.
Loss of gag reflex
most common
Respiratory Only when bulbar In severe cases Sometimes Absent
insufficiency and bulbospinal
involving
respiratory muscles
CSF WBCs High WBCs. <10 Normal Normal
proteins Normal or slightly High Normal or Normal
increased slightly elevated
Bladder Absent Transient Present Never
dysfunction
Nerve Abnormal, anterior Abnormal, Normal of Abnormal in
conduction horn cell disease demyelination abnormal has no sciatic nerve
velocity in 3rd diagnostic value

EMG 3rd week Abnormal Normal Normal Normal

Sequelae at 3 Severe Symmetrical Flaccid Moderate
months and up asymmetrical atrophy of distal atrophy only in
to a year atrophy, skeletal muscles, diplegia, affected lower
deformities may atrophy after years limb
develop later

laboratory in good condition (i.e., no desiccation, no

3. Confirmation
An AFP case is confirmed as Polio only by the
isolation of wild poliovirus from any stool
specimen.An AFP case is classified as non-polio
AFP if wild poliovirus is not isolated from
adequate stool specimens.If stool specimens are
inadequate, final classification of the AFP case as
either nonpolio AFP or compatible with Polio will
depend on the results of 60 days follow-up
examination. If the 60 days follow-up examination
shows no residual weakness, the case is classified as
non-polio AFP. The final classification of the case
as compatibleor discarded as non-polio AFP is
determined by the National Expert Review
Committee (ERC) which meets every month in New
Delhi to review all such cases.
3.1 Adequate stool: Two specimens collected within
14 days of paralysis onset and at least 24 hours
apart;each specimen must be of adequate volume (8-
10 grams) and arrive at a WHO-accredited
or salt/sand packs to prevent rotation.
If transient urinary retention occurs
When pain subsides passive movements of
alternate hot and cold compresses over the
suprapubic region.
(Caution: No massage or intramuscular injections as
it may further precipitateparalysis. Watch for
progression, particularly for the involvement of the
respiratorymuscles.)
Warm water fomentation using hot packs with
soaked towels wrapped around the affected partsfor
about 10 minutes, 2-3 times a day help in
leakage, with adequate documentation and evidence
that the cold chain was maintained.)
4. Treatment for acute POLIO
like illness
All cases should be treated as below except patients
with isolated single lowerlimb involvement and
reporting after 4 days of onset of paralysis and
currently not progressing for more than 48 hours.
4.1 Nonpharmacological
Complete bed rest and correct positioning of the
affected limbs in the optimal
Position as follows:
Hipslight flexion, knee5 flexion, foot90
with support against the soles. Both legs should be
supported from the lateral sides with pillows or
rolled towels
relieving painthe jointsfor about 10 minutes, 2-3
times a day.
4.2 Pharmacological
There is no specific drug therapy for polio. For fever
and pain, use paracetamol or ibuprofen (see section
on Fever in Chapter 1). Referral to a tertiary care
centre witha ventilatory support facility, if there is
progression of paralysis, respiratory distress,bulbar
involvement, paralysis of upper limbs which is <3
days old (there is higherrisk of diaphragmatic
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involvement in such cases), marked drowsiness or Note: Post-polio residual paralysis should be
any other complication. referred for rehabilitative services to an appropriate
centre.
Patient/parent education No dietary restrictions,
however, continue breastfeeding or other
regular feeding.
5 Action expected on
Paralysis progresses usually for about 4-7 days admission of suspected
after onset. Recovery may startthereafter over AFP case:
days to weeks with little recovery of strength - Report to higher authority immediately
after 6 months ofillness. A regular
physiotherapy facilitates recovery of muscles. - Take adequate stool sample
- Send the stool sample maintaining cold chain to
district headquarte

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 29. FEBRILE SEIZURES
1. Introduction
Febrile seizures are brief (2-5 min), generalized
tonic-clonic and self-limited seizures followed by a
brief post-ictal period of drowsiness, in an otherwise
healthy, febrilechild of 6 months to 5 years of age,
without any evidence of underlying
neurologicaldisease. They are the most common
seizure disorder during childhood, with a
uniformlyexcellent prognosis. They occur rarely
before 6 months and after 5 years of age. The peak
age of onset is approximately 14-18 months of age,
found in 3-4% of young children. There is a strong
family history of febrile convulsions in siblings and
parents, suggesting a genetic predisposition. Except
for the cases at high risk, simple febrile seizures
rarely develop into epilepsy.
2. SALIENT FEATURES
Febrile seizures usually occur when the temperature
is rising rapidly, to generally 39C (102F) or more
of core temperature. They are of two types:
(i) Typical (simple) febrile seizure occurs on day 1
of fever, does not last formore than 10 minutes;
generalized tonic-clonic; generally not more than
oneepisode within 24 hours.
(ii) Atypical or complex febrile seizure may persist
for more than 15 minutes;it could be focal in nature;
more than one episode of seizure in 24
hours;associated with abnormal neurological
findings or deficits. An organiccause such as an
infectious or toxic process should be considered
andinvestigated.Late onset febrile seizures,
persistent febrile seizures, generalized epilepsy
andfebrile seizure plus (GEFS+) and febrile status
epilepticus (FSE) are part of thespectrum of febrile
seizures
3. Investigations
3.1 Lumbar puncture: A lumbar puncture with
examination of CSF is essential to rule out
possibility of meningitis in cases with first episode
of febrile seizures.
3.2 EEG has no role in case of simple febrile
seizures. However, in cases withatypical febrile
seizure or in a child with high risk for developing
epilepsy, itmay be helpful.
4. High risk for developing
epilepsy,
It include a positive family history of epilepsy,initial
febrile convulsion prior to 9 months of age,
aprolonged or atypicalfebrile seizure, delayed
developmental milestones and an abnormal
neurologicalexamination.
5. Treatment
Most febrile seizures are brief and would be over by
the time a child is brought to the doctor or health
facility. Management includes definitive diagnosis,
restraint in investigations, treatment of an acute
episode, prophylaxis for future episodes and family
counselling. Role of defervescence in preventing
febrile seizures is questionable.
5.1. Nonpharmacological
Clear the airway, semi-prone lateral position and
oxygen therapy.
5.2. Pharmacological
5.2.1 In cases presenting with seizures, the mainstay
of management is prompt administration of
anticonvulsants.
5.2.2 Thebest drug
isDiazepam/Midazolam/Lorazepam in a dose of 0.3
mg/kg by slow intravenous or rectal route. It can be
repeated, if seizures do not subside (per rectal dose
may be given up to 0.5 mg/kg/dose).
5.2.3 Intermittent prophylaxis (during febrile
illness)
5.2.4 It is a safe and effective method of prophylaxis
but does not reduce the risk of future epilepsy.
Tab Clobazam 0.75 mg/kg for 2-3 days in 2 divided
doses during fever or Tab/Syr. Diazepam 0.3
mg/kg/dose every 8 hours (1 mg/kg/day) for 2-3
days of febrile illness,started on the day of onset of
fever. Dose can be adjusted, if over sedation or
ataxia noted.
5.3 Continuous prophylaxis
Febrile status, complex and recurrent febrile
seizures (>6/year in spite of intermittent
prophylaxis) may need EEG, neuroimaging and
continuous prophylaxis with AED.Phenobarbitone
and valproate may be used in infants and older
children, respectively, for 1-2 years. Carbamazepine
and phenytoin are not useful.
6. Patient/parent education
The parents and caretaker should be assured of
the benign nature of the disease andshould be
told that no neurological deficit or mental
retardation occurs as a result ofsimple febrile
seizure. They should be taught about control of
fever at home. They can be taught to give
diazepam per rectally at home.
Page 235
 Routine immunization as per schedule should
be followed. After DPT vaccination, oral
paracetamol 15 mg/kg/dose every 6 h for 2 or 3
days and similarly, after measles vaccination,
oral paracetamol in the same dose started on the
4th day from the day of vaccination and given
for 3 to 4 days to avoid precipitation of febrile
seizures.
Page 236
 30. ACUTE NEPHRITIS

1. Introduction:
It follows streptococcal infection of throat or skin by 1-2 weeks. Glomerular injury will clinically present as acute
nephritis In majority of pediatric patients it is PSGN Age group 3-12 years. Disease is self-limiting and generally
resolves in one moth; however, microscopic urinary changes may perists up to one year.

2. Signs &Symptons:
Hematuria, Oedema, Hypertension, Varying degree of oliguria or anuria May present with CCF Many primary or
secondary Glomerular diseases will present as acute Nephritis.

3. Lab Investigations:
3.1 Urine exam: RBCs, RBC casts, significant proteinuria2+/3+
3.2 ASO titre increases
3.3 Chest X-ray:
Cardiomegaly, Pulmonary vascular congestion, Effusion
3.4 Hemogram: Normocytic normochromic anaemia
3.5 BUL, SerCreatinine raised

4. Complication:
Congestive heart failure, encephalopathy may occur in a few patients.

5. Treatment
5.1 Diet-Proteins,
Sodium, potassium should be restricted. Urine output should be measured accurately.

5.2 Daily monitoring of weight.

Protein restriction up to 0.6mg/kg/day

5.3 Drugs:
Oral Penicilline 25000-50000u/kg/Day OR
Inj Penicliilne 25000-50000 u/kg/Day im/iv in 4 divided doses x 7 days
OR
5.4 Erythromycin 40mg/kg/dayin 4 divided doses X 7 days
5.5 Diuretics: Frusemide1-2mg/kg/day in 1-2 divided doses
5.6 Antihypertensives: Nifidepine 1 to 2 mg per kg/ Atenolol 0.08 mg per kg/Enalapril 50 mg per day
5.7 Rest

6. Refer patient to higher center

CCF
Uncontrolled HTN or its complications

Page 237
 31. NEPHROTIC SYNDROME
1. Introduction:
Nephrotic syndrome ischaracterized by massive
proteinuria, hypoalbuminemia and edema.
Hyperlipidemia is usually associated; hematuria,
hypertension and impaired renal function are
occasionally seen.
More than 90% of childhood nephrotic syndrome is
primary (idiopathic). Other causes are amyloidosis,
vasculitis, SLE; post-infectious GN and hepatitis B
nephropathy.Nephrotic syndrome in children can be
divided into two groups based on renal histological
characteristics:
i)Minimal change nephritic syndrome(MCNS).
This is usually sensitive to steroids with a
satisfactory long-term outcome.
ii) Nephrotic syndrome with significant lesions.
It is usually associated with less satisfactory
course, tends to be steroid resistant and a significant
proportion progress to chronic renal failure.
2. Clinical Features:
The onset is insidious with edema first noticed
around the eyes and subsequently around the
legs.Gradually edema may become generalized,
with ascites, hydrothorax and hydrocele. A severe
muscle wasting is seen. It is a triad of
hypoproteinemia, hypercholesterolemia and
proteinuria.
3. Investigations:
Urine >3+ proteinuria
No RBCs/ Casts
Azotemia not significant
Serum proteins< 3.2gm/dL
Serum cholesterol raised
4. Management
4.1 1st Episode
The child should receive a high protein diet no extra
salt is given.
Prednisolone (2mg/kg/Day)in 2-3 divided doses
along with antacid Given till patient goes into
remission(Urine Albumin 1+/absent for 5 days)
OR up to 8 weeks and then tapered to
2mg/kg/alternate day x3-6 months and then stopped
Ideal calculation 60mg/m2 BSA
4.2 Relapse:
Urine Albumin 2+ >5 days / oedema
Sometimes resolves in a week if precipitated by
infection, then infection is treated. If not resolved
continue Prednisolone 2mg/kg/day in 2-3 doses till
urine is protein free for 5 days then taper alternate
day x 4 week and then stop
General care
Ca++ & K+ supplement if on frusemide
Frusemide1-2mg/kg/day for edema with expert
advise
4.3 Treatment of frequent
relapses:
i) Long term alternate day prednisolone. Following
completion of treatment for relapse, alternate day
prednisolone is slowly taoered to minimum
maintenance dose (0.3 0.7mg/kg). The dose is
maintained for 9-12 months.
ii) Levamisole: After inducing a remission,
levamisole is administered at a dose of 2-2.5 mg/kg
on alternate days. Alternate day prednisolone is
given in decreasing doses, until a dose of 0.3-
0.5mg/kg is reached, for 2-3 months.
Cyclophosphamide and cyclosporine A are used in
some cases.
Page 238
 Persistence of Hypertension /azotemia/ Hematuria
5. Refer to higher center
Steroid dependent or resistant or frequent relapse
For confirmation of diagnosis

Systemic features: arthritis/ Rash /

Hepatospleenomegaly

Page 239
 32. CONGESTIVE HEART FAILURE (CHF)

1. Rheumatic fever and RHD

Introduction:
Every Cardiac patient has potential to develop CHF. 2. CHD complicated by anemia infection
It is not a diagnosis; it is a clinical syndrome due to
an underlying anatomical or pathological cause 3. Hypertension
which is the primary diagnosis.
4. Mycarditis
Definition:
5. Upper respiratory obstruction.
Congestive cardiac failure is defined as inability of
the heart to maintain an output, at rest or during Symptoms:
stress , necessary for the metabolic needs of the
body(systolic failure) and inability to receive blood Slow weight gain, easy fatiguiability, persistant
into the ventricular cavities at low pressure during horse crying, wheezing, excessive perspiration,
diastolic(diastolic failure) . puffiness of face, edema.

Etiology
The causes of diastolic failure are given below:
i) Mitral or tricuspid stenosis.
ii)Constrictive pericarditis
iii)Restrictive cardiomyopathy
iv)Acute volume over load (acute aortic or mitral
regurgitation)
v)Myocardial ischemia
vi)Marked ventricular hypertrophy
vii)Dilated cardiomyopathy
The causes of systolic failure or mixed systolic
diastolic failure can be divided into two groups
according to age (refer to causes of CCF below).
The commonest cause of CCF in infants is
congenital heart disease, whereas in the older
children it is rheumatic fever and rheumatic heart
disease.
Causes of Congestive Cardiac Failure
Signs:
Left sided failure is indicated by tachypnea and
tachycardia, Persistant cough, wheezing, crepts in
the chest.Right sided failure signs are hepatomegaly,
facial edema, edema on feet.
Treatment:
It is based on following principles:
i)Reducing cardiac work.
ii)Augmenting myocardial contractility.
iii)Improving cardiac performance by reducing the
heart size.
iv)Correcting the underlying cause.
Control of excessive salt and water retention with
diuretics. Improve cardiac contractility with
digoxin. Prevent and reverse neurohormonal
changes that lead to progressive worsening of
cardiac status with beta blockers, ACE inhibitors.

Infants: Digoxin
Drug of choice in chronic CHF with atrial
1. Congenital heart disease fibrillation

2. Myocarditis and primary myocardial disease In CHF with sinus rhythm it gives
symptomaticbenefit
3. Paroxysmal tachycardia Dose
Total digitalizing dose in children 30 - 40 mcg/kg
4. Anemia the total dose stat: after 8 hrs; after 16 hrs Daily
maintenance dose of total digitalizing dose. Once
Children in day or two divided doses.

Page 240
Note: Enalapril: 0.1 mg/kg/dose oral every 12 - 24 hourly
Hypokalemia may aggravate digitalis toxicity upto 0.5 mg/kg/day or
especially with concomitant diuretic administration.
-blockers is an integral part of congestive heart
Use oral Kcl supplement or use potassium sparing
failure therapy nowadays.
diuretics such as spironolactone.
Metaprolol or carvedilol is also used
Oral Diuretics Diet Calories
Frusemide: 1 - 2 mg/kg/day or Recommended daily dietary allowance plus 20 -
30% in shunt lesions Avoid salty foods and
Hydrochlorothiazide: 1 - 1.5 mg/kg/dose every 12 -
additional salt in cooking Iron supplementation
24 hours or
When to refer
Spironolactone: 1 - 2 mg/kg/day
Severe respiratory distress
ACE inhibitors
Acute pulmonary oedema
Indicate for all patients with congestive heart
failure. Refractory CCF
Captopril: 0.1 to 0.5 mg/kg/dose oral every 8 to 12 Cardiogenic shock
hourly upto 4 mg/kg/day or

Page 241
 33. PICA

1. Introduction: 3. Treatment
Pica involves repeated and chronic ingestion of non- - Pica below two years does not need any
nutrient substances including mud, plaster, paint, intervention.
earth, clay, etc. Children with PICA usually have
- Children with pica are at increased risk of lead
history of neonatal insults. Most of the time, it is
poisoning, iron deficiency, and parasitic
self-limiting and represents manifestations of family
infections. They should be investigated for
disorganization, poor supervision, and affectional
these problems and if present, treated suitably.
neglect. Testing or mouthing of strange objects is
normal in infant and children up to age of 2 years. - Education, guidance and counselling of the
Common in children from lower socieoeconomic family.
strata and at times in the malnourished and mentally
- The child has to be kept occupied in other tasks
subnormal children.
and provided with the environmental
stimulation.
2. Signs &Symptoms:
Pallor and chronic abdominal pain are main
complaints.

Page 242
 34. NOCTURNAL ENURESIS
1. Introduction:
Enuresis is defined as normal nearly complete
evacuation of the bladder at a wrong place and time
at least twice a month after the fifth year of life.
Bedwetting at night is known as nocturnal
enuresis.Enuresis may be primary or secondary:
2. Primary enuresis:
Repeated passage of urine into clothes/bed during
night in a child more than 5 years of age. Most
common cause in primary enuresis is inappropriate
toilet training. Other causes could be genetic, sleep
disorder, reduced ADH at night. In some cases there
may be organic etiology such as obstructive
uropathy or UT. There may be associated with
mental retardation or spinal cord abnormalities.
3. Secondary enuresis:
The child has been dry for several months and again
starts bedwetting. Too enthusiastic and immature
toilet training, emotional stress, parent child
maladjustment, urinary tract infections, diabetes
mellitus or diabetes insipidus. can cause secondary
enuresis.
4. Signs &Symptoms:
SALIENT FEATURES
Involuntary discharge of urine after the age at
which bladder control should have been
established (5 years).
In primary nocturnal enuresis, child has never
been dry at night while in secondary, child has
been continent for at least 6 months before the
child begins to wet again.
5. Investigations:
Full medical history
Genital and neurological examination
Urine for albumin, sugar, microscopy, specific
gravity and culture.
USG voiding cystourethrogram and
urodynamic studies.
6. Treatment
6.1. Nonpharmacological
(Effective in 30% cases)
Rule out organic causes. Restrict fluid intake in
the evening.
Bladder exercises:
(i) Hold urine as long as possible during the day.
(ii) Practice repeated starting and stopping the
stream at the toilet bowl.
(iii) Emotional supportto child.
(iv) Behaviour modification- Child should not be
given liquids after meal in the evening. Practice
getting up from bed and going to the bathroom at
bedtime before sleep.
(v) Alarm device- alarm device is used to elicit a
conditioned response of awakening to the sensation
of a full bladder.
6.2. Pharmacological
Indicated only in children > 6 years where sufficient
trial of non pharmacological management has failed
with following:
Tab. Imipramine: (0.9-1.5 mg/kg/day/PO) 6-8 year
(25 mg), 9-12 year (50 mg), >12 year (75 mg) once
a day at bedtime. Success rate 30-60%, relapse rate
90%. or
Tab. Desmopressin: 0.1-0.5 mg at bedtime.
Or
Desmopressin acetate (nasal spray, 10 mcg per
spray): Start with 10 mcg given at bedtime daily and
increase gradually by 10 mcg/per week to a
maximum of 40 mcg per day. If effective, it should
be used for 3-6 months. Success rate is 40-60%,
relapse rate is 90%.
(Caution: Not effectively absorbed in rhinorrhoea. If
not used properly may cause hyponatraemia)
7. Referral
Refer the patient to a higher centre, if organic cause
is suspected or when
Diagnosis is in doubt.
8. Parent education
Reassure the parents that condition is self-limiting.
Ask the parents to maintain a diary record of dry
nights; reward the child for such nights. Avoid
punitive measures.
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 35. THRUSH / CANDIDIASIS
1. Introduction:-
Candida fungal infection in the oral cavity is
common and may be seen as early as 7_10 days
of age (peak 4th week of life).
After infancy it is usually secondary to
treatment with broad-spectrum antibiotic.
Chronic or recurrent oral candidiasis is seen in
children having immuno-deficiency. HIV
AIDS, undergoing cancer therapy and in severe
malnutrition.
Hypoparathyrodism, Addison's disease,
autoimmune disorders are other rare causes.
Fig. 1: Candidiasis / oral thrush.
3. Treatment:
Drugs
In case of breast fed baby, the medicine has to be
applied to mothers nipples also to prevent cross /
re-infection.
3.1 clotrimazole 1% cream, gel or lotion, oral
application 3-4 times/day after feeding for 5-7
days (or 1-2 days beyond recovery).
Or
Gentian violet 1% aqueous solution, 1-2 times a
day, for 5-7 days (can stain tissues and clothes).
2. Salient Diagnostic Features:
Thick white patches on an angry red base in the
mouth may spread to involve the lips, buccal
mucosa, tongue and palate.
Asymptornatic or may cause pain in the mouth,
discomfort, anorexia and feeding difficulty.
Diagnosis is confirmed by the fact that on
removing the plaques, spots of bleeding are
seen on the mucosal surface.
Avoid bottle feeding. Faulty sterilization of
bottle and nipple causes persistent or recurrent
infections / thrush.
In resistant/ chronic cases (patients with major
underlying disease)
Tab. Fluconazole 3-6 mg/kg once daily for 5-7
days.
Prevention:
Emphasize on avoiding bottle feeding
/bottle hygiene, care/ hygiene of the nipple and
treatment of vaginal candidiasis in expectant
mother.
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 36. CONGENITAL HYPOTHYROIDIM

Aim: to normalize serum T4, avoid

1. Introduction: hyperthyroidism,promote normal growth and
It may be familial or sporadic, goitrous or development
nongoitrious. In about 85% cases the etiology is
dysgenesis. All new born babies should be screened.
4.3 Repeat T4 and TSH at 2 and 4
2. Signs &Symptons: weeks after initiation of
At birth hypothermia/bradycardia, shock therapy.
Develop with passage of time
Large tongue After one year tests to be done 1-2 monthly
Hoarse cry
Facial Puffiness Between 1 and 3 years do tests 2 to 3 monthly
Umbilical Hernia
Hypotonia Over 3 years do tests yearly till growth is complete
Mottling
Cold hands and feet
Lethargy
ProlongedUnconjugated Hyperbilirubinemia
Constipation
Hypothermia
Large Anterior fontanelle
Posterior fontanellemore than 0.5 cm

3. Investigation:
TSH level should be estimated after 72 hours of life
if TSH is more than 20 mu / L then
Hypothyroidism is considered and Eltroxin should
be started.
Second screening at 2 to 6 weeks (routinely in
VLBW and NICU graduates)

4 Treatment of Congenital
Hypothyroidism
As soon as possible diagnosis.

4.1 Counseling of Parents

4.2 Eltroxin 10-15 microgram/kg---

start higher dose
Do NOT use liquid preparation

On above dose, T4 Normalises in 1 weekand TSH in

one month

Page 245
 37. URINARY TRACT INFECTION (UTI)
1. Introduction :
Approximately 8% of girls and 1 - 2% of boys are
likely to get UTI during childhood. A significant
proportion of children less than 2 years developing
UTI have underlying urinarytract anomalies, most
often vesico ureteric reflux (VUR). UTI in a setting of
VUR may lead to renal scarring, an important cause of
chronic renal disease. Early recognition and treatment
of UTI and urinary anomalies is essential to
preventsuch complications.
2. Signs & Symptoms
2.1 Neonates
Sepsis like features with fever or hypothermia,
lethargy, poor feeding, poor weight gain, aundice and
shock; urinary symptoms may be absent.Infants and
children below 2 yearsUnexplained fever; urinary
symptoms minimal or absent.
2.2 Adolescents
Mostly related to lower urinary tract such as dysuria,
frequency, urgency and suprapubicpain. Renal
parenchymal involvement is indicated by high fever,
chills, rigors and flankpain.
3. Investigations:
3.1 Urine analysis
May suggest UTI in the form of increased leukocytes
in urine. Gram stain of centrifugedurine specimen may
show bacteria.Dipstick for nitrite reduction and
leukocyte esterasemay help in rapid diagnosis.
3.2 Urine culture
This is the only confirmatory test for UTI. Every
effort must be made to properly collect and senda
urine sample before antibiotic is started. In infants and
young children UTI should be suspected if there is
unexplained fever.A midstream clean catch specimen
is ideal. Soap or antiseptic solution should not be used
beforecollection. In infants urine can be obtained by
suprapubic aspiration.
4. Common organisms
responsible for UTI are
E. coli, Occasionally Klebsiella, Staph epidermidis or
Strep fecalis may be responsible.
A colony count of > 105 colony forming units (CFU)
/ ml of single species in a clean catchspecimen
indicate significant bacteriuria. Presence of any
bacteriuria in suprapubic specimenis significant. For
the purpose of management UTI is divided into
complicated and uncomplicated UTI.
5. Complicated UTI
Temperature > 39C, persistent vomiting, renal
angle tenderness and systemic toxicity are featuresof
complicated UTI Infants below 3 months of age and
those with complicated UTI should receive parenteral
antibiotics initially.
6. Treatment
6.1 In young infants (< 3 months) entire treatment is
parenteral
1. Cefotaxime 100 - 150 mg/kg/day in 3 div doses, or
2. Ceftriaxone 75 mg/kg/day in 1-2 doses, or
3. Gentamycin 5 - 7.5 mg/kg/day single dose, or
4. Amikacin 15 - 20 mg/kg/day single dose, or
In young infants (< 3 months) entire treatment is
parenteral
6.2 For older children, after first 2 - 3 days, oral
antibiotics may be started based on
antimicrobialsensitivity Total duration of treatment is
10 - 14 days.
Oral antibiotics
Amoxicillin 20 - 40 mg/kg/day in 2 - 3 doses, or
Cefadroxil 30 mg/kg/day in 2 doses, or
Cephalexin 50 mg/kg/day in 3 doses, or
Cefixime 8 mg/kg/day in 2 doses, or
Ciprofloxacin 10 - 20 mg/kg/day in 2 doses
7. Uncomplicated UTI
Children > 3 months of age and those who do not have
features of complicated UTI can be treated withoral
amoxicillin (10 to 15 mg per kg) or cefadroxil (5 to
10 mg per kg) for 7 to 10 days (based on sensitivity).
Though fluoroquinolones are effective and safe for
UTI, they are not the first-line antibiotics
Page 246
 OBSTETRICS
AND
GYNAECOLOGY

Page 247
 1.NORMAL PREGNANCY
Antenatal period is the most crucial period as the
services provided during this period can have positive
impact on health of both the mother and her child.
1. Essential obstetric care to
every pregnant woman
Registration of all pregnant women before 12
weeks.
2. Detailed history at first visit
Menstrual histor y: Regularity of cycles, date of
LMP, calculate EDD and record on Mother
Child Protection (MCP) card
Obstetric history:Number of prior pregnancies
and outcome of each pregnancy (full term birth,
preterm birth, abortion), place and mode of
delivery, weight of baby, Live birth/stillbirth,
Table 1: Examination at antenatal clinic
*Height
*Weight : Compare with previous visit (calculate
BMI in first trimester)
*Pallor, icterus
*Edema over feet, hands, face
*Blood pressure
* During first check up
The last two visits are important as many of the
pregnancy complications are detected during last
trimester. For 'high risk' mothers more frequent
examinations will be required.
complications during after delivery (PPH,
Retained Placenta, Infection)
Past history: Hypertension, Diabetes Mellitus,
Tuberculosis, Asthma, Heart disease, any other,
surgical procedures undergone, medications
taken during pre conceptional period, history of
bleeding.
H/O current symptoms, perception of fetal
movements if pregnancy> 16 weeks.
3. Schedule of Examination
Ideally all the ANCs should be examined monthly
after registration. If it is not possible to attend ANC
clinic monthly, then checkup should be carried out at
least five times during the pregnancy. First 8-12
weeks, second between 14-20 weeks, third at 22-26
weeks, fourth at 28-32 weeks and fifth at 36-40
weeks.
*Breast examination
*Systemic examination : Auscultate chest
*P/A: Fundal height & its correlation with period of
amenorrhoea (POA)
*Fetal presentation and position after 32 weeks
*Fetal heart rate
Medical officer should perform at least one
checkup during the third trimester and auscultate
her chest to r ule out any systemic abnor mality.
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4. Investigations
Table 2:
Hemoglobin estimation VDRL
Urine Analysis: Protein and s ugar Voluntary HIV testing
Test for sickling in selected tribal area Blood sugar testing
Blood grouping, Rh typing Hepatitis B surface antigen (HBsAg)
Ultrasonography (16 to 18 weeks) Malarial parasite in Ende mic area.

5. Examination and action to be taken during ANC check up

Table 3:

Examination Action

Ede ma Examine whether ede ma is on one leg or both legs and is it pitting. Look for
edema over face, hands, and abdomen. Check for proteinuria and
hypertension.
High blood pressure and albuminuria, refer to specialist as she has pre-
eclampsia.
History of kidney disease, if yes refer to specialist.
If edema is on one leg, refer to specialist.
If bilateral pedal edema without albuminuria and normal BP: Reassure
mother, c heck for anemia and give IFA tablets as required

Weight gain Record monthly weight on MCP card of mother, calculate weight gain since
the previous visit
Weight gain more than 3 kg. in a month: Suspect pre-eclampsia
Weight gain less than 1 kg. in a month: Suspect fetal growth retardation.

Blood Pressure If 140 / 90 mm Hg or more, advise mother to rest for half hour and then
repeat the BP recording. Check for proteinuria
If systolic between 140-160 and /or diastolic 90 or above: advise extra rest
and refer to MO PHC
If systolic 160 or more or diastolic > 100 : refer to specialist

Fundal Height Examine fundal height in weeks and compare with calculated duration of
pregnancy as per LMP. If it is greater or lesser refer to specialist. Causes of fundal
height less or more than expected are given in table below.

Fetal Presentation Noncephalic (correction can be attempted at 36 weeks in suitable cases)

byObs/Gyn specialist.

Fetal Heart Rate FHR < 120 or > 160 /minute : Refer to specialist.

Hemoglobi n % Hb 11 gm% or more: IFA 100 tablets

Hb between 7-11 gram%: Start IFA double dose* and re-examine after one month
- If improvement of Hb by more than 1gm%, continue IFA. Give tab

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 Examination Action
Albendazole(during second trimester)
Hb< 7 gm % - Refer anemia treatment guidelines

Proteinuria If proteinuria present suspect pre-eclampsia and refer to specialist.

Risk factors All high-risk pregnancies should be checked by MO and then referred to specialist
if necessary for further checkup or during delivery depending upon the risk factor.

* For better absorption, IFA tablets should be taken 1.30 hours before meals
Table 4:
Fundal height < Period of Amenorrhea Fundal height > Period of Amenorrhea
Wrong dates Wrong dates
Infrequent periods prior to conception Poly hydramnios
Intrauterine Growth retardation(IUGR) Twins
Oligohydramnios Big baby
Intrauterine fetal death. Hydatidiform mole
Uterine fibroids

discharge per vaginum, blurred vision, excessive

6. Education and counseling
regarding care during
pregnancy
6.1. First and second trimester:
Diet: More than one meal a day and evening
snacks (mos t impor tant), inclusion of sprouted
legumes, pulses, green leafy and other
vegetables, seasonal fruits.
Rest: 2 Hours in afternoon and 8 hours at night
in lateral position.
Exercise: Walking for 30 minutes daily.
Habits: Avoid tobacco in any form, avoid
alcohol.
Practicing safe sex.
Self-reporting of danger signals, e.g.Abdominal
pain, severe headache, giddiness, palpitations,
easy fatigability, breathlessness, fever,
generalized edema, vaginal bleeding, watery
vomiting, reduced fetal movements.
Consumption of iron folic acid 100 tablets for
anemia prophylaxis.
Tetanus Toxoid 2 doses/booster dose.
Calcium through diet and Calcium carbonate
tablets 1.2 Gm daily.
6.2. Third trimester:
Avoid heavy work and jerky travel on bad roads.
Importance of institutional delivery, safe
delivery, inform TOLL free No.102 and 108 for
free ambulance service, JSY, JSSK and other
benefits, Plan for place of delivery, preparation
for delivery.
Importance of early initiation of colostrum
feeding within Half an hour of birth & exclusive
breast-feeding for 6 months, child immunization
and contraception especially PPIUCD.
Ask about birth companion.

Page 250
1. Identify high-risk mothers:
Table 5:

Risk factors detectable during Abnormalities developing during

first check up Current pregnancy

Age : Teenage/ elderly primi, Anemia

Para 4 and above Hypertension, proteinuria
Short stature, limping gait, vertebral spine Vaginal bleeding during pregnancy
abnormalities
Premature rupture of membranes (PROM)
Bad obstetric history: H/O stillbirth, neonatal
death, LBW baby, recurrent abortions Gestational diabetes mellitus (GDM)
Fundal height < POA or > POA
Previous Caesarean delivery
H/O PE/eclampsia, PPH, retained placenta Uterus over distension: Twins,
Polyhydramnios
during previous pregnancies
Fetal malpresentation persisting near term
Preexisting medical conditions : Heart
disease, diabetes mellitus, renal disease Pregnancy > 41 w eeks
HIV /VDRL positive gravida Reduced fetal movements
Rh negative gravida

2. Actions sugge sted for some high risk indicators:

RISKS
1. Elderly Primi
Hypertension during pregnancy
Gestational diabetes
Difficult labour - Chances
caesarean section are higher
Fetal abnormalities.
2. Teenage primi
Table 6:
ACTION
Refer to specialist soon after registration for evaluations to
exclude fetal anomalies (biochemical markers and
ultrasonography)
of Regular ANC: B.P, urine analysis every month
Pelvic assessment at or after 36 weeks.
Institutional delivery under care of specialist.

Hypertension during pregnancy Regular antenatal care

Anemia Hb%, BP, urine analysis more frequently
Pre-term labour Adequate rest
Fetal growth retardation. IFA tablets, nutrition guidance
Difficult labour Pelvic assessment at 36 weeks
Hospital delivery.
3. Primi : Height less than 145 cms Regular ANC check. Assessment of place of delivery by

Page 251
 RISKS ACTION
specialist. Observe progress of labourpartographically.
4.Primi having vertebral /limb deformity Regular check up at PHC, Assessment by specialist for place of
delivery.
5. Grand multipara (para 4 and more)
Anemia Supplement IFA, nutrition guidance
Malpresentation At 34 and 36 weeks look for fetal malpresentation
Atonic PPH Hospital delivery - Avoid Injudicious use of oxytocics for
augmenting labour
Uterine rupture
Active management of 3rd stage of labour - Keep IV line
ready

Page 252
 2.NORMAL LABOUR
1. Pelvic Assessment
Table 1:

Parameter Adequate Suggestive of abnormality

Sacral promontory Not felt Felt easily
Diagonal Conjugate* >11.5 cms < 11.5 cms
Sacral curvature Well curved Flat
Lateral Pelvic walls Parallel Converging
Ischial spines Both cannot be palpated simultaneously Both spines can be palpated
simultaneously
Subpubic Angle Accommodates two fingers (850) Acute
Inter tuberous diameter Accommodates closed fist (4 Knuckles) Cannot accommodate 4 knuckles
* If sacral promontory is felt, the distance between the sacral promontory and the lower border of pubic symphysis
is measured.

Push the head into the pelvic inlet and note

2. Clinical Examination for
CPD
Place the woman in dorsal position.
Hold the fetal head by left hand.
Place two fingers of gloved right hand into the
vagina at the level of ischial spines.
Place the thumb of right hand on the pubic
symphysis.
3. Monitoring during active phase
Table 2:
whether it descends into the pelvis (felt by
fingers in vagina) or overhangs on the public
symphysis.
If head descends with no overlap at public
symphysis: No inlet CPD.
If the head is engaged it indicates that the pelvic
inlet is adequate.
Get urine sample tested for protein, sugar and note
volume.

Examination / Observation Periodicity

Maternal pulse and FHR Every 30 minutes

Uterine contractions Every 30 minutes

Maternal temperature, BP, urine volume Every four hours

Vaginal Examination Every four hours

Note the time of rupture of membranes and To assess cervical dilatation, station and position
perform va ginal examination immediately of vertex.
To rule out cord prolapse and see the color of Assess and monitor the progress of LABOUR by
liquor. using Simplified Partograph adopted by GOI to

Page 253
record FHR, liquor, cervical dilatation, uterine
contractions, medications administered during labour,
maternal pulse, blood pressure and temperature.
Points to Reme mber
This graph is used only during active phase of
labour.
The complications requiring immediate
interve ntion need to be excluded first.
3.1. Partograph
On this graph, one square represents one hour on
horizontal axis. On vertical axis, one square
represents cervical dilation of one centimeter.
3.1.1 Phases of first stage and alert and action
line:
Latent phase: Cervix dilates very slowly up to 4
centimeters. It may take up to eight hours for
this.
Active phase: 4 cm onwards; cervix dilates
rapidly at the rate of about 1 centimeter per hour.
Alert Line: An obl ique line on the graph from 4
to 10 centimeters progressing at the rate of 1
centimeter per hour.
Action Line: Parallel line Four hours to the right
of alert line
3.1.2 Recording o n partog raph:
Initiate recording when cervix is 4 cm dilated
and immediately if the cevix is > 4 cm dilated on
admission to the Labo ur ward.
Record the dilatation in cm (symbol x) on the
alert line and record the time at which
observation has been made on the horizontal axis
below this point.
Perfor m vaginal examination every 4 hours and
note the cervical dilatation and mark it on the
graph.
Join the points and interpret the observations.
3.1.3 Interpretation:
Satisfactory progress: Cervical dilatation lies
on left side of alert line, active phase progression
> 1 cm/ hour, Fetal and maternal health
parameters are normal.
Slow progress: Alert line crossed, careful
monitoring to note the progress. At subcentre
and PHC the arrangements for referral to FRU.
Action line reached or crossed: Careful review
to find the cause for delay followed by
appropriate interventions.
a) First stage of labour showing satisfactory
progress: Continue observation till second stage
starts.
b) Second stage of Labour:
Cervix is fully dilated.
Signs of imminent delivery: Mother starts
pushing (bearing down). Fetal scalp seen at
vulva, perineum bulges, anus gapes. Mother gets
sensation of defecation.
Encourage the mother to push only during
contraction.
Monitor progress and fetal wellbeing during
second stage.
Note FHR every 15 minutes.
Assess descent of presenting part (fetal station)
every 15 min.
Look for caput, molding, meconium staining of
liquor.
Suppor t the perineum and de liver the head gently
Deliver the shoulders
Keep the baby on mothers abdomen on a pre-
warmed towel and give immediate care.
Conduct delivery. Follow universal bio safety
precautions.
Delivery of baby takes place usually within 30
minutes in a multi and 60 minutes in a primi
para.
Give mediolateral episiotomy under local
infiltration anesthesia by Injecting 1%
lignocaine, if mother is unable to push or if there
is undue delay.
c) Third stage of Labour: Deliver the placenta by
active management of third stage of LABOUR
4. Active Management of Third
Stage of labour (AMTSL)
Active management of 3 rd stage of LABOUR reduces
the amount of blood loss due to uterine atony,
reduces the chances of having atonic PPH and
requirement of blood transfusion significantly
thereby helping to reduce maternal mortality due to
severe PPH.
It is an integral part of skilled attenda nce at birth and
is mandatory for all deliveries (vaginal and
abdominal). The steps are as follows:
After the childbirth, exclude presence of another
baby by abdominal palpation
Give Inj. oxytocin 10 IU IM. immediately after
birth (Oxytocin should be kept in refrigerator).
When oxytocin is unavailable, tabletmisoprostol
600 mcg (3 tablets) may be given orally.
Page 254
 Check for uterine contraction.
Clamp and cut the cord.
Deliver the placenta by controlled cord traction.
When the uterus is well contracted , give gentle
downward traction on cord while giving counter
Figure 1: Controlled Cord Traction
5. After delivery
Examine the perineum, vulva, lower vagina for
tears.
Examine the placenta and membranes carefully
for completeness and any abnormality.
Observe the mother every 15 minutes for two
hours for general condition, pulse, vaginal
bleeding, pallor, uterine contraction.
Repeat uterine massage every 15 minutes for 2
hours.
Encourage mother to take the baby to breast
within hour of delivery.
6. Augmentation of Labour
6.1. Care of woman showing slow
/unsatisfactory progress of
Labour
Alert line crossed or the action line reached
Causes: Hypotonic uterine action, occipito
posterior position, deflexed head, CPD etc. Refer
the case to higher level of care.
Labo uraugmentation by amniotomy (artificial
rupture of membranes) and oxytocin infusion are
offered as per the clinical situation.
Labo uraugmentation should be done in places
where clinical expertise and facilities for
operative delivery are available.
traction by other hand pushing the uterus
upwards towards umbilicus. Repeat this during
contraction as required.
After delivery of placenta, give uterine massage
to keep the uterus contracted.
If vertex is engaged and cervix is well applied to
the vertex then controlled ARM can be
performed to hasten the progress.
After ARM review progress after two hours. If
progress is still slow, assess uterine contractions.
If uterine contractions are infrequent and weak
then consider oxytocin augmentationafter
excludi ng contraindications.
If there is no progress after augmentation or if
signs of fetal distress develop, an emergency
caesarean section might be required. Hence such
a woman should be referred to a well-equipped
maternity unit.
6.2.Oxytocin Augmentation: (only
where specialist is available)
Exclude contraindications before starting oxytocin
CPD, Fetal distress
Grandmultiparity, Malpresentations, Scar on the
uterus
6.2.1 Dose and Administration
Add 2.5 IU to 500 ml of normal saline or
Ringers lactate. Start infusion at the rate of 8-10
drops/min. Observe uterine contractions.
If contractions are mild increase the drip rate by
8-10 drops /min every 30 min until she gets 3
contractions in 10 minutes, each contraction lasts
Page 255
 for 40-45 seconds and there is good relaxation of
uterus in between the contractions (optimum
response).
Drip rate can be increased maximum up to 60
drops/minutes. If the contractions are inadequate
at this rate, prepare another drip with 5 IU /500
ml and start it at the rate of 30 drops/min,
increase by 5 drops every 30 minutes and
observe the response
6.2.2 Monitoring:Monitorfollowing parameters
every 15 minutes,
Drip rate, Uterine contractions frequency and
intensity
FHR and Maternal pulse
Progress of labour
6.2.3 Complications:
Hyperstimulation : > 5 uterine contractions / 10
minutes, each lasting for > 60 sec
Uterus failing to relax between the contractions
Fetal bradycardia (distress)
Uterine rupture if drip is not supervised
vigilantly.
Water intoxication if too much of electrolyte free
infusion is administered.
Neonatal hyperbilirubinaemia
6.2.4 Treatment of Hyperstimulation:
Discontinue the drip
Maternal repositioning (left lateral position),
Oxygen therapy
Terbutaline 250 mcg can be given IV slowly for
tocolysis if required
Caution:
For augmentation of Labour oxytocin should
never be give n intramuscularly.
Cautious use in multiparous women as the uterus
tends to rupture.
6.2.5 When to discontinue the drip:
If six hours of strong stimulated uterine activity
is unable to bring progress of labour, discontinue
the drip and review the case.
If there are signs suggestive of fetal distress.
If after initial satisfactory progress, cervical
dilatation does not progress for two hours or
more in established active phase of Labo ur then
review her. This could be due to cephelo-pelvic
disproportion or large head with deflexion. Such
patient may need operative intervention.
Prolonged second stage
If second stage is prolonged for more than 2 hours in
primi and for > 1 hour in multi, then
Assess size of baby and pelvis again.
See whether fetal head is still palpable in
suprapubic region.
Page 256
 3. CLINICAL CARE OF HIGH RISK
PREGNANCY
Common Risk Indicators:
Bad obstetric history: Previous history of pre-
term Labo ur, stillbirth, early neonatal death,
recurrent pregnancy loss.
Post caesarean pregnancy.
Vaginal bleeding during pregnancy.
Rh negative pregnant woman , husband Rh +ve
Fetal malpresentation (Breech/transverse lie)
persisting at 36 weeks.
Diagnosed twins, polyhydramnios.
Pregnancy be yond 41 w eeks.
Medical diseases: Anemia, diabetes mellitus,
cardiac disease, chronic hypertension, kidney
disease, tuberculosis.
Refer to other high risk indicators mentioned in
earlier chapter.
1. Bad Obstetric History
Bad obstetric history is a term used in day to day
practice for describing unsuccessful pregnancy
outcome in previous pregnancies. A variety of
unsuccessful outcomes are included in this such as
previous H/O stillbirth, preterm delivery, recurrent
midtrimester/early abortions.
1.1. Recurrent Pregnancy Loss
(RPL)
1.1.1 Definition:Three or more consecutive
pregnancy losses
1.1.2 Causes:
Genetic
Environmental and occupational exposure to
organic solvents, ionizing radiation, toxins,
tobacco, alcohol
Uterine anomalies, Cervical incompetence,
Uterine synechiae (adhesions), Uterine fibroids
Infections
Endoc rine Dysfunction: Polycystic ovary
syndrome (PCOS), Luteal phase inadequacy
(LPI), Diabetes mellitus, Thyroid dysfunction,
Prolactin disorders.
Antiphospholipid antibody syndrome (APLAS)
Unexplained: In some cases no cause can be
detected.
1.1.3 Risk Factors:
Risk is highest among couples where the age of
woman is 35 years.
The risk increases after each successive
pregnancy loss, reaching approximately 40%
after three consecutive pregnancy losses.
1.1.4 History:
Detailed obstetric history about each pregnancy.
Duration of pregnancy at mishap. Whether USG
documented cardiac activity was seen, fetus was
live born/stillborn ( fresh/macerated stillbirth),
baby normal/abnormal.
H/O Consanguinity, history of infertility,
menstrual abnormality, infections, STD.
Personal history: Tobacco, alcohol, caffeine,
medications.
Personal/familial H/O thrombosis, autoimmune
disorder.
1.1.5 Physical examination:
a) Look for obesity, hirsutism, acanthosis, thyroid
enlargement, galactorrhoea
b) P/S & P/V examination: Look for uterine
fibroids, double uterus, bicornuate uterus, genital
infection, torn or short cervix
c) Investigations: Carry out the relevant
investigations as indicated and available
depending on whether the woman has presented
during pregnancy or after the mishap.
d) During pregnancy:
Hematology, blood group and Rh typing, VDRL
Urine analysis
Rule out diabetes
Antiphospholipid antibody testing
USG: For uterine abnormalities, Monitoring
early pregnancy
Thyroid function, Prolactin
e) Non pregnant state:
Pelvic USG for polycystic ovaries (PCOS),
Hysterosalpingography(HSG), Hysteroscopy for
uterine abnormalities
Parental karyotype
Mid luteal serum progesterone and
thrombophilia profile if available
f) Soon after miscarriage:Chromosomal studies of
conceptus
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1.1.6 General Measures:
Quitting cigarette smoking, tobacco, alcohol and
caffeine consumption
Weight reduction in PCOS cases
Therapies depending upon cause.
Psychological counseling & support is extremely
helpful.
50% Success even if no treatment is given.
Some common conditions are as follows:
2. Cervical incompetence
Premature softening and dilatation of internal
cervical os during pregnancy can lead to
protrusion of membranes, rupture of membranes
and fetal expulsion during second trimester or
early third trimester
Typical obstetric history is diagnostic: Repeated
midtrimester or early third trimester pregnancy
terminations, relatively painless, rapid, often
preceded by rupture of membranes followed by
expulsion of fresh or live fetus
Symptoms : Low backache, mucoid vaginal
discharge
P/S: Bag of membranes may be seen through the
cervical os
Vaginal examination: Internal cervical os dilated
in absence of uterine contractions, cervix may be
short.
2.1 Investigation:
USG may show short cervix, funneling of
cervix, membranes dipping into the cervical
canal.
USG assessment of cervical length (25mm or
less) bytransvaginal scan before 24 weeks in
women having previous history of preterm
LABOUR is considered significant for
prediction of preterm LABOUR.
2.2 Treatment: PHC:
Refer the case to specialist soon after
registration.
At RH/DH:Prophylactic cervicalos tightening at
16 weeks by McDonald method under short
general anesthesia.
Follow up: Extra rest, avoid exertion.
Stitch removal at 37 weeks or at the onset of
LABOUR whichever is earlier. Anticipate rapid
delivery.
3. Infections
Generally cause sporadic pregnancy loss.
Toxoplasmosis, rubella, cytomegalovirus, herpes and
listeria infections do not cause recurrent pregnancy
loss and routine TORCH screening is not indicated.
Active syphilis during pregnancy can lead to
recurrent pregnancy loss.
3.1. Syphilis during pregnancy
3.1.1 Effects: Late abortions, stillbirths, neonatal
deaths, infant having active congenital
syphilis.
3.1.2 Diagnosis is serological: VDRL at booking.
Note titers, titers 1:8 or more are significant.
Treponemal test (TPHA) is confirmatory.
3.1.3 Treatment: Treatment of maternal disease
can prevent fetal infection and also treat
established fetal disease
Benzathine penicillin single Injection 2.4 Mega
units deep IM after sensitivity test as Penicillin is
the only antibiotic that can cross the placenta in
adequate amounts to treat the fetus.
For latent disease > 1 year duration, 3 Injections
at weekly interval.
Penicillin sensitive individuals require
desensitization.
Erythromycin 2 gms daily in divided doses for
14 days can be considered however Penicillin is
more effective.
Infant of a VDRL positive mother needs care by
specialist.
Safe sex counseling.
4. Hypothyroidism
Hypothyroidism can be due to iodine deficiency
or thyroid autoantibodies.
Infertility, menstrual problems due to Ovulation
disturbances.
Increased risk of miscarriage due to luteal phase
insufficiency.
Anemia, gestational hypertension, placental
abruption and postpartum hemorrhage are
common.
Fetal/neonatal problems: Preterm birth, low birth
weight, congenital malfor mations, neonatal
respiratory distress, perinatal death. Cretinism.
TSH. If elevated thyroid function tests and
antibod y testing.
Treatment by thyroxine can correct ovulatory
dysfunction and help achieving pregnancy and
successful outcome.
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 Counsel pregnant women for consumption of
iodized salt.
Targeted case finding approach is followed.
Universal TSH screening is currently not
recommended.
5. Rh Negative Pregnant
Woman
A major cause of hemolytic disease of newborn
(HDN) is Rh blood group incompatibility between
the mother and her fetus. When Rh negative mother
bears Rh positive fetus, the Rh antigen from fetal red
cells enters the maternal circulation and results in
antibody formation in mother. These antibodies cross
the placenta and cause destruction of fetal red cells
resulting in fetal Anemia. Prevention of such
sensitization is pos sible by antenatal screening and
appropriate care.
5.1. Pregnancy outcome
First child usually escapes. Subsequent babies suffer
from mild hemolytic anemia, rapidly increasing
hyperbilirubinemia within 24 hours of birth or
hydrops fetalis resulting in intrauterine fetal death.
The adverse perinatal outcome occurs earlier during
pregnancy with each subsequent pregnancy.
5.2. Management
Every pregnant woman should be tested for Rh
typing at registration.
Those testing negative should have their
husba nds Rh typi ng done.
Take detailed histor y about every pregnancy and
its outcome. H/O neonatal jaundice, hydrops,
stillbirths etc.
Note history of receiving anti D
immunoglobulin, time, dose during/following
every pregnancy.
Perform indirect Coombs test (ICT) on blood
sample to detect maternal sensitization.
5.2.1Nonsensitized woman:
Negative ICT indicates that the woman does not
have detectable antibodies against Rh antigens.
Refer her to gynecologist at FRU. ICT is
repeated monthly.
Do not perform external cephalic version for
malpresentations. Any episode of bleeding or
manipulation, procedure such as amniocentesis
should be followed by administration of anti D
immunoglobulin.
It is recommended to give 300 mcg anti D
immuno globulin during pregnancy at 28 weeks
for reducing the risk of antepartum sensitization.
At delivery, cord blood sample to be tested for:
Infants Rh, ABO grouping, hemoglobi n and
hematocrit.
Direct Coombs test, Direct and indirect bilirubin
estimation.
Administration of 300 mcg of anti D Ig IM to
mother within 72 hours of delivery (earlier
within 24 hours is still better). 300 mcg
neutralizes 15 ml of fetoplacental hemorrhage
(FMH). If it has not been given within 72 hours,
should be given up to one week with some
benefit.
The baby is referred to neonatology specialist
and is observed for icterus, anemia.
5.2.2 Sensitized woman:
If ICT is positive, it indicates that the woman is
sensitized and has got antibodies against Rh
antigen in her blood. Note the titres reported.
There is no use of giving Anti D Ig to sensitized
mother.
Sensitized woman must be referred to a tertiary
care centre having equipment and expertise for
cordocentesis and intravascular fetal transfusion.
6. Post Caesarean Pregnancy
Pregnancy with h/o previous caesarean section (CS)
is a high risk condition as there is increased risk of
complications during childbirth after each caesarean
section (Scar rupture, placenta previa, adherent
placenta, PPH)
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6.1 Risks
Table 1: Risk Factors
Maternal
Scar dehiscence during Labour
Scar rupture leading to severe
haemorrhage& shoc k
Chances of repeat CS are high
All cases having CS in previous delivery should be
referred to specialist at FRU/district hospital during
third trimester. At 36 weeks she should have a
review by specialist regarding plan for delivery
either by repeat elective CS or trial for vaginal birth
after CS which depends on indication of prior CS
and assessment of scar integrity.
6.2 History
Indication for CS, elective or emergency, when
in labour it was done.
Place and person operating , performed at term
or preterm.
Type of CS :Lower segment transverse incision
or classical .
(Vertical scar is very weak having high chances
of scar rupture which is likely to happen during
late pregnancy and during labour with increased
risk to the mother and fetus hence elective
caesarean section should be performed at term in
such cases)
Review operation notes regarding
complications, inverted T extension of incision,
lateral extension of tears, post-operative
infection, blood transfusion, prolonged hospital
stay.
Inter pregnancy interval < 24 months increases
the risk.
6.3 Examination
Anemia:Correction before term is important as
the chances of requiring repeat CS are high.
Note the size of baby, presentation, presence of
any other risk factor or complication in current
pregnancy.
Pregnancy complication: Twins,
polyhydramnios, APH.
Look for scar tenderness.
Fetal/neonatal
Fetal distress
Fetal death due to scar
rupture
Neonatal asphyxia
Perform clinical pelvic assessment at or after 36
weeks.
6.4 Investigations
USG assessment of fetal weight, localization of
placenta. Look for morbidly adherent placenta if
placenta previa.
6.5 Selection for Trial of Labour
after caesarean section
Indication for previous CS non recurrent (fetal
distress, breech, placenta previa.)
Only one prior low transverse CS delivery. No
other uterine scars or previous rupture.
Vertex presentation, Clinically adequate pelvis.
No other obstetric complication ( APH, breech
presentation)
Surgeon, anesthetist immediately available for
emergency CS.
Repeat CS: Women not eligible for vaginal trial will
need an elective repeat CS. which should be
performed at 39 weeks for the best neonatal
outcome, if there is no maternal or fetal indication to
perform it earlier.
All post caesarean pregnancies should only be
managed in equipped hospitals with personnel
readily available for emergency caesarean section
when needed carefully selected women can be
allowed to have trial of vaginal birth under expert
supervision.
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6.5.1 Manage ment of labour following caesarean
section:
Refer post caesarean delivery to higher centers.
Counseling and informed consent for trial of
Labo ur.
Keep operation theatre ready for CS, arrange
blood.
Monitor progress of labour.
Watch for early signs of fetal distress, scar
dehiscence and perform immediate caesarean
section if these signs appear.
If satisfactory progress, cut short the second
stage of labour and deliver.
After vaginal delivery, watch for PPH/intra
peritoneal hemorrhage.
6.5.2 Symptoms & Signs of impe nding rupture
during labour:
Suprapubicpain persisting in between uterine
contractions.
Slight fresh vaginal bleeding.
Unexplained tachycardia, tenderness over
uterine scar.
Alteration in fetal heart rate, sudden signs of
fetal distress.
Hematuria.
Falling BP with increasing pallor is a late sign
of uterine rupture.
6.5.3 Contraception:
Counseling for contraception for increasing inter
pregnancy interval.
Postpartum IUCD insertion at operation before
closure of uterine incision is safe.
7. Twin Pregnancy
7.1 Antenatal Diagnosis and
Management
The incidence of twin gestation is increasing as a
result of infertility treatment. With modern assisted
reproduction techniques higher order of multifetal
gestation is common.
7.1.1 History:
Ovulation induction by clomiphene or
gonadotropin Injections for infertility.
Maternal family histor y of twins, adva nced age,
high parity.
7.1.2 Signs:
Suspect twins when the fundal height is greater
than the period of amenorrhoea and multiple
fetal parts are felt.
Palpation of 2 heads, 3 major poles
May have associated polyhydramnios
Two pe rsons simultaneously hearing FHS at two
different locations with a difference of > 10
beats/min.
7.1.3 Investigation:
Ultrasonography. Early sonographyin second
trimester helps in assessing chorionicity

7.2Risks
Table 2: Risk to baby according to type of complication
Pregnant Woman Baby

Hyperemesis gravidarum Prematurity

Anemia IUGR
Pre-eclampsia Malpresentations
Antepartum haemorrhage due to Placenta previa and Fetal asphyxia
also abruptio placentae is likely
Preterm LABOUR Twin-to-twin transfusion
Hypotonic uterine action, prolonged LABOUR Fetal malformations
Postpartum haemorrhage Fetal death

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 Difficult delivery Perinatal mortality is high

7.3 Management during pregnancy 8.2. Causes

Detection and correction of anemia. Fetal anomalies: Anencephaly, esophageal
Nutrition counseling, extra nutrients to meet the atresia.
need of two fetuses.
Maternal diabetes, Multiple pregnancy.
Avoiding exertion, extra rest in left lateral
position. Idiopathic, Placental chorioangioma.
Early diagnosis of preeclampsia.
Can be mild, moderate or severe. Development can
Refer to specialist for antenatal care and delivery be acute or chronic
at FRU.
Explaining warning signals for preterm Labo ur.

8. Polyhydramnios
8.1. Definition 8.3 Risks
Excessive volume of amniotic fluid
Table 3: Risk according to complication type

Pregnant Woman Baby

Hypertension Prematurity
Risks due to associated diabetes mellitus Malpresentations
Risks due to associated twins Fetal asphyxia due to cord prolapse or placental
abruption
APH : Placental abruption Fetal malformations
Preterm labour, PROM, cord prolapse Problems due to associated complications :
twins/preeclampsia/APH
Hypotonic uterine action, prolonged labour
Postpartum haemorrhage

Difficult delivery

8.4. Diagnosis Hydramnios should be differentiated from ascites

and large ovarian cyst.
Fundal height is > POA. Abdomen is over
distended.
Fluid thrill can be demonstrated.
8.5 Management
Fetal parts are not well felt if the abdomen is
tense. FHS may not be clearly heard. Mild cases: No intervention required. Extra rest in
USG confirms the diagnosis by demonstrating comfortable position.
large amount of amniotic fluid. Amniotic fluid
Symptomatic women need to be hospitalized.
index (AFI) 24-25 cm
Association with twins and fetal malformations Specialist can offer following interventions
need to be looked for. depending upon the case.
Severe hydramnios can lead to edema, severe
Tablet Indomethacin: 50-100 mg stat followed
breathlessness, inability to sleep and may require
by maximum 200 mg in 24 hrs for 24-48 hrs. at
immediate attention by specialist.
< 30-32 weeks of pregnancy (As there is risk of
Maternal diabetes mellitus needs to be excluded. premature closure of fetal ductusarteriosus)

Page 262
 Amniocentesis to relieve the maternal distress.
The success is transient and repeated fluid
removal is required. Complications such as
preterm Labo ur, rupture of membranes,
chorioamnionitis, and placental abruption are
likely.
Delivery in a well-equipped institution under
care of a specialist.
Oxytocin augmentation if contractions are weak.
Risk of placental abruption is high when the
membranes rupture and a large volume of
amniotic fluid is drained sudde nly. Preserving
membranes is important. When required,
controlled ARM is done.
Active management of third stage as there is a
risk of atonic PPH.
Examine the baby for congenital malformations
(Esophageal atresia or trachea- esophageal
fistula)
9. Prolonged Pregnancy
9.1. Definitions
Post term pregnancy: Pregnancy that has crossed 42
weeks.
9.2. Risks
Post maturity syndrome: In about 20 % cases
of prolonged pregnancy there is placental
insufficiency which results in a pathologic
syndrome in which there is fetal growth
retardation associated with meconium stained
amniotic fluid, oligohydramnios and fetal
distress. The newborn is at risk of meconium
aspiration syndrome. The baby shows loss of
subc utaneous fat, wrinkled, dry, cracked skin
(old man look). It has long thin body and long
nails. Associated oligohydramnios increases the
likelihood of postmaturity.
In other cases not complicated by placental
insufficiency, there is continued growth of the
fetus leading to macrosomia, with increased risk
of abnormal labour, shoulder dystocia, and
Injuries to baby.
Increased perinatal mortality in pregnancies
continuing > 42 weeks.
Mother: Difficulties in labour due to fetal
macrosomia, Shoulder dystocia.
Increased chance of caesarean delivery.
9.3 . Risk Factors
Primiparity, pervious history of post term
pregnancy, sedentary life style, anencephalic
fetus. Genetic predisposition
9.4 Prevention
Accurate calculation of EDD. Ask whether
menstrual cycles before conception had been
regular.
Instruct ASHA, ANM to refer a woman who has
crossed her EDD to the medical officer.
At 40 weeks: Check for any complications. In
pregnancies complicated by hypertension,
preeclampsia, IUGR the fetus is at greater risk of
asphyxia. Hence these women should not be
allowed to cross their EDD. They should be
referred to specialist as they need to be delivered
early.
Uncomplicated pregnancy: Wait until 41 weeks.
Instruct the woman to report if fetal movements
are reduced.
Vaginal examination: Assess whether the cervix
is ripe or unripe (Bishop Score).
Sweeping of membranes should be done during
this examination as it decreases the chances of
post term pregnancy.
At 41 weeks: At PHC, once pregnancy has
reached 41 weeks, refer her to FRU for further
evaluation and i nterve ntions.
9.5 Management of post term
pregnancy at FRU
There are two options of managing 41 weeks
pregnancy: Immediate induction of labouror
expectant management until 42 weeks, while
monitoring the fetal wellbeing.
9.5.1In low-risk pregnancies routine induction of
labour at 41 weeks is associated with reduction in
perinatal mortality. The risk of fetal distress is
reduced by induction of labour.
9.5.2 Follow up:If expectant management option is
chosen, the mothers should be advised to come for
fetal surveillance test at 41 weeks and twice between
41 and 42 weeks.
History:
a) Accurate assessment of gestational age to
avoid delivery of a preterm baby. Errors likely if
prior irregular menstrual cycles or if she has
conceived soon after cessation of oral contraceptive
pills.
Page 263
Review the early USG reports and the date of
detection of positive UPT.
Ask about history of di minished fetal movements.
b) On examination:
Less amount of liquor on abdominal palpation,
Baby may be of large size.
c) USG:
Look for oligohydramnios: Amniotic fluid index
(AFI) 5 cm or less or there is no vertical pocket > 2
cm. This is a marker for fetal compromise. Note:
estimated fetal weight and check for macrosomia.
d) Nonstress test:
Reactive or nonreactive. [FHR increased by > 15
beats lasting for 15 seconds in response to fetal
movement is assuring]
Fetal compromise is indicated by reduced AFI,
nonreactive NST, reduced fetal movements when
immediate delivery is indicated.
e) At 42 weeks:Labour is induced. If the baby is too
large or severely compromised, caesarean section is
performed.
9.6 Induction of labour
Cervix unfavorable (Bishops score < 6):
Vaginal misoprostol 25 mcg 6 hourly for
induction of Labo ur. Oral misoprostol 25 mcg 2
hourly can be used.
Pre induction cervical ripening can also be
achieved by intra cervical PGE2 gel or by Foley
catheter. Cervix is reassessed for improvement in
bishop score. Induction can then be carried out
with oxytocin infusion.
Favorable cervix: Induction with oxytocin
infusion and ARM.
9.7 During labour (Induced or
spontaneous)
Partographic monitoring of Labo ur. Monitor
FHS and color of liquor, (electronic monitoring
if available). watch for signs of fetal distress.
CS is indicated for intra partum fetal distress and
for large baby.
Second stage : Risk of shoulder dystocia.
Episiotomy, assisted delivery may be performed
as required.

Table 4: Bischop score

Parameters 0 1 2 3

Cervical dilatation in cm Closed 1-2 3-4 5+

Cervical effacement in % 0-30 40-50 60-70 80+

Fetal station -3 -2 0 +1 +2, +3

Cervical consistency Firm Medium Soft

Cervical position Posterior Middle Anterior

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 4. OBSTETRIC COMPLICATIONS
1. Preeclampsia and Eclampsia Proteinuria: One plus or more.
Pre-eclampsia is a condition specific to pregnancy,
Oedema of hands, face, abdominal wall (generalized
arising after the 20th week of gestation, characterized
by hypertension and proteinuria. edema) may be present but it is not a diagnostic
Eclampsia is pre-eclampsia with convulsions. feature. Excessive weight gain. 1 kg or more in a
week or 3 kg in a month could be a warning signal.
1.1. Signs of preeclampsia
1.2 Classification of pre-eclampsia
Hypertension: BP 140/90 mmHg or more on at
least 2 occasions 4 hours apart after 20 weeks of Mild and severe.
gestation.
Table-1: Classification of PIH

Finding Mild Pre-eclampsia Severe Pre-eclampsia

Blood Pressure (BP) BP > 140/90 but <160/110 BP 160/110 mm Hg or
mmHg more

Proteinuria Present, 2+ or less *3+ or greater

GeneralisedOedema (including in the face & hand) May or may not be Present
present
Headache Absent Present

Visual Disturbances Absent Present

Upper abdominal pain Absent Present

Oliguria Absent Present

Fetal growth restriction (IUGR) Absent Present
Pulmonary Oede ma Absent Present

Decreased foetal Movement Absent Present

Platelet count Nor mal Less than 1 lac

It is not necessary that all these signs are present in all cases

1.3. Diagnosis At each prenatal visit, check the woman's BP, urine
for presence of protein; look for oedema and record
There are no symptoms in mild preeclampsia. Look her weight. If there is a rise in BP, monitor the
for signs woman's BP weekly.

Page 265
 Table-2: Dangers
Maternal
Eclampsia
Cerebral haemorrhage, thrombosis, oedema
Acute renal failure
Aspiration bronchopneumonia, Pulmonary oedema,
HELLP syndrome (haemolysis, elevated liver enzymes, low platelet count)
Disseminated intravascular coagulopathy (DIC) leading to hemorrhage
1.4 Management of mild pre-
eclampsia
1.4.1 Gestation more than 37 weeks:
Admit the woman to a hospital. Check BP. Test
for proteinuria. Monitor FHR.
Assess cervix. Induce labour if cervix is ripe. Do
not allow her to cross her EDD.
In mild cases when maternal and fetal condition
is well, can await spontaneous onset of labour
until 37-38 weeks.
1.4.2 Gestation less than 37 weeks
Advise her to avoid exersion. Encourage her to rest in
left lateral position. Counseled her about diet. She is
allowed to take normal salt in food but no extra salt
should be added to the food.
Hospitalization.
Check BP, urine protein, urine output, weight
daily.
Check for generalized body oedema.
Exclude symptoms of severe pre-eclampsia
Monitor foetal growth, ask the woman about
foetal movements, check daily fetal movement
count (DFMC), FHR.
Fetal/Neonatal
IUGR
Stillbirth
Neonatal asphyxia
Biweekly LFT, KFT, Platelet count, NST,
umbilical artery doppler weekly if available.
Antihypertensive drugs are not beneficial in mild
hypertension.
Diuretics are not recommended.
During observat ion if BP starts rising,
(diastolic BP 100 mm Hg or more) start
antihypertensive .
Tab Alpha methyl dopa 250-500 mg 6-8 hourly
orally (maximum up to 2 gm in 24 hours) OR
Tab Nifedipine sustained release preparation 10
mg orally twice a day (maximum up to 80 mg in
24 hrs) OR
Tab Labetalol 100 mg orally twice a day
Terminate pregnancy if there are signs of fetal
compromise, BP is persistently rising or if there
is worsening protienuria.
Mode of delivery: Vaginal or caesarean section
depending on gestational age, cervical status,
maternal and fetal condition.
During observation anytime if systolic BP is 160
mm Hg &/or diastolic BP 110 mm Hg: Manage as
severe preeclampsia. She should be referred to a
district hospital/ medical college for further care.
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1.5. Management of Severe pre-
eclampsia
Hospitalize patient.
Control hypertension: Give anti-hypertensive
drugs. Maintain diastolic blood pressure between
90-100 mmHg.
Nifedipine 10 mg orally. After 30 minutes, if BP
is not brought under control, another 10 mg of
the drug can be repeated. Caution needed while
using Nifedipine as there may be a sudde n and
massive fall in B P.
Labetalol can be given.
Monitor vital signs, reflexes & fetal heart rate.
Auscultate lung bases frequently and look for
signs of pulmonary edema. If rales are heard give
Frusemide 40 mg IV.
Perform bedside clotting test.
Watch for warning symptoms and signs which
may appear before getting fits. Sharp rise of BP,
increased proteinuria, exaggerated knee jerk.
Severe headache, drowsiness, mental confusion,
visual disturbances (e.g. blurred vision, flashes
of light, double vision) epigastric pain, nausea,
vomiting, decreased urinary output.
Prevent fits: Give prophylactic Magnesium
Sulphate( full loading & maintenance dos e as in
Eclampsia )
Encourage the woman for delivery at the FRU
1.6. Investigations
Urine- Albumin, sugar, culture & sensitivity, 24 hrs
urine protein.Hb%, PCV, Platelets, bleeding time,
clotting time, serum fibrinogen, Blood urea, serum
creatinine, serum uric acid, serum bilirubin, serum
proteins, SGOT, SGPTFundoscopy.
1.7. Obstetric management
Gestation < 24 wks: Fetal salvage is difficult so
proceed with termination of pregnancy.
If gestation > 24 wks - < 34 wks : Treatment
should be individualized.
Give Inj Dexamethasone 6 mg 12 hourly 4
doses.
If BP controlled keep woman under regular
maternal & fetal surveillance.
Deliver the woman at 37 wks. Induce LABOUR
before 37 weeks if BP uncontrolled or worsening
of clinical/ biochemical parameters or
appearance of signs of fetal compromise.
Assess cervical status. If cervix is unripe
induction by oral or vaginal misoprostol. 25 mcg
or intra cervical dinoprostone gel can be used for
preinduction ripening of the cervix.
If cervix is ripe induce with oxytocin infusion
and amniotomy.
LSCS may be done for deteriorating maternal
condition, adverse fetal condition, failed
induction or other obstetric indications.
2. Eclampsia
Eclampsia is characterized by hypertension and
proteinuria. (Preeclampsia) and convulsions/fits
followed by coma.
Convulsions may occur in the antepartum, intra
partum or the postpartum period.
Status eclampticus: Convulsions continue one after
the other.
2.1. Differential diagnosis of
convulsions during pregnancy
Eclampsia: Hypertension, proteinuria.
Epilepsy: Past H/O fits, normal BP.
Cerebral malaria: Fever, Anemia, jaundice,
Malaria tests positive.
Meningitis/encephalitis, Tetanus.
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2.2. Management of Eclampsia 2.2.2 Controlling fits

Principles: Magnesium sulfate is the drug of choice.

i. General care Loading Dose: Give Inj. Magnesium sulphate 4 g

(20 ml of 20% solution) slow IV in 5 min. (not to
ii. Control fits
be give n as a bol us rapidly). Then administer Inj.
iii. Control blood pressure Magnesium sulphate 10 gm deep IM, 5 g in each
iv. Expedite delivery gluteus muscle ( 10 ml of 50% solution, in each
buttock) with 1 ml of 2% Lignocaine in the same
v. Maintain fluid balance
syringe.
vi. Postpartum care If convulsions recur after 15 minutes, give
2.2.1 General care additional 2 g of Magnesium sulphate (10 ml of
20 % solution) IV over 5 minutes.
Keep the patient in a quiet room in a bed with
Maintenance Dose: Give 5 g of 50% Magnesium
padded rails on sides. Place the woman on her
sulphate solution IM with 1 ml of 2 %
left side.
Lignocaine every 4 hours alternately in each
Evaluate vital signs.
buttock.
Clean the mouth & nos trils by appl ying gentle
Magnesium sulphate to be continued till 24 hours
suction.
after delivery or the last convulsion whichever
Give oxygen.
occurs later.
Prevent Injury to tongue by putting airway or by
Before giving the next dose of Magnesium
placing padded tongue blades.
sulphate, e nsure:
Start IV line with Ringer lactate/ normal saline :
The Urine output is at least 100 ml in previous 4
60 ml/hour.
hours.
Catheterize patient. Monitor hourly urine output.
Knee jerk reflexes are present
Send investigations as for severe pre-eclampsia
The respiratory rate (RR) is at least 16
If not breathing check airway and give ba g and
breaths/min.
mask ventilation.
Postpone the next dose if the above criteria are
not met.

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 Table-3: Magnesium sulphate solution for loading dose

Preparation of 20 % Magnesium sulphate solution for loading dose

Inj. Magsulf is supplied as a 50 % solution in 2 ml vial. 1 amp of 2 ml = 1 g Magsulf

4 amp of 2 ml 50% solution = 4 g Magsulf in 8 ml solution

Add 12 ml distilled water or saline to make 20 ml 20 % Magsulf solution and
Give slowly IV in 5 min
For initial intramuscular dose:
5 amp of 2 ml 50% solution =5 g MgSO4. Give 10 ml deep IM in each buttock

Table-4: Magnesium sulphate for maintenance dose

Preparation of 50 % Mag nesium sulphate for maintenance dose

1 amp 2 ml 50% solution = 1g. 5 amp = 5 g Magsulf.

Give deep IM in alternate buttock every 4 hourly

Table-5: Precautions
Precautions:
Do NOT give 50 % Magnesium sulphate solution IV without diluting it to 20 %
Do NOT give rapid IV infusion of MgSO4 as it can cause respiratory failure or death.
If respiratory depression occurs (RR < 16 breaths/minute) do not give the next dose.
Give antidote Calcium gluconate 1 g IV (10 ml of 10 %) over a period of 10 minutes.

2.2.3 Controlling bloo d pressure 2.2.4 Delive ring t he baby

Nifedipineis the drug of choice for controlling BP.
Tab. Nifedipine 10 mg orally, followed by 6 hrly
after taking BP.
Labetalol: Intravenous Labetalol (1 blocker) is
another commonly used dr ug for severe hypertension.
It is given in a dose of 20 mg IV initially. If BP has
not decreased to the desirable level in 10 min then 40
mg is given. If the BP has still not decreased in the
next 10 minutes, an incremental dose of 80 mg may
be given. This may be followed by another 80 mg
every 10 min if needed till a maximum of 220 mg has
been administered. Cardiac monitoring is required.
Avoid in bronchial asthma and in cardiac disease.
The mode of delivery should be decided depending
on whether or not the woman has gone into labour
and the stage and progress of labour. In eclampsia,
delivery should occur within 12 hours of the onset of
convulsions.
If woman is in active labour: Monitor the
progress of labour and deliver. Watch for signs
of fetal distress. Augment labour by amniotomy
and oxytocin infusion as required.
Cut short the second stage of labour.
Do not give Inj Methyl ergometrine.

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 If woman is not in labour: Assess condition of
cervix and induce labour with va ginal or oral
misoprostol 25 mcg or ARM & Oxytocin
infusion.
Mode of delivery depending on fetal condition
and condition of cervix.
Perform LSCS if: Cervix unfavorable, Fetal
distress, Fits are not controlled, labour is not
progressing well despite induction/ augmentation
or for any other obstetric indication.
2.2.5 Maintaining the fluid balance
Monitor urine output. It should be at least 30
ml/hour.
Record the fluid intake. Give all the necessary
fluids slow IV @ 60 ml per hour. (Urine output +
500ml) fluid DNS.
Maintenance of proper fluid balance is essential
to prevent water intoxication, dehydration,
hyponatraemia, or pulmonary oedema.
Diuretics should not be used unless there are
signs of pulmonary e de ma.
2.2.6Post Partum Care
Fits can also occur for the first time in the immediate
postpartum period. Monitor BP and the urine output
after delivery. Continue antihypertensives to maintain
diastolic BP between 90 100 mm Hg. Advise the
woman to have her BP checked regularly until BP
returns to nor mal. If BP remains high at 12 weeks
diagnose her as chronic hypertension and refer her to
physician for evaluation.
3. Vaginal Bleeding During
Early Pregnancy
1.1. A woman may present with history of a short
period of amenorrhea followed by
Vaginal bleeding.Abortion, vesicular mole and
ectopic pregnancy are the common underlying
conditions, while an occasional woman may simply
have a delayed menstruation.
3.1 Ask patient following
Period of amenorrhea, LMP, symptoms
suggestive of pregnancy.
Amount and duration of bleeding, it may be
scanty in threatened and missed abor tion and
profuse in incomplete / inevitable abortion. Prior
H/O abortion, ectopic pregnancy.
Nature and severity of pain (severe in ruptured
ectopi c pregnancy)
Clinical presentation may be asThreatened
abortion, Inevitable abortion, Incomplete
abortion, Complete abortion, Missed abortion or
Septic abortion.
Arrange for ultrasonography and pr egnancy test.
Arrive at the diagnosis with the help of following
chart.
Refer to specialist for further management.
3.2 Different diagnosis

Table 6: Differentiating features according to condition

Particulars Threatened Incomplete Missed abortion Vesicular/H Ectopic

abortion abortion Mole pregnancy

Uterine Size Equal Smaller Smaller Bigger Smaller

to POA Intos open
Internal os closed

Vaginal Slight Profuse Absent or Recurrent Slight

bleeding brownish small
discharge

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Pain Mild or Absent Cramping pain Absent Absent Severe,
significant continuous

G.C. pallor Fair Proportional to Fair Fair Out of

/tachycardia blood loss proportion to
visible blood
loss.

Tenderness Absent Absent (Unless Absent Absent Marked

Abd/vag infected)

USG Intrauterine viable Some products in Nonviable Snowstorm Empty uterus

pregnancy uterine cavity pregnancy appearance pelvic / adnexal
mass

Risks Preterm Hemorrhage Blood Hemorrhage Shoc k

coagulation
/IUGR Sepsis
failure

Manage ment Expectant Surgical evacuation Termination of Suction Laparoscopy or

pregnancy evacuation
Antibiotics Laporotomy,
Blood
Blood
transfusion if
transfusion
required

3.3. Management of Threatened Uterus is < 12 weeks: Manual/electrical vacuum

abortion
Avoiding exertion, sexual abstinence and regular
follow up to monitor the growth of the fetus are
recommended. The role of progesterone therapy or
human chorionic gonadotropin is unproven.
Follow up: Regular ANC check up every 15 days.
The pregnancy has higher risk of having recurrent
episodes of bleeding, bleeding in late pregnancy due
to APH, fetal growth retardation and preterm
delivery.
3.4. Management of Missed
Abortion
Investigation: Ultrasonography. Bleeding time,
clotting time, prothrombin time, platelet count (risk
of coagulation failure with prolonged retention of
dead fetus).
Treatment: The pregnancy needs to be terminated
for maternal anxiety and for risk of blood coagulation
failure leading to excessive bleeding.
aspiration.
Uterus > 12 weeks: Pregnancy termination by
misoprostol.
3.5. Septic abortion
Unsafe abor tion. Anemia, delay in emptying the
uterus in cases of incomplete abortion, failure to
follow adequate aseptic precautions.
Symptoms and signs: Fever, tachycardia, lower
abdominal pain, offensive vaginal discharge and
pelvic tenderness.
Investigations - Bleeding time, clotting time,
prothrombin time, platelet count are done as there is
risk of coagulation failure.
Treatment: Antibiotics. Inj.Ampicllin 1gm stat IV
followed by Inj. ampicllin 500 mg.6 hourly,
Inj.Gentamicin 80 mg 12 hourly, Inj.Metronidazole
100 ml IV 8 hourly slowly.
Surgical evacuation of uterus if there are retained
products.

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Cases having severe sepsis with complications need
to be referred to district hospital.
3.6. Ectopic pregnancy
The commonest site of ectopic pregnancy is the
fallopian tube.
Clinical presentation: Unruptured tubal pregnancy;
tubal abortion or tubal rupture with severe
intraperitoneal bleeding leading to shock.
3.6.1 Unruptured ectopic pregnancy: Diagnosis
requires a high inde x of suspicion. The woman can
reveal some of the risk factors for ectopic pregnancy,
will present with signs and symptoms of pregnancy,
may have a unilateral adnexal mass.
UPT positive; ultrasonography reveals an empty
uterus.
Refer to specialist for laparoscopic surgery.
Medical management for selected cases: Inj
Methotrexate under careful monitoring.
3.6.2 Tubal abortion: Symptoms:
Significant pain in lower abdomen, vaginal bleeding
could be slight or even absent.
Signs: Tenderness in lower abdomen.
P/V: Cervical movements extremely painful and
tenderness in fornices.
Pallor and tachycardia depending on the amount of
internal bleeding.
Clinical condition usually stable.
Investigations: Ultrasonography reveals free fluid in
abdomen.
Treatment: Referral to gynecologist for surgical
management.
3.6.3 Ruptured ectopic pregnancy:
Severe and acute pain in abdomen with severe
intraperitoneal bleeding which is continuing.
Signs: The patient presents with tachycardia, severe
pallor and hypotension. The abdomen is tender and
distended. Signs of free fluid in abdomen (shifting
dullness). Vaginal examination is extremely painful
and an ill defined mass may be felt in posterior and
lateral fornix.
USG: Free fluid in abdomen and vague ill defined
mass may be seen.
Culdocentesis: Blood is aspirated which fails to clot
on observation.
Treatment: Management of shoc k. Urgent surgical
exploration to stop the bleeding. Blood transfusion as
required.
3.7 Hydatidiform Mole
An abnor mal pregnancy where there is no fetus, no
amniotic sac and the uterus is full of proliferated
trophoblastic tissue.
Symptoms: The pregnancy vomiting is often
exaggerated and there is recurrent vaginal bleeding
rarely with passage of grape like vesicles.
Signs: Uterus is larger than the POA and soft /
doughy in consistency Tachycardia, pallor.
Investigation: Ultrasonography reveals snow storm
appearance, absence of fetus, amniotic fluid. The
ovaries may be enlarged with multiple cysts.
Pregnancy hormone Beta HCG is markedly elevated.
Treatment: The pregnancy is terminated by suction
evacuation under general anesthesia. Blood is
arranged.
Complications:
Severe hemorrhage and uterine perforation
during evacuation.
Infection.
Development of gestational trophoblastic
neoplasia.
Follow up: Baseline X ray chest and beta HCG
levels tested before discharge. Regular beta HCG
monitoring till it falls to normal level and for 6
months thereafter as there is risk of development of
gestational trophoblastic neoplasia.
It is important to avoid pregnancy by using reliable
contraception during this follow up period. Oral pills
can be give n. Intrauterine contraception is not
recomme nded.
During follow up: Look for abnormal vaginal
bleeding, enlarged soft uterus, evidence of any
metastasis (lungs, brain, anterior vaginal wall)
Pregnancy is allowed when beta HCG remains
normal for 6 months. Referral to tertiary care centre
is indicated for chemotherapy if Beta HCG levels
show initial decline followed by a rise or it remains
static (plateau).
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4.Antepartum Haemorrhage
(APH)
4.1. Definition:
Bleeding from vagina after 20 weeks of pregnancy
and before the birth of child. Two major causes:
Abruptio placentae: Bleeding from premature
separation of normally located placenta in the
upper uterine segment.
Placenta Previa: Bleeding from premature
separation of low lying placenta located in lower
uterine segment.
4.2. Dangers:
Maternal mortality is high due to hemorrhagic shoc k
and its complications like acute renal failure (ARF),
coagulation failure due to DIC. There is increased
risk of atonic PPH after delivery. Lacerations of
friable cervix also cause bleeding. Operative delivery
rates are high.
Fetal and neonatal mortality is high due to
prematurity (Spontaneous & iatrogenic), LBW and
asphyxia.
4.3.Case Management of APH
4.3.1 History:
Ask the period of amenorrhoea, fetal
movements, Time of onset of bleeding, amount,
prior H/O warning hemorrhages.
Abdominal pain present or absent and its
severity.
4.4 PlacentaPrevia
Figure 1: Placenta previa
Passage of urine.
Prior USG reports if available.
H/O trauma, internal examination/ coitus
aggravating the bleeding.
2.4. Examination:
Note pallor, tachycardia, general condition,
record blood pressure.
In concealed accidental hemorrhage, although
the woman is in shock, her BP may be nor mal as
she could be having hypertension. Therefore
degree of pallor and tachycardia are more
important for assessment of amount of bleeding
and general condition.
P/A :
Uterus is relaxed, contracting and relaxing or
hard.
Uterine tenderness present/absent (localized or
generalized)
Presentation, FHS
No vaginal examination to be done until placenta
previa is ruled out
4.3.3 Investigations:
Urgent USG to locate placenta and assess the
fetal condition and its gestational age.
Blood tests: Hb, PCV, Coagulation profile
(Bleeding & clotting time, clot observation test,
platelet count, prothrombin time.
Liver function and renal function tests.
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4.4.1 Differentiate between Placenta Previa a nd Abruptio placentae
Table-7: Differentiation between placenta previa and mixed abruotio placentae
Particular Placenta previa Concealed or mixe d abruptio placentae
Pain Painless recurrent vaginal bleeding Painful bleeding

General Pallor, tachycardia, restlessness proportional Pallor, tachycardia disproportionately more

condition to visible amount of blood lost than the visible amount of vaginal bleeding
Uterus Relaxed, non-tender, fetal parts felt well Tense, tender, woody hard, fetal parts
cannot be felt
Presentation May be abnormal or head may be high floating Presentation cannot be made out
Fetus Fetal condition usually well if mother not in Fetus often distressed or dead. FHS may not
shoc k be heard
Maternal Hypovolemic shock Shoc k, acute renal failure, DIC
Dange rs
Action No P/V examination. IV fluids, referral IV fluids, referral, monitor

4.4.2 Complications: If pregnancy duration is > 36 weeks or if there is

life threatening bleeding then pregnancy is
Maternal:Hypovolemic shock, malpresentations,
terminated.
operative delivery, PPH
Expectant management For clinically stable
Baby: Prematurity, low birth weight, fetal/neonatal patient with moderate blood loss having fetus
asphyxia alive and preterm until 36 weeks.
4.4.3. Manage ment: P/S : Exclude local genital causes (cervical
growth, polyps, vascular ectropion)
Even if bleeding is only a very small amount,
Pregnancy is terminated in maternal interest at
hospitalization is required.
any time during the observation period if there is
Assess the blood loss.
furious uncontrolled bleeding or when pregnancy
Full blood count and clotting studies. > 36 weeks.
Arrange cross matched blood
4.4.4 Mode of delivery:
Perform gentle palpation of abdomen to assess the
gestational age of fetus, presentation and position. Caesarean section for major degree placenta
previa and for cases having type II posterior
Assess fetal condi tion. Arrange urgent
placenta previa with a salvageable fetus.
ultrasound.
Previous CS & anterior placenta previa: There is
Rh negative woman: With every episode of
risk of morbidly adherent placenta leading to
bleeding, give prophylactic anti-D
furious hemorrhage. Refer such case to tertiary
immunoglobulin.
care centre. Such case needs to have 4 units of

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 blood to be kept ready and preparations for CS amniotomy followed by oxytocin infusion.
hysterectomy if required. Arranging blood and the delivery at well
Cases having low lying placenta, (type II equipped institution is necessary.
anterior) can be delivered vaginally by

4.5 Abruptio Placentae

Figure 2: Abruptio placentae

4.5.1 Diagnosis:

May present with va ginal bleeding and USG shows placenta in upper uterine segment
abdominal pain. and may show retroplacental hematoma.
Ask H/O trauma, prior hypertension. Errors in diag nos is
Assess blood loss: Look for pallor, tachycardia,
The case could be misdiagnosed as preterm
general condition, urine output, record BP. Labo ur.
Hypertension and pr oteinuria may be present. A patient of concealed accidental hemorrhage
can be misdiagnosed as patient in labour with
P/A uterus hard, tender, not relaxing severe anemia with fetal death.
(Hypertonus) In Labo ur, uterine rupture can be misdiagnosed
as concealed accidental hemorrhage.
In cases of severe abruption, fetal parts may not
be felt well, fetus may be distressed/dead. When 4.5.2 Manage ment:
the fetus is dead at least 1,500 ml of blood is lost,
hence shoc k is usual, uterus is firm-to-hard and If fetus is alive and salvageable an urgent CS is
performed, hence referral to nearest facility is
very tender. Blood pressure may be normal in indicated.
spite of being in shoc k as the initial BP may be If fetus is dead, it indicates massive
retroplacental hemorrhage. Hemodynamic
high. Coagulation failure leading to severe stability is assessed (pulse, BP, pallor). Foley
bleeding is common.

Page 275
 catheter is introduced and hourly urine output is
monitored. Coagulation profile is checked.
Correction of hypovolemia: Ringer lactate
infusion and by blood transfusion.
Refer the woman to tertiary level of care having
facility of providing blood and blood products
for treatment of DIC.
Induce labour by ARM and oxytocin infusion.
4.5.3 DuringLabour:
First stage of Labo ur is augmented by ARM and
oxytocin infusion.
If fetus is alive, watch for signs of fetal distress .
Second stage of Labo ur is cut short.
Active management of third stage of labour.
Placenta is examined and the retro placental clot
is weighed.
Hemoglobin and hematocrit estimation following
delivery.
5. Preterm labour
Prematurity and low birth weight is the important
causes of neonatal deaths in India.
Preterm labour is onset of labour from 24 weeks to
37 completed weeks of gestation.
From survival point of view, the gestational age of 34
weeks is important as after this period the fetal lungs
are mature enough for independent survival outside
the uterus.
A single course of antenatal corticosteroids
administered between 24 to 34 weeks of pregnancy
has been shown to reduce the neonatal mortality
significantly in preterm bor n babies.
5.1. Risk Factors for preterm
Labour
Maternal weight < 40 Kg in first trimester. (BMI
< 19.8 kg/m2), Obesity ( BMI> 30 kg/m2).
Teenage pregnant women, Short inter pregnancy
interval.
Short stature, maternal under nutrition ,anemia.
Inadequate weight gain during pregnancy
Strenuous working, long hours of work, inability
to take adequate rest.
Tobacco, smoking, heavy alcohol use, illicit drug
use.
Previous H/O preterm birth, mid trimester
abortion. Risk increases with each additional
preterm birth.
Incompetent cervix, uterine malformations.
Vaginal infections : Bacterial vaginosis.
Overdistended uterus (Twins, polyhydramnios),
Vaginal bleeding during pregnancy,
Chorioamnionitis.
Diabetes, hypothyroidism, heart disease, chronic
hypertension, HIV illness, urinary tract
infection(UTI), periodontal infections.
Fall, psychological stress, abdominal surgery
during pregnancy.
5.2. Prevention
Treatment for UTI, correction of anemia,
improving oral hygiene.
Nutritious diet and consumption of IFA tablets.
Counseling: Avoid strenuous work, take extra
rest, quitting tobacco, alcohol.
Women with previous history of preterm birth:
Refer to specialist.
Vaginal sonography to see the length of cervix.
Weekly Injections of 17 hydroxy progesterone.
Cervical os tightening in selected cases are some
of the preventive interventions.
5.3. Prediction by warning
symptoms
Cramping discomfort/pain in lower abdomen,
low backache.
Increased mucoid vaginal discharge.
Intermittent uterine contractions felt during
discomfort.
Heaviness in pelvis (something descending
down).
5.4. Diagnosis
Assess pregnancy duration accurately
Confirm onset of Labo ur: Intermittent painful uterine
contractions (4 in 20 min or 8 in 60 mins) along with
progressive change in the cervical dilatation and
effacement assessed over 2 hours
5.5. Management principles
5.5.1 If pregnancy is < 34 weeks
Antenatal Dexamethasone therapy
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 Inhibition of preterm labour by administering
tocolytic medicine.
In Utero transfer.
Safe conduct of preterm labour.
Special care of preterm neonate.
a) Antenatal corticosteroid therapy
Inj Dexamethasone administered between 24- 34
weeks of pregnancy in cases of threatened
preterm labour is effective in lowering the risk of
respiratory distress syndrome (RDS) & neonatal
mortality if birth was delayed by at least 24
hours after initiation of therapy. The effect
persists for 7 days after completion of course of
steroid therapy.
Injection Dexamethasone 6 mg IM 12 hourly for
48 hours, total 4 doses. Repeated courses should
not be give n.
Who can receive the therapy?
All women having spontaneous onset of preterm
labour and those having complicated pregnancies
(Severe preeclampsia, antepartum hemorrhage
etc).
Preterm rupture of membranes before the onset
of labour pains (PROM)
Which women should not receive corticosteroid
therapy?
If there is chorioamnionitis, (infection of fetal
membranes) delivery is not to be postponed.
Early delivery is safer for both mother and her
baby. Signs are.
Fever, lower abdominal pain, Tenderness over
the uterus
Fetal tachycardia (FHR > 160/minute), Foul
smelling liquor
b) Inhibition of uterine contractions by tocolytic
drugs:
Tocolyticdrugs stop contractions temporarily but
rarely prevent preterm birth. However the
delivery is delayed long enough for getting the
benefits of administration of Dexamethasone.
Indication for Tocolysis
If Labo ur starts between 24 weeks to 34 weeks.
The cervix is <3 cm dilated.
There is no foetal distress.
Tocolysis is not indicated in Amnionitis, pre
eclampsia, active bleeding &foetal distress.
Nifedipine 20 mg oral stat followed by 10 mg 4
hourly till contractions stop or maternal pulse
exceeds 120 beats/min. Continue drug till steroid
cover is complete or for 8 hours after last
contraction. Then taper the dose slowly.
Alternatively, beta adrenergic receptor agonists
(Ritodrine, Turbutaline, Isoxusprine) can be
given. Turbutaline is a selective beta agonist
having lesser cardiovascular side effects that can
be administered subcutaneously. However their
value is not proven.
Cardiac disease needs to be excluded before
giving these drugs. While administering tocolytic
drugs careful monitoring is required for side
effects. Monitor pulse, BP, signs of respiratory
distress, uterine contractions, loss of amniotic
fluid or blood, FHR, fluid balance, blood
glucose. Watch for maternal acute pulmonary
oedema when combination of steroids and
tocolysis is used.
Do NOT give tocolytic drugs for more than 48
hours.
c) In Utero transfer: If the period of gestation is <
34 weeks, and Labo ur continues despite tocolysis, or
if the woman is already having cervical dilatation >3
cm, refer to district hospital/medical college with
NICU/ SNCU facility for delivery. Before referral
always give at least the initial shot of steroid
mentioning the time on the referral note. Record BP,
urine test result on referral note.
d) Safe conduct of preterm labour
Do not inhibit preterm labour and allow it to
progress if
The cervix is >3 cm dilated.
There is active bleeding, severe pre-eclampsia,
amnionitis
Fetus is distressed, dead or has an anomaly
incompatible with survival.
If a woman presents with preterm labour which
is progressing rapidly, there may not be adequate
time available for referral. Still give the first dose
of Inj. Dexamethasone as even 1 dose few hours
before delivery has some beneficial effects.
Check fetal presentation as possibility of
abnormal presentations is higher in preterm
labour needing skilled attendance.
Monitor the progress of Labo ur.
Prevent birth trauma and birth asphyxia while
conducting breech delivery.
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 Avoid delay in second stage by giving
episiotomy to prevent trauma to the babys head.
Do not use vaccum extractor as the risk of
intracranial bleeding is high.
If Labo ur continues and the gestation period is <
37 weeks; although evidence is not in favour of
prophylactic antibiotics but as woman is coming
from hygienically poor area, antibiotics can be
given to reduce the chances of infection in the
neonate. (Cap. Ampicillin, Tab Metronidazole
and Inj Gentamicin)
e) Special care of preterm neonate
If needed, refer neonate to the nearest NICU/
SNCU after appropriately stabilizing new born
Intrapartum Complications
Abnormal Presentations:
Diagnosis of fetal malpresentation during Labour:
Vaginal examination
6.1 Breech Presentation
In complete breech presentation the presenting part is
buttocks with feet, in frank breech buttocks only and
in footling presentation only feet are felt.
The chance of cord prolapse is highest in footling
breech while it is lowest in frank breech. It is
necessary to avoid rupturing membranes during
vaginal examination.
6.2 Transverse lie
Fetal shoulder felt. After rupture of membranes hand
prolapse occurs, cord prolapse may occur. These
cases need to be referred to FRU urgently for
caesarean delivery.
6.3 Face presentation:
Chin and face felt. If the chin is anterior (left or right
mentoanterior position) vaginal face delivery is
possible specially in a multipara having average sized
baby. However in mentoposteriorposition caesarean
delivery is often required. Refer these women to
FRU, however a midwife should accompany with a
delivery tray during referral.
6.4 Brow presentation:
`Babys forehead and part of the face is felt and chin
is not easily felt. A good sized babys head is unable
to get engaged in the pelvis and the LABOUR is
likely to get obs tructed. Such woman should be
referred to FRU for caesarean section.
7. Breech delivery
If the full term breech presentation is diagnosed in
early labour the case should be referred to higher
centre. Decision to deliver by caesarean section or
allowing va ginal delivery needs to be taken after
careful evaluation by specialist. Maternal age, parity,
pelvic capacity, status of membranes, type of breech,
estimated weight of baby, other complicating medical
/obstetrical conditions, scar on uterus are some of the
important considerations for this decision.
However sometimes woman arrives in advanced
labour when you are required to conduct her delivery
by performing the following steps:
Check the delivery tray, episiotomy tray, baby
tray and newbor n resuscitation equipment
Start IV infusion
Tell the woman to bear down with contractions
only when the cervix is fully dilated and the
buttoc ks are in the va gina
Wash hands with soap and water and put on
sterile gloves.
Take the woman to the edge of the table
Clean the vulva with antiseptic solution and
drape the mother.
Catheterize the bladder, if necessary.
Give pudendal block or local perineal infiltration
for episiotomy.
Give episiotomy when the buttocks distend the
perineum.
Do not pull the baby or interfere in any way
When the baby is bor n up to umbilicus, pull a
loop of cord and keep it aside. Cover the baby
with a clean sheet and gently hold the buttoc ks of
the baby but do not pull.
If the legs do not deliver spontaneously, deliver
one leg at a time.
Ask the mother to continue pushing with
contractions.
Check whetherr arms are on the chest. Allow the
arms to get rotated and disengage spontaneously.
If the arms are stretched above the head or folded
around the neck (Winging of the scapulae
indicates extension of arms) use
Lovsetsmanoeuvre to deliver arms.
Deliver the head by Burns Marshal manoe uvre or
Mauriceau-Smellie-Veitmanoeuvre (jaw flexion
and s houlder traction).
Observe babys breathing and initiate
resuscitation as required (Breech born baby takes
longer time to start normal breathing)
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 Perfor m active management of the third stage of
Labo ur.
Check the birth canal for tears and repair
episiotomy.
8. Twins delivery
A case of diagnosed twin pregnancy arriving in early
labour should be referred immediately as the babies
are often LBW and require special care. However, if
the mother is admitted in advanced labour the
following steps should be taken to deliver her.
Check presentation of first baby , check FHS
Start IV Ringer lactate
If first baby is presenting by vertex allow
LABOUR to progress and deliver the first baby.
Leave a clamp on the maternal end of the cord of
the first twin and do not give Oxytocin.
Palpate abdomen to determine the lie of second
fetus. If it is breech or transverse attempt to
perform external cephalic version.
Check the presentation of second baby by
vaginal examination. If vertex, allow labour to
progress and deliver the baby.
If the uterine contractions become weak and
delivery of second baby is getting delayed start
oxytocin drip slowly.
If the presenting part is breech conduct breech
delivery. If delivery is getting delayed or if fetus
shows signs of distress, perform breech
extraction carefully.
If second baby is transverse refer to FRU for CS.
(If the baby is small and very preterm sometimes
it may deliver spont aneously, hence it is
necessary to accompany her with preparations to
conduct delivery during transfer)
Give Oxytocin soon after delivery of second
baby and conduct active management of third
stage of labour.
Anticipate risk of PPH and check for hardness of
uterus and massage the uterus. Start IV Oxytocin
infusion ( 20 I U in 500 ml of Ringer lactate)
Weigh both babies and take steps for special care
needs if the babies are LBW.
9. Cord Prolapse
Cord prolapse is more common if the presentation is
breech or transverse. In vertex presentation cord gets
severely compressed as head descends and baby gets
severely asphyxiated and needs urgent delivery and
prompt resuscitation
Determine the lie and the presenting part
Note the fetal heart rate
P/V to determine the stage of Labo ur and the
presenting part
Gently feel for the cord pulsations. Push the cord
in the va gina
If first stage; push the head upwards to relieve
pressure by presenting part on cord and give
head low position to mother. Alternatively, insert
a Foleys catheter in urinary bladder and rapidly
fill the bladder with 300-500 ml Normal Saline
to elevate the fetal presenting part. Clamp the
catheter. The clamp must be released and the
bladder drained before any delivery attempt.
Refer immediately to FRU for Caesarean
Section.
If in second stage; expedite delivery with
episiotomy and vacuum/forceps delivery.
Perform breech extraction, if the baby is
presenting by breech.
Check for breathing and resuscitate the newborn.
If the baby is very premature or dead
spontaneous delivery can be awaited.
10. Shoulder Dystocia
If the baby is big the chances of shoulders getting
stuck after delivery of head are high. Many babies die
within few minutes of the head being delivered. It is
important, therefore, to manage the problem
efficiently and carefully so as to avoid Injuries to the
baby or mother.
Call for help
Discourage maternal bearing down effort
Apply Mc Roberts maneuver, bring knees as far
as possible up to the chest and abduct and rotate
legs outwards
Appl y firm suprapubic pressure using the heel of
the hands
Make adequate episiotomy
Rotate the babys body so that the posterior
shoulder moves anteriorly.
If these measures fail to deliver shoulders,
attempt internal rotation maneuvers to deliver
anterior or posterior shoulder. ( Application of
pressure to the anterior/posterior shoulder in the
direction of the babys chest)
Check babys breathing and initiate resuscitation
Complications: PPH, vaginal/perineal tears and
Injuries to baby.
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11. Obstructed Labour
11.1 Causes
Cephalopelvic disproportion due to contracted
pelvis or large head.
Transverse lie, Brow presentation, mento
posterior face presentation, Deep transverse
arrest of fetal head.
11.2 Diagnosis
Non progressive Labo ur, prolonged Labo ur.
Maternal exhaustion: Tachycardia, restlessness,
sweating, mild fever, signs of dehydration.
Signs of fetal distress or death.
11.3 Signs of obstruction
Lower uterine segment over stretched
Bandles ring seen which is rising progressively
towards umbilicus.
Suprapubic bulge Edematous bladder.
Presenting part High, abnormal or showing
excessive moulding.
On catheterization, scanty high colored/ blood
stained urine.
Early signs include edematous cervical lip,
increasing moulding of fetal head.
11.4 Action
Urgent referral. IV infusion during referral will help
in correcting dehydration. Delay in referral can result
is uterine rupture, infection due to prolonged labour
and foetal death.
Vesico-vaginal fistula may develop if presenting part
is deep in the pelvis for prolonged period as in deep
transverse arrest.
At the institution the patient will be delivered mostly
by caesarean section.
12. Uterine Rupture
12.1 Causes
Scarred uterus (previous caesarean section,
uterine perforation etc.)
Obstructed Labo ur
Incorrect use of oxytocic agents like Oxytocin,
prostaglandi ns
Internal podalic version, manual removal of
placenta.
12.2 Diagnosis
Cessation of uterine contractions after prolonged
obstructed Labo ur.
Continuous pain in abdomen.
Maternal tachycardia, restlessness, increasing
pallor, hypotension, fresh va ginal bleeding,
haematuria.
Fetus dead.
Abdomen distended, tender all over, fetal parts
may be felt easily.
Signs of free fluid in abdomen.
In LABOUR, presenting part may recede
upwards.
12.4 Dangers:
Maternal shock and death due to severe internal
hemorrhage.
12.4 Action
Urgent referral to tertiary care centre where
blood transfusion facility is available.
IV infusion of 1 liter of fluids, start antibiotics,
monitor vitals.
Exploratory laparotomy, blood transfusion.
At laparotomy: Hysterectomy or repair of tear.
If only repair of the rent is done, there is risk of
uterine rupture in subsequent pregnancy and an
elective caesarean section is required.
13. Third Stage Complications
13.1 Postpartum Hemorrhage
13.1.1Definition:
Excessive vaginal bleeding > 500 ml after delivery.
Even moderate amount of bleeding could lead to
shoc k in women who are anemic or have
preeclampsia.
13.1.2 Types: Within first 24 hours after childbirth.
(Immediate PPH)
After 24 hours up to 42 days after childbirth (Delayed
PPH).
Although PPH is more common in cases of twin
pregnancy, APH, over distended uterus, grand
multiparas, it is an unpredictable complication and
can occur in any low risk woman.
13.1.3 Probable cause of Excessive Bleeding and
Shock after childbirth.
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 Table 8: Causes of excessive bleeding and shock after Childbirth.
Clinical Presentation
Uterus is flabby, not contracted, fundus is rising.
Uterus is well contracted. Speculum examination of cervix and va gina
reveals cervical/vaginal lacerations/tears.
Placenta not delivered within 30 minutes after delivery.
Placenta incomplete, torn vessels in the membranes.
Bleeding continues even after treatment. Blood does not clot for > 15
minutes.
Uterine fundus not felt per abdo minally. Inverted uterus seen in va gina or
outside vulva.
Delayed PPH. Uterus is larger for the postnatal day, soft, may be tender,
bleeding may have foul smell.
13.1.4 Initial Manage ment of Atonic PPH:
The management includes, uterine massage,
bimanual compression of uterus, administering
uterotonic drugs along with blood volume
replacement and evaluation to look for other causes.
Check for flabby uterus, retained placenta, tears
and lacerations in vagina and cervix.
If the uterus is flabby/soft, give continuous
uterine massage and bimanual compression of
uterus immediately.
Secure intravenous access and collect blood
samples Two 16 or 18 gauge cannulae are
inserted in two veins for correcting hypovolemia
by rapid infusion of IV Ringer lactate/Normal
Saline.
Start Oxytocin infusion 20 IU in 500 ml of
Ringer lactate@ 40-60 drops/minute. Other
Oxytocic agents (Inj Methyl ergometrine 0.2 mg,
Inj 15 methyl PGF 2 , tablets Misoprostol) can be
given in dos age give n in table if uterus remains
flabby.
Send blood sample for cross matching of 3-4
units of blood
Send blood sample to laboratory for full blood
count, coagulation profile, baseline urea and
electrolytes testing.
Inspect placenta if she is recently delivered.
Auscultate lung bases frequently to rule out
pulmonary ede ma.
Oxygen is given by face mask: 8 L/min
Keep the woman warm. Elevate the legs.
Wash hands and wear surgical glove s.
Insert Foleys catheter and monitor hourly urine
output. Urine output less than 20 ml /hour
indicates poor perfusion of tissues.
a) Oxytocics for Management of Atonic PPH
Probable diagnosis
Atonic PPH
Traumatic PPH
Retained placenta
Retained lobe of placenta
Coagulation failure
Acute Uterine Inversion
Uterine infection, retained
lobe/fragments of placenta
Monitor womans GC, pulse, blood pressure,
respiratory rate, temperature every 15 minutes.
Note pallor. Assess whether the woman has
heavy bleeding and s he is in shoc k.
Uterine temponade with condom catheter may be
tried.
If bleeding is controlled by drugs, repeat uterine
massage every 15 minutes for 2 hours.
Monitor vitals closely every 10 minutes for 30
minutes, every 15 min for next 30 mins, and
every 30 min for next 3-6 hours or until.stable.
Continue oxytocin infusion. (max 100 IU in 24
hours)
If the bleeding does not stop, explore uterine
cavity for retained placental bits/lobe.
If the uterus is hard, explore the lower genital
tract in good light to look for genital trauma and
repair any tears followed by firm packing of
vagina to stop the oozing from lacerations.
If the blood sample fails to clot, reversal of
coagulation defects needs to be achieved by
administering blood and blood products. Execute
urgent referral to higher facility.
Arrange urgent referral to FRU, with
accompanying HCW and relatives. Continue
oxyt ocin infusion & oxygen during transit.
If the woman is in shoc k manage shoc k. The first
drip should be fast and timed for approximately
1 litre in 20 min. Estimated replacement is
usually 3times the blood loss. Attempt
compressing the abdominal aorta by firm
pressure with a closed fist just above the
umbilicus during transit.
If it is delayed PPH, look for signs of infection
and administer the first dose of antibiotic.
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 Table-9: Manage ment of Atonic PPH

Oxytocin Methyl Ergo metrine Misoprostol 15 Methyl

PGF2alfa
Dose & Route IV infusion 20 I U in 0.2 mg IM or IV slowly. 800 micrograms 0.25 mg IM Can
500 ml of RL/NS @ Can be repeated after 15 (4 tablets of 200 be repeated
40-60 drops/min mins, thereafter 4 mcg each) per every 15 minutes
hourly if required rectally
Maximum dose 100 IU in 24 hours 5 Injections (Total 1.0 800 micrograms 8 doses (Total 2
mg) mg)
Precautions & Do not give as IV Preeclampsia, Safe drug Rule out Asthma
contraindication bolus Inj hypertension, heart
s disease
Side effects Hypotension if Vomiting Nausea, vomiting, Nausea,
given IV bol us chills vomiting,
diarrhea
Remarks Safe and effective Causes sustained Stable at room Refrigeration is
retraction of uterus temperature, cheap required
Refrigeration is
required Refrigeration is required

First Oxytocin,if not responded Methyl Ergometrine,
if not responded Misoprostol, if not responded 15
Methyl PGF 2alfa.
b) Uterine Temponade with a sterile condom is a
simple procedure which can be carried out by any
SBA as a life saving measure before referral. After
putting the patient in the lithotomy position, under
aseptic precautions a sterile rubber catheter is
inserted within the condom and tied near the mouth
of the condom by a silk thread and introduced in the
uterine cavity. The condom is inflated with 250-500
mL normal saline. The uterine condom kept tight in
position by ribbon gauze pack placed in the vagina.
The condom catheter is kept for 24-48 hours,
depending upon the initial intensity of blood loss. It
is gradually deflated when bleeding is controlled.
Uterine contraction is maintained by oxytocin drip
for at least 6 hours after the procedure. Antibiotic
cover is given.
For uncontrolled PPH surgical procedures may be
required.
13.2 Retained Placenta
13.2.1 Definition:When the placenta fails to deliver
for 30 minutes after the birth of baby in spite of
routine measures including administration of
oxytocin Injection and controlled cord traction, it is
necessary to perform manual removal of placenta
(MRP)
13.2.2 Manage ment (Manual re moval of placenta)
Check womans pulse, blood pressure,
respiration. Assess the amount of blood loss.
Check whether she is in shoc k.
Wash hands, Wear plastic apron, gown, mask
and long surgical glove s.
Start IV Ringer lactate, start Oxytocin infusion.
Catheterize the bladder and monitor urine output.
Give premedicationClean the perineum and the
vagina with antiseptic solution.
Hold the cord with left hand and introduce the
whole right hand in the vagina, pass it through
the cervical canal into the uterine cavity. Suppor t
the fundus with left hand. Locate the edge of the
placenta, separate it completely by slicing
movement, remove the separated placenta and
explore the uterine cavity to check that it is
empty Continue oxytocin drip, massage the
uterus.
Inspect the birth canal for any Injury.
Give antibiotics. Monitor the vital signs.
If the placenta cannot be removed completely, if the
woman is in shock or needs blood transfusion refer
her to tertiary care centre immediately. Morbidly
adherent placenta causes furious bleeding requiring
urgent lifesaving hysterectomy.

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13.2 Acute Inversion of Uterus
13.3.1 Definition:
Uterus turns inside out and may protrude outside
vulva.
The woman gets very severe hemorrhage and goes in
profound shock.
Usually occurs due to mismanaged third stage, giving
traction on cord when placenta is yet not separated
and the uterus is relaxed.
13.3.2 Manage ment:
O/E: Pulse feeble and fast. Hypotension.
P/A: Cupping of fundus, fundus may not be felt at all.
Inverted uterine fundus may be seen at vulva or in
vagina.
Check whether placenta is separated and delivered or
is still attached.
No oxytocics to be given until the fundus is
manually reposed.
Start IV infusion preferably in two veins, give Ringer
lactate infusion, arrange Blood transfusion and treat
Shoc k.
The freshly inverted uterus can be often replaced in
pos ition by pushing up on the fundus with the hand
immediately after inversion. In case of delayed
diagnosis short uterine relaxant inhalation anesthesia
helps successful reposition.
After reposition, inhalation anesthesia is discontinued
and Oxytocin 20 IU in 500 ml of Ringer lactate is
given along with bi manual compression of the uterus
to maintain the uterine retraction and the reposition.
Correct management of third stage of LABOUR is
important for preventing this dangerous
complication. Do not give any traction on cord until
the uterus is firmly contracted and retracted which
indicates the onset of placental separation.
13.4 Puerperal Sepsis
About 8% of maternal deaths are attributed to post
abortal or postpartum sepsis. It is a preventable
complication. Early detection and prompt treatment
can save a lot of morbidity associated with it.
13.4.1 Causes of Fever in Puerperium:
Wound infection: Episiotomy, Caesarean
section.
Puerperal sepsis due to postpartum
endomyometritis, pelvic cellulitis, septicemia,
Urinary tract infection, Mastitis, breast abscess.
Thrombophlebitis, deep vein thrombosis
Malaria, pneumonia, typhoid, HIV related
infections.
13.4.2 Symptoms:
Fever with chills and rigors, Foul smelling
lochia.
Malaise, headache, nausea, anorexia, vomiting.
13.4.3 Signs:
Depending upon severity of infection
Tachycardia, fever, hypotension in septic shock,
swelling in one leg, calf tenderness. (DVT)
P/A: Subinvol uted tender uterus, tenderness in
iliac fossae, distension, guarding, absent
peristalsis in peritonitis.
Local examination: Episiotomy oedematous, pus
discharge, foul smelling lochia.
Vaginal examination: Uterus subinvol uted,
tender, fornices tender, Bogginess in posterior
fornix if pelvic abscess.
13.4.4 Risk Factors:
Prolonged labour, PROM, Unclean delivery.
Anemia, under nutrition, Diabetes Mellitus, HIV
infection.
13.4.5 Investigations:
CBC with WBC total and differential count.
Smear for malarial parasite.
Urine routine, microscopy, culture & sensitivity
in suspected cases of UTI.
USG for retained products, collection in pelvis.
Chest X-ray.
High vaginal and cervical swab smear, culture
sensitivity.
Blood culture in seriously ill cases.
13.4.6. Manage ment:
a) Genital sepsis
On examination patient has pallor, tachycardia,
uterus is soft, tender, sub involuted (i.e. large for the
day of puerperium), abdomen soft, non-tender.
Mild sepsis can be treated at PHC level by giving
oral antibiotics for 7 days.
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Cap Ampicillin/Amoxicillin orally 500 mg 6 hourly
for 7 days, Tab Metronidazole 400 mg orally 3 times
a day.
Give Hematinics. Review after 48 hours.
If response is seen, continue treatment for 7 days. In
case of deterioration, refer the patient. Antibiotics
includi ng Inj Gentamicin 80 mg IM should be
initiated by ANM/MO at the first suspicion of sepsis
before referral.
b) Pelvic peritonitis
If P/A examination reveals tenderness in lower
abdomen (iliac fosse) with or without distention and
guarding, suspect pelvic peritonitis and refer to FRU
after giving loading dose of antibiotics. Inj.
Ampicillin 1 gm IV, Inj. Gentamicin 80 mg, IV
Metronidazole 500 mg.
This patient needs hospitalization and parenteral
antibiotics for 7-10 days. Inj. Ampicillin 1 gm IV
followed by 500 mg 6 hourly. Inj. Gentamicin 80 mg
twice a day I.M. IV Metronidazole 500 mg 8 hourly.
IV fluids are given. After 48 hours if patient
improves and resumes oral intake, Cap Ampicillin
and Tab Metronidozole can be given orally.
Change in antibiotics as per results of antibiotic
sensitivity testing is required if there is no response to
treatment within 48 hours.
c) Generalized peritonitis or septicemia:
If a patient of puerperal sepsis is looking very ill,
febrile, restless, has marked tachycardia and has
distention of abdomen, guarding, tenderness over
abdomen, peristalsis is sluggish or absent then such
patient is having generalized peritonitis. She may
have septicemia. Refer her to tertiary care center, as
she requires special care in critical care unit, higher
antibiotics and may need surgical interventions.
There is risk of death due to endotoxic shoc k, acute
renal failure, DIC.
Any degree of puerperal sepsis when associated
with severe anemia, there is risk of rapid
deterioration. Hence refer such patient to a
specialist at district hospital.
d) Surgical treatment:
Retained products in uterine cavity: Evacuation
of uterine cavity.
Pelvic abscess is drained by colpotomy.
General peritonitis may require laparotomy.
Breast abscess: Incision and drainage.
13.4.7 Preve ntion of sepsis:
During pregnancy: Nutrition, IFA prophylaxis,
anemia correction, Diabetes control.
Intranatal and postnatal: Strict aseptic measures,
minimum number of vaginal examinations, early
delivery in PROM cases & antibiotic
prophylaxis.
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 5. MEDICAL DISORDERS COMPLICATING
PREGNANCY
1. Anemia in Pregnancy 1.1. Definition:
Anemia during pregnancy is a major contributory Anemia in pregnant women is haemoglobi n level of
cause for maternal deaths. Nutritional deficiency is less than 11 g/dL.
the commonest cause.
Table-1: Anemia Classification

Degree Hb(gm/dl)
No Anemia 11
Mild 9 -10.9
Moderate 7- 8.9
Severe Less than 7

1.2. Causes of Anemia During Precordial soft systolic murmur.

Pregnancy Signs of cardiac failure, crepitations at the base of

lungs.
i. Nutritional (Iron, folic acid, proteins)-
deficiency anemia commonest cause. 1.5. Investigations
ii. Wor m infestations.
iii. Twin/ multifetal pregnancy. Hb estimation, Haematocrit, Blood counts.
iv. Malaria. Peripheral blood smear (PBS) to know whether
v. Urinary tract infection, tuberculosis. Iron deficiency or B 12/ Folate deficiency.
vi. Blood loss. Haematological indices- MCV, MCH, MCHC.
vii. Acquired hemolytic anemia.
viii. Hemoglobinopathies: Sickle cell disease, To find out the cause of anemia.
Thalassemias. Examination of stool for worms and occult
ix. Rare causes : Aplastic anemia, leukemia. blood.
Urine examination routine, microscopic, culture
if required.
1.3. Symptoms PBS (thick and thin smear) for malarial parasite.
Weakness,Lassitude and fatigue,Anorexia and Sickling test: Solubility test.
indigestion,pa lpitation,dyspnoea,giddi ness and Serum bilirubin: Hemolysis, megaloblastic
swelling of legs. anemia.
Hemoglobin electrophoresis in suspected
1.4. Signs hemoglobinopathy.
Pallor,glossitis and stomatitis, edema, signs of 1.6. Complications
nutritional deficiencies, Koilonychias, platynychia.
Anemia contributes to 20 % of maternal death

Table 2: Complications

Maternal Baby
Increased risk of cardiac failure. Fetal growth retardation. (IUGR)

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 Inability to withstand third stage hemorrhage, can go in
shock with moderate blood loss.
During Puerperium: Risk of puerperal sepsis, Poor
establishment of lactation.
Puerperal venous thrombos is , Pulmonary embol ism.
1.7 Treatment
Treatment depends upon:
Severity of anemia, cause of anemia and gestational
period at which anemia is detected.
1.7.1 Nutritional deficiency ane mia
a) Prophylaxis (Hb =/> 11 G/dl):
Oral IFA tablets (Elemental iron 100mg with Folic
acid 0.5mg/day) one tablet daily for 6 months during
pregnancy and 6 months during lactation.
b) Mild/Moderate anemia: (Hb< 11 G/dl):
Therapeutic double dose: Oral IFA one tablet twice a
day. For better absorption it should be taken before
meals. Check response after 4 weeks. The treatment
should be continued till the Hb becomes normal, then
one tablet daily is to be continued to replenish the
iron stores.
Nutritional guidance is given. Protein is
supplemented.
Tab Albendazole (400mg) single dose after first
trimester.
c) Response of therapy is evidenced by
Sense of well-being, increased appetite within 3-
4 days.
After a lapse of 2 weeks hemoglobin starts rising
at the rate of 1gm % per week.
If no significant improvement is evident
clinically and haematologically after 4 weeks
refer the woman to FRU as diagnostic re-
evaluation is needed.
d) Parenteral iron therapy is indicated if:
Intolerance to oral iron.
Patient not co-operative to take oral iron.
Poor responders to oral iron.
Severely anemic mothers.
Iron sucrose is safe. It helps in replenishing iron
stores faster than oral iron.
Calculated dose: (2.4 W D +500mg for storage
iron) where W= weight in kg (Prepregancy), D =
(target Hb in gm% - actual Hb in gm %), rounded up
to the nearest 100 mg. Total iron is given in divided
doses. Oral iron is to be stopped before 24 hours.
Prematurity
Poor stores of iron at birth, risk of
anemia during infancy.
200 mg iron sucrose in at least 200 ml of normal
saline is given over a period of 30 minutes on
alternate days. Keepi ng emergency dr ugs is a must at
every clinic.
e) Severe anemia:
Patients with Hb level <7gm% or moderately anemic
patients with associated obstetrical or medical
complications should be referred to specialist for
evaluation and management. Hospitalization helps in
complete evaluation for cause of anemia.
Bloo d transfusion is indicated if
Hb< 5 gm/dl any time during pregnancy
Severe anemia seen after 36wks of pregnancy
Refractory anemias
Patients needing operative delivery
Continued bleeding
Packed red cells are transfused slowly and under
supervision, diuretics are given to avoid circulatory
overload.
17.2 Treatment of other causes for
anemia
Should be given as indicated: Antimalarial treatment,
appropriate care for bleeding piles etc.
17.3Management during Labour
a)1st stage:
The patient should be in bed, propped up
position, Oxygen inhalation.
Strict asepsis. Monitor vitals, auscultate lung
bases.
c) 2nd stage:
Avoid exersion and delay: Episiotomy,
prophylactic low forceps or vacuum delivery.
d) 3rd stage:
Active management of 3 stage of labour with
prophylactic oxytocin.
Blood t ransfusion if required
Precaution against post partum overloading of
heart.
d) Puerperium
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 Prophylactic antibiotics
Pre delivery Anemia therapy continued till 3
months after nor malization of Hb.
Baby:
Prone to sepsis in neonatal period.
Special care if low birth weight. Iron suppl ements as
stores are poor.
17.4 Patient education and
counseling
Proteins, Iron and vi tamin rich diet
Correct cooking habits
Precaution against malaria
Spacing between pregnancies
2.2.Effects of GDM on the mother & on the fetus
Table-3: Effects of GDM
Mot her
Pre-eclampsia
Polyhydramnios
Caesarian section more common due to fetal
macrosomia and CPD.
Shoulder dystocia, maternal Injuries due to
macrosomia.
Chorioamnionitis and postpartum endometritis.
Miscarriages in uncontrolled diabetes.
Recurrent UTI, fugal vaginitis, skin infections.
Long term risk of type-2 diabetes mellitus.
The risk of fetal anomalies is high in pregestational
DM. It is not increased in GDM patients. However,
the risks of unexplained still births (during the last 4-
8 weeks of gestation) is similar to pre-gestational
diabetes.
2.3. Screening and diagnosis of
Diabetes in pregnancy
All Indian women should be screened for gestational
Diabetes Mellitus as they belong to a high risk
ethnicity.Screening is initiated between the 24th and
2. Diabetes Mellitus (DM) in
Pregnancy
Due to lifestyle factors and dietary habits, incidence
of type 2 DM is increasing. Gestational Diabetes
Mellitus (GDM) results in higher maternal and
perinatal morbidity and requires meticulous control
and special care. Of all GDM patients, > 50%
develop type 2 DM in later life.
2.1. Two types of cases
Pregestational DM: DM diagnosed before
pregnancy.
Gestational DM: Glucose intolerance detected
for the first time during pregnancy.
Baby
Unexplained s udde n fetal death during third trimester.
Congenital abnormalities.
Macrosomia (big baby > 4 Kg ) , Birth trauma. (due to
shoulder dystocia)
Neonatal hypoglycemia
Hyaline membrane disease. (RDS)
Hypocalcemia, hypomagnesemia.
Prematurity, Jaundice, Apnea and bradycardia.
Polycythemia/hyperviscosity syndrome.
28th weeks of pregnancy or earlier if any of the risk
factors are present.
One step screening and diagnostic test is very
convenient for pregnant women in Indian scenario.
As advised by DIPSI (Diabetes in Pregnancy study
Group India) and WHO 75 gm Glucose load is given
to women attending ANC irrespective of meal status
and blood sugar is estimated after 2 hours.
A value of 140 mg and above is considered
diagnostic of GDM. A value of < 120 mg/dl is
normal. Value between 120 139 mg/dl is
considered as gestational glucose intolerance.
Page 287

2.4. Management of Diabetes in
Pregnancy
The woman should be referred to gynecologist at
district hospital. A team of specialists including
diabetologist, sonologist and neonatologist should
manage the case in consultation.
2.4.1 Medical nutrition therapy:
Calories calculation for 24 hours according to weight
and occupation.
30-35 kcal/ kg body weight and for obese women 25-
30 kcl/kg/day.
Composition of diet It should include carbohydrates
(50-55%), proteins (20-30%) and fats 20-30%) with
saturated fat <10%.
Three major meals and 3 snacksare advised.
2.4.2 Exercise:Walking 3- 4 times weekly for 20-30
min/session.
Blood sugar monitoring should be done after 1-2
weeks of starting diabetic diet.
Recomme nded glycemic goals:Fasting blood
glucose < 90 mg/dl;
2 hour postprandial blood glucose < 120 mg/dl
BSL monitoring 2 weekly from 28 weeks onwards,
weekly from 32 weeks. More frequently as required.
2.4.3 Insulin Therapy:IfMNT fails to achieve
glycemic goals within two weeks of therapy.
Insulin requirements increase as pregnancy advances.
Consult a physician or endoc rinologist for insulin
administration. The starting insulin dos e can be
calculated on the basis of the patient's weight. For
non obese patients usual doses are 0.8 U/kg and for
obese 0.9-1.0 U/kg. Calculate total dose. Give 2/3 in
morning and 1/3 in evening. Adjust dose with blood
sugar levels.
2.4.4 Obstetrical Management:
Antepartum foetal monitoring: Nonstress test and
Amniotic fluid index are performed periodically
during third trimester to prevent IUD and plan
delivery. Umbilical artery doppler studies help in
timing the delivery. More frequent monitoring is
done if there is history of stillbirth, hypertension, and
uncontrolled blood sugars.
For well controlled uncomplicated cases can waitupto
40 weeks. Do not allow to cross EDD in any case.
Elective induction is done at 38 completed weeks or
earlier if indicated by fetal monitoring tests.
Caesarean section: Large baby and other obstetric
indications.
2.5. Care of Pregestational diabetes
mellitus
2.5.1 Before pregnancy:To reduce the risk of fetal
malformations and fetal macrosomia, counsel for
planning pregnancy when glycated hemoglobi n levels
are normal. Advise pre conceptional Folic acid.
2.5.2 During pregnancy: Special investigations for
detecting fetal malformations, as
practicableBiochemical screening (10 weeks) PAPP
A, -hCG, USG (11-12 weeks) for nuchal
translucency.
Triple screen (16-18 weeks), level II scan (18-22
weeks) foetal echocardiography (20-22 weeks)
2.5.3 Third trimester: Assess fetal growth and
liquor volume by USG. NST and umbilical artery
doppler studies to decide time and mode of delivery.
2.5.4 Delivery:For uncomplicated pregnancy with
well controlled diabetes one can wait until 40 weeks.
However, in view of adverse perinatal outcomes
associated with poor control, induction of labour at
38 -39 weeks is a safe practice unless indicated
earlier.
Elective LSCS if foetal weight 4 kg.
a) Management during Labo ur:
Regular glucose monitoring Urine testing for
sugar and ketones.
Regular insulin: Low-dose infusion depending
upon blood sugar levels.
Prophylactic antibiotics.
Baby needs monitoring and special care.
2.5.5 Postpartum management:
After delivery insulin requirement decreases hence
dose needs to be adjusted. Fasting and postprandial
blood sugar should be checked before discharge.
Patients who are diagnosed to have GDM during
pregnancy are subjected to oral glucose tolerance test
with 75g glucose at 6 -12 weeks.
2.5.6 Contraception:
Condoms. Intrauterine device safe
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3. Pregnancy with Cardiac
Disease
Cardiac disease complicates around 1% of
pregnancies. The disease worsens during pregnancy,
delivery and postpartum period. It is one of the
important indirect cause of maternal mortality.
Rheumatic valvular disease (Mitral stenosis,
regurgitation) is common for m in India. Currently
congenital heart disease cases are being diagnosed
early and surgically corrected. Such women are also
presenting during pregnancy.

3.1. Risks
Table-4: Maternal and foetal Risks in Cardiac Disease

Maternal Fetal/Neonatal
Cardiac failure, Acute pulmonary ede ma Prematurity

Subacute bacterial endocarditis IUGR leading to LBW

Thromboembolic complications

Atrial fibrillation & other arrhythmias

Twins, polyhydramnios
3.2. Risk of failure Tachycardia due to any cause: Physical exertion,
emotional upset
The cardiac patient faces greater risk of cardiac
failure at each of the time points when there is 3.3.Diagnosis
significant rise in cardiac output.(at around 12-16
weeks, 28-32 weeks, during labour with each Normal pregnancy is associated with fatigue,
successive stage of labour, soon after delivery and dyspnea, decreased exercise capacity, peripheral
first 24 hours after delivery). edema, and jugular venous distention. Most pregnant
women have audible physiologic systolic murmurs
Obstetric and medical complications increase the risk
and a physiologic third heart sound (S3).This makes
of cardiac failure.
diagnosis of heart disease during pregnancy di fficult.
Infection: Urinary, respiratory, dental.
Anemia, hypertension, preeclampsia,
hyperthyroidism.
Table-5: New York Heart Association (NYHA) Functional Classification

NYHA Class Symptoms

I No symptoms on ordinary physical activity such as walking or climbing stairs.

II Mild symptoms and slight limitation during ordinary activity.

III Marked limitation in activity due to symptoms, even during less-than-ordinary

activity such as walking short distances (20-100 m). Comfortable only at rest.

IV Severe limitations. Experiences symptoms even while at rest.

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3.4. Symptoms Around 28-32 weeks depending on social
circumstances.
In grade 1 and 2 the woman may not have any 3.7.4 Care during labour:Await spontaneous
symptoms. LABOUR. Induction only for obs tetric indications
Grade 3: Breathlessness on accustomed exertion,
fatigue, syncope, chest pain. a) First stage:
Grade 4: Breathlessness even at rest, nocturnal Rest in propped up position; Avoid fluid
cough, hemoptysis. overload.
Prophylactic antibiotics depending upon risk of
3.5. Signs complications: Ampicillin, Gentamicin.
Pain relief.
Cardiac murmurs: Systolic grade 3 or more , any
diastolic murmur. Monitor pulse, respiratory rate, BP, temperature,
lung bases.
Abnormal heart sounds , Arrhythmias.
Monitor oxygen saturation; Oxygen as required.
Signs of cardiac failure : Progressive dyspnoea,
Neck veins engorged, Palpable tender liver, HJR Keep cardiac drug tray ready.
positive. Monitor Labo ur progress, fetal condition.
Pitting oedema over feet. b) Second stage:
Crepitations at the lung bases.
Do not allow the woman to have strenuous
3.6. Investigations bearing down effort.
Cut short the 2nd stage by prophylactic
ECG, 2D Echo cardiography vacuum/forceps delivery.
3.7. Management: c) Third stage:

3.7.1 Before conception-Women with preexisting Do not give Inj Methyl ergometrine. Provide
cardiac lesions should receive preconception physiologic management.
counseling regarding maternal and fetal risks during Give Inj Oxytocin IM 10 IU if there is excessive
pregnancy and long-term maternal morbidity and bleeding.
mortality. Women with NYHA class III and IV face a
high mortality and morbidity. These women should d) During Postpartum period:
be strongly cautioned against pregnancy. Monitor vitals. Watch for signs of failure.
3.7.2Care during pregnancy: Encourage ambulation to preve nt
thromboembolism.
Every pregnant woman should be completely Watch for signs of puerperal sepsis and give
examined between 4-6th month by the medical antibiotics.
officer. Chest auscultation is a must during this
examination. Suspected cases must be referred to Breast feeding is advisable.
physician. 3.7.5 Contraception:
Complete evaluation by physician/ cardiologist.
Risk determination, counseling Combined oral contraceptive pills are
Watch for signs of cardiac failure. contraindicated.
Care of teeth, treatment of urinary tract infection. Condom is safe.
Prevention or early correction of anemia.
After completing family tubal ligation can be
Monitoring blood pressure. performed at district hospital or in tertiary care
Early detection and prompt treatment of centre. Male partner may be encouraged to
pregnancy complications. undergo vasectomy.
3.7.3 Hospitalization: MTP ( if requested) can be performed at district
Grade 3 & 4 dyspnoea kept in hospital hospital after stabilizing cardiac condition.
throughout pregnancy.
Women with obstetric or medical complications.

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4. Peripartum cardiomyopathy
This is an idiopathic dilated cardiomyopathy that
develops in the last month of pregnancy or within 5
months of delivery and is characterized by left
ventricular systolic dysfunction with ejection fraction
(LVEF) <45%.
4.1 Risk factors:
Advanced maternal age, multiparity, multiple
gestation, obe sity, malnutrition, gestational
hypertension, preeclampsia, cesarean section, family
history, abuse of tobacco, alcohol, or cocaine.
The mortality rate is 25% to 50%, half of those die
within the first month of presentation and the
majority die within three months postpartum. Death
results from progressive cardiac failure,
thromboembolic events, and arrhythmias. Of the
patients who survive, approximately 50% recover
normal left heart function. Prognosis is related to left
ventricular dysfunction at presentation.
4.2Management
Medical management includes fluid and salt
restriction, Digoxin, Diuretics, Vasodilators, and
Anticoagulants. These women need to be in a tertiary
care centre having cardiac ICU facility under care of
cardiologist.
5. Women receiving
anticoagulation for
surgically corrected heart
disease and Pregnancy
Women with prosthetic valves are receiving warfarin,
a vitamin K antagonist orally for anticoagulation.
Warfarin freely crosses the placenta and causes
adverse fetal effects. The risk of warfarin
embr yopa thy is highest when warfarin is
administered during 6 to 12 weeks gestation.
Heparine does not cross the placenta and is safe for
the fetus.
Anticoag ulat ion: Warfarin must be discontinued
and heparin should be administered during this
period. After 12 weeks heparin is stopped and
warfarin is restarted and continued until 36
weeks. After 36 weeks again LMWH or
unfractionated heparin is started which is
stopped 4-6 hours before delivery and restarted 6
hours after delivery if there are no bleeding
complications (24 hours after caesarean section).
There is risk of profuse bleeding hence delivery
should always take place in tertiary care
institution. Protamin sulfate is antidote.
These cases need regular Laboratory monitoring
to adjust the dose of medications. Also they
might need fresh frozen plasma for bleeding
hence they should be under care of specialists at
the tertiary care centre during pregnancy and
delivery.
Breast feeding is allowed.
Combined oral contraceptives are
contraindicated.
6. Malaria during Pregnancy
Malaria during pregnancy is more common, more
atypical, can be more serious and can be fatal.
6.1. Effects on Pregnancy Outcome
The chances of spontaneous abortion, preterm
birth, fetal growth retardation,foetal distress and
still birth are increased.
Rarely transplacental spread to the foetus
resulting in congenital malaria.
6.2. Complications
Profound Anemia may develop rapidly as there is a
reduction in haemoglobi n. Anemia can have serious
consequences during Labo ur. In the last two decades
in India, an increasing proportion of P. falciparum
infections is proving to be resistant to Chloroquine.
6.3. Clinical presentation
Fever, Spleenomegaly
Anemia may be the presenting feature of
malaria, therefore all cases of anemia should be
tested for M.P.
Fetal growth retardation.
6.4. Diagnosis
Microscopy of stained thick & thin smear is the
gold standard.
Rapid diagnostic tests. All fevers particularly in
malaria endemic areas should be tested for
malaria.
In endemic areas the pregnant woman should be
routinely tested for malaria at all antenatal visits
by RDT even if she does not manifest any
symptoms of malaria.
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 Table-6: Treatment of Uncomplicated Malaria during Pregnancy

Day 1 Day 2 Day3

P. Vivax CQ 250 mg CQ 250 mg CQ 250 mg

(150 mg base) 4 tablets 4 tablets 2 tablets

P. Falciparum

First trimester Quinine Quinine Quinine 10mg/kg 3

times daily Continue
10mg/kg 3 times daily for 7 days. 10mg/kg 3 times
upto 7 days.
daily.

2nd, 3rd AS 200 mg 1 tablet SP 2 tablets ( 750 + AS 200 mg 1 tablet AS 200 mg 1 tablet
trimester 37.5mg each)

P. Vivax + P. AS 4 tablets of 50 mg 3 SP tablets AS 4 tablets of 50 AS 4 tablets of 50 mg

Falciparum mg
(500mg + 25 mg each)
(Mixe d)

CQ: Chloroquine 250 mg tablet containing 150 mg

base; 25 mg/kg body weight divided over three days
i.e.10 mg/kg on day 1, 10 mg/kg on day 2 and 5
mg/kg on da y 3.

AS: ArtesunateSP:Sulfadoxine+ Pyrimethamine 6.5.3 Mixe d infections(P .vivax + P.

6.5. Treatment
6.5.1 Vivax Malaria:Chloroquine for 3 Use of personal protection measures includi ng
days.Primaquine is contraindicated in pregnant
women. To prevent the relapse, suppressive
chemoprophylaxis with Chloroquine 300mg base,
once a week until delivery.
6.5.2 P.falciparum Malaria:As pregnant women
having falciparum malaria are more prone to develop
complications, they should be referred to nearest
FRU immediately.
Treatment during first trimester: Quinine. It may
induce hypoglycemia; do not give quinine on
empty stomach and tell the woman to eat
regularly, while on quinine treatment.
ACT is not to be given in first trimester of
pregnancy
During 2nd & 3rd trimester: ACT-SP
falciparum)treated as falciparum malaria
6.6 Prevention:
insecticide treated bed nets (ITN) / Long lasting
insecticidal nets (LLIN) should be encouraged.
7. HIV Infected Pregnant
Woman
Every pregnant woman during her first visit should
be counseled for voluntary HIV testing at an ICTC to
know her HIV status.
7.1. Care of HIV positive pregnant
woman during pregnancy
7.1.1 Points to be noted in history:
High risk be havior in her and her spouse

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Pregnancy duration, number of previous pregnancies,
live children, receipt of any antiretroviral medicines
earlier.
If pregnancy is unwanted and is < 20 weeks refer her
to MTP centre.
7.3
If she wishes to continue current pregnancy, refer her
to PPTCT centre soon after confirmation of
pregnancy to start the antiretroviral medicines for
reducing the risk of vertical transmission. ART centre
will be initiating HIV medicines from 14 weeks and
will be doing CD4 testing and other evaluations.
Screen for TB and STI at every visit.
7.1.2 Specific education & counseling
regarding:
7.4
Nutritious diet, consumption of micronutrient
suppl ements.
Safe sex practices for preventing new STIs and
other strains of HIV which could harm the baby.
Adherence to HIV medicines.
Follow up at ART & PPTCT centers as
instructed.
Institutional delivery.
Safe infant feeding practices, infant care.
7.2 Care during delivery
Insist on institutional delivery at a PPTCT centre as
she requires ARV medicines during labour which
need to be continued postpartum. If she is in
advanced labour, conduct her delivery by following
principles:
Do not rupture membranes.
Follow universal safety precautions during
conduct of delivery.
Avoid: Episiotomy, perinealInjuries, vacuum
delivery.
Table-7:Dosage Schedule and Associated Side Effects of ARV Medicines
Give ARV medicines as per protocol.
Immediate clamping of umbilical cord.
Clean the baby of the maternal blood and body
fluids before handing over to the relatives.
Care of mother after delivery
Refer to PPTCT centre for care of mother and
baby.
Watch for signs of sepsis.
Nutritious diet, nutrient supplements.
Encourage to use reliable contraception; safe sex
practices.
Treatment at PPTCT/ART
centre
The new protocol consists of triple ART to
pregnant woman and extended nevirapine
therapy for the exposed infant.
Baseline investigations: Hb, urine, VDRL,
screening for hepatitis B and C, ALT, CD4,
urea/creatinine, blood sugar, lipid profile.
Triple antiretroviral therapy (ART) initiated
irrespective of CD4 count and continued
lifelong.
If CD4 is < 250 Cotrimoxazole (CPT) 1 ds tab
daily.
ART drugs at ART centre: Given in table below.
If there is no prior exposure to EFV/NVP, triple
ARV regime consisting of Tenofovir,
Lamivudine and Efavirenze is started from 14
weeks onwards to be continued throughout
pregnancy and Labo ur.
If there is H/O prior exposure to NVP/EFV then
EFV is not given and a protease inhibitor is
given (Lopinavir/Ritonavir).

Name of ARV Dose Major Side Effects

Tenofovir (TDF) 300 mg OD Nephrotoxicity, hypop hosphatemia
Lamivudi ne (3 TC) 300mg OD Very few
Hypersensitivity, rarely pancreatitis
Efavirenz (EFV) 600 mg OD Neuropsychiatric symptoms (hallucinations, suicidal
ideation, nightmare
*Lopinavir/Ritonavir 400/100 mg BD GI disturbance, glucose intolerance, lipo-dystrophy &
(LPV/r) hyperlipidemia
* For prior exposure to EFV or NVP; LPV/r FDC tablet of LPV 200 mg/r 50 mg: 2 tablets BD

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Laboratory tests:
After 2 weeks of initiating ARV Hb, ALT.
At 4 ,8,12 weeksHb testing.
Every 6 months BUN, S Creat, ALT, CD4,
Urine analysis (imp in TDF based regimes).
If on PI based treatment: BSL & Lipid profile
every 6 months.
7.5 Care of HIV exposed infant:
7.5.1 Infant is give n Nevirapine (NVP) syrup
for 6 weeks.
7.5.2 Appropriate infant feeding is initiated
asper informe d choice (following AFASS
counseling): Upto 6 months: Exclusive
breast feeding. No mixed feeding.
7.5.3 At 6 weeks :
Start cotrimoxazole (CPT) prophylaxis,
Early infant diagnosis (EID) by dry blood spot
test (DBS); if DBS +ve Whole blood spot (WBS)
confirmatory testing.
EID +ve babies are started on ART irrespective
of CD4
7.5.4 After 6 months, if breast feeding option has
been chosen, breast feeding is continued as
per EID stat us:
EID ve babies: Continue BF upto 1 year +
Complementory feeding; No abrupt stopping
of breast feeding
EID +ve baby on ART: Breast feeding
continued upto 2 years
7.5.5 Growth & nutrition monitoring,
immunization as per schedule.
7.5.6 Repeat HIV testing at 6, 12 months and 6
weeks after stoppage of breast feeding; (If
rapid test + ve DBS followed by WBS).
At 18 months: Confirmation of HIV status
by 3 rapid antibody tests.
7.5.7 Counseling: Counsel for adherence to ARV
and AKT if co-infected with tuberculosis.
Encourage safe infant feeding practices.
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 6. COMPREHENSIVE ABORTION CARE:
MEDICAL TERMINATION OF PREGNANCY
Unsafe abortion still accounts for nearly 9 %
maternal deaths. Provision of easily accessible, free
safe abortion service can reduce the burden of
maternal morbidity and mortality.
6.1. Legal limit
Is 20 weeks of pregnancy. A trained medical officer
at Primary Health Center is authorized to perform
MTPs up to 12 weeks.
6.2. Indications
Pregnancy likely to enda nger womans life or
likely to cause grave Injury to her physical or
mental health.
Child is likely to suffer from serious physical or
mental disability.
Pregnancy caused by rape.
Pregnancy following contraceptive failure.
6.3. Consent for MTP:
An adult woman who is not mentally ill can undergo
MTP with only her ow n consent. Consent of legal
guardian is required for minors and mentally ill
women.
6.4. Record and register
Consent in for m C of the MTP Act.
Certify MTP within 3 hours on for m I specifying
the indication.
Admission register (Form III). This register is a
secret document.
6.5. Clinical evaluation:
Medical history, date of LMP, complete physical
examination. Determine size of uterus on va ginal
examination.
6.6. Investigations:
Hemoglobin, blood group, Rh typing, urine testing
for sugar and protein.
Ultrasonography is not manda tor y. It may be helpful
for knowing the pregnancy duration in women having
irregular cycles, lactationalamenorrhoea, when on
examination the uterine size is uncertain or discrepant
with the period of amenorrhoea and to exclude an
ectopic gestation.
6.6 Methods for first trimester
MTP
6.6.1 Surgical methods:
Manual vacuum aspiration (MVA) is the safe
recommended technique for pregnancy up to 12
weeks.
Electrical vacuum aspiration is also safe and
effective.
D&C should not be used as a method for MTP.
Give antibiotics prophylaxis: Cap. Doxycycline
100 mg orally twice a day for seven days may be
given.
Follow adequate infection control practices.
a) Before MVA:
Check the eligibility and consent
Give pain relief
Start prophylactic antibiotics
If uterus is > 9 weeks size, cervical softening can
be achieved by administering 400 mcg (2 tablets)
of misoprostol orally/vaginally 3-4 hours before
MVA.
Keep the charged syringe ready, perfor m the
MVA procedure.
b) Complications:
Incomplete abortion, hemorrhage, infection,
Uterine perforation
Anesthesia related complications.
Failed termination with continuation of
pregnancy. Woman should be counseled to
report if she continues to be amenorrhoic after
MTP. Repeat termination of pregnancy can be
undertaken.
6.6.2 Mifepristone-misoprostol abortion
(MMA):
In India, MMA is permitted up to 49 days. However
by using combi pack it can be performed up to 63
days by protocols given below:
a) Information to Women:
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MMA is safe and effective. Efficacy up to 95%
Three visits are necessary, day 1 Mifepristone,
day 3 Misoprostol tablets and day 14 for post
treatment evaluation
Table-1:Protocols for Mifepristone-Misoprostol Abortion
Mifepristone
Day 1
Gest Age Dose Route
Upto 49 days 200 mg (1 tab) oral
49-63 days* 200 mg (1 tab) Oral
* The Central Drugs Standard Control Organization,
Director general of health services, Govt of India has
approved a combi pack of one 200 mg tablet of
mifepristone and four 200 mcg tablets of misoprostol
for MTP for gestation between 49-63 days.
WHO recommends MMA upto 63 days
In the event that vomiting ensues within 30 minutes of
oral misoprostol the medication should be repeated.
There is no need to keep a woman in the facility till
she aborts.
Misoprostol given by vaginal route has lesser side
effects, is absorbed slowly and is effective for a
longer time whereas by oral route it is absorbed
quickly, is effective for a shorter time and leads to
more gastrointestinal side effects.
c) Contraindications:
Ectopic pregnancy, either confirmed
suspected, or undiagnosed adnexal mass
Hemorrhagic disorder.
Allergy to mifepristone, misoprostol
another prostaglandi n.
Current anticoa gulant therapy, Current use of
long-term systemic corticosteroids.
Intrauterine device in place (remove before
giving Mifepristone).
Chronic adrenal failure. Inherited porphyria.
Caution: Haemoglobin<8 gm %.
If treatment fails, surgical termination is
necessary; pregnancy cannot be continued, as
there is risk of fetal malformation.
Vaginal bleeding and uterine cramping may
occur for 7-14 days.
b) Protocol
Misoprostol
Day 3
Dose Route
400 mcg (200 mcg, 2 tablets) Oral/vaginal
800 mcg (200 mcg, 4 tablets) Vaginal
Uncontrolled hypertension, BP > 160/100
Uncontrolled seizure disorder.
d) Contraception after MMA:
OC pills or Inj DMPA can be started on day 3 or day
15 when abortion process appears to be complete.
IUCD insertion after one normal menstrual period.
Tubal ligation after next cycle.
e) Counseling:
Early abortion is safer. MTPs should not be
performed repeatedly. Using contraception is
important. Concomitant female sterilization or IUCD
insertion at the time of surgical abortion is safe.
Inform the woman to report early for symptoms
suggestive of complications.
6.7 Methods for Second Trimester
or
MTPs
6.7.1
or a) Mifepristone Misoprostol:
These drugs are recommended by WHO for second
trimester MTPs. Combination improves the efficacy.
The suggested protocol is 200 mg mifepristone
followed after 36 48 hours by 400 micrograms of
vaginal, sublingual or oral, misoprostol every 3 6
hours up to 5 doses. Before 18 weeks 3-4 hourly
interval is preferred. At or after 18 weeks consider 6
hourly dosing interval.
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Vaginal misoprostol is more effective than oral
Cautious use in cases having scarred uterusCheck and
record vital signs 4 hourly until onset of strong
contractions, thereafter 2 hourly.
b) Use of Misoprostol alone
Is less effective as compared to combination
400 mcg 3-6 hourly upto 5 doses.
If fetal expulsion does not occur after 24 hours from
initial dose perform abdominal examination and USG
to rule out uterine rupture.
c) Extraamniotic Instillation of Ethacridine Lactate,
0.1 %, 150 ml
Safe method, however the drug is not currently
available.
d) Abdo minal Hysterotomy:
Major surgery done only in selected cases. Eg.
Cancer cervixSecond trimesters MTP procedures
require hospitalization for few days. They are likely
to be associated with more bleeding, more chances of
incomplete abortion and other complications.
Provi der needs to make sure that the woman is not
seeking a sex selective abortion.
Additional legal requirements: MTP centre approved
for 2nd trimester MTP, experienced RMP as stated in
MTP Act, and the requirement of opi nions of two
registered medical practitioners are necessary.
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 7. COMMON GYNECOLOGICAL PROBLEMS
1.2.2 Congestive Dysmenorrhoea:
1. Dysmenorrhoea
a) Common causes: Chronic pelvic inflammatory
2. Abnormal Uterine Bleeding: disease (PID), endometriosis, Genital tuberculosis,
pelvic adhesions.
a. Menorrhagia
b) Symptoms: Chronic pelvic pain. Pain is
b. DUB experienced few days before period and is usually
relieved with the onset of menstrual bleeding. It is
3. Post-Menopausal Bleeding continuous dull aching pain in lower abdomen and
low backache. Often associated with dysparunia,
a. Endometrial Cancer vaginal discharge, menorrhagia and i nfertility.

b. Cervical Cancer c) Signs of chronic PID:

P/A: Tenderness in lower abdomen

4. Infertility
P/S: Discharge from cervical canal in STIs
5. Pelvic Organ Prolaps
P/V: Retroverted fixed uterus, cervical movements
painful.
1. Dysmenorrhoea
1.1 Definition: Tenderness in fornices and tender adnexal mass
Nodularity in posterior fornix in endometriosis.
Dysmenorrhoea is painful menstruation.
d) Investigations:
1.2 Types:
Ultrasonography to detect pelvic pathology
Spasmodic (Primary) and Congestive (Secondary). (adnexal mass, ovarian cyst).
Diagnostic laparoscopy helps in diagnosis of
1.2.1 Spasmodic Dysmenorrhoea genital TB, endometriosis, adhesions.

a) Symptoms:Colicky pain in lower abdomen starts e) Treatment:

on first da y of menstruation and usually lasts for a
day. Nausea, vomiting may occur. Assurance and treatment of cause.
b) Treatment: NSAIDs for pain relief: Mefenamic acid,
Ibuprofen.
Usually reassurance is adequate. Antibiotics for treatment of PID.
Majority get relief with antispasmodics Progestins for endometriosis.
(Dicyclomin) or antiprostaglandi ns Specialist referral for treatment of
likeMefenimic acid 500 mg tds as needed. endometriosis, genital TB.
If no response: Combined oral contraceptive pills Laparoscopy for diagnosis of cause for chronic
for 3 cycles. pelvic pain and treatment of adhesions,
Rarely pain may be very severe not responding endometriosis.
to medicines and may need further evaluation
and management by specialist.

c) Investigations: If pain is persistent, USG to rule

2. Abnormal Uterine Bleeding
out endometriosis and uterine anomalies. Abnormal uterine bleeding (AUB) accounts for 20%
of all gynecologic visits.

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2.1 . Definitions
Menorrhagia:Excessive uterine bleeding
occurring at regular intervals or prolonged
uterine bleeding lasting > 7 days.
Dysfunctional uterine bleeding (DUB):
Abnor mal uterine bleeding occurring in the
absence of identifiable pathology. It can be
ovulatory or anovulatory DUB.
Metrorrhagia: Acyclical menstrual bleeding
occurring at irregular intervals.
Breakthrough bleeding: Unpredictable
bleeding that occurs while on exogenous
hor mones (eg hor monal contraception).
Oligo menorrhea: A menstrual cycle interval of
more than 35 days.
Polymenorrhea: A menstrual cycle interval of
less than 21 da ys.
Postmenopausal bleeding: Vaginal bleeding
occurring more than 12 months after the last
menstrual period.
Amenorrhea: Absence of menstrual bleeding.
2.2. Differential diagnosis of AUB
Abnormal uterine bleeding can occur in all age
groups. The diagnostic testing and treatment
approach should take into consideration the age
group a nd fertility choices of the woman.
Adolescent girls: Anovular DUB is common.
Pregnancy related conditions should be kept in
mind. Bleeding disorders can be present in some
cases.
Women between 20-40 years: Pregnancy related
conditions, ovular DUB, pelvic infection and
benign neoplasia like fibroids are common.
Perimenopa usal AUB is commonly due to
anovulation and fibroids. However it is necessary
to exclude polyps, endometrial hyperplasia and
malignancies.
Postmenopa usal bleeding: Malignancy needs to
be excluded.
2.3. History
Detailed menstrual history, sexual histor y, past
medical history, gynecologic and obstetric
histor y. Note any change in the patient's weight,
and exercise pattern.
History of bleeding disorders, possible
pregnancy.
H/O Drugs, IUCD.
Antipsychotic medications (Dopamine
antagonists), Phenothiazines and antidepressants
can cause hyperprolactinemia and AUB.
Combination OC pills can cause breakthrough
bleeding.
Prolonged use of high doses of progestational
agents.
Anticoagulant medications.
Digitalis, Phenytoin, and Corticosteroids.
Copper- intrauterine devices.
2.4. Physical Exam
Note pallor, thyroid examination.
Breast examination: Galactorrhoea.
P/A examination: Pelvic mass (fibroids),
tenderness in lower abdomen. (PID)
Speculum examination: Cervical pathology.
(growth, ulcer, polyp)
P/V: Cervical motion tenderness, size and
contour of uterus, and presence of any palpable
adnexal masses or tenderness.
2.5. Investigations
Complete blood count
Ultrasonography abdomen and pelvis and
transva ginal ultrasonography (TVUS) for
diagnosing fibroids, polyps, adnexal mass.
Thickness of endometrium can be measured.
Intrauterine pregnancy and ectopi c pregnancy
can be excluded.
Endometrial biopsy in women over age 35 and
women having risk factors for endometrial
cancer. It helps in diagnosing ovular or anovular
bleeding, endometrial hyperplasia, endometrial
precancerous lesions and endometrial carcinoma.
Endometrial sampling is a rapid, safe, and cost-
effective procedure that can be performed in the
office to evaluate AUB. A potential drawback is
that the biopsy does not sample the entire
endometrium and a localized lesion may be
missed.
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 Dilation and Curettage (D&C) can be both
diagnostic and therapeutic.
Hysteroscopy is the gold standard for evaluating
the endometrial cavity. It provides direct
visualization of the endometrial cavity and can
be performed in the office setting or operating
room. It can be both diagnostic and therapeutic,
allowing for directed biopsies and excision of
polyps and small sub mucus myomas.
Saline infusion sonohysterography for detecting
endometrial polyps or uterine leiomyoma.
Thyroid stimulating hor mone (TSH) and
Prolactin estimation: Hypothyroidism and
hyperprolactinemia can lead to anovulation and
DUB.
Bleeding disorders should be evaluated if
historical or clinical features suggest specific
conditions.
2.6. Dysfunctional Uterine Bleeding
Dysfunctional uterine bleeding (DUB) is a
diagnosis by exclusion of other causes of AUB
without a demonstrable pathologic cause. The
predominant causes of DUB are anovulation or
oligo ovulation.
Long-term anovulation, polycystic ovary
syndrome: Resulting unopposed estrogen state
increases the risk of endometrial hyperplasia.
Morbid obesity with associated elevated estrogen
levels. Can also cause DUB.
In some cases DUB may be associated with
ovulator y cycles.
2.6.1 Medical therapy: Treatment of Anemia should
be initiated. Women who are severely anemic or not
responding to medical treatment should be referred to
specialist.
a) Nonsteroidal anti-inflammator y dr ugs (NSAIDs)
may reduce menstrual blood loss by about 30% in
women with menorrhagia and can be given as the
first line therapy. They need to be taken during
menses only. The options are:
Mefenamic acid 500 mg three times a day for 5
days during menstruation.
Ibuprofen 600-1200 mg /day.
Naproxen sodium 500 mg 1, then 250 mg
every 6-8 hourly.
b) Hormones:
Oral Progestins: Useful in anovulatory bleeding.
For acute heavy bleeding: Medroxy progesterone
acetate 10 mg tablet 2-3 times a day till bleeding
stops. It is tapered and continued 1 tab daily for a
total duration of 21 days. Withdrawal bleeding
starts in few days. Further cyclical therapy (10
mg daily) is given from day 5 to 25th day for 2
more cycles. Response is awaited.
Norethisterone tablet 5 mg can be used similarly
for a period of 21 days, initially 1 tab 3 times a
day until bleeding stops, then 1 tab twice a day
for few days and then tapered to 1 tab daily
thereafter. Side effects of progestins include
breast tenderness, weight gain, and headaches.
Combined oral contraceptive pills can be given
from day 5 to 25 for 3-6 cycles in women
between 20-40 years of age not having
contraindications for estrogens and who also
wish to have contraception.
c) Antifibrinolytic medications(e.g. Tranexamic acid)
decrease menstrual blood flow by 50%, and need to
be taken during menses only. However, there are
concerns about their pro-thrombotic potential.
2.6.2 Surgical Treat ment for DUB:
Diagnostic D&C may have some therapeautic
effect. However it does not have a sustained
therapeutic effect.
Endometrial ablation: Endometrial ablation is not
recommended in women who desire future
fertility.
Hysterectomy provides definitive treatment for
menorrhagia and may be a reasonable option in
women with severe menorrhagia, who have
completed their childbearing and are refractory
to medical and less invasive surgical therapy.
The women not responding to medical line of
treatment should be referred to specialist at
FRU/DH for surgical treatment.
2.7 Menorrhagia
2.7.1 Causes of Menorrhagia
1. General medical causes associated with
me norrhagia: Hypertension, cardiac failure, hepatic
dysfunction can be associated with AUB.
2. Genital Infection: Chronic PID and genital
tuberculosis.
3. Endometrial Pathology & Genital Neoplasia:
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a. Endometrial Polyps can present as menorrhagia
ormetrorrhagia. Diagnosis is by saline infusion
sonogram and hysteroscopy. Endometrial polyps can
be removed by operative hysteroscopy.
Cervical polyps can be removed by grasping with
forceps, twisting them off, and cauterizing the base.
b. Endometrial Hyperplasia: A precursor to
endometrial carcinoma. It is classified into simple or
complex, based on architectural features, and typical
or atypical, based on cytologic features. Endometrial
hyperplasia tends to occur during periods of long-
term unopposed estrogen exposure, either secondary
to anovulatory cycles or exogenous use. AUB is the
most common presenting symptom.
Diagnosis by endometrial biopsy
Treatment depends upon age, desire for future
fertility and presence of atypia in the pathology
specimen.
Simple hyperplasia can be treated with
progestogens.
Cyclic Medroxyprogesterone Acetate (MPA 10
mg/day for 12 to 14 days/cycle for 3 to 6
months) in young anovulator y women to i nduce
monthly withdrawal bleeding.
Local Progesterone administration:
Levonorgestrel-releasing intrauterine system.
(Mirena)
Atypical endometrial hyperplasia is more likely
to progress to carcinoma or may coexist with
endometrial carcinoma. Hence hysterectomy is
advised.
c) Uterine Fibroids: Menorrhagia is the most
common presenting symptom. Diagnosis is by
Table-1: Differential diag nosis of postmenopausal vag inal bleeding.
Endometrial causes
Endometrial Hyperplasia
Endometrial carcinoma
DUB
Endometrial polyp
Senile endometritis
TB endometritis
Cervical causes :
Cancer cervix, Polyp,
Decubitus ulcer on prolapse
Cervicitis
USG. Symptomatic fibroids need surgical
treatment by a specialist.
d) Endometrial Cancer: It is mostly seen in
postmenopausal women and is rare in patients
younger than 40. Postmenopausal bleeding is the
presenting symptom which should be assumed to
represent endometrial cancer until proven
otherwise. The women should be referred to
specialist for further evaluation and treatment.
e) Cervical Cancer: Bleeding patterns associated
with cervical carcinoma are intermenstrual and
postcoital bleeding. Cervical biopsy is
diagnostic. The woman should be referred early
to district hospital or a cancer treatment centre.
f) Ovarian Cancer: Estrogen-producing ovarian
tumors, can produce endometrial hyperplasia and
AUB. USG will reveal the tumor. The woman
should be referred to district hospital or a cancer
treatment centre for surgical treatment.
3. Postmenopausal Bleeding
3.1 Definition:
Vaginal bleeding occurring one year after cessation
of menses.
Uterine bleeding is often due to endometrial cancer,
polyps or endometrial hyperplasia. Genital tract
malignancy and precancerous.conditions need to be
excluded in these cases. Hence immediate referral to
gynecologist is necessary for further evaluation and
treatment.
3.2 Differential diagnosis:
Ovarian causes
Benign tumors of ovary
Malignant tumors of ovary
Hormone secreting tumors of Ovary
(Granulosa- theca cell tumor)
Exogenous Estrogens
HRT for menopa usal symptoms can cause
irregular bleeding
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 Vulvo-Vag inal causes:
Senile atrophic vaginitis
Foreign bod y in va gina like pessary
Malignant lesions on vulva
3.2.1 Endometrial Cancer
a) Risk Factors for Endometrial Cancer:
Conditions associated with excessive estrogens
unopposed by cyclical progesterone are
commonly responsible for postmenopausal
bleeding. Estrogens could have been produced in
the bod y (endogenous) or given in medicinal
for m ( exogenous)
Age at menopa use > 52 years
Nulliparity, infertility.
Obesity, hypertension, diabetes mellitus
Family history of uterine, breast, colorectal
cancer
Drugs: Estrogen therapy, Tamoxifen
b) Management:
At PHC:
History:
Ask symptoms: Irregular bleeding, spotting,
brown discharge, post-coital bleeding, number of
bleeding episodes
Age of woman, late menopause (> 52 years),
nulliparity,
H/O receiving hor mones
(estrogen/progestogen), dr ugs (tamoxifen)
Family history of endometrial cancer
Diabetes mellitus, hypertension
Examination:
Look for obesity, hypertension
Examination of vulva for any lesion, ulcers,
growth, atrophy, polyp.
P/S examination of va gina and cervix to look for
any growth, polyp, ulcer, estrogenization,
infection. If cervical pathology is seen refer to
gynecologist for cervical biopsy, polypectomy as
necessary
Vaginal examination: Look for uterine
enlargement, Suspect pyometra if soft uniformly
enlarged tender uterus with intermittent offensive
Non ge nital causes:
Hypertension
Bleeding diathesis
Urethral and rectal bleeding can sometimes
be misreported as vaginal bleeding
vaginal discharge. Suspect uterine myoma or
malignancy if firm irregularly enlarged uterus
Refer the woman to the gynecologist for further
evaluation.
Refer for USG includi ng transva ginalsonography
for assessment of endometrial thickness and
other uterine and ovarian pathology.
c. Management
At RH/DH:
If gross cervical pathology seen cervical biopsy,
polypectomy
Pap smear if no gross lesion seen
Colposcopy for unhealthy cervix, abnormal Pap
smear, vulval lesions
Ultrasonography : TVS or Saline infusion
sonography
Hysteroscopy and directed biopsy is the gold
standard for evaluation: It permits direct visual
inspection of uterine cavity with greater accuracy
of diagnosis as focal lesions are not missed. It is
superior to blind dilatation and curettage in
which neoplasia may be missed.
Fractional curettage under GA if hysteroscope
unavailable
Treatment is planned according to pathology
found.
Endometrial hyperplasia: Abdominal total
hysterectomy with bilateral salpingo
oophorectomy
Cervical/Endometrial malignancy: Treatment as
per stage
Ovarian tumors: Staging laparotomy (Total
hysterectomy + bilteralsalpingo oophorectomy
for benign tumors. Tretment as per stage for
malignant tumors)
Senile vaginitis: Vaginal estrogen therapy
d. Screening for endometrial cancer:
TVS for endometrial thickness is a simple, non-
invasive, reliable screening technique for the
diagnosis of Ca endometrium. All postmenopausal
women should have annual trans vaginal sonographic
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assessment for endometrial thickness. Women having
endometrial thickness > 4 mm need further
evaluation to rule out endometrial cancer.
3.2.2 Cervical Cancer
Cervical cancer is the second most common cancer
among women in India, the first being breast cancer.
In 2012, about 1,23,000 new cases of cancer cervix
were detected in India and 67,000 women died due
to cervical cancer, but this cancer can be prevented.
Human papillomavirus (HPV) is the causal agent for
cervical cancer and about 15 high-risk types of HPV
are known. HPV infection is a very common
infection. Those women who cannot clear this
infection by their natural immunity are at risk of
cervical cancer.
a. Screening for Cervical Cancer:
Cervical cancer is preceded by a long phase of
premalignant lesion called as cervical intraepithelial
neoplasia (CIN). This stage may last for about 10-20
years before developing into a frank malignancy.
When the abnormal cells are limited to the lower
third of the epithelium it is labeled as CIN 1, when
lower two thirds of the epithelium is involved, it is
termed as CIN II and when the entire thickness of the
epithelium is involved, it is termed as CIN III. CIN
can be diagnosed by a pathologist on
histopathological examination of cervical biopsy
specimen. CIN lesions can be treated by simple
treatment modalities and cervical cancer can be
prevented.
The World Health Organization (WHO) has
recommended that at a minimum, as a priority,
screening is recomme nded for every woman 3049
years of age at least once in a life time. Screening
should be initiated at 30 years of age. For HIV-
infected women screening should be initiated as soon
as the infection is diagnosed.
Cervical cancer screening can be done by following
different tests:
Figure 1 Scraping from ectocervixFigure 2 Endocervical sampling
ii) Visual inspection of cervix with acetic acid
(VIA):
Pap smear (cytology screening)
Visual inspection of cervix with acetic acid
(VIA)
HPV testing for high risk types (it is expensive
and available only in some centres. Useful in
increasing the screening interval in women
above 30 years age)
i) Pap s mear (cytology screening):
Pap smear requires LABOURator y infrastructure,
quality control, a system for informing the results to
the women and further referral for colposcopy.
Material:Cuscos bivalve speculum, Ayres spatula,
endo-brush, fixative spray or jar containing fixative
solution, 95% ethanol or ether-alcohol mixture, glass
slides.
Procedure:
Schedule the procedure following abstinence for
24 hours and when there is no vaginal bleeding.
Confirm that no va ginal examination has been
done in previous 24 hours. No vaginal antiseptics
should be used
Use speculum to inspect the cervix
Do not take smear if there is vaginal bleeding or
active infection
Place the Ayres spatula against the cervix and
rotate it firmly against the cervix through 360
degrees to scrape the transformation zone.
Spread the sample on the spatula evenly on a
glass slide. Endocervical cells are obtained by
endo-brush or cotton tipped applicator rolled in
cervical canal. Place the sample on another glass
slide
Fix the smears by putting in fixative jar or by a
fixative spray. Send the smears to an expert
cytopathologist
Currently Bethesda system (2001) is used for
repor ting of smears.
VIA involves application of 5% acetic acid on the
cervix for one minute and visual inspection of
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colour change s in the cervi x. VIA is simple, cheap,
it can be performed by trained health care workers
and provides an opportunity to treat screen positive
women during the same sitting thus reducing the
challenges of lost to follow up.
Materials and equipme nt needed for screening:
Sterile gloves and Cuscos speculum
Autoclaved cotton balls and sponge holding
forceps/ autoclaved cotton-tipped swabs
Freshly prepared acetic acid solution (5%)
Procedure:
Insert a bivalve speculum, get the view of the
cervix
Remove any discharge, blood or mucus from the
cervix by a saline moistened cotton swab
Ide ntify the squamo-columnar junction (SCJ)
and the area around it
Figure 3 VIA positive cervix
After screening
If the test is negative, repeat test in 3-5 years.
For HIV infected woman repeat testing within 3
years.
b) Treatment strategy for screen positive cases:
GOI-WHO (2006): Screening women between age
30 -59, by VIA by trained HCW at PHC. Referral of
VIA positive to DH.
At DH repeat VIA followed by pap smear,
colposcopy, directed biopsy from abnormalareas
followed by cryotherapy /LEEP as required at the
same sitting.
Apply acetic acid to the cervix for one minute
and simultaneously obs erve if any color change
develops
Observe any changes in the color/ appearance of
the cervix after one minute. Give special
attention to abnormalities close to the SCJ
Look for any raised and thickened white plaques
or acetowhite epithelium.
Use a fresh swab to remove any remaining acetic
acid solution from the cervix and vagina. Gently
remove the speculum.
The test results are reported as follows:
VIA positive - when there is a dense white,
opa que lesion touching the squamo-columnar
junction (SCJ)
VIA negative when such lesion is not seen
VIA positive-invasive cancer when there is a
clinically visible growth which turns dense
aceto-white and bleeds on touch.
WHO guidelines (2013):
Screen and Treat approach, using a screening test
giving immediate results (like VIA) followed by on
the spot treatment (cryotherapy) of detected lesions
to eligible women, without any further tests, when
there is no suspicion of cancer. This has been shown
to be an effective strategy. This is a single visit
appr oach which is conve nient for rural women.
A comprehensive approach to cervical cancer
prevention and control invol ves health education and
screening of all women and treatment before
progression to invasive disease. Awareness among
women and doctors that cervical cancer can be
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prevented by early detection and treatment of CIN is
critical for the success of cervical screening.
Primary prevention of cervical cancer is now
possible by HPV vaccination of girls between 9 to 13
years of age before initiation of sexual activity. But
HPV vaccines are currently expensive and not yet
available in the government programs.
4. Infertility
4.1 Definition:
Infertility is defined as failure to conceive after one
year of regular, unprotected sexual intercourse. It can
be primary or secondary:
i. Primary: The woman has never conceived in
past.
ii. Secondary: The woman has previously
conceived but is subsequently unable to
conceive for 12 months.
Infertility affects 10 15% of the general population.
It is the problem of the couple. Male factor is
responsible in 30%, Female factor responsible in
50%, and the combined factors are responsible in
10%. Unexplained infertility in observed in 10%.
To develop into mature
Table 2: Minimum normal criteria for semen
analysis: WHO revised criteria.
Parameter WHO 2010
Volume 1.5 ml
Sperm
15 million/ml
concentration
Progressive
32%
motility
Nor mal for ms 4%
d) Counselling for male:
Regular intercourse 2-3 times/week, stop smoking,
alcohol & any addictive drugs, wear loose fitting
underwear and trousers, and avoid Occupational or
social situations that might cause testicular heating.
Treat any ps ycho-sexual problem if present.
4.1.1 Infertility Male Factor
a) History in Male Partner: Age, occupation,
previous marriage if any, substance abuse, coital
histor y (Frequency of intercourse / Knowledge of
fertile period / Coital difficulties related to erection /
penetration / ejaculation).
Past history:
Mumps/Genital trauma/STIs/Surgery/Tuberculosis),
Current histor y: Any illness, dr ug treatment.
b) Physical Examination - Rule out hernia,
hydrocele, undescended testis, absence of testis. Note
the size of testis. Look for varicocele in upright
position.
c) Investigations:
Bloo d and urine routine testing
Semen Analysis: Sample collected after 2-3 days of
abstinence and examined within 2 hours of
collection.
Male partner should be evaluated first by
performing semen analysisIn humans ittakes
about 75 days for spermatogonia.
If semen report is abnormal, the test should be
repeated twice at least at 2-4 weeks interval before
considering it as abnormal. Ideally a
period of 3 months should be considered for
evaluation of any improvement as a result of therapy.
Persistently abnormal semen parameters require
further evaluation at speciality infertility clinic.
e) Male Partner- Treatment
i. Medical therapy: Antioxidants, clomifene
citrate, gonadotropins.
ii. Intra-uterine Inse mination (IUI): Mild male
factor infertility.
iii. Donor inse mination: For azoospermia
(Primary testicular failure)
iv. Adoption: For cases with recurrent
unexplained failed IVF cycles.
v. Surgical restoration of duct patency: For
obstructive azoospermia (previous vasectomy).
vi. Intra-cytoplas mic Sperm Injection (ICSI):
For severe male factor or for recurrent
unexplained failed IVF cycles.
4.1.2 Infertility Female Factors
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a. Causes of fertility in females
Anovulatory infertility-
i. Anorexia nervosa / Stress related / Exercise
induced.
ii. Hyperprolactinemia , Thyroid disorders.
iii. Polycystic ovarian disease.
iv. Decreased ovarian reserve, Premature ovarian
failure.
Tubal infertility:
Genital tuberculosis, PID, Tubectomy
Uterine factors:
Submucous fibroids, Tubercular endometritis,
Endometrial polyps, Intrauterine adhesions.
Peritoneal factors: Endometriosis, Chronic PID
Cervical factors:
Immunologic, infections, surgical trauma
(amputation, conization, deep cauterization of
cervix).
b) History in female Partner:
Age, years since marriage, occupation, substance
abuse. History suggestive of reproductive tract
infections (Vaginal discharge/Pruritus
vulvae/Chronic pelvic pain), Tuberculosis,
Endoc rinopa thy (Weight & Hair changes/Discharge
from nipples/cold intolerance/dryness of skin),
Premature ovarian failure (H/O Mumps, hot
flushes/oligomenorrhoea/amenorrhoea), Abdo minal
Surgery. Coital frequency & knowledge of fertile
period, dyspareunia
H/Oprevious pregnancies, pregnancy outcome, post
partum infection.
Family history: egTuberculosis
Menstrual history:
Menarche, regularity of cycles, dysmenorrhoea, flow,
LMP.:Regular cycles, dysmenorrhoea,
mittelschmertz (mid cycle pain), premenstrual breast
heaviness and mastalgia are suggestive of ovulatory
cycles.
c) Examination of female partner:
Look for obesity or gross underweight (BMI),
lymphadenopathy, thyroid enlargement, hirsutism,
galactorrhoea, acanthosisnigricans.
Systemic exam
Speculum & per va ginal exam: Look for anatomic
abnormalities.
d) Investigation in Female Partner
Pelvic USG:Diagnosis of PCOS, uterine fibroids,
adnexal mass, uterine malfor mations,
endo metrioma.
Serial trans-vaginal sonography for confirmation
of ovulation and timing of ovulation.
Hormonal assay: Mid luteal serum progesterone..
TSH, Prolactin, FSH & LHin selected patients
with anovulation
Endometrial sample collected by premenstrual
curettage is sent for histopathological and
microbiological evaluation to exclude
endometrial tuberculosis in suspected cases.
Laparoscopy helps in diagnosis.
Hysterosalpingography (HSG)-Performed
between Day 6 Day 11 of the menstrual cycle,
at the Radio- diagnosis department.
Contraindicat ions:
Current PID, suspected Genital TB, cervicitis.
HSG also helps in detecting intra uterine pathology.
Laparoscopy with chromot ubat ion
This is an invasive surgical procedure indicated
when HSG is abnormal, there is failure to
conceive within 6 months in spite of a nor mal
HSG, and for suspicion of endometriosis.
Usually done in the pre ovulatory period.
Diagnostic laparoscopy helps in diagnosing
tubal, uterine pathology and also helps in
detecting endometriosis, pelvic adhesions, pelvic
tuberculosis. Surgical treatment for adhesions,
endometriosis can be done laparoscopically.
Hysteroscopy:
Endoscopic direct visualization of the uterine
cavity.Submucous fibroids, endometrial polyps,
adhesions, malformations and foreign bodies can
be visualized.Hysteroscopic, resection of uterine
septum, submucusmyoma and adhesiolysis for
intrauterine adhesions can be offered.
Laparoscopy can be combined with
hysteroscopy.
e) Counselling for Fe male Partner:
Regular intercourse 2-3 times/week. stop smoking,
alcoholand addictive drugs, and follow a supervised
weight loss programme if obese. Treat psycho-sexual
problem if present.
f) Treatment of Fe male Partner:
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Induction of Ovulation:
For women with ovulator y dysfunction.

Clomiphene citrate is the first line drug for Surgical Treat ment
ovulation induction.
50 mg orally daily for 5 days from day 2 to day 6 i. Laparoscopic adhesiolysis
of menstrual cycle. Ovulation is monitored by ii. Hysteroscopic tubal cannulation, resection of
USG follicle monitoring. If ovulation doe s not intrauterine adhesions, pol yp or
occur, the dose can be increased by 50 mg daily submucusmyoma.
in successive cycles up to 150 mg daily. Risk of iii. Laparotomy for tubal reconstructive surgery.
multiple pregnancies should be explained.
Failure of ovulation or conception after treatment
for 3 cycles requires careful review and
evaluation. 5. Pelvic Organ Prolapse
Women with polycystic ovary syndrome who
have not responded to clomifene citrate should Pelvic organ prolapse (POP) is a common
be offered laparoscopic ovarian drilling gynaecological problem in women above the age of
Gonadotropins for ovulation induction requires 40 years. POP includes anterior vaginal prolapse
special expertise and careful monitoring. There is (cystocele), uterine prolapse, and posterior vaginal
risk of multiple pregnancy prolapse (rectocele, enterocele).
Hyperprolactinaemia: Treatment with
bromocriptine.
Hypothyroidism: Thyroxine therapy restores
ovulator y cycles
5.1 Symptoms
Intra-uterine Insemination (IUI): Unexplained
infertility and cases with minimal endometriosis.
Table-3: Symptoms

Lower urinary t ract symptoms Bowel symptoms Sexual symptoms Other symptoms

Incomplete emptying, Constipation Interference with Pelvic pressure,

sexual activity heaviness, pain
recurrent UTI, frequency, urgency
nocturia

Stress urinary incontinence Straining Dyspareunia Presence of vaginal

bulge/mass

Voiding difficulty: may require to Incomplete Decreased sexual Low back pain
reduce prolapse before passing evacuation desire
urine

5.2. Signs
P/A:Look for any lump, ascites, obesity

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 Local exam: Inspection of the vulva with
coughing and straining demonstrate severe
prolapse and may demonstrate stress
incontinence ( provided the bladder is full)
Examination using Sims speculum: Note type of
prolapse, degree of uterine descent, anterior and
posterior vaginal wall prolapse. Look for
decubitus ulcer on cervix, elongation of cervix
Vaginal examination: Note uterine size, pos ition,
adnexal mass
Rectal examination, to differentiate rectocele
from enterocele
Assess anal sphincter tone, assess levator tone,
perineal body
5.3. Predisposing factors
Injuries to supports of pelvic organs during
childbirth
Obesity, chronic cough, chronic constipation,
Atrophy and loss of tone due to aging, estrogen
deficiency
Congenital weakness of tissues can lead to
nulliparous prolapsed
5.4. Management
5.4.1 At PHC:Preoperative care given at PHC can
help in shortening the hospital stay and reduce the
number of visits to the district hospital.
Treat urinary tract infection. Correct Anemia,
control diabetes
Treat the decubitus ulcer before surgery:
Reposition of prolapse and maintaining it in
reposed position helps in healing of ulcer.
Glycerine-acriflavin vaginal packing daily helps
in healing. In older women having severe vaginal
atrophy, vaginal application of estrogen cream
helps in rapid healing. The ulcer will usually
heal within 7 da ys.
5.4.2 At FRU/DH: The women should be evaluated
completely for planning the treatment modality. Most
women will be candidates for surgical treatment. In a
young woman following childbi rth conservative
measures should be advised for 3 to 4 months.
a) The nonsurgical treatment is useful in following
women Women having mild degree of prolapse
Pregnancy and Postpartum
Unfit or unwilling to undergo surgery.
Kegel exercises to strengthen the pelvic supports.
Ring pessary: Woman unfit for surgery, can provide
temporary relief.
b) Surgical treatment:
Surgery can be of two types. Vaginal hysterectomy
with vaginal wall prolapse repair and uterus
conserving surgical repair. Choice of surgical
procedure depends on age, parity and wish for further
pregnancy and medical fitness. In younger women
desirous of retaining fertility, conservative surgical
repair operations are indicated, whereas in the
perimenopausal and menopausal women, vaginal
hysterectomy with repair of the pelvic floor is
performed.
5.5. Prevention
Antenatal physiotherapy, relaxation exercises
and due attention to weight gain and Anemia are
important.
Proper management of second stage of Labo ur.
Avoiding undue prolongation of second stage by
timely assisted delivery.
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 Immediate and accurate suturing of perineal tear Provision of adequate rest for the first 6 months
after delivery. after delivery
Postnatal exercises and physiotherapy are Contraception: Too many births at too short
beneficial. intervals are avoided.
Early postnatal ambulation.

Page 309
DERMATOLOGY

Page 310
 1. INFECTIONS OF SKIN

1. Bacterial infections of Skin

d. Furuncle
It is infection of skin caused by bacteria. Persons
Erythematous, painful, tender
with poor personal hygiene, old age, Diabetes and
Immunocompromised patients are prone to bacterial Form discrete follicular nodules with
infection of skin. Perifollicular edema.

1.1. Pyoderma
1.1.1 Types
a. Impetigo
Starts as an erythematous Macule
Develops into a vesicle with erythematous halo
Vesicle breaks down with oozing
Dries to form golden yellow crust Spreads by
auto i noc ulation

b. Ecthyma
Deeper infection
An ulcer covered with adherent crust e. Carbuncle
Heals with scarring Infection of multiple adjoining hair follicles
Rule out Diabetes Mellitus in case of recurrent Presents with painful, tender plaque with
furunculosis and carbuncle. ulceration.
Rule out Diabetes Mellitus in case of recurrent
c. Folliculitis furunculosis and carbuncle
Follicular oriented pustules without peri-
follicular oedema.

1.1.2 Investigation: - CBC, BSL (R) Systemic antibiotics Erythromycin (250 or

1.1.3 Treatment guidelines:
Good personal hygiene
Wash with soap and water
Topical antibacterial cream Neomycin 0.5 %
/ Framycetin1 % / Mupirocin / Fusidicacid -
Local application two times in a day for 7
days.
500 mg QID) / Cefadroxil (250 or 500mg BD)
for 7 days
Azithromycin 250 mg bd for 7 days
For recurrent pyo derma:
Topical application of mupirocin 2 % to carrier
sites especially anterior nares and natal clefts
for 2 weeks.
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1.1.4 Erysipelas H/o minor injury may be present
Erysipelas is a superficial form of bacterial Present as sharply defined erythematous tender
cellulitis Swelling.
Usually seen over the face

Treatment:
Systemic antibiotics- Azithromycin 250 bd for
5-7 days / Cloxacillin / Amoxicillin-
Clavulanicacid - 625 mg bd for 7 days.
IV antibiotics for severe cases -Inj.Cefotaxime
1 gmIvbd for 7 days.
Non steroidal anti-inflammatory drugs - Tab.
Brufen 1 bd for 7 days.
1.1.5 Cellulitis
Cellulitis is a deep subcutaneous infection with
lymphangitis and adenopathy
Borders of the lesion are poorly demarcated
Vesicles and bullae may be seen over the
surface in both conditions.

Treatment:
2.1.1 Tineacapitis
Non steroidal anti-inflammator y drugs - Tab. Presents with different clinical types and is
Brufen 1 BD for 7 days. more common in children.
Amoxycillin + Clavulinic acid 625mg BD / a. Gray patch
Cloxacillin for7-10 days Well defined scaly circular patches

IV antibiotics for severe cases - With partial alopecia showing broken off hair.
Inj.Cefotaxime 1 gm IV BD for 7 days.

2. Fungal infections of skin

2.1 Dermatophyte infections
Superficial fungal infections of keratinized tissue
caused by dermatophyte fungi. Persons with
diabetes, Obesity and Immunocomprised patients
are prone to infections.
Dermatophytosis is classified according to the body
part involved.

Page 312
b. Black dot
Broken off hair near the surface give
appearance of black dot.
Diffuse and poorly circumscribed lesions with
low grade folliculitis.
c. Kerion
Boggy purulent inflammator y nodules and
plaques with sinus for mation and pus discharge
which leads to thick crusting & matting of
adjacent hairs.

d. Fav us Systemic antibiotics in case of secondary

Perifollicular erythema and matting of hair
with fetid odour
Heals with scarring alopecia.
e. Investigation: - CBC, BSL (R)
f. Treatment
g. Topical anti-fungals (lotions / creams)
Clotrimazole - 1% Local application BD for 15
days 1 month.
Miconozole - 2% Local application BD for 15
days 1 month.
h. Systemic anti-fungals
Tab. Griseofulvin 10mg/kg/da y for 4 to 6
weeks
infection - Azithromycin 250 BD for 5-7 days
/ Cloxacillin / Amoxicillin-Clavulanic acid -
625 mg BD for 7 days.
Tab. Fluconazole 150 mg / week for 4 to
6weeks.
2.1.2 TineaCorporis
Dermatophytosis of the skin with the exclusion
of palms, soles and groin is called
TineaCorporis
Well defined scaly annular patches
With or without vesicles, pustules at margin
Single or multiple scattered lesions
Itching Present

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2.1.3 TineaCruris
Infectionof groin area and includes infection of
genitalia, pubic area, perianal and perineal skin.

Treatment:
Topical cream
Clotrimazole - 1% Local application BD for 4-
6 weeks.
Miconozole - 1% Local application BDfor 4-6
weeks.
Systemic
Tab.Griseofulvin 250 to 500 mg BD for 3
weeks
Tab.Fluconczole 150mg one per week X 4 -6
weeks
2.1.4 TineaPedis
Dermatophyte infection of the feet.

Treatment:
Topical cream
Clotrimazole 1% Local application BD for 4-
6 weeks.
Miconozole - 2% Local application BD for 4-6
weeks.
Systemic
Tab. Griseofulvin 250 to 500 mg BD for 3-6
weeks
Tab.Fluconczole 150mg one per week for 4 -6
weeks
2.1.5 TineaManum 2.1.6 TineaUnguium
Dermatophyte infection of palms and inter-digital Dermatophyte infection of nail plate whitish or
areas of hand. brownish yellow discoloration of nail.Separation of
nail bed and nail plate

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 Nails becomes friable and discolored
Treatment:
Griseofulvin 1 gm per Day for 4-6 months for
finger nails and 12-18 months for toe nails
Tab.Fluconczole 150mg one per week for 6
months for finger nails & 12 months for toe
nails.
2.1.7 Candidiasis:
Caused by yeast like fungi candida albicans
a. Chronic paronychia
Infection of nail fold
Erythema and swelling of finger tips
b. Intertrigo
Seen over intertrigenous areas,groin,inbetween
toes, be low the neck in children
Sharply demarcated pol ycyclic erythematous
eroded patches with satellite pustules
Rule out underlying Diabetes Mellitus.

c. Diagnosis
KOH mountDirect examination of scrapings
under microscope from lesions with KOH
mount will reveal budding yeasts with hyphae
or pseudo hyphae.
d. Treatment
Keep intertrigenous areas dry
Treat underlying Diabetes mellitus
Clotrimazole 1% Local application BD for 4-
6 weeks. 2.1.8 Tineaversicolor
Miconozole 2% Local application BD for 4-6
Chronic superficial fungal infection caused by
weeks.
malassezia furfur. Lesion vary color from white,
Tab. Fluconazole 150 mg per week for 4 weeks. pink to brow n usually consisting of coalescing
macules, pa tches with fine scales on trunk and neck.

a. Treatment:
Oral Fluconazole given as single dose of 400
mg
b. Locally apply:
Ketoconazole 2% shampoo Local application
half an hour before bath for 4 weeks.
Selenium Sulphide suspe nsion - Local
application half an hour before bath for 4
weeks.
Clotrimazole 2% solution local application for
4 to 6 weeks

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 Disseminated herpes zoster occurs in
3. Viral infections immunocompromised individuals
3.1 Herpes Zoster 3.2 Herpes simplex
3.2.1 Infection occurs in two types
a. HSV1 usually responsible for cutaneous,
oropharygeal and ocular infections.
b. HSV2 invol ved in genital infections and
infections of new bor n.
Oral Infections shows vesicle, erosions are
seen on buccal mucosa or perioral skin with
severe pain and high fever.
Vulvovaginitis in female and painful penile
lesions in men with appearance of vesicles and
erosions seen.

3.1.1 Prodromal Symptoms

Pain at the site
Closely grouped reddish papules, vesicles
and pustules in continuous or interrupted
band in one or adjacent dermatomes
Usually unilateral and does not cross the
midline
Thoracic segments most commonly
involved.
3.2.2 Treatment:
Orally Acyclovir 200 mg 5 times daily for 7 days
(1-1-1-2)

3.3 MolluscumContagiosum
3.3.1 Clinical manifestations:
Molluscumcontagiosum A viral infection of the
skin caused by a poxvirus. It is a contagious disease
particularly common in young children. After
approximately two to three months of the virus
incubating, small, round growths begin to emerge.
These are light pink or tan colour and can look
similar to warts. They can sometimes become red
and irritated or have a tiny white depressed spot in
the centre.
3.3.2 Treatment:
Needling
3.1.2 Treatment Curette most commonCryotherapy with
liquid Nitrogen
Tab Acyclovir 800mg 1-1-1-2 x5-7 days. Electrocautery
3.1.3 Herpes Eye:In herpes zoster Topical 50% trichloroacetic acid Twice a
week till resolution
opthalmicus, refer to ophthalmologist for
further management.
3.4 Warts
Fillform or digitate warts
Plantar warts
Page 316
a. Common warts:
Firm keratotic papules with rough hor ny
surface

b. Plane warts
Multiple smooth, flat or slightly elevated round
or polygonal papules (1 to 5 mm)
c. Filiform or Digitate
Composed of one or more finger like
projections 2 to 10 mm in length.

d. Planter Warts e. Treatment:

Sharply defined rough keratotic lesion. Spontaneous resolution possible

Topical keratolytics
Surrounded by a smooth collar of thickened 16.7 % salicylic acid and 16.7% lactic acid in
hor n. collodion baselocal application daily till
resolution or
50% Trichloroacetic acid applied weekly
tillresolution or
Topical 5% flurouracil ointment local
application daily till resolution.
Electrocautery or liquid nitrogen therapy
Podophyllin 25 % for genital wart twice
weekly tillresolution.
Cryotherapy with liquid nitrogen for genital
wart

Page 317
 Scrofuloderma
4. Cutaneous Tuberculosis
It is infection of skin caused by mycobacterium
tuberculosis. Persons with malnutrition and 4.1.1 Lupus vulgaris:
Immunocompromised patients are prone to Reddish brown plaque which spreads with foci
tuberculosis. of scarring
4.1 Clinical types Has an active advancing edge and areas of
Lupus vulgaris Scarring.
Tuberculosis verrucosa cutis

4.1.2 TuberculosisVerrucosa Cutis: 4.2 Investigations

Indurated warty papule or nodule or a plaque,
with surrounding erythema. TT (Tuberculin Test )
There may be fissuring and di scharge from the Xray chest PA view Screen for pulmonary
surface. tuberculosis.
Irregular extention leads to serpigenous Skin biopsy to confirm diagnosis.
margin.
Treatment after confirmation.
4.1.3 Scrofuloderma:
It occurs over the underlying focus of 4.3 Treatment
tuberculosis like caseating lymph Antituberculous treat ment 6 months
gland,bone,joint etc. 4 Drugs 2 months
Present as painless bluish red swelling which 2 Drugs 4 months
breaks down to from sinus orundermined Refer RNTCP guidelines.
ulcer.

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 2.Non Infectious Skin conditions
1. Urticaria 1.1. Provoking factors
Elevated erythematous itchy swelling i. Drugs

Transient in nature ii. Food

iii. Infection
Worsened by scratching
iv. Stress
Acute < 6 weeks
v. Systemic Diseases
Chronic >6 weeks
Angio-oedema involves the deeper structures

Figure 1 Urticaria

1.2. Treatment 2. Psoriasis

Eradication of the etiological factor
2.1 Clinical features
In acute urticaria with laryngopharyngeal
edema 0.5 to 1 ml of subcutaneous i. Erythematous well defined scaly plaques
epinephrine.
ii. Predominantly extensor aspect of the bod y
iii. Scales are silvery and loosely attached to the
Antihistamines lesion
Cetrizine 10 mg /day for 2 to 4 weeks or iv. Koebner phenomenon (it is isomorphic reaction
to trauma or injury) in which positive new
T. Levocetrizine 5 mg per day for 2 to 4 weeks
lesion occurs at the site of trauma
or
Loratidine 10 mg /day for 2 to 4 weeks.

Severe extensive cases or unresponsive cases

Predinisolone 0.5 to 1 mg /kg per day and
gradually tapered
T.Albendazole 400 mg single dose
Ref to higher centre if no response

Figure 2 Psoriasis

Page 319
Scalp:
Scaling that extends be yond the hair line
Nails:
Collection of keratotic material under the nail lifting
the distal part of the nail from the nail bed and Nail
pitting
Joints may be involved
2.2 Treatment
i. Potent topical steroids for localized lesion
Clobetasol Propionate 0.05 % local application
twice daily for 2 weeks.
ii. Topical keratolytics Salicylic acid 3% or 6%
twice daily for 2 weeks.
iii. Liquid paraffin for external use or use of any
other emollients local application twice daily
for 2 weeks.
3.2 Treatment
Topical steroids - Clobetasol Propionate. 0.05
% local application twice daily for 2 weeks.
Tab. Cetrizine 10 mg daily for 2 weeks.
Generalized forms - Systemic steroids like
Tab. Prednisolone 0.5 mg/kg per day.
Gradually tapered over the next 4-6 weeks
Refer to higher centre for extensive lesions.
4. PityriasisRosea
4.1 Clinical features
Initial lesion 2 to 6 cm circular asymptomatic
erythematous scaly plaque called herald patch
Within days crops of papules and oval patches
with wrinkling surface and a bor der of fine
scales
Trunk and proximal extremities are commonly
involved {covered part}
Lesion heal with hyper or hypo pigmentation

iv. Tab.Cetrizine 10 mg per day if itching persists

v. 5% Coal tar ointment local application twice
5. Acne
daily for 2 weeks. 5.1 Clinical features
vi. Calcipotriol cream local application twice daily Common in adolescents
for 2 weeks. Present as comedones, papules, pustules, nodules,
Patients with extensive involvement, abscess, cysts, scars
arthropathy, pustular psoriasis, erythrodermic Sites Face, chest, back, shoulder
psoriasis refer to higher centre.
Note: avoid use of systemic steroids.

3. Lichen Planus
3.1 Clinical features
Welldefined,violaceous,polygonal flat topped
papules
Itching present
Common Sites : legs and forearm
Koebner Phenomenon + ve
Involvement of hair leads to alopecia Figure 4 Acne
Oral mucosa : lacy network of whitish patche
Differential diagnosis:
Psoriasis
Secondary syphilis
Tineacorporis
Note - Systemic Steroids should be avoided
Treatment:
Mostly do not require treatment
Symptomatic treatment like topical
moisturizers local application BD for 7 days.
Tab. Cetrizine 10 mg per day if itching is
Figure 3 Lichen Planus present
Daily Sun exposure of covered part if possible.

Page 320
Sequelae: Hyper pigmentation and scarring.
5.2 Treatment
5.2.1 Grade I
Comedones / Occasional papules.
Washing of Face with soap and water when it
becomes oily.
Removal of comedones by Comedone extractor.
Topical Retinoic acid (0.025%) local
application HS for half hour for 2 to 4 weeks.
Benzoyl Peroxide(2.5%) local application HS
for half hour for 2 to 4 weeks
5.2.3 Grade III
Predominant,pustules,nodules,abscesses;
Washing of Face with soap and water when it
becomes oily.
Topical benzoyl peroxide local application HS
for half hour for 2 to 4 weeks.
Retinoic acid local application HS for half hour
for 2 to 4 weeks.
Azithromycin 500 mg OD 3 days per week,
may be repeated; maximum duration 3 months,
or
Doxycycline 100 mg OD for 2 to 6 weeks, or
Isotretinoin 0.5mg/kg/day for 16 to 24 weeks
(only after expert opi nion)
5.2.4 Grade IV
Mainly cysts,abscess,widespread scarring
Washing of Face with soap and water when it
becomes oily.
Systemic antibiotics and Isotretion as in grade
III
Aspiration of cysts
Intra-lesional steroids for cysts
Triamcinolone acetonide 10 mg / ml weekly.
5. Pityriasis Alba
6.1 Clinical features
Asymptomatic round or oval hypo-
pigmented scaly patches usually on the
face.
Single or multiple
Spontaneous resolution may recur.
Age group 3 years to puberty
5.2.2 Grade II
Papules, comedones, pustules:
Washing of Face with soap and water when it
becomes oily.
Topical antibiotics Clindamycin local
application BD for 2 weeks.
Erythromycin 2 to 4% local application BD for
2 weeks.
Benzoyl peroxide local application HS for half
hour for 2 to 4 weeks.
Retinoic acid local application HS for half hour
for 2 to 4 weeks.
6.2 Differential diagnosis
Early vitiligo
Pityriasisversicolor
Leprosy
Post inflammatory hypo pigmentation
6.3 Treatment
Reassurance
Bland emollients for external application like
liquid paraffin local application BD.
Multivitamins like SypCalcivit 1 tsf HS for 1
month.
Treatment of worm infestation if any Tab
Albendazole 400 mg HS single dose.
Cap Vit A 50,000 IU OD for 4-6 wks.
6. Miliaria
7.1 Clinical features
Small discrete itchy non follicular erythematous
confluent macules or papules forming sheets
Inj.
Pricking sensation
Occurs more in summer and heat condition.
7.2 Treatment
Avoidance of excessive exposure to heat
Calamine lotion local application BD for 5
days.
Antihistamines Tab. Cetrizine 10 mg HS for 5
days.
Tab. Vitamin C 500 mg OD for 5 days.
Loose cotton dresses
Plenty of oral fluids etc.

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8. Eczema
8.1 Stages
These are synonymous terms signifying
inflammator y response of skin to different
factors
8.1.1 Acute Stage-Characterised by erythema, oedema, vesicles Azithromycin 250 bd for 5-7 days /
and oozing
8.1.2 Subac ute stage Erythema, oedema,
vesicles decrease and are replaced by
moderate oozing, crusting & Scaling
8.1.3 Chronic Stage Mainly consists of hyper
pigmentation and lichenfication. Highly
pruritic in all stages.
8.2 Treatment
Treatment is according to stage of dermatitis.
8.2.1Acute eczema
Wet soaks / compresses of Potassium
permanganate (4-5crystals in 500ml water)
local application 3 times in a day.
Antihistaminics Tab cetrizine 10 mg BD for 5
days.
Topical corticosteroids- Clobetasone 0.05 %
local application 3 times in a day.
Systemic Antibiotics if secondary infections.
8.2.2Subacute eczema
Wet compresses for crust removal like acute
Eczema local application 3 times in a day.
Betamethasone or mometasone topical
application in cream form local application 3
times in a da y.
Systemic Antibiotics if secondary infections.
8.2.3Chronic eczema
Corticosteroid ointments - Clobetasone
0.05 % local application 3 times in a day.
Tab Cetrizine 10mg BD for 5 to 10 days.
8.2.4Acute infected Eczema
i. Wet dressing with light weak pink potassium
permanganate soaks for 5 days where
indicated
ii. Whenever infection is present. It has tobe
treated with appropriate antibiotics like
Figure 5 ECZEMA / DERMATITIS
Caused by exogenous or endogenous factors
Generally, 3 stages acute, subacute and
chronic
Cloxacillin 500mg three times a day 5 to 7
days / Amoxicillin-Clavulanic acid - 625 mg
bd for 7 days.
iii. Emollients like liquid paraffin applied daily.
iv. Mild cases Hydrococortisone 1% ointment
daily
v. Moderate cases Betamethasone 0.1% cream
or ointment twice daily
8.2.5 Symptomatic relief by anitihistamines
Tab Chlorpheneramine (4 mg) TID as needed or
Tab Promethazine (10-25 mg) 6-8 hourly as needed
in severe cases.
Refer to higher centre to confirm diagnosis and for
management of complicated cases.
8.2.6 Management as per severity
Mild or moderate infectedEczema
Soaks or compresses of plain tepid water or
normal saline
Severe
Tab Prednisolone (5 or 10 mg) 0.5 to 1mg/kg
with gradual tapering, if infection present Tab
Erythromycin (250 to 500 mg) one tablet QID
for 5 to 10 days
Tab.Chloropheniramine Maleate (4 mg) one
tablet TID for 5 to 10 days.
9. Dermatitis
9.1 Atopic Dermatitis Diagnostic
Feature
Chronic pruritic dermatitis over face, neck and
flexures. Seen mainly in infants &children
9.2 Treatment Guidelines
Tab Chlorpheniramine (4 mg) one tablet TID for
3 Days Topical steroid (Clobetasone Butyrate
cream (0.05%)) local application BD for 3
Page 322
 weeks.
Tacrolimus 0.03 % BD X 3 months topically

9.3 General Guidelines Figure 6 Atopic Dermatitis

Use soft non irritating cotton clothing
Use emollients such as oils applied over wet skin.
Avoid foods which tend to aggravate lesions e.g.
nuts, eggs, wheat, cows milk, fish.
Accentuation under Woods lamp
Skin as well as mucous membranes can get
involved.

9.4 Treatment
Moderately potent corticosteroids - fluticasone
/ mometasone cream topically for 6 weeks
Tacrolimus 0.03% for face ; 0.1% for trunk and
extremities for 3 months
Extensive/ resistant cases refer to higher
centre

10. Alopecia areata 10.2 Treatment

10.1 Diagnostic features Moderately potent corticosteroids
Loss of hair in patches (Mometasonefuroate, Fluocinloneacetonide,
Patches of non-scarring alopecia especially over the Fluticasone) for 6 to 12 weeks
scalp and the beard area. Usually round or oval in
shape with a normal appearing superficial skin. 11. Androgenetic alopecia
Asymptomatic, Exclamation mark appearance of the
Underlying susceptibility of hair follicles to
hair
androgenic miniaturization.
Avoid irritating strong soap chemicals
Affects up to 70% of men and 40% of women
Exclusive breast feeding in infants
Treatment:
Review patient after 2 weeks. Topical Minoxidil solution (2 to 5%)BD application
for 4 to 6 months.
9. Vitiligo
9.1 Diagnostic feature
Depigmented macules and patches which can
occur anywhere on the body

Figure 7 Vitilligo

Page 323
 3. Sexually Transmitted Infection (STI)
1. Syphilis Tab Erythromycin 500 mg orally QID x 2 weeks

1.1 Early Syphilis c. Follow Up:

1.1.1 Primary Syphilis After treatment the patient should be examined
clinically and serologically once a month for first 3
Causative agent Treponemapallidum months and quarterly till the end of second year
Incubation period -9 to 90 days
Genital ulcer (primary chancre) classical lesion 1.2 Late Syphilis
Regional lymphadenopathy in 50 % of cases In untreated early syphilitic patients will have the late
Primary chancre resolves in 3 to 6 weeks syphilitic manifestations after 5-15 years from the
After 3 weeks of appearance of chancre,VDRL onset of infection.
becomes reactive 1.2.1 Late latent syphilis
Treponemapallidum can be demonstated from the After 2 years from the onset of infection No signs and
chancre symptoms
In the case of untreated primary syphilis, patient may Non-infectious
develop secondary syphilitic lesions in 3-6 months 1.2.2 Late benign syphilis(Gumma)
interval. After 5-7 years from the onset of
infection,Visceralgumma
1.1.2 Secondary Syphilis: 1.2.3 Cardiovascular syphilis
Skin Rash After 10-15 years from the onset of infection
Maculopapular Uncomplicated aortitis
PapulosquamousPsoriatiform Aortic regurgitation, Coronary ostial stenosis Aortic
Annular Pustular Follicular aneurysm
Rash is generalized, bilaterally symmetrical non 1.2.4 Neuro-syphilis
itchy After 10-15 years from the onset of infection
meningitis, meningo-vascular General Paresis of
Mucosal lesion
Insane (GPI),Tabesdorsalis
Snail track ulcers
CNS gumma
Condylomatalata
Painless discrete, rubbery lymphnodes, systemic 1.2.5 Treatment:
manifestations a. Late latent Syphilis and Late Benign Syphilis
Highly reactive VDRL (Gumma)
Inj. BenzathinePenicilin 2.4 mega units IM
Treponemapallidum can be demonstrated from the Weekly for 4 consecutive weeks or
skin lesions, Cutaneousgumma
Inj. Procaine Penicilin 1.2 mega units IM daily
1.1.3 Early latent Syphilis: for 21 days
No Signs and symptoms b. Cardiovascular syphilis and neuro syphilis
2years period is demarcation between early and Inj. Procaine Penicilin 1.2 mega units IM /day for
late latent syphilis 21 days under the cover of steroids.

1.1.4 Treatment:
a. Penicillin treatments c. In Penicilin allergic patients
For all the above 3 conditions Cap.Doxycycline 100 mg orally BD x 4weeks
Injection: Benzathine penicillin 2.4 mega units deep Cap.Tetracycline 500 mg orally QID x 4 weeks
IM after test dose (or)
Tab.Erythromycin 500 mg orally QID (4 Weeks)
b. In Penicillin allergic patients: d. Follow-up
The patient should be monitored at 6 months interval
Cap Doxycycline 100 mg orally BD x 2 weeks clinically and serologically along with repeat cerebro
(or) spinal examination.
Cap Tetracycline 500 mg orally QID x 2 weeks
(or)

Page 324
1.3 Congenital syphilis 2. Chancroid
Untreated early syphilitic mother may deliver a
congenital syphilitic child. 2.1 Clinical features
Causative agent Haemophilusducreyi
1.3.1 Early: Incubation period Usually 3 to 5 days but it can
Skin lesions, Rash,Bullae,Condylomatalata extend upto 14 days.
Lymphadenitis,Hepatosplenomegaly,Osteochond Multiple, painful, non indurated ulcers with
ritis ragged and undermined edges. Floor is covered
CNS, Kidneys, Lungs, Testes involvement. by a yellowish grey necrotic exuda tes ove rlying
1.3.2 Late: granulation tissue that bleeds on manipulation.
Interstitial keratitis In 50% of the patients, a tender inguinal adenitis
Neuros yphilis (usually unilateral) occurs (Inflammatory Bubo)
Bone and joint involvement School of fish appearance in smears
Sensori-neural deafness
Gummatous lesions
Cardiovascular syphilis involvement.
1.3.3 Stigmata:
Bulldog facies
Hutchinsons teeth
Rhagades Salt and pepper Fundus Gummatous
scars.
1.3.4 Treatment:
a. Early:
Inj. Benzathine penicillin 5000 units /kg/day
divided in 6 hourly doses for 7 days.
b. Pat ient Education:
To seek early and appropriate treatment
To avoid sexual contact until the treatment is Figure 1 Chancroid
completed
Insisting epidemiological treatment of sex
partners with regular follow-up
c. Preve ntion: 2.2 Treatment
Sexual abstinence Cap. Doxycycline 100mg oral BD for 14 days or
Avoid high risk behavior Tab. Erythromycin 500 mg orally QID for 14
Consistent and correct usage of condoms days or
Safer sex practices Tab. Azithromycin 1 gm oral stat or
Tab. Ciprofloxacin 500 mg oral BD for 3 days

Page 325
3. LymphogranulomaVenereum 5. Gonorrhoea
(LGV) 5.1 Clinical features
Causative agent Neisseria gonorrhoeae
3.1 Clinical features Incubation period 1 to 14 days
Caused by Chlamydia trachomatis serovars
Presents as urethritis in male and cervicitis in
L1,L2, L3
female
Incubation period 3 to 12 days
Primary Transient genital ulcer Lymphnode s
(bubo)

Figure 3 Gonorrhoea

5.2 Complications
5.2.1 Male:
Posterior urethritis
Figure 2 LymphogranulomaVenereun Infection of cowpers and tysons gland Epididymitis
Prostatitis
Tertiary complications include:
Seminal Vesiculitis
Elephantiasis of genitalia
Fistulae Strictures Peri-urethral abscesses
5.2.2 Fe male:
3.2 Treatment Salpingitis, Peritonitis, PID
Cap. Doxycycline 100mg oral BD for 3 weeks (
or) Bartholinitis,Proctitis
Tab. Erythromycin 500mg oral QID for 3 weeks Chronic urethritis
4. Venereal granuloma 5.2.3 Other forms:
(Donovanosis) Disseminated gonococcal infection
Gonococcal arthritis
4.1 Clinical features Meningitis
Causative agent- Anorectal and
Calymmatobacteriumgranulomatis Pharyngeal gonorrhea
Incubation period 1 to 3 months
Granulomatous ulcer 5.3 Treatment
Calymmatobacteriumgranulomatis (Donovan Tab.Azithromycin 2 g oral stat (or)
bodies)seen inside large mononuclear cells in InjCeftriaxone 250 mg IM stat
tissue smears.
6. Non gonococcal urethritis
4.2 Treatment
6.1 Clinical manifestation
C. Doxycycline (100mg)BD or T.Cotrimoxazole
(800mg + 160 mg) BD or Causative agent
InjCeftrioxone 250 mg single dose IM Chalmiydia trachomatis ureapalsmaurealyticum,
14 to 21days or Mycopa smagenitalium
T. Erythromycin (500mg) 4 times a day in Urethritis
pregnant women for14 Days or Increased polymorphononuclear leucocytes in
Inj. Ceftriaxone (1gm) daily IM injection for 7 uretheral smear or sediment of first voided urine.
days 7. Chlamydial infections
Page 326
 Agent Chlamydia trachomatis 9.3 Treatment
Incubation period -1 to 3 weeks
Tab. Metronidazole 400 mg bd for 14 days (or)
7.2.1 Male: Tab. Secnidazole 2g stat dose
Urethritis
Littritis 10. Candidiasis
Epididymitis
Prostatitis 10.1 Clinical features
Proctitis Predominantly caused by candida albicans
Reiters syndrome
Predisposed by pregnancy, diabetes, HIV and
immunosuppression
7.2.2Female:
Cervicitis, Urethritis,Bartholinitis
Endometritis,Salpingitis
Fitz HughcurtisSyndrome (It is fever with lower
abdoman pain after cervical movement. There are
adhesions in pelvic cavity, may lead to infertility.)

7.3 Treatment
Tab.Azithromycin 1 gm oral stat (or)
Cap Doxycycline 100 mg oral BD for 14 days
(or) Tab Erythromycin 500 mg QID for 14 days.

8. Bacterial Vaginosis
8.1 Clinical aspects
Polymicrobial Syndrome
GardnellaVaginalis
Mycoplasma hominisBacteroids
Excessive,homogenous,unifor mlyadherent
vaginal discharge, elevated Vaginal pH > 4.5
Positive Amine test (Whiff test)
Presence of Clue Cells (Epithelial cells
studde d with organisms)
8.2 Treatment
Tab Metronidazole 400 mg BD for 14 days (or)
Tab Secnidazole 2g stat dose
9. Trichomoniasis
9.1 Epidemiology
Caused by trichomonasva ginalis
Incubation period 4 to 28 days
9.2 Clinical features diagnosis
Copious, homogenous, malodorous, yellowish
green va ginal discharge
Punctuate hemorrhages over cervix Strawberry
cervix
Demonstration of motile trichomonads in wet
film smears under direct microscopy
Culture gold standard for diagnosis
Figure 4 Warts (CondylomataAcuminata)
Causes Balanoposthitis in males
Clinically erythema and swelling with a macular
/papular rash over glans penis.
A white Subpreputial discharge ,increased skin
Marking, Fissuring of the glans and Fore skin
occasionally regional lymphadenopathy may be
present
Causes vulvo vaginal candidiasis in females -
oedema, fissures, erosions, curdy white
discharge.
Demonstration of candidiasis by 10 % KOH
Yeast cells, mycelia seen.
10.2 Treatment
Commonly used antifungals include oral fluconazole
and topical clotrimazole.
Vaginal candidiasis a single dose of oral fluconazole
(150mg)
Clotrimazolepessary for 7 days daily
Clotrimazole cream (1%) or miconazole cream (2%)
daily bd
Application for 7 to 14 days
11. Warts(CondylomataAcuminata)
11.1 Clinical features
Page 327
Caused by Human papilloma Virus
Incubation period 1 to 8 month
Skin coloured multiple verrucous lesions
11.2 Treatment
Predominantly By HSV -2 also by HSV 1
Incubation period 5 to 14 days
Ballooning degeneration and giant cells seen in
HPE

Topical podophyllin 25 % local application twice Primary Severe associated with systemic
weekly. symptoms starts as grouped vesicles ulcerate -
pol ycyclic margin
Cryotherapy
Cautery Recurrence less severe
Surgery

12. Herpes Genitalis

12.1 Clinical features
12.2 Complications
CNS involvement dissemination Secondary infection
Recurrence
Transmissible during pregnancy and de livery

11.3 Treatment
11.3.1 For Primary
Tab Acyclovir 200 mg 5 times a day for 7 days

Figure 5 Herpes Genitalis 11.3.2 For Recurrence

Tab Acyclovir 400 mg 3 tims a day for 5 days

Page 328
 4.SYNDROMIC MANAGEMENT OF STD

1. Syndromic Approach 2. Why Syndromic

Provision of STI/RTI care services is a very
important strategy to prevent HIV transmission
and promote sexual and reproductive health
under the National AIDS Control Programme
(NACP III) and Respective and Child Health
(RCH II)
Syndromic case management (SCM) with
appropriate laboratory tests is the cornerstone of
STI/RTI management under NACP III.
SCM is a comprehensive approach for STI/RTI
control endorsed by the WHO.
Diagnosis is based on the identification of
syndromes, which are combi nations of the
symptoms the client repor ts and the signs the
health care provider observes.
The provision of the most effective therapy at
patient's first contact with a health or medical
facility.
The recommended treatment is effective for all
the diseases that could cause the identified
syndrome.
Provides single does treatment as far as
possible.
Comprehensive to include patient education on
risk reduction, counseling, condom promotion
and provision, partner notification, follow up.
Management
STI signs and symptoms are rarely specific to a
particular causative agent.
Laboratory services may not be available.
Dual infections are quite common and both
clinician and labor atory may miss one of them.
Waiting time for lab. Results may discourage
some patients.
Failure of cure at first contact.
3. The common STD
Syndromes
Genital ulcer diseases
Urethral discharge
Vaginal discharge
Bubo ( inguinal Swelling)
Lower abdominal pain in female
Scrotal swelling
Ophthalmianeonatorum
Syndromic approach for STI s is useful and practical
strategy for offering , high quality, effective and
acceptable care for prevention and treatment of
sexually transmitted infections (Guidelines from
National Aids control Organization (NACO) has
been used)

Table 1:NACO Guidelines

Kit Color Compostionof kit Syndrome / disease

1) Gray Tab.Azithromycin 1 g stat + Tab. Urethral discharge (UD), Cervical, discharge (CD),
Cefixime 400 mg. anorectal discharge (ARD), Presumptice treatment
(PT), Painful scrotal swelling.

2) Green Tab.Secnidazole 2 g stat + cap. VD {Vaginal discharge.}

Fluconazole 150 stat

3) White Inj.BenzathinePenicilin 2.4 MU IM Genital ulcerative disease (GUD); non herpetic)

stat + Tab Azitromycin 1 g stat

4) Blue Cap Doxycycline 100 mg BD for15 (GUD); non herpetic)

days + Tab Azitromycin 1 g stat

5) Red Tab Acylovir 400 mg TDS for 7 (GUD); herpetic)

days

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6) Yellow Tab Cefixime 400 mg stat + Tab. Lower abdominal pain (LAP)
Metronidazole 400 mg BD for 14
days + Cap. Doxycycline 100 mg
BD for 14 days.

7) Black Cap doxycycline 100 mg BD for 21 IB { Inguinal Bubo}

days + Tab Azitromycin 1 g stat

Page 330
 5. HIV AIDS
1. HIV
Invades the helper T cells (CD4 cells) in the body of 2. AIDS
the hos t (defense mechanism of a person)
Acquired Immunodeficiency Syndrome HIV is the
Human Immunode ficiency Virus A unique type of virus that causes AIDS
virus (a retrovirus)
Disease limits the bodys ability to fight infection
Preventable, managable but not curable. due to markedly reduced helper T cells.
Patients predisposed to multiple opportunistic
infections leading to death.

Figure 1 The Viral genome

Lasts for an average of ten years

3. Modes of HIV/AIDS This stage is free from symptoms
Transmission There may be swollen glands
The level of HIV in the blood drops to low
Through Bodily Fluids levels
Blood products Semen and Vaginal fluids HIV antibodies are detectable in the blood

Sharing Needles without sterilization Increases

the chances of contracting HIV 4.3 Stage 3 Symptomatic
Unsterilized blades The immune system deteriorates
Through Sex Unprotected Intercourse Oral, Opportunistic infections and cancers start to
sexual, Anal appear.
Mother-to-Baby - Before Birth, During Birth,
After Birth 4.4 Stage 4 - HIV AIDS
The immune system weakens too much as CD4
4. Stages cells decrease in number.
4.1 Stage 1 Primary
Short, flu-like illness - occurs one to six weeks
after infection 5. Opportunistic Infections
Mild symptoms associated with AIDS
Infected person can infect other people
CD4<200
4.2 Stage 2 Asymptomatic Bacterial infections, Tuberculosis (TB), Herpes

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Simplex, Herpes Zoster, Vaginal candidiasis, Hairy
leukoplakia, Kaposis sarcoma
5.1 Tb & HIV Co-Infection
TB is the most common opportunistic infection in
HIV and the first cause of mortality in HIV infected
patients (10-30%)
10 million patients co-infected in the world.
Immuno-suppr ession induced by HIV modi fies the
clinical presentation of TB: Subnormal clinical and
roentgen presentation
High rate of MDR/XDR
High rate of treatment failure and relapse (5% vs<
Blood Detection Tests :Table No: 1
HIV enzyme-linked immunosorbent assay (ELISA)
Western Blot
HIV rapid antibody test
Absolute CD4 lymphocyte count
HIV viral load tests
7. Treatment Options
7.1 Treatment of opportunistic infection
Table 1 : Managing Ols before starting ART
Drug reaction
Acute diarrhea which may reduce absorption of ART
Non-severe anemia ( Hb<8g/ liters)
Skin conditions such as PPE and sebor rhoeic
dermatitis, psoriasis, HIV-related exfoliative
dermatitis.
Suspected MAC , cryptosporidiosis and
microsporidiosis
Cytomegalovirus infection
1% in HIV)
6. Testing Options for HIV
6.1 Anonymous Testing
No name is used
Unique identifying number
Results issued only to test recipient
6.2 Blood Test
Screening test for HIVSensitivity> 99.9%
Confirmatory test
Specificity> 99.9% (when combined with ELIZA)
Screening test for HIV
Simple to perform
Predictor of HIV progression
Risk of oppor tunistic infections and AIDS when
<200
Best test for diagnosis of acute HIV
infection correlates with disease
progression and response to HAART
Do not start ART during an acute reaction
Diagnose and treat first, start ART when diarrhea is
stabilized or controlled
Start ART if no other causes for anemia are found (
HIV is often the case of anemia ): avoid AZT
Start ART (ART may resolve these problems)
Start ART (ART may resolve these problems)
Treat if drugs available; if not, start ART
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 Table 1 : Managing Ols before starting ART
Toxoplasmosis Treat; start ART after 6 weeks of treatment and when
patient is stabilized.

Figure 2 HAART = highly active anti retroviral treatment

7.2 Antiretroviral Therapy Regimens
Currently, the national programme provi des the
following drugs/ combinations for first-line
regimen.
Fixed- dose combinations (FDCs) are preferred
because they are easy to use, have distribution
adva ntages (procurement and stoc k management),
improve adherence to treatment and thus reduce
the chances of development of drug resistance.
The current national experience show that bid
(twice a day) regimens of FDCs are well tolerated
and complied with.

Page 333
 Table 2 : Revised NACO ART Regimen 2012
Regimen I Zidovudine + First line Regimen for patients with Hb 9 gm/dl and not on
concomitant ATT
Lamivudi ne +
Nevirapine
Regimen I (a) Tenofovir + First line Regimen for patients with Hb< 9 gm/dl and not on
concomitant ATT
Lamivudi ne +
Nevirapine

Regimen II Zidovudine + First line Regimen for patients with Hb 9 gm/dl and not on
concomitant ATT
Lamivudi ne +
Efavirenz
Regimen II (a) Tenofovir + First line Regimen for patients with Hb< 9 gm/dl and not on
concomitant ATT. First line for all patients with Hepatitis B and /
Lamivudi ne +
or Hepatitis C co-infection First line Regimen for pregnant
Efavirenz women,with no exposure to sd-NVP in the past.

Regimen III Zidovudine + Regimen for patients on AZT containing first line regimen, who
develop toxicity to both NVP and EFV Also second line regimen
Lamivudi ne +
for those who are on TDF containing first line regimen if Hb 9
+ Atazanavir/ gm/dl
Ritonavir

Regimen III (a) Tenofovir + For patients of regimen III who develop severe Atazanavir
toxicity First line regimen for patients with HIV-2 infection with
Lamivudi ne +
Hb 9 gm/dl
+ Lopinavir /
Ritonavir
Regimen IV Tenofovir + Second line regimen for those who are on AZT / d4T containing
regimen in the first line. Also for patients on TDF containing first
Lamivudi ne +
line regimen who develop toxicity to both NVP and EFV.
Atazanavir / Ritonavir

Regimen IV (a) Tenofovir + For patients on regimen IV who develop severe Atazanavir
toxicity First line Regimen for patient with HIV 2 infection with
Lamivudi ne +
Hb 9 gm/dl First line Regimen for all women exposed to sd-
Lopinavir /
NVP in the past.
Ritonavir

Regimen V Stavudine + Second line for those who are on TDF containing regmen in the
Lamivudi ne + first line if Hb 9 gm/dl
Atazanavir / Ritonavir
Regimen V (a) Stavudine + For patients on Regimen V who develop severe Atazanavir
Lamivudi ne + toxicity.
Lopinavir /
Ritonavir

Page 334
Antiretrovi ral Drugs Higgly active anti 9. Post Exposure Prophylaxis
retrovovival treatments
(PEP)
Nucleoside Reverse Transcriptase inhibitors
(NRTI) Steps to be taken on exposure to HIV
AZT (Zidovudine), Lamividine, Ditanosine, infected blood, body fluids and contaminated
Abacavir, Empricitadine, Tinofavir (Nt RTI) sharps etc
Non-Nucleoside Transcriptase inhibitors 1. Actions to be taken
(NNRTI) Immediately following on expos ure:
Viramune (Nevirapine), Effvirenz
Protease inhibitors (PI) i. Needles pricks and cuts should be washed
Ritonavir, Lopinavir with soap and water
ii. Splashes to the nose, mouth or skin should be
8. Primary Prevention flushed with water
Five ways to protect yourself: iii. Eyes should be irrigated with clear water,
saline or sterile irrigant
Abstinence
iv. Do not pa nic
Monogamous Relationship
Protected Sex v. Pricked finger should not be put in to mouth
Sterile needles by reflex
New shaving/cutting blades vi. Do not squeeze the pricked finger to expel
the contaminated blood
vii. PEP should be started within 72 hours of
expos ure, within 2hrs is ideal.

2. Post Exposure Prophylaxis (PEP)

The decision to start PEP is made on the basis of

degree of expos ure to HIV and the HIV status of
the source from where the expos ure infection has
occurred.

2.1 Exposure Code Determination

Page 335
 Figure 3 Exposure Code Determination

Is the source of material blood, body fluid, other potentially

infectious material (OPIM) or an instrument contaminated with one
of these substances

YES No No PEP Needed

OPIM Blood or Body Fluid

What Type of Exposure has occured

Mucous membrane or Skin Intact Skin only Percutaneous

integrity contaminated Exposure

Volume No PEP needed Severity

Small i.e. Few drops, Large e.g. several Less severe e.g. solid More severe e.g.
short duration drops major blood needle superficial large base hollow
splash and / or scratch needle, deep
longer duration punctures, visible
(i.e. several blood or device,
minutes or more) or needle used in
source patients

EC1 EC2 EC2 EC3

Page 336
2.2 Determination of HIV status of source :

Figure 4 Exposure Source

THE HIV STATUS OF THE EXPOSURE SOURCE

HIV NEGATIVE HIV STATUS SOURCE

POSITIVE UNKNOWN UNKNOWN

NO PEP
NEEDED

LOWER TITRE HIGHER TITRE EXPOSURE

EXPOSURE (e.g. (e.g. ADVANCED AIDS
ASYMPTOMATIC AND PRIMARY HIV INFECTION &
HIGH CD4 COUNT ) HIGHER INCREASING VIRAL
LOAD OR LOW CD4 COUNT )

HIV SCI
HIV SC2
HIV SC
UNKNOWN

Page 337
2.3 Pep recommendation based on exposure code & source code
Figure 5 PEP

EC HIVSC PEP Recommendation

1 1 PEP may not be warranted

1 2 Considered basic regimen

2 1 Recommend basic regime

(mos t expos ures are in this category)

2 2 Recommend expanded regimen

3 1 or 2 Recommend e xpa nded regimen

2/3 Unknown If the source (in the case of an unknown source) the settings were the exposure
occurred suggested a possible risk for HIV
exposure and ec 2 or 3 consider PEP basic regimen

*- Details of Exposure code at Annexure 1

** - Details of HIV Source Code at Annexure 2

a. In case of intolerance to Efavirenz, regimen a. containing Tenofovi r + Lamivudine + Pl

b. (ATV/r or LPV/r) can be used after expert dose should be given at bed time with clear
consultaion by an experienced physician. instruction to take it 2-3 hours after dinner & to
avoid fatty food in dinner.
2.4 PEP regimen
c. Wherever PEP is indicated and source is ART 2.5 In case of Sexual Assault :
nave or unknown: recommended regimen is
3 PEP should be provided to exposed person in case
Tenofovir 300 mg + Lamivudine 300 mg +
of sexual assault as a part of overall package of
Efavirenz 600 mg once daily for 28 days.
post sexual assault care.
Wherever available, single pill containing these
formulations should be used. Dual drug regimen
should not be used any longer in any situation for
PEP.The first dose of PEP regular should be
administered as soon as possible, preferably
within 2 hours of expos ure and the subsequently

Page 338
PSYCHIATRY

Page 339
 1.MENTAL ILLNESS
1. Introduction
15 to 20 % of general population suffers from
major or minor type of psychiatric illness
causing significant degree of morbidity &
mortality in society.
It is therefore necessary to know about
commonly occurring mental illnesses & their
primary management.
2. Classification of Psychiatric
Disorders
2.1 Psychiatric illnesses can be
broadly divided into two
categories:
2.1.1 Major psychiatric illnesses (Abnormality in
thinking,e motions, and behavior leading
tosevere impairment in Social and
Occupa tionalfunctioning).
Schizophrenia.
Bipolar Mood Disorder.
Major Depressive Disorder.
2.1.2 Other disorders
a) Anxiety disorders -
General Anxiety disorders.
Phobias.
Obsessive & Compulsive Disorders.
Somatoform Disorder and Conversion Disorder.
b) Special Group Disorders -
Dementia/ Alzheimers Disorder.
Substance use disorder.
Children and Adolescent Disorder.
Intelligence Disability Disorder.
Psychiatric Emergencies ex. Suicide, violence.
Page 340
 2. EVALUATION: HISTORY& MENTAL
STATUS EXAMINATION (MSE)
History: Data from patient (subjective) / from procedures, head injury, Epilepsy and Medico-
reliable informant (objective) Legal issues.
Demographic details:- Family h /o of ps ychiatric illness, addictions,
o Name suicide.
o Sex/Age Developmental history.
o Address Level of education.
Presenting complaints:-Onset/duration/progress. Occupational history.
Past h /o of psychiatric illness/treatment. Marital history.
Past h/o of medical illnesses (Hypertension, Personal history - anyaddiction.
Diabetes, TB, Enteric Fever etc) / surgical Premorbid personality.

Table No 2.1: Mental Status Examination For mat

1. Appearance Tidy untidy

Appropriately dressed Over dressed
2. Attitude Cooperative Uncooperative
3. Behavior (psychomotor DullNor malIncreased
activity)
4. Eye to eye contact PresentAbsent
5. Rapport Established Difficult to Establish
Not Established
6. Speech NormalMute Speaking very few wordsOver talkative
CoherentIncoherent
RelevantIrrelevant
Flight of ideas Thought block
7. Mood Euthymic AnxiousIrritable
Elevated SadDepressed
8. Affect NormalCheerfulHappy Tearful
Depressed Blunt
9. Hallucinations (Abnormal AuditoryVisual OlfactoryTactile
perception without external Gustatory
stimulus)
10. Delusions (Firm & false Persecution Grandiosity Reference Infidelity
belief)
11. Obsessive Cleaning WashingArranging
thoughts/compulsive RitualsVerbal
behaviors
12. Suicidal/Homicidal ideation PresentAbsent
13. Level of consciousness Alert DrowsyStuporous
14. Orientation TimePlace Person
15. Attention & concentration SustainedNot sustained
16. Memor y IntactImpaired
17. Intelligence Average Below average
18. Judgment IntactImpaired
19. Insight PresentAbsent
**Delusions and Hallucinations are the cardinal features of Schizophrenia / Psychosis

Page 341
 3. SCHIZOPHRENIA
Anxious and fearful affect.
1. Introduction Poverty of speech.
Delusion of Persecution and/or Reference.
Schizophrenia is a mental disorder of chronic nature
in which there is primary impairment of thought s, Audi tory Hallucinations.
emotions and behavior which leads to sever socio- Lack of Insight.
occupational impairment and personality Impaired Judgment.
deterioration.
4. Investigations
2. Symptoms No diagnostic investigations available.
Suspiciousness. Complete Haemogram, Blood Sugar, Renal
Fearfulness. Function Test, Liver Function Test, Serum
Social withdrawal. Electrolytes, Urine Routine, Chest X-Ray (If
Muttering / smiling to self. necessary).
Poor self care.
Disturbed sleep.
5. Complications
Work impairment. Severe agitative behavior,
Homicidal tendencies,
3. Signs Self harm / Suicidal behavior.
Unkempt appearance. Catatonic Stupor/Excitement.
Increased or decreased Psychomotor activity.

6. Treatmentand Management:
6.1 Antipsychotics:Primary care phys ician can start single drug a nd titrate it up to o ptimum level
Table No3.1 Antipsychotics

Name Strength Recommended doses** Duration/ Remark

Trifluoperazine 5mg 10-40 mg/day Drugs to be started in low
Trihexyphenidyl 2mg 2-6 mg/day dos es and gradually
Haloperidol 5mg 10-30mg/day increase till 80 %
Risperidone 2mg 4-8mg/day improvement.
Olanzepine 5mg 5-20mg/day
Quetiapine 50/100mg 50-300mg/day Maintenance doses to be
Clozapine 50mg 50-200mg/day continued long term
Chlorpromazine 50mg 50-200mg/day
To be given in divided doses:- It is to be monitored by ps ychiatrist.

6.2 Sedatives:
Table No3.2 Sedatives

Name Strength Recommended doses Duration/ Remark

Lorazepam 2mg 1-4mg HS Drugs to be started in low
Diazepam 5mg 5-10mg HS doses preferably at night
Clonazepam 0.5mg 0.5-1mgHS and to be tapered off
Nitrazepam 5mg 5-10mg HS within 2 weeks

Page 342
6.3 Modified Electro-Convulsive
Therapy:
Minimum of 8-15 sessions of modified ECT are
required.
6.4 Treatment and Management of
Complications:
Inj. Haloperidol 10mg BD/ SOS for 2/3 days. OR
Inj. Promethazine* 50 mg BD/ SOS for 2/3
days
6.5 Maintenance Therapy:
All patients with Schizophrenia have to be
maintained on long term antips ychotics oral or
injectable treatment.
Depot Inj:
Inj Haloperidol Decanoate 50mg once a month deep
IM
Inj Fluphenazine 25mg once a month deep IM.

(*Not to exceed 100mg/da y.) OR

Elecro-convulsive Therapy. Inj Flupe nthixol 40mg once a month deep IM.
Inj. Diazepam 10mg or Lorazepam 4mg if
required.

6.6 Side effect & management:

Table No3.3 Common Side Effects and Management

Side Effect Manage ment Durat ion/ Remark

Tremors at extremities/ Salivation
Dystonic Reaction/ Rigidity
Dry Mouth/Constipation
Neuroleptic Malignant Syndrome
(Rigidity, Fever, Disorientation,
Reduced urine output)
Trihexyphenidyl 2-6mg along with antipsychotic
drugs.
Inj. Promethazine 50mg Stat / SOS SOS
Reduce dos e of Trihexyphenidyl 1 week
Stop Antipsyc hotics Till patient recovers and CPK level
comes to normal.
Inj Lorazepam, Tab.
Bromocriptine, Supportive
Management

6.7 Counseling and Psychotherapy

Refer to higher centre if needed.

Page 343
 4. BIPOLARMOOD DISORDER
1. Introduction 5. Signs of Depression
Distinctive episodes of abnormally and Dull, withdrawn.
persistently elevated, expansive, irritable or Poor eye contact.
depressive mood. Decreased productivity of speech.
Patient may be in Mania or Depression or Crying spells.
present with mixed features. Feelings of guilt.
Suicidal thoughts, ideas & plans.
2. Symptoms of Mania Decreased appetite.
Over talkative. Sleep disturbances.
Hyperactive.
Over familiar/ Over religious/
Overspending/Over grooming. 6. Investigations
Big talks. No diagnostic investigations available.
Decreased need for sleep. Complete Haemogram, Blood Sugar, Renal
Work Impairment. Funtion Test, Liver Function Test, Serum
Electrolytes, Urine Routine, Chest X-Ray (If
necessary).
3. Signs of Mania
Increased psychomotor activity.
Pressured speech/ flight of ideas.
7. Complications
Grandiosity. 7.1 Mania:
Easily distractible/ irritable. Severe agitative behavior,
Hypersexual behavior. Homicidal tendencies.
Audi tory hallucinations of God/ Actors talking to
him. 7.2 Depression:
Self harm / Suicidal behavior.
4. Symptoms of Depression
Persistent and pervasive low/ sad mood.
Lack of energy/interest/initiative.
8. Treatment and Management
Hopelessness/ worthlessness/ helplessness. of Mania
Feeling of guilt, agitation. 8.1 Antipsychotics:
Suicidal ideas/ attempts. Primary care physician can start single drug a nd
Decreased sleep, appetite and libido. titrate it up to optimum level
Sometimes hearing of voices.
Work impairment.

Table No 4.1 Antipsychotics

Name Strength Recomme nded doses** Durat ion/ Remark

Trifluoperazine 5mg 10-40mg/da y Drugs to be started in low
Trihexyphenidyl 2mg 2-6 mg/day dos es and gradually
Risperidon 2mg 4-8mg/day increase till 80 %
Olanzepine 5mg 5-20mg/day improvement.
Quetiapine 50/100mg 50-300mg/day
Chlorpromazine 50mg 50-200mg/day Maintenance doses to be
continued long term
**To be given in divided doses

Page 344
8.2 Sedatives:
Table No 4.2 Sedatives

Name Strength Recomme nded doses** Durat ion/ Remark

Lorazepam 2mg 1-4mg HS Drugs to be started in low
Diazepam 5mg 5-10mg HS doses preferably at night
Clonazepam 0.5mg 0.5-1mg HS and to be tapered off
Nitrazepam 5mg 5-10mg HS within 2 weeks.
**To be given in divided doses

8.3 Mood Stabilizers

Table No 4.3 Mood Stabilizers

Name Strength Recomme nded doses** Durat ion/ Remark

Carbamazipine 100/200mg 100 to 600mg/ da y Drugs to be started in low
Lithium 300mg 300 to 900mg/da y dos es and gradually
Divalproex 250/500mg 500 to 1500mg/da y increase till 80 %
improvement.

Maintenance doses to be
continued long term .
**To be given in divided doses

8.4 Side effects of mood Modified Electro-Convulsive

stabilizer:
Carbamaz epine- Giddiness, blurred
vision, rash, hypotension.
Lithium- Tremors, muscle twitching,
disorientation.
Divalproex Sodium-Gastric irritation,
weight gain, lethargy, confusion,
tremors.
Therapy: Minimum of 8-15 sessions of modified
ECT are required.
9. Treatment and Management
of Depression
9.1 Antidepresent:
Primary care physician can start single drug a nd
titrate it up to optimum level.

Table No 4.4 Treatment and Management of Depression

Name Strength Recommended doses** Duration/ Remark

Imipramine 25mg 50 to 150mg/da y To be started in low doses
Amitriptyline 25mg 50 to 150mg/da y & gradually increase till
Sertraline 25/50mg 25 to 100mg/da y 80 % improvement. To
Escitalopram 5/10mg 5 to 20mg/da y continue at least 6 months
Mirtazapine 7.5/15mg 15 to 30mg/da y & more if necessary
Desvenlafaxin 50mg 50 to 100mg/da y
**To be given in divided doses
9.2 Sedatives
Table No 4.5 Sedatives

Name Strength Recommended doses** Duration/ Remark

Lorazepam 2mg 1-4mg/HS Drugs to be started in low
Diazepam 5mg 5-10mg/HS doses preferably at night
Clonazepam 0.5mg 0.5-1mg/HS and to be tapered off
Nitrazepam 5mg 5-10mg/HS within 2 weeks

Page 345
9.3 Modified Electro-Convulsive
Therapy:8-15 sessions if needed.
9.4Treatment and Management of
Complications during Mania:
Inj. Haloperidol 10mg BD/ SOS for 2/3
days.
Inj. Promethazine* 50 mg BD/ SOS for 2/3
days ( *Not to exceed 100mg/day)
Elecro-convulsive Therapy.
Inj. Diazepam or Lorazepam 1 amp stat if
needed.
In case of Depression,Elecro-convulsive
Therapy 8-12 sessions if patient shows
suicidal tendencies.
9.5 Precautions for Suicidal patients
24 hrs continuous supervision.
Do not isolate the patient.
Do not keep any sharp objects, ropes,
blades near patient.
Do not allow patient to lock room/
bathroom from inside.
Note - Reduce doses of mood stabilizers if above
side effects are seen.
9.6 Counseling and Psychotherapy
Refer to higher centre if needed.
Page 346
 5.MAJOR DEPRESSIVE DISORDER (MDD)
Sometimes psychotic symptoms like
1. Introduction hallucination and reference ideas.
Depression is major public health problem.
Atypical symptoms,
By 2020, it will be the major cause of worldwide o Overeating
morbidity and mortality. o Oversleeping
MDD is a disabling condition that severely o Agitation
affects a persons family work, sleeping, eating o Decreased libido
habits and general health
It is the leading cause of suicide.
4. Investigations
2. Types: Mild, Moderate, No diagnostic investigations available.
Severe. Complete Haemogram, Blood Sugar, Renal
Funtion Test, Liver Function Test, Serum
Electrolytes, Urine Routine, Chest X-Ray (If
3. Signs and Symptoms of necessary).
MDD
Pervasive and persistent low mood.
Low self esteem.
5. Complications:
Self harm / Suicidal behavior.
Loss of interest or pleasure in normally enjoyed
activities.
Lack of energy and e nthusiasm, easy fatigue.
Loss of appetite, weight loss
6. Treatment and Management
Disturbed sleep. of Depression
Hopelessness, Helplessness, worthlessness.
Suicidal thoughts, ideas or attempts. 6.1 Antidepressants:

Table No6.1 Treatment and Management of Depression

Name Strength Recomme nded doses Durat ion/ Remark

Imipramine 25mg 50 to 150mg/da y To be started in low doses &
gradually increase till 80 %
Amitriptyline 25mg 50 to 150mg/da y improvement. To continue at least
Sertraline 25/50mg 25 to 100mg/da y 6 months & more if necessary.
Escitalopram 5/10mg 5 to 20mg/da y
Mirtazapine 7.5/15mg 15 to 30mg/da y
Desvenlafaxin 50mg 50 to 100mg/da y

6.2 Sedatives:
Table No6.2 Sedatives

Name Strength Recomme nded doses** Durat ion/ Remark

Lorazepam 2mg 1-4mg/HS Drugs to be started in low doses
preferably at night and to be
Diazepam 5mg 5-10mg/HS

Page 347
Clonazepam 0.5mg 0.5-1mg/HS tapered off within 2 weeks
Nitrazepam 5mg 5-10mg/HS
**To be given in divided dosesIf Psychotic features are present, add low dose antipsychotics.

6.3 Modified Electro-Convulsive

Therapy:8-15 sessions are required.
6.4 Treatment and Management of Precautions for Suicidal patients
24 hrs continuous supervision.
Complications Do not isolate the patient.
Elecro-Convulsive Therapy Do not allow patient to lock room/ bathroom
Daily ECTs(if needed), minimum for three from inside.
days.
Counseling and Psychotherapy play a major role.

Refer to higher centre if needed.

Page 348
 6. ANXIETY DISORDER
1. Introduction
Anxiety is a nor mal emotion experienced by
everyone at times of stress.
Symptoms of anxiety are psychological, physical
or mixture of bot h.
Anxiety becomes a disorder when symptoms
become severe, disabling and reduce quality of
life.
Anxiety spectrum disorders tend to be chronic.
2. Presentation
2.1 Generalized Anxiety Disorder
(GAD):
This involves excessive, unrealistic worry and
tension without any definite reason.
Signs and Symptoms
Palpitation, dry mouth, tremors, sweating,
difficulty in breathing, frequency of urination,
abnormal feeling in the gut, muscle tension,
dizziness.
2.2 Panic Attacks:
Can occur in pa tients with GAD
Signs and Symptoms include all of the above
with severe choking sensation and s hortness of
breath with impending feeling of death or going
crazy. The attack lasts for few minutes and
subsides on its own.
If panic attacks occur frequently, then it is called
as Panic Disorder.
2.3 Phobia:
Intense and irrational fear of a specific object or
situation leading to phobic avoidance. E.g. Fear
of public places, closed spaces, heights, animals,
water etc.
2.4 Post Traumatic Stress Disorder
(PTSD):
Disabling fear, intrusive flashbacks or vivid
dreams and emotional disturbances after
traumatic life event causing avoidance of similar
situations.
2.5 Obsessive Compulsive Disorder:
Frequent intrusive thoughts producing
apprehension and fear or worry and leading to
compulsive, repetitive behavior aimed to reduce
the anxiety.
E.g. Frequent thoughts of contamination leading
to compulsive washing. Frequent checking of
locks, gas knobs, counting money etc.
2. Investigations
No diagnostic investigations available.
Complete Haemogram, Blood Sugar, Renal
Funtion Test, Liver Function Test, Serum
Electrolytes, Urine Routine, Chest X-Ray (If
necessary).
3. Complications
Any of the anxiety spectrum disorder can lead to
Major Depressive Disorder making person vulnerable
to suicide.
4. Treatment and Management
IncludesDrug and Non Drug Treatment.
Page 349
4.1 Drug Treatment
Table No 6.1 Drug Treatment

Drug Treatment Durat ion/ Remarks

SSRIs (Any O ne) As anxiety disorders tend to be chronic, treatments
1. Escitalopram 10-20mg/day should be give n for long duration.
2. Paroxetine 12.5-25mg/day
3. Mirtazepine 7.5-15mg/day
4. Fluvoxamine 50-150mg/day (Preferred in OCD)
5. Sertraline 25-50mg/day
TCA
Clomipramine 25-75mg/day

Anxiolytic Drugs(Any O ne)

6. Clonazepam 0.5-1mg/da y
7. Lorazepam 1-2mg/da y
8. Diazepam 5-10mg/day

-Blocker
Propranolol 10-40mg only in panic disorder

4.2 Non Drug Treatments

Table No 6.2 Non drug Treatment

Reassurance
Supportive Therapy
Relaxation Therapy
Expos ure and Response Preve ntion Therapy
Cognitive Behavior Therapy
Yoga and Exercises
Self help techniques

*Comprehensive treatment including drugs and psychotherapies are most effective .

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 7. SOMATIZATION DISORDER
1. Introduction
Excessive thoughts, feelings or behavior related
to the somatic symptoms or associated health
concern.
Persistently high level of anxiety about health
symptoms.
Excessive time and energy spent over these
symptoms and their investigations and
treatments.
2. Signs and Symptoms
Pain in different areas-
Head/Back/Stomach/Joint etc
GI symptoms like nausea, vomiting
One pseudo-neurological condition (Paresis,
Loss of Voice, Loss of Vision).
Symptoms cannot be explained by a medical
condition.
3. Conversion Reaction
Altered voluntary motor or sensory function with
incompatibility between the symptom and
recognized medical/neurological condition.
Causes significant distress in social, occupational
and other important areas of functioning.
Possession Attack is an example of Conversion
Reaction.
4. Investigations
Psychiatric assessment
Laboratory Investigation
o No diagnostic investigations available.
o Complete Haemogram, Blood Sugar, Renal
Funtion Test, Liver Function Test, Serum
Electrolytes, Urine Routine, Chest X-Ray (If
necessary).

5. Management
5.1 Antidepressants (Any One)
a) Tab Sertraline 25-200mg/day in divided doses For 10
b) Tab Amitriptyline 25-100mg/day in divided days.Review
doses
after 10 days
c) Tab Escitalopram 5-20mg/day in divided doses
& then taper
5.2 Anxiolytics (Any One)
a) Tab Lorazepam 2mg HS/SOS Gradually.
b) Tab Clonazepam 0.5-1mg HS/SOS
c) Tab Diazepam 5-10mg HS/SOS
5.3 Counseling and Psychotherapy- Supportive, Cognitive Behavioral, REBT
5.4 Stress Management andLifestyle changes.

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 8. ORGANIC BRAIN SYNDROME

1. Introduction 2.1.3Risk factors are:

Primary biochemical or structural disturbances Old age, preexisting dementia, very young,
(damage) to the brain resulting in impairment of postoperative, burns victim, alcoholic and
mental functions affecting memory, orientation Benzodiazepine dependence.
and cognition.
2. Types of organic brain 2.1.4 Signs and Symptoms:
syndrome Confusion.
Acute organic brain syndrome- Delirium Clouding of Consciousness.
Chronic organic brain syndrome- Dementia Visual illusion and hallucination.
Other/ Sub-Acute Organic Brain Syndrome- Labile affect.
Amnestic syndrome. Disorientation to time, place, person.
Hyperactivity or hypoactivity.
2.1 Delirium: 2.1.5 Investigations:
2.1.1 Definition: Complete Haemogram, Blood Sugar, Renal Function
It is a clinical syndrome of fluctuating global Test, Liver Function Test, Serum Electrolytes, Urine
cognitive impairment of consciousness, attention Routine, Chest X-Ray (If necessary).
and orientation. 2.1.6 Manage ment:
Additional disturbances in memor y, language Ide ntify and treat the precipitating cause.
and perception may occur.
Provide environmental & supportive care.
Commonly occurs in hospitalized patient with
Avoid sedation. But for severely agitated
history of major preexisting medical,
patients it may be necessary to induce sedation in
neurological or surgical illnesses.
order to facilitate investigations and treatment.
2.1.2 Causative Factors: Regular clinical review, close vigilance.
Substance intoxication (alcohol, cannabis, opioid
2.1.7 Medication:
etc).
Important:
Substance withdrawal. Watch for level of consciousness before giving
Medicine induced. injectables.
Delirium due to preexisting medical conditions
e.g. Hepatic Encephalopathy. Use single medication - Start low, go slow.

Haloperidol - 1-4mg /da y

Lorazepam - 0.5-1mg daily Initially for 3 days,
Risperidone - 1mg daily review & titrate
Quetiapine - 25mg 100mg daily the dose.
(To be given in divided doses)

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All anti psychotics and sedatives to be tapered
gradually, once symptoms are relieved.
2.1.8 Refer to higher center.
For Counseling and Psychotherapy.
2.2. Dementia:
2.2.1Definition:
Itis a syndrome characterized by progressive, usually
irreversible, global cognitive deficits primarily
characterized by me moryi mpairme nt and
dysfunction in Activity of Daily Living (ADL).
2.2.2 Common Causes of Dementia
Vascular dementia (20%).
Substance Use Disorders (10%).
Subdural hematoma.
Vitamin B12 deficiency.
Metabolic causes,Hypothyroidism.
All Anti psychotics and Sedatives to be tapered
gradually once symptoms are relieved.
Refer to higher centre for Counseling and
Psychot herapy.
2.2.3 Signs and Symptoms:
Memory impai rme nt.
DysphasiaDeficiency of words, name
generation.
Agnosia Inability to recognize parts of body.
Aprax ia Inability to perform purposeful action
and draw objects.
Impaired exe cutive function Inability to plan
and take action accordingly.
Personality disintegrationResulting
maladaptive behavior.
2.2.4 Investigations:
Complete Haemogram, Blood Sugar, Renal
Funtion Test, Liver Function Test, Serum
Electrolytes.
Urine Routine.
Chest x Ray.
Thyroid Function Test.
HIV.
Vit B12,Folate levels.
ECG.
CT brain, MRI.
EEG abnor mal dependi ng upon the cause.
2.2.5 Treatment and Manage ment
a. Cog nitive Enhancers
(ACE inhibiter)
Oral Donepezil 2.5-10mg / day lifetime.
b. NMDA antagonist
Oral Memantine 5mg.
Associated Psychosis/agitation
Tab. Quetiapin 25mg - - 1
OR
Tab. Risperidone 1mg /day Titrate the dose, regular
follow up and then stabilize the dose for two years.
Taper the dose after two years.
c. Associated Depression/Insomnia
Tab Sertraline 25mg/day, for 2 months & then
titrate the dose.
Tab Escitalopram 10mg/day, Lorazepam 0.5
mg/da y.
Anti-psychot ics and Anti-depressants to be
discontinued once symptoms relieve d.
2.2.6 Treatment of co-morbid medical illnesses:
a.Supportive
High doses of Multi Vitamins.
b. Assistance
For routineactivitieslike bath, food etc.
in Keep surroundings of patient safe and calm and
well lit.
c. Psychological support
To both patient and caregiver.
d. Functional manage ment
Maximize mobility & independence, assist
communication.
e. Social management
Shelter homes, recreational activities, assistance
in financial and legal matters.
Page 353
 9. DRUG ABUSE&SUBSTANCEUSEDISORDER
consequences in physical, social, legal aspects of
1. Introduction life.
When substances like alcohol, caffeine,
cannabis, inhalants, opioids, sedatives and Patients of addictions, especially of alcohol, are
hypnotics etc are taken in excess quantities, they the most commonly treated cases in rural set up.
produce intense activation of the brain and
disinhibition.
2. Common Substance
Addiction- Repeated, compulsive use of a Disorder
substance that continues in spite of negative

Table No 9.1 Common Substance Disorders

Condition Sign & Symptoms Manage ment Durat ion

Alcohol intoxication Aggressive behavior, mood No active treatment Till symptoms
Caused by excessive lability, slurred speech, needs to be given. recover.
consumption of Alcohol incoor dination, unsteady gait, Manage
nystagmus, impaired symptomatically.
judgment.
If excited-
Inj.Haloperidol 5mg +
Inj.Phenergan 50mg
IM.
IV fluids SOS.
Alcohol withdrawal Autonomic hyperactivity, Inj.Thiamine 100 mg 5-7 doses on alternate
tremulousness, insomnia, and Multivitamin days
Caused by Cessation or
psychomotor agitation, infusion.
reduction of alcohol use that
nausea/ vomiting, transient
has been heavy and Inj. Lorazepam 1 2-3 days
visual, tactile, auditory
prolonged earlier. ampule BD/ HS.
illusion or hallucinations.
4-5 days and taper
Shift to Tab.
gradually.
Loazepam 1mg TDS
/SOS.
IV Fluids As necessary.

Delirium Tremens Tremors, disorientation, 1. IV Inj.Thiamine 10 days

It is a severe form of confusion, hyperactivity, 100mg /day in 100
Withdrawal insomnia, illusions, ml NS.
severe anxiety, seizures 2. IV 5% Dextrose As needed.
Close monitoring of vital hallucinations. and DNS.
functions like pulse, BP, 3. Inj.Diazepam 5mg 5 days.
temperature, input and IM TDSor Inj
output is very essential. lorazepam 2 mg
IM/IV TDS.
4. Tab.Diazepam 5mg As needed.
TDS or Tab.
Lorazepam 6-12
mg/day in divided
doses.

Page 354
 5. Inj. 6 days.
MVI(MultiVitmin
Injection) + 5%
Dextrose drip.
6. If severe agitation Till psychotic symptoms
or perceptual recover.
abnormality present
Tab.Olanzapine
2.5-10mg or
Tab. Risperidone
2-4mg per da y in
divided doses.
Cannabis intoxication Dryness of mouth, 1. Supportive As needed.
tachycardia, reduced motor treatment and IV
skills, euphoria, sleepiness, Fluids.
apathy, laughter, paranoia, 2. Benzodiazepines
hallucinations. eg. Clonazepam
0.5mg / Lorazepam
1mgTDS.
3. Tab Olanzapine 5 days.
5mg HS.
Cannabis withdrawal Anxiety, irritability, 1. Supportive 3-5 days.
depressed mood, restlessness, treatment and IV
insomnia, loose motions, Fluids
2. Benzodiazepines
eg. Clonazepam
0.5mg / Lorazepam
1mgTDS.
Opioid withdrawl Dysphoric mood, 1. Lorazepam 1-2 mg 2-3 times a day for 1 st
Heroin, Gard, Afeem, MD, insomnia, muscle aches, oral/I.M./I.V. for Week.
Brown Sugar, Inj. Fortwin nausea or vomitting, anxiety and
diarrhea, lacrimation or decreased sleep.
rhinorrhea, yawning.
2. Tab. Brufen 400mg As needed.
or Tab. Naproxen
250 500mg Or
Paracetamol TDS.

3. Tab. Clonidine As needed.

0.1mg can be give n
2-3 times a day
during
detoxification.
4. IV fluids and As needed.
Supportive Care.
Remark:
All patients with substance addiction should be motivated to enroll in de-addiction centres and to attend support
groups like Alcohol Anonymous(AA) and Narcotic Anonymous(NA).
All other Substance Use Disorder patients should be treated symptomatically and referred to higher centre.

Page 355
 10. INTELLECTUAL SUBNORMALITY
A state of mind with intellectual and functional iii. Postnatal - CNS infections, trauma,
deficits commonly known as Mental Retardation. uncontrolled epilepsy.

1.Incidence 3. Types of Mental Retardation

3 to 4 cases per 1000 population.
1. Borderline
2. Etiology: 2. Mild
3. Moderate
i. Prenatal (1 in 1000 live birth) due to genetic,
4. Severe
intrauterine viral infections, injuries, maternal
5. Profound
metabolic disorders
Refer to the table for details and management.
ii. Perinatal - All causes leading to hypoxia
during birth.

Table No 10.1 Mental Retardation Classifications

Types Borderline Mild Moderate Severe Profound

Dull Slow
Nor mal Learner
I Q range 80 to 90 70 to 80 50 to 70 35 to 50 35 to 15 up to 15
Salient - Scholastic - Can tell rightleft - May not be - May not be able - Cannot feed self.
backwardness in laterality able to tell to name or gans
Clinical - Cannot protect
some subjects but laterality
- Can recognize - May notable to self.
features may complete
coins. - May not recognize
- 10th Standard with recognize all
extra years
- Can use money.
coins Colors
- Can do simple Coins
- And additional
calculation .
- May not tell Count
coaching. all colors
- Can tell relations. - May not
- May not count recognize own
- Can pass 10th beyond 10. family members
std. in selected
- May not be but recognize
subjects.
able to
recognize familiar faces.
relations like
cousins,
uncles.
ADL - Independent - Independent - May need -Needs assistance -Needs to be fed,
help for for bath, bathed,
(Activities of - Can travel on own. - Can use
grooming, protected.
telephone. cleanliness but
Daily bath.
- Good social Can feed self.
Living) - May be able
skills.
to move in
e.g. bath, village but
food, not faraway.

Page 356
grooming etc.

Trainability - Trainable. - Trainable. - Trainable for - Non trainable - Non trainable

- Can earn. - Can earn. - Repetitive - Soremains - So remains
work dependent for life dependent for
long. life long.
- Under
supervision.
-May be able to
earn as
shepherd,
helper
% Disability <50 but eligible for > 40 % > 50 % > 75 % 100%
subject selection.

4. Management
Anti-Psychotics in low doses for behavioral 5. Special Guidance
disturbances. Get IQ assessment certificate and Disability
Anti-Epileptics if the patient has co-morbid certificate from concerned Civil Hospital.
Epilepsy.
ADL training. Enrollment in government employment facility for
Vocational training. gainful employment.
Caregiver education.

Page 357
 11. CHILD& ALDOLESCENT PSYCHIATRY
1. Introduction
Child & adolescent form a major percentage of
population
Many psychiatric problems are present in this
age group.
Early detection and treatment of these conditions
will prevent complications and significantly
reduce the morbidity.
Commonly seen disorders are behavior
disorders, anxiety disorders and depressive
disorders.
2. The child Usually presents as poor
scholastic performance, disobedience, somatic
pain.
2.1 Assessment:
History to be taken from parents, school teacher
and care taker as well as other colleague
children.
Child to be taken into confidence by talking to
him alone.
A large number of these age group patients belong to
the intellectual sub normality disorder.
2.2 Important childhood
disorders:
2.2.1 Psycho-developmental disorders :
A. Learning Disorders or Dyslexias
IQ of the child is normal but still he lags in scholastic
performance due to specific learning disability i. e.
Writing dyslexia - wrong spellings and
grammatical mistakes.
Reading dyslexia - unable to read sentences
and words with proper pronunciations.
Arithmetical dyslexia - conf usion in
mathematical symbols e. g. +, -, x, 3, 6,
i. e. geometrically reverse symbols, resulting
into poor performance in solving and
understanding mathematics.
Global dyslexia - all of above.
Detection of dyslexia is usually done by the school
teacher and confirmation has to be done by
government approved agency such as special units in
teaching hospitals / medical colleges.
Certified patients can avail the provision of a writer
and extended time to write a paper in 10th std. and
12th std. board examinations. Remedial teaching by
specially trained teachers either one to one or in
groups of a few children is very effective.
B. Pervasive Developmental Disorder of
Childhoo d or Autism
Such children do not mix or communicate verbally or
emotionally even with their parents. They are self-
engrossed in non goal directed activities. Usually non
complaining & self-sufficient. Odd motor
movements, peculiar speech pattern,attracted by
music. Those with normalIQ may excel in some arts
like music, dr awing.
Some such patients may need small dose
antipsychotic if self-destructive. Tab. Haloperidol
1.5 mg half tablet HS.They need special training in
one to one setup.
2.2.2 Psycho e motional disorders :
A. Attention Deficit Hyper Activity Disorder -
ADHD/ADD. not uncommon.
Clinical symptoms
InattentionI.e. not able to mentally focus at a
given task adequate enough to understand it or
perform it. Easily distractible & so, forgetful.
Hyper activity Always driven by some
move ments; cannot sit still; runs around; climbs
windows; cupboards.
Impulsivity Acts before thinking; shifts from
one activity to another; disruptive.
Plenty of complaints from the school, neighbors.Most
of the children show good response to psycho
stimulant medicine.
Tab. Methylphenidate 5 to 10mg OD
or
Cap Atomoxetine 10 to 25mgOD.
B. Childhoo d Depression common.
C. Nocturnal Enuresis due to environme ntal
stress.
Common.
Shows good response to Tab. Imipramine
25mgHS.
Page 358
2.2.3 Performance Anxiety, Phobia, Oppositional disobedient, negativistic, temper
Childhoo dDepression, Tension headac he, tantrums, argumentative, stubborn, not yielding to
Somatization disorderare also commonly rules.
seen among children facing stress at home or
Manage ment:
at Aashramshala or in the school . They need to
Small doses of antidepressant e.g.Tab. Imipramine
be managed with medication (discussed
25mg 0-0-1 or Tab. Sertraline 25 mg - 0 0 to 1-
already) and along with counseling.
0-0 for a short period. Benzodiazepines should be
Clinical symptoms:
avoided.
Headache, pain in abdomen, migraine, loose
motions, vomiting, exacerbations of asthma, Behavioral modification using positive/negative
fever, skin rash. reinforcers,
Irrational fear and phobia of animals, ghosts,
Childhood psychoemotional disorders are
darkness, school which ultimately resulting
usually secondary to environmental stress. So,
into avoidance to school.
modification of the stressful environment and
Sleep disturbances, nightmares, enuresis. improving childs coping capacity must be
Child remains withdrawn and introvert, not taken care to relieve symptoms. Medication is
playing, crying spells, excessively shy, as mentioned, to be given only till symptoms
Temper Tantrums. active, and in dosages appropriate to weight.
Small doses of antidepressant e.g.Tab.
Imipramine 25 mg HS or Tab. Sertraline 25
mg - 0 0 to 1-0-0 for a short period. Note:All suspected cases need exhaustive evaluation
Benzodiazepines should be avoided. by psychiatrist, so must be referred if not
responding to above medication.
2.2.4 Conduct disorder
In adolescents Antisocial behaviors like violating
rules, showing aggression, running away from home,
lying, stealing, lack of guilt feeling.

Page 359
 12.PSYCHIATRICEMERGENCIES
1.Suicidal Attempt
4. Catatonic Stupor
1.1 Causes: Patient develops complete mental and physical
Severe depression - associated with financial inactivity, becomes statue like and non
burden, crop failure, love affair failure. communicative. Does not eat for many days and
Schizophrenia. develops dehydration.
Drug induced ps ychoses like alcoholic
hallucinations. 4.1 Causes:
Impulsive act. Depression.
Psychotic illness.
1.2 Management: Organic brain disorder.
Immediate physical resuscitation.
Treatment for psychiatric illness ECT and 4.2 Management:
medicines. I.V. fluids.
24 hrs continuous supervision. Inj. Lorazepam 1mg slowly BD till
Do not isolate the patient. symptoms reduce.
Do not keep any sharp objects, ropes, blades Ryles tube feeding.
near patient. ECTs.
Do not allow patient to lock room/ bathroom Low doses of antipsychotic.
from inside.
Counseling and ps ychotherapy.
6. Dystonic Reaction
Sustained muscles contractions causing twisting
2. Psychotic excitement and repetitive movements or abnormal postures.
2.1 Causes: e.g. neck dystonia, tongue protrusion.
Schizophrenia.
Mania. 5.1 Causes:-Use of antipsychotics like
Psychoactive drug abuse like charas, ganja, Haloperidol,Trifluoperazine,Risperidon,
alcohol. Olanzapine.

2.2 Management: 5.2 Management:

Injection Haloperidol 10mg IM twice a day
Injection Promethazine 50mgIM twice a day
till excitement controlled.
Restrain the patient to avoid injuries to self
or others or destruction of property.
I.V. fluids if patient not eating / R. T.
feeding to maintain hydration and nutrition.
Oral antipsychotics.
ECTs.
3. Delirium
Management as given under topi c of same name.
Taper off the anti psychotic.
Injection Phenergan 50mg IM twice a day
to be tapered off over next 4-5 days
depending upon symptom relief.
Tab. Benzhexol 2mg 1-1-1 till symptoms
subside.
I.V. fluids till patient able to eat orally.
Change of antips ychotic by Psychiatrist.
Note: all patients of psychiatric emergencies need to
be referred to psychiatrist as early as possible, once
they are fit to travel.

Page 360
 13. PROCEDUREFOR ADMISSIONTOA
MENTAL HOSPITAL
1. Introduction:
All admissions to any government or private mental
hospital are governed by the Mental Health Act-
1987.
The act provides guidance for - admission
and discharge procedures of civil & criminal
patients.
Management of prope rty of the patients.
Safeguarding human rights of the patients.
2. Admissions
2.1 Voluntary Boarder -Patient himself
signs the application requesting the
superintende nt of a mental hospital to allow him
to stay in the hospital for treatment of his mental
illness. Maximum stay 90 days.
2.2 U/s. 19 (Mental health Act)-When
patient not capable of signing above application
due to his mental illness then, he is examined by
2 Psychiatrist indepe nde ntly and if found to need
admission, can be admitted for maximum 90
days.
2.3Detention Order - A suspected mentally
ill person can be admitted to a mental hospital
for 10 days of observation period by the
Detention Order of the Hon. District Civil Judge
or the CP of the area.
This section usually used for admission of
wandering mentally ill people suffering of
schizophrenia, mental sub normality, delirium,
dementia etc. Also for criminal people behaving
abnor mally.
On certification after observation period,the stay
in the hospital for treatment can be extended by
the Reception Order from the concerned (i.e
the district of the patients residence) court.
2.4 Reception Order - By the concerned
District Civil Court is issued only on
confirmation of the mental illness and then, the
patient can stay beyond 90 days till recovery.
such a patient eve n on discharge can extend his
order with the leave of absence facility for 60
days forever (i.e. he can be readmitted with the
original R.O. any time in future without further
legal procedures).
3. Documents required
Documents required for above legal procedures:
3.1 Address proof of the patient or his caretaker.
3.2 Photographs of the patient and his caretaker.
3.3 Undertaking to pa y hospital charges by the
caretaker unless exempted by court order or by
provisions under the GR ---
3.4 Medical Certificates by 2 Psychiatrist for U/s.
19 and for obtaining R. O. if patient admitted as
D.O.
3.5 Medical Certificates in prescribed format by
one Medical Officer in government service and
by any Registered Medical Practitioner for
application for R.O.
Note:
i. All court procedures to be done during court
timing i.e between 10 am to 5.45 pm.
ii. Patient and all documents to be presented to the
court.
iii. No legal procedures needed for admission at a
Civil Hospital or a General Hospital, as the
patient is not isolated from society. Hence, such
admissions to be encouraged.
Page 361
ENT

Page 362
 1.ACUTE OTITIS MEDIA (AOM)
1. Definition -
Fig 1. Congestion of eardrum
1.2 Symptoms& Signs -
1. Pain, Fever
2. Congestion of the eardrum (Tympanic membrane)
& loss of normal light reflex
3. Hearing Impairment
4. Bulging Tympa nic Membrane & tinnitus
In Children - Fever, Vomiting, Loose motion,
Irritability.
Common childhood disease by age of 5 yr,
- (80 % of children. will get at least one episode of
AOM)
- If not diagnosed & treated may lead to ASOM/
CSOM
1.3 Treatment -
1. Counselling- advice to mother about correct
feeding techniques
2. No ear drops, ear mopping to be done only with
good illumination facility, not to blow nose
3. Symptomatic - Analgesic (Tab.Diclofenac -50 mg
t.i.d x5days)or Ibuprofen 200mg t.i.d, Antipyretic
(Paracetamol-325 mg t.i.d x5days)
1.4 Treatment levels -
An acute inflammatory condition of the middle ear
space. Common in children usually associated with
fevers.
Level 1 (PHC)& Level 2 (Rural Hospital): Diagnosis
& above mentioned treatment with regular checkup.
Non improvement or detoriation,then refer to higher
center.
At Level 3-Distrtict Hospital Referral Hospital
1.Diagnosis, Investigations and Treatment of the
case.
2. Referred case from Level 1 & Level 2,
Reassessment & further treatment.
3.2. Treatment:-
1. If the tympanic membrane is bulging Or if
complication are suspected myringotomy should be
done by ENT specialist under microscope with a
coverage of antibiotics (Ampicillin/Amoxycillin 5 to
10 mg/kg in child for 5 days. Adult dose 500mg TID
for 5 days/Amoxycillin + ClavunicAcid 625 mg BD
for 5 days.
Decongestants - Oxymetazoline nasal drops, 0.1%
Nasal drops, 2-3 in each Nostril thrice daily/
Xylometazoline Nasal Drop 0.05% in children.
2. Mastoid exploration may be required in cases
of coalescent mastoiditis or other
complication.
3. Neurological/Pediatric Physician
Opht halmologists Consultation may be
required in unresolved cases & management in
accordance with them.
Page 363
 1. Dry moppi ng/ Suction Clearence
2. Acute Suppurative Otitis
2. Antibiotic (ampicillin/amoxycillin 500 mg thrice
Media (ASOM) daily or , Amoxycillin + Clavunic Acid 625 mg
bd x 5 days). If needed parenteral antibiotics IV
2.1. Definition - cefotaxime 1 gm 12 hourly in adult for 5 days.
An Acute inflammatory condition of middle ear cleft 3. Anti inflammatory drugs( TabIbuprofen 200 mg
which includes Eustachian tubes, middle ear, Antrum + Paracetamol 325 mg b.i.d)
(opening of mastoid air cells in middle ear) with pus
discharge from external auditory canal due to 4. Decongestant - Oxymetazoline nasal drops,
bacterial infection or following exanthematous 0.1% nasal drops, 2-3 in each nostril thrice daily/
fevers. It is also called safe ear if infection limited to Xylomatazoline Nasal Drop 0.05% in children.
lower part of Eardrum.
2.3.3Stages
2.2. Symptoms- a) Inactive stage -
1. Severe Pain, Fever Antibiotic not required and ear toileting may be done
regularly Antibiotic ear drops (Ciprofloxacin ear drop
2. General malaise
2 drops BID) may be needed.
3. Vomiting/Loose Motions
b) Quiescent stage may not require any active
4. Irritability treatment as the ear is dry
5. Discharge from ears: c) In active case of the disease Symptoms and Signs:-
Mucopurulant discharge after dry mopping or 1. Ear Discharge - Non foul,
suction Tympanic membrane may show smelling/intermittent/profuse and associated
congestion, perforation and pulsatile discharge with uppe r respiratory tract infection.
6. Signs of upper respiratory tract infection like 2. Hearing Loss - conductive in nature and
sinus, nasal & throat involvement. gradually progressive

2.3. Treatment- 3. May be associated with tinnitus,Autophony

4. Otoscopic examination - shows central
2.3.1 Level 1 (at PHC level) & Level 2 (Rural perforation in the tympanic membrane with
Hospital):- pulsatile dishcharge coming out to external
1. Dry mopping, suction, clearance of ear discharge canal.

2. Treatment of other septic focus - Eg. Acute 4.5. Active stage:

Adeno Tonsillitis, Rhinosinusitis with
antibiotics, anti inflammatory drugs and
decongestant (mentioned earlier)
a. Systematic antibiotics - antibiotics
(Ampicillin/Amoxycillin) 5 to 10 mg/kg in child
for 5 days. Adult dose 500mg TID for 5 days.
b. Anti inflammatory/Anti pyretic
Ibuprofen(200mg) with Paracetamol ( 325 mg)
in divided doses for 5 days.
c. Decongestant - Oxymetazoline nasal drops,
0.1% nasal drops, 2-3 in each nostril thrice
daily/ Xylometazoline Nasal Drop 0.05% in
children.
Level 3 (Referral Hospital/Dist. Hospital):-
Diagnosis is generally clinical. History with
otological findings of central perforation is
characteristic. Patient is advised to avoid risk factors
- in the form of avoiding excessive cold. Treatment is
as mentioned above. Patient advised to keep ear dry
and avoid water going into the ear.
TREATMENT:
1. Antibiotic treatment as per the culture and
sensitivity reports.
2. Regular ear cleaning and antibiotics ear drops
in addition to oral/parental drugs.(Ampicillin
/Amocycillin 500mg TDS x 5 days or
Amoxycillin + Clavunic Acid 625 mg BD x 5
days. Parental drugs. Inj.Cefotaxime 1gm IV
12 hourly x 5da ys.

2.3.2 Treatment -

Page 364
3. Treatment of the foc us of infection - Indications of Tympanoplasty - There should be
Chronicadeno Tonsillitis, Deviated nasal
(i) Well sensorineural hearing preserved
septum and any sinus pathology.
(ii) Eustachian tube should be patent
4. The corrective surgery:- The myringoplasty /
Tympanoplasty can be performed once the ear (iii) Stapes mobile
is dry with perforation with no disease activity.
iv) Repeated attacks with no healing of disease.

Page 365
 2. CHRONIC SUPPURATIVE OTITIS MEDIA
(CSOM)

2.1. Definition: 2.4. Investigations and

It is a chronic inflammatory disease characterized by Treatment:
foul smelling ear discharge with cholesteatoma 2.4.1 -At Level 1:
formation in atticoantal region. If attic involved, it is
Ear toileting if unresolved refer to higher centers.
called as unsafe ear (infection may get routed to
nearby structures leading to complications. The 2.4.2 At Level 2:
cholesteatoma is aggressive in nature and has got
tendency of bone erosion leading to intracranial and Essentially aggressive treatment in the form of ear
intratemporal complications. It is also called as Atti toileting, antibiotics (Ampicillin/Amoxycillin 500 mg
co antral disease or unsafe type of CSOM. thrice daily or Amoxyclav 625mg b.i.d x
5 days) to avoid complications.
2.2. Symptoms and signs: 2.4.3 At Level 3:
1. Scanty, foul smelling, continuous ear
a) Investigations
discharge,occasionally blood stained.
1. Oto microscopy
2. Hearing loss- conductive or sensorineural in
nature 2. Aural swab for culture and anti bacterial
sensitivity test
3. Vertigo- if inner ear is involved eg-labyrinthitis
3. X-ray mastoids/CT-scan/MRI to confirm the
4. Patient may have:
destructive pathology and spread of disease
a. Fever- Due to acute mastoiditis, meningitis,
4. Pure tone audiometry
lateral sinus thrombosis (fever chill and rigors)
b. Headache- Due to meningitis, extradural abscess 5. Investigations to assess the co-morbid
c. Vertigo,tinnitus, vomiting - Due to labyriynthitis, conditions.(Biochemical & other Lab
brain abscess, increased intracranial tension, investigations)
meningitis
d. Facial weakness or paralysis b) Treatment
e. Post aural swelling due to mastoiditis. Cholesteatoma being aggressive and destructive in
nature-definitive management is surgery- in the for m
2.3. Complications: of Tympanoplasty OR Modified Radical
Mastoidectomy
1. Facial Nerve palsy
Aim: Removal of disease.
2. Labyrinthitis
Aims of modified radical surgery are
3. Meningitis
1. To make ear safe to patient by removing the
4. Brain abscess - Extradural, subdural abscess
cholesteatoma by surgery.
5. Lateral sinus thrombosis
2. To make ear dry and prepare a self cleansing
6. Mastoiditis mastoid cavity
7. Petrositis 3. To prevent complications of CSOM.
4. Establishing hearing mechanism of the ear
(Reconstruction).

Page 366
 3. ACUTE PAROTITIS -VIRAL/BACTERIAL
secondary infections), results in bacterial parotitis . It
1. Viral Mumps(Viral is prevalent in debilitated patients.
Parotitis)
2.2. Symptoms & signs
Caused by Paramyxovi rus. Disease is contracted by
droplet infection and fomites. Children were Severe Pain
commonly affected. Incubation period 2 -3 weeks. Swelling over parotid
Tenderness
1.1. Symptoms & Sign- Indurations of gland
1. Parotid swelling - Unilateral or Bilateral Erythema of skin and or al mucosa
Fever.
2. Pain over gland, ear pain
3. Low-grade fever Arthralgia Malaise
2.3. Management
Headache Appropriate antibiotics - ampicillin/amoxycillin
500 mg thrice daily (5 to 10 mg/kg of body
1.2. Complication - weight for paediatric patients for 5 days).

Orchitis with painful and tender testis Adequate hydration

AspticMenigitis or meningoencephalitis may
occur with or without the salivary gland
invol ment
Unilateral sensorineural hearing loss
Other complications-
Thyroiditis,myocartitis,nephritis and arthirits.
1.3. Investigation -
Haemagglutination inhibition test
Complement fixation test
1.4. Treatment -
Supportive Measures - Bed rest, adequate
hydration, Antipyretics
Prevention MMR(Mumps,Measles,Rubella)
vaccine at 10 months of age
2. Bacterial Parotitis
2.1. Definition
Infection leading to Mechanical blockage of salivary
duct (stasis of salivary secretions coupled with
Oral antiseptic gargles.
Good Oral hygiene
Warm compression over gland
Bimanual massage to milky purulent discharge /
calculi from the gland
Stone in the distal duct - can be manully
expressed & remove d by pushing in mouth
ope ning of gland
Abscess drained out with a small incision.
organised Abscess, to be confirmed by
Sialography,CT scan Or USG. Needs open
surgical interve ntion.
Surgical drainage: Elevation of anteriorly - based
flap over super facial parotid fascia, Parallel to
branches of facial nerve with placement of
external drain.
Rule out tumor mass by CT/MRI before surgical
excision.

Page 367
 4. FURUNCLE

1. Definition: 4. Investigation:
Infection of root of hair follicle usually caused by
Hb, CBC, Blood sugar & culture & sensitivity test of
staph aureus. This infection occurs in cartilaginous
discharge/pus.
ear canal.

2. Symptoms: 5. Treatment:
Severe earache 5.1 Local-packing the ear with
Movement of pinna painful antibiotic ointment
Blocking sensation
5.2 Systemic:
Antibiotics (Ampicillin/Amoxycillin 500 mg thrice
3. Signs: daily (5 to 10mg/kg of body weight for pediatric
Tragal cartilage area tenderness patients for 5 days)or amoxyclav 625 mg bid in adult
Otoscopy- swelling in ear canal for 5 days) Analgesics (Diclofenac 50mg BD for 5
Post auricular lymphadenitis (swelling) Days)Recurrent furunculosis: rule out diabetes

Page 368
 5. OTO-MYCOSIS

1. Definition: 3. Treatment:
Fungal infection of ear canal caused by fungus like Removal of fungal debris by ear toileting (mopping
Candida albicans or Aspergillusniger or suctioning)Antifungal ear drops
(Clotrimazole/Flucanozole 2 drops TID for 5
2. Symptoms & signs: Days)Analgesics Tab Diclofenac 50 mg bid for 5
days.Application of gentian violetTreatment of
Severe irritation and itching in the earSevere diabetes (If associated)
earacheWhitish wet paper like discharge
(candida)Black spores (aspergilous) or combination 4. Preventive:
of both fungus.
Keep ear dry,Avoid swimming in polluted water,Care
in rainy season.

Page 369
 6. NECK SWELLING
Differential diagnosis depends on swelling occupying Pain: Present-acute inflammation
particular (Anterior& Posterior) triangle of neck.
Absent-granulomatous disease or malignancy
1. Classification: Size: rapid increase malignancy
Cervical lymph nodes:classified as 7 groups
Level la: submental
3. Diagnosis:
Blood investigations:CBC, ESR, HIV
Level lb: submandibular Cytology: FNAC (Fine Needle Aspiration
Cytology)Chest X-ray, Ultrasound
Level ll :upper jugular
CT/MRI
Level lll: middle jugular Lymph node diagnostic excision biopsy
Level lV: lower jugular
Level V: posterior triangle 4. Treatment:
Level Vl: pretracheal, prelaryngeal
4.1 7 to 14 days course of
Level Vll: mediastinal
antibiotics
Ampicillin/Amoxycillin 500mg thrice daily (5 to 10
mg/kg for paediatric patients for 5 days)/Amoxyclav
625 BD 5 to 7 days and follow up evaluation
2. Symptoms and signs:
Neck swelling-lymph node consistency: 4.2 Surgical excision of neck
1. Stony hard: malignancy/metastatic swelling
2. Firm to rubbery: lymphoma
3. Soft: infection /inflammation 4.3 Malignancy
Search for primary and treat accordingly, as neck
4. Matted: tuberculosis nodes appears secondary (Metastatic)to primary
malignant focus.

Page 370
 7. A TROPIC RHINITIS

Nasal irrigation and removal of crusts -

1. Definition: byretracted Nasal douching with saline,
glucose, glycerine solution.
Chronic inflammation of nose characterized by
atrophy of nasal mucosa and turbinate bones. The Nasal douching - The patient must be asked to
nasal cavities becomes roomy and full of foul- douche the nose at least daily with
smelling crusts. Saline solution:
Sodium Bicarbonate - 28.4 gm and
SodiumChloride - 56.7 gmmixed in 280 ml of
2. Clinical Symptoms and luke warm water thrice a day till crust
signs: disappears.
25 % glucose in glycerin: - After crusts
Commonly seen in females and s tarts around removal nose painted with 25% glucose in
puberty. glycerin twice a day for 1 month.
Foul smelling form nose Potassium iodide can be prescribed orally to the
Feeling of Nasal Obstruction patient in an attempt to increase the nasal
secretion.
Formation of crusts in the nose
Epistaxis may occure after crusts removal Placental extract injected submucosally in the
nose has been attempted with varying degrees
Roomy nasal cavitiy
of success.
Anos mia
Atrophy of Nasal turbinates,nasal mucosa looks
pale and atrophied 3.2. Surgical management:
Saddle nose deformity( destruction of cartilage) 1. Sub mucous injections of paraffin
Sometimes nasal septal perforation ( erosion of 2. Teflon strips, and autogenously cartilages
cartilage) grafting
3. Wilson's operation - Sub mucosal injection of
50% Teflon in glycerin paste.
3. Management: 4. Young's operation - This surgery aims at
closure of one or both nasal cavities by plastic
3.1. Conservative: surgery in rare cases.

Aims at maintainaing nasal hygiene by removal

of crusts and lessening.putrified smell due to
erocian& destruction.

Page 371
 8. NASAL MYASIS
Nasal Myasis commonly known as maggots in the iii. Cellulites of the nose and face may develop.
nose. It is an infestation of the nose by maggots iv. Fever and toxaemia may be present.
which are larvae of fly. Maggots are living foreign
bodies in the nose.
3. Treatment:
1. Causes: i. Remova l of maggots by installing Liquid
paraffin may be used to stifle the worm. Liquid
Poor hygiene, Leprosy, atrophic rhinitis & other nasal
diseases which forms crust with foul purulent paraffin bloc ks or chokes the lung of the
discharge and loss of nasal sensation attracts flies to maggots, thereby killing them. The killed worms
the nose. can easily be removed.
ii. Turpe ntine packs can be kept in the nose which
irritate the maggots. Nasal saline douching is
2. Clinical Features: done for removal.
i. Maggots are seen crawling in the nose. They iii. Surgical procedure: nasal endoscopic complete
come out of the nose. removal of the worms & infected parts of nose.
ii. Foul nasal discharge is present.

Page 372
 9. FOREIGN BODIES IN NOSE
1. There are two types of
foreign bodies in nose
(i) Non-living: Organic like seeds and grams.
Inorganic like beads, paper or buttons.
(ii) Living: Maggots.
(iii) Iatrogenic: Cotton wool, pledgets or swabs may
be left behind accidentally.
(iv) Commonestoccurrence by mishaps in children,
age group 0-5 years (self insertion)
2. Clinical Features:
History of insertion of the foreign bod y may be
available from patient/pain in the nose bleeding.
Blocking of the nose.
Sneezing may be present.
Unilateral Foul Smelling Bloo d stained
Discharge - oneshould suspected old foreign
body in the nose.
3. Investigation:
(i) Anterior Rhinos copy gives site of foreign body
in the nose.
(ii) Nasal endoscopy will locate exact site of the
body.
(iii) Xray will detects only radio-opaque foreign
body.
4. Treatment:
(i) Generally Blowing the nose or induction
sneezing may expel the foreign bod y.
(ii) Removal of foreign body by Eustachian tube
catheter, which is inserted behind the foreign
body.(without destructing nasal mucosa &
touching F.B. Otherwise bleeding may obs cure
visibility. It is performed under local
anaesthesia.
(iii) Endoscopy:underGeneral Anaesthesia
Page 373
 10. DEVIATED NASAL SEPTUM
1. Introduction:
The septal deformities are of the following
types:-
(i) Deviations are smooth deflections which are
upper or lower, anterior or posterior. I.e. C-
shaped deviation
(ii) Spurs are isolated thickenings at the junction of
the bone and the cartilage.
(iii) Thickening may result from trauma leading to
ove rriding of the cartilaginous fragments, which
grow later in double layers.
(iv) Dislocation:The anterior edge of the septal
cartilage may be displaced to one side causing
the widening of the coluella of the nose.
v) S Shaped Deformity
vi) Bony posterior deformity of vomarine/ethemoid
bone.
2. Clinical features:
Unilateral or bilateral blocking of the nose.
Headache due to sinusitis.
Recurrent Colds.
Epistaxis.
Anos mia.
External deformity associated with deviation of
the septum.
3. Investigation:
History, examination of the nose by anterior
rhinoscopy& posterior rhinoscopy. X Ray PNS
waters view/CT scan PNS.
4. Treatment:
Required only if the patient has persistent or
recurrent symptoms due to the deviated septum or
blockage of nose. Permanent relief is obtained by the
Submucous Resection of the Nasal Septum or
Septoplastysugery.
4.1. Sub mucous resection of
nasal septum:
Indications for sub mucous resection of nasal septum:
1. Marked septal deviation occurring behind the
vertical line passing between the nasal processes
of the frontal and maxillary bones. This deviation
must be the cause for the patient's symptoms.
2. Closure of septal perforations
3. Source of grafting material
4. To obtain surgical access in hypophysectomy, and
vidianneurectomy
4.2. Septoplasty:
Indicated as tailor-made operation without disturbing
nasal mucosa of other nasal fossa,where only
obstructing part is removed.It can be associated with
Rhinopl asty surgery.
Page 374
 11. NASAL OBSTRUCTION
1. Introduction: 4. Management:
The common causes of nasal obstruction are DNS,
nasal polyps, hypertrophied turbinates& old nasal
4.1. Medical:
foreign bod y like rhinolith. Local nasal decongestants Xylometazoline 0.1 %
2drops BID for 3 days,
2. Clinical feature is nasal Local nasal steroid spray like Fluticasone once daily,
Antibiotics (Ampicillin/Amoxycillin 500 mg thrice
obstruction daily / Amoxycillin + ClavunicAcid 625 mg BD (5
to 10 mg/kg of body weight for paediatric patients for
5 days), Antihistaminic (Cetrizine 5mg BD for 7
3. Investigations: days)
History, examination of the nose by anterior
rhinoscopy& posterior rhinoscopy& functional nasal
endoscopy (FESS). 4.2. Surgical:
Cottles test used to check the nasal obstruction is Nasanpolypectomy
due to abnormal nasal valve.
Radiological : XRay PNS/ CT PNS region Turbinopl asty, turbinectomy
Septoplasty
Endoscopic sinus surgery

Page 375
 12. TONSILLITIS

1. Acute tonsillitis 2. Chronic tonsillitis

Definition:
1.1. It is acute infection/
inflammation of palatine tonsils.
1.2 Pathological types:
a. Acute parenchymatous tonsillitis
b. Acute follicular tonsillitis
c. Acute membranous tonsillitis
. 2.2.1 Symptoms:
1.3. Clinical features:
1.3.1 Symptoms-
Sore throat
Odynophagia.
Fever, malaise, headache may be present.
Pain may be referred to the ears
1.3.2 Signs-
Patient may look toxic and febrile.
Tonsils are enlarged and congested; may be
studded with follicles or membrane.( Scanty pus
may come out)
Anterior pillars are congested
Tongue is coated
Jugulodiagastric lymph nodes are enlarged and
tender.
1.4 Treatment:
Bed rest.
Soft bland warm diet
Avoid cold, oily, spicy food
Antibiotics for 5-7 days.: Amoxycillin500mg-
3times/day, Amoxycillin with clavulenic acid
625 mg twice/day x 5 days
Anti-inflammatory analgesics to reduce pain,
fever and i nflammation: Ibuprofen with
Paracetamol ( 200+325)mg 2 times/day x 5 days
Antiseptic gargles
Multivitamins orally BD x 5da ys.
2.1 Definition:
It is chronic inflammation/ infection of palatine
tonsils.
It is characterized by recurrent episodes of acute
tonsillitis. A history of 3-4 episodes of acute
tonsillitis in a year should be labelled as Chronic
tonsillitis
2.1. Clinical features:
Recurrent history of sore throat, Odynophagia
and fever with symptom free interval between
the two attacks
Halitosis
Change of taste
Dry cough: Hawking due to irritation in throat.
Failure to thrive: Seen in children
2.2.2 Signs:
Tonsils may be enlarged ( Parenchymatous type )
or Fibrotic and small (Fibrotic type)
Yellowish cheesy material is seen in tonsillar
crypts which oozes out when the tonsils are
pressed by tongue depressor.
Enlarged jugulodiagastric lymph nodes.
Occasionally, yellowish cystic swelling
(retention cyst ) may be seen on the surface of
tonsil.
Redness of the ante pillar
2.3 Investigation:
Hematological:Hb%, CBC,ESR,BT,CT, PT, XRAY
neck lateral view for adenoiditis &Xray chest for
preoperative evolution.
2.4 Treatment:
Tonsillectomy by dissection method under
general anesthesia.

Page 376


13. ADENOIDITIS

1. Introduction: 2.3 General symptoms: (Adenoid

Inflammation of adenoids is called adenoiditis. Facies)
Failure to thrive.
Adenoids are also called as nasopharyngeal tonsils. It High arched palate
is group of lymphoid tissue situated at the junction of Crowded and protruding teeth
the roof and posterior wall of nasopharynx.Adenoids Halitosis
usually atrophy by the age of 13-14
Pinched and narrow nose
(puberty).However in some patients it may be
Mask like face
hypertrophied and produce symptoms, then treatment
is required.
3. Investigations:
2. Symptoms: X ray soft tissue nasopharynx: It shows enlarged
Symptoms and signs occur due to the following: adenoids and compression of airway.

2.1 Due to nasal obstruction- 4. Treatment:

Mouth breathing 4.1 Medical Treatment
Snoring
Drooling of saliva Acute infection is treated with:
Difficulty in breathing Antibiotics: Antibiotics of choice are-
Change of voice Amoxycillin 500mg TID, Amoxycillin with
Rhinitis and sinusitis Clavulenic acid 625mg BD for 5 days.
2.2 Due to Eustachian tube Anti-inflammator y agents like Ibuprofen 200 mg
BD for 5 days
obstruction: Nasal decongestants: Xylomethazoline 0.05%
Ear pain (adult : 0.1%)
Ear blockage due to secretory otitis media. Antihistaminic: Levocetrizine 5 mg OD for 5
Decreased hearing. days
4.2 Surgical treatment:
Adenoidectomy under G.A.

Page 377
 14. PERITONSILLAR ABSCESS (QUINSY)
the tonsillar region. CervialIymphadenopathy is
1. Introduction: commonly seen.
It is collection of pus in the peritonsillar space which
is in between the capsule of tonsil and the superior
constrictor muscle. 4. Investigation:
It usually follows acute tonsillitis. As mentioned in chronic tonsillectomy section.

2. Clinical Features: 5. Treatment:

These are generally due to septicaemia and resemble
any acute infection. Symptoms like fever, chills &
5.1 Medical management:
rigors, general malaise,bodyaches,headache, nausea IV antibiotics Inj.Ampicilin 500mg 12 hourly for 5
and constipation are present. Local symptoms like days, IV fluids, and analgesics like Paracetamol 500
unilateral severe throat pain, odynophagia, muffled mg bid for 5 days, good oral hygiene
thick speech like hot patato voice. Foul breath,
Ipsilateral earache, trismus. 5.2 Surgical Management:
Incision and drainage of abscess (I & D)
3. Examination findings: Interval tonsillectomy
On examination tonsil, pillars & soft palate on the
involved side are congested and swollen, uvula is
swollen and oedematous, bulging of the soft palate
and anterior pillers. Mucopus may be seen covering

Page 378
 15. ACUTE PHARYNGITIS
Oede ma, congestion and i nflammation of
1. Definition: posterior pharyngeal wall and soft palate
It is acute infection / inflammation of pharynx.
Ulcerative pharyngitis:Ulceration and sloughing
of the posterior pharyngeal wall. It is rare and
2. Etiology: may occur in immune compromised patients.
Granular pharyngitis:Red granulations over the
a. Infective posterior pharyngeal wall. (due to hypertrophied
b. Associated with Tonsillitis, Rhinitis, Sinusitis. lymphoid tissue)

c. Associated with Gastro-oesophageal reflux. 4. Treatment:

3. Clinical features: Bed rest and improvement of oral hygiene.
Soft bland diet with plenty of fluids
3.1. Symptoms- Antibiotics: Antibiotics of choice are.
Amoxycillin500mg 3 times/day x 5, Amoxycillin
Sore throat or raw sensation in throa t with with clavulenic acid 625 BD x 5days.
halitosis
Antacids : Tab. Ranitidine 150 mg/Cap.
Fever, malaise
Omperazole 20 mg daily in case of reflux.
Odynophagia ( Pain during swallowing )
Anti-inflammator y agents like Diclofenac and
Dry, irritating cough Paracetamol (50+325mg) BD x 5days.
Antiseptic gargles like Betadine or
3.2. Signs- Chlorehexidine.
Catarrhal pharyngitis:

Page 379
 16. HOARSENESS OF VOICE

1. Introduction: 4. Treatment:
Hoarseness is term used to describe changes in voice 4.1. For habitual dysphonia
quality. It result from changes in vocal cords. Main stay of treatment is prevention by easing vocal
A hoarse voice is rough and unpleasant, and it results abuse
from lesions of the vocal cords. The causes of
hoarsense may range from innocent acute laryngitis 4.1.1 Things to do
to larynegal diphtheria and malignancy. Rest to the voice
Drink plenty of water
2. Evaluation of hoarseness:
In the absence of upper respiratory tract infection any 4.1.2Things to avoid
patient with hoarseness persisting for more than two Tobacco
weeks needs evaluation. Shouting
Drinking alcohol
3. Physical examination: Trying to talk excess when there is cold or laryngitis
Whispering loudly or for very long
1. Thorough head and neck examination. Trying to c hange naturally speaking voi ce
2. Assessment of hearing acuity
3. Upper airway mucosa, tongue mobility. 4.1.3 Voice therapy-
Cranial nerve examination. Maladaptive vocal habit and techniques are replaced
4. Laryngeal examination. with appropriate use of vocal mechanism.
If not responded to this then surgery may be advi sed
a. indirect laryngoscopy
b. Flexible nasolaryngoscopy 4.2. For organic causes
Treatment of the cause, mostly surgical interventions,
c. Strobolarygoscopy followed by speech therapy
5. Examination for signs of systemic disease
such as hypothyroidism or neurologic 4.3. For psychogenic
dysfunction such as Tremors or Parkinson's Suppor t and i nstructions on how to cope with
disease. emotional and stressful conditions. Speech therapy to
patient.

Page 380
 17. STRIDOR
3. Cough
1. Definition: 4. Hoarseness
It is an auditory manifestation of disordered 5. May have difficulty in de glutition
respiratory functions due to airflow changes within 6. Dysphonia
larynx, trachea or bronchi.
It may be-
4. Investigation:
Xray neck lateral view, x-ray chest, direct
1. Inspiratory- When obs truction is at the level of
laryngoscopy, bronchoscopy & C.T.scan to find out
supraglottis and above.
cause & level of stridor.
2. Expiratory- When obs truction is at the level
bronchioles.
3. Biphasic- i. e. Both during inspiration and
5. Treatment:
expiration and obstruction is at the level of
trachea or sub glottis.
5.1. General measures:
1. Humidified oxygen
2. Types: 2. Steroids (Prednisolone up to 40mg/day x 7 days.
3. Antibiotics- Ampicillin 500mg TDS x 5days
1. Congenital 4. Intubation or tracheostomy is indicated if stridor
2. Acquired is severe to relieve airways obstructions
3. General features of stridor: 5.2. Surgical
1. Stridor is not a disease but a symptom or sign. With the help of investigation, cause & level to be
2. Noisy breathing which may be wheezing, find out & depends upon that cause, surgical
crowing, whistling, croaking, sighing,rattling or interve ntion is needed.
snoring.

Page 381
 18. FACIAL PALSY (BELL'S PALSY)

1. Introduction: 3. Clinical Features:

It is an Idiopathic condition leading to peripheral
facial paralysis or paresis which is of acute onset.
High Risk cases ofBells palsy are diabetics and
pregnant women.
2. Causes:
Viral infection due to herpes simplex,herpes zoster or
E.B.virus& other condition leading to external
pressure on facial canal.
Sudde n onset
Patient is unable to close his eyes completely
Dribbling of saliva from angle of mouth
(weakness of angular oris muscle)
Face become asymmetrical
Epiphora - Tears flow down from the eye
Pain in the ear
Noise intolerance due to stapedial paralysis
Loss of taste due to involvement of chorda
tympani.

Fig 1. Facial palsy

Reassurance,pain relief by analgesics

4. Investigation &Diagnosis:-
It requires careful history, completeotological
and head a nd neck examination
X-ray studies, blood test- CBC, ESR,blood sugar
and serology
Nerve conduction & excitability tests to monitor
nerve degeneration
Topodiagnosis - localize site of lesion
5. Treatment:-
5.1 General
(Tab.Diclofenac 50mg BID for 7 days), eye care,
physiotherapy, massage of facial muscles, use of
eye pads.
Acyclovir - 200 - 400 mg 5 times a day for 5-7
days
Medical
5.2 Steroid therapy -
Prednisolone 1 mg/kg per day in a divided doses
for 5 da ys, if paralysis recovers with the dose of
prednisolone, then it is tapered for next 5 days,if
paralysis remains the same dose continued for
Page 382
 next 10 days and thereafter tapered in next 5
days
Contraindications for Steroid therapy - Pregenancy,
Diabetes, Hypertension, Peptic ulcer, Pulmonary 5.3 Surgical Treatment-
tuberculosis and glaucoma. If there are no signs of recove ry within 7 da ys then
opt for surgical interve ntion.
5.2.2 Ascorbic acid 500Mg OD for 7 days Facial nerve decompression exploring fallopian canal
where facial nerve is encased to release pressure.
5.2.3 Multivitamins
vit B1, B6, B12 1BD for 7 days

Page 383
 19. SENSORINEURAL HEARING
LOSS AND ITS MANAGEMENT
1. Sensorineural hearing loss
(SNHL) 4. Management:
Result from lesions of the cochlea, VIII thnerve &
Early detection of SNHL is important as measures
central auditory pathways. It may be present at birth
can be taken to stop its progress, reverse it or to start
(congenital) or start later in life (acquired).
an early rehabilitation & interventions.
2. The characteristics of 5. SPECIFIC FORMS OF
sensorineural hearing loss HEARING LOSS
are:
5.1 Inflammations of labyrinth
1. A positive Rene test i.e. air AC>BC. (Bone
conduction impaired) 1. Viral labyrinthitis
2. Bacterial
2. Weber test lateralized to better ear (better 3. Syphilitic
hearing ear).
3. ABC test: Bone conduction reduced on absol ute 5.2 Ototoxicity
bone conduction tests. 1. Amino glycoside antibiotics - Neomycin,
4. More often involving high frequencies. Kanamycin, Amikacin,Streptomycin and
Dihydrostreptomycin are cochleotoxic drugs
5. No gap between air and bone conduction curve with Selective destruction of outer hair
an audiometry. cellsPatients particularly at risk those are having
6. Loss may exceed 60 dB. impaired renal function.
2. Diuretics- Frusemide and Ethacrinic acid
7. Speech discrimination is poor.
3. Salicylates - Symptoms of salicylate ototoxicity
8. There is difficulty in hearing in the presence of are tinnitus and bilaterial sensory neural loss.
noise. (Hearing loss particularly affecting higher
frequencies.)
3. Diagnosis: 4. Quinine - Ototoxic symptoms due to quinine are
1. History tinnitus and sensorineural hearing loss
2. Duration of illness - sudden or slowly 5. Chloroquin - Effect is similar to that of quinine
impairment or since birth. and permanent deafness can result.
3. Severity of deafness 6. Cytotoxic drugs - Nitrogen mustard, cisplatin
and carboplatin can cause cochlear damage.
4. Type of audiogram, whether loss is high
frequency, low frequency, mild 7. Miscellaneous -Erythromycin, Ampicillin, and
Chloramphenicol,indomethacin,
Frequency or flat type.
Phenylbutazone,Ibuprofen, Tetanus antitoxin,
5. Site of lesion i.e. cochlear, retrocochlear or Propranolol PropylthiouracilAlchohol, Tobacco
central by BERA test. & Marijuana also cause damage to the inner ear
6. Brainstem Evoked Response Audiometry 8. Topical Ear drops -Chlorhexidine drop
(BERA) helpful in profound sensorineural loss. containing amino- glycoside antibiotics. E.g.
Neomycin, Framycitin& Gentamycin.

Page 384
 1. Infection - Mumps, Herpes zoster, Meningitis,
Encephalitis, Syphilis, Otitis media.
2. Trauma - Head injury, Ear operations, Noise
trauma, Barotraumas, Spontaneous rupture of
5.3 Noise Trauma cochlear membrane.
3. Vascular Haemorrhage, Embolism or
Hearing loss associated with exposure to noise has Thrombos is of labyrinthine or Cochlear artery or
been well-known in boiler operators, iron & their vasospasm.
coppersmiths & artillery men. Lately, noise trauma 4. Ear (otologic) - Meniere's disease, Cogan's
has assumed greater significance because its being an syndrome
occupational hazard, the compensation asked for & 5. Toxic - Ototoxic drugs.
the responsibilities thrust upon the employer & the 6. Neoplastic - Acoustic neuroma. Metastases in
employee to conserve hearing. High level of sound cerebellopontine angle, carcinomatous
pollution, use of speaker walls leads to Noise truama. neuropathy.
TYPES 5.4.3 Manage ment -
1) Acoustic trauma-Very high sound decibel level for 1. Bed rest.
short duration 2. Steroid therapy- Prednisolone 40-60 mg in a
2) Noise Induced Hearing Loss- Over period of time single mor ning dos e for one week & then tailed
off in a period of 3 weeks.
5.4 Sudden Hearing Loss 3. Inhalation of carbogen- (combination of CO2 &
O2) It increases cochlear blood flow & improve
5.4.1 Definition: oxygenation.
It is defined as Sensory neural hearing loss that has 4. Low molecular weight de xtran
developed over a period of hours or a few days. Loss 5. Hyperbaric oxygen therapy
may be partial or complete. Mostly it is unilateral. it 5.4.3 Preve ntion as pects-
may be accompanied by tinnitus or temporary spell
of vertigo. 1. Immunisation of child & ANC mothers.
2. Avoidance of ototoxic drugs.
5.4.2 Etiology - Most often the cause of sudden 3. Use of driving saftygazets.
deafness remain obscure, in which case it is called 4. Ear infection prevention & treatment in time
the idiopathic variety. 5. Avoiding sound pollution areas

Page 385
 20. VERTIGO
1. Definition: 2.2.2 Central Vestibular Disorder
Revolving around or spinning around. 1. Vertebrobasilar insufficiency
2. Posterior inferior cerebellar artery syndrome
2. Disorder of vestibular 3. Basilar migraine
system cause vertigo & is 4. Cerebellar disease- Cerebellum may be affected
divided into: by haemorrhage infraction, infection or
tumours.
2.1 Peripheral 5. Multiple sclerosis - It is a demyelinating disease
Which involve vestibular end or gans& their first affecting young adults. Vertigo & dizziness are
order neurons. The cause lies in the internal ear or the common complaints.
8thnerve. They are responsible for 85% of all cases of 6. Tumours of brainstem & floor of IVth ventricle
vertigo. - Gliomas, astrocytomas may
2.2 Central arise from pons & midbrain, epidermoid cysts
or teratomas may arise from floor of IVth
Which involve central nervous system after the ventricle.
entrance of vestibular nerve in the brainstem and
involve vestibulo-ocular, vestibulo-spinal and other 7. Epilepsy
central nerves system pathways. 8. Cervical vertigo - Vertigo may follow injuries
2.2.1 Peripheral Vestibular Disorders of neck 7-10 days after the accident

1. Meniere's disease (endolymphatichydrops) -It is 3. Investigations:

characterized by trio of vertigo, fluctuating
hearing loss, tinnitus with sense of pressure in 3.1Examination:-
the involved ear. Vertigo is of sudden onset,
lasts for a few minutes to 24 hours 3.1.1History:
2. Benign paroxysmal positional vertigo (BPPV) History of diagnosis,
giddiness,deafness,tinnitus,othorrhoea,cvs&
It is related to positional changes. Certain neurological symptoms. Past history of
provoked position leads to attack of vertigo. giddiness,injury,diabetes,hypertension, medication
3. Vestibular neuronitis and surgery should be noted. Histor y of Tabacco and
alcohol consumption should be noted.
4. Labyrinthitis
3.1.2 Otoscopy:
5. Vestibulotoxic drugs - Drugs like
Gentamicine&Amikacin cause ototoxicity by 3.1.3 For attic perforation with cholesteatoma to be
damaging the hair cells of the inner ear. rule out.
6. Head Trauma - Head injury may cause 3.1.4Blood pressure measurement, CVS & CNS
concussion of labyrinth, completely disrupt the exam includes tests for co-ordination, gait,
bony labyrinth or VIII th nerve or cause a past-pointing test, Romberg's test and corneal
perilymph fistula. reflexes.
7. Perilymph fistula 3.2 Ear Function Test:-
8. Syphilis (i) Hearing test tunning's forks test,Audiometry
etc.
9. Acoustic neuroma - It has been classified in (ii) Labyrinthine tests: Caloric test, ENG
peripheral vestibular disorders as it arises from
CN VIII within internal acoustic meatus

Page 386
 4.2.1 The manoeuvre consists of five positions.
3.3 X-Ray mastoid cervical spine Position 1 - With the head turned 45 degrees, the
patient is made to lie down in head hanging position.
and skull: (Dix Hallpikemanoe uvre). It will cause vertigo and
3.4 Lab investigations nystagmus. Wait till vertigo and nystagmus subside.
3.4.1 CBC with Hb%
Position 2 - Head is now turned so that affected ear is
3.4.2 Glucose tolerance test for diabetes
up.
3.4.3 Serum cholesterol
3.4.4 V.D.R.L Position 3 - The whole bod y and head are now
3.4.5 Thyroid Function tests. rotated away from the affected ear to a lateral
3.5 Electrocardiogram. recumbent position in a face-down position.

3.6 CT Scan & M.R.I. of the head.
4. Management:
4.1 Medical:
4.1.1 Reassurance regarding the nature of the
disease,no jerks,avoidance of provocative
posture
4.1.2 Labyrinthine sedatives like prochlorperazine
5mg BD for 7 days
4.1.3 Vasodilators like Cinnarizine 25/75 mg BD for
7 days or vestibular sedatives like betahistidine
8/16 mg BID for 7 days or for a long time.
4.1.4 Vitamins like B1,B6 and B12 can be used in
supplementary doses
4.1.5 Diuretics (Frusemide 20/40Mg for 3 to 5 days)
and low salt diet for reducing the tension of
endolymph.
4.2. Labyrinthine Exercises are
helpful in regaining the
confidence of the patient:
Position 4 - Patient is now brought in a sitting
position with head still turned to the unaffected side
by 45 degrees.
Position 5- The head is now turned forward and chin
brought down 20 degrees.
There should be a pause at each position till here is
no nystagmus or there is showing of nystagmus,
before changing to the next position. After
manoeuvre is complete, patient should maintain an
upright for 48 hours. Eighty percent of the patients
will be cured by a single manoe uvre. If the patients
remains symptomatic, the manoeuvre can be
repeated. A bone vibrator placed on the mastoid bone
helps to loosen the debris.
4.3 General:
Smoking and alcohol should be avoided.
4.4 Surgical:
(i) Operations which reduce the tension of
endolymph
(ii) Vestibular nerve section.
(iii) Labyrinthectomy

Page 387
 21. FRACTURE INVOLVING NASAL BONE
1. Introduction: 4. Investigation:
Two all pieces of nasal bone present on nasal bridge 1. Imaging study like X-ray nose lateral view, X-
which usually get fractured in Head andsm Facial ray PNS, CT scan.
trauma, assault, RTA, sport or industrial accident. 2. Anterior & Posterior rhinoscopy
3. Routine Biochemical & Serological Laboratory
2. Symptoms and Signs: Test.
4. Preinjury photographs if available.
1. History of Trauma
2. Nasal deformity with swelling. 5. Management:
3. Pain
4. Bleeding nose 5.1. Medical:
5. Nasal blockage
6. Discoloration of nasal skin Head up position, cold compression to reduce
oedema.
3. Signs: Suturing of open wound
1. Epistaxis (active or clots in nasal cavity) Anti inflammatory drug (Tab. Diclofenac 50 mg BD
2. Crepitus on palpation over nasal bone area. x 7 da ys.
3. Deformity
4. Oedema on and around nose Antibiotics (Amoxy 500mg TID x 5 days or
5. Nasal obstruction. Parenteral Amoxyclav 1.2gm I.V. 12 Hourly
6. Associated traumatic injury
7. Black eye 5.2. Surgical:
5.2.1. Closed reduction under General Anesthesia
with septal elevation.
5.2.2. Open reduction with wiring in case of multiple
fractures.

Page 388
 22. FRACTURE INVOLVINGMAXILLA

1. Introduction: Laboratory Test.

Maxillary bones are present on either side of nose & 5. Types of Maxillary fracture:
are part of skull bone. Fracture maxillary bone occurs
in Head and Facial trauma, assault, RTA, sport or Le fort type I - Floating fracture
industrial accident. Le fort II - Midlevel/ sub zygomatic fracture
2. Symptoms: Le fort III - Craniofacial fracture at supra
zygomatic, zygomaticomaxillary complex
1. History of Truama
2. Nasal deformity with swelling. fracture or Tripod fracture.
3. Pain
4. Bleeding nose 6. Management:
5. Nasal blockage
6. Discoloration of nasal skin 6.1 Emergency care -
Airway maintenance, control of oral & nasal
3. Signs: bleeding.
1. Epistaxis (active or clots in nasal cavity) 6.2 Medical Management -
2. Crepitus on palpation over nasal bone area.
3. Deformity Includes emergency care &stabilisation of general
condition.
4. Oedema on and around nose
5. Nasal obstruction. Anti inflamatory drug (Tab. Diclofenac 500mg BD x
6. Associated traumatic injury 7 days.
7. Black eye Antibiotics (Amoxy 500mg TID x 5 days or
Parenteral Amoxyclav 1.2gm IV 12 Hry
4. Investigation:
6.3 Surgical-
1. Imaging study like X-ray nose lateral view,
X-ray PNS, CT scan PNS. Multi displinary approach with involvment of ENT
2. Anterior & Posterior rhinoscopy surgeon, Maxillofacials& Neurosurgeon may needed
3. Routine Biochemical & Serological depending upoun types & severity of fracture.

Page 389
 Figure 1Flowchart of fracture involving Maxilla

History of Trauma to Face: 1. Vitals

Assault 2. Check for ventilation/Circulation
RTA Le fort I/ Floating fracture
Gunshot wounds
Sports 3. Mobility of maxillary alveolar segment (floating
fracture)
Falls 4. Pain and tenderness while speaking or
Industrial accidents clenching
Any Other 5. Ecchymosis or laceration in labial or buccal
vestibule
6. Swelling and oedema of upper lip
7. Mal occlus ion
8. Bilateral epistaxis
Suspect Fracture Involving Maxilla 9. Brusing o f palatal tissues (15-20% of cases)
10. On palpation tenderness over buttress area
11. Percussion of teeth cracked pot sound
Le fort II/ Pyramidal fracture/ Mid level
i. Zygomaticomaxillary fracture/ Subzygomatic fracture
complex # (tripod fracture)
LeFort I, II, III # 1. Oedema mid third of face (Moon face) (Panda faces)
2. Paresthesia of cheek
ii. Zygomatic arch # 3. Bilateral circumorbital ecchymosis
4. Bilateral subconjunctivalhaemorrhage
iii. Alveolar process of maxilla # 5. Dish face deformity
6. Depressed nose
iv. Smash fractures # 7. Epistaxis
8. CSF rhinorrhea
9. Limited ocular movement (Diplopia)
10. Mal occlus ion
11. Inability to ope n mouth
Percussion of teeth cracked pot sound

Le fort III/ Craniofacial dysfunction/

High level fracture/ Suprazygomatic
fracture

1. Oedema of face (Panda faces)

2. Bilateral periorbital edema
Emergency Care: 3. Bilateral circumorbital ecchymosis (Racoon eyes)
1. Airway imme diately evaluated for obstruction 4. Bilateral subconjunctivalhaemorrhage
5. Dish face deformity
6. Depressed nose, flattening of nose
If not maintaining SPO2 - ETT / Tracheostomy 7. Epistaxis
8. CSF rhinorrhea
9. Limited ocular movement (Diplopia, Enophthalmos)
If Cervical Spine fracture - No endotrac heal intubation
10. CSF otorrhoea
Tracheostomy Rather than ETT
11. Mal occlus ion posterior gagging of occlusion
Cervical collar 12. Inability to ope n mouth
Control of oral or nasal bleeding by- 13. Mobility of fractured fragment at NF, FZ sutures
If active Anterior/ Posterior nasal bleeding -AN / PN 14. Tenderness over zygomatic bo ne, arch and FZ suture
Packing Ecchymosis at mastoid process (Battles sign
1. Start Secured IV line for Fluids Replace ment

Page 390
 23. PENETRATING NECK INJURY
1. Causes: 4. Immediate Treatment:
Gunshot
Airway
Stab
Breathing
Penetrating shrapnel with or without speed.
Circulation maintenance
2. Levels: These requires immediate intervention.
Includes skin and pl atysma.
5. Investigations:
Includes importunt structures like major vessels
CT neck/Angiography/ Laryngoscopy/
(carotid & jugular vein), trachea, oesophagus,
Bronchoscopy/GI scopy.
cranial & other nerves.
Involvement of spine &vertibrae. 6. Treatment:
3. Look for 6.1 Emergency medical interve ntion to maintain BP
through IV fluid, airwaymaintenance throgh
Dysphasia, Hoarseness of voice, oropharyngial plastic airway in mouth or intubation.
bleeding, neurological deficit, Hypotension, sub 6.2 Surgical intervention includes Haemostasis of
cutaneous emphysema & air bubbles through wound major bleeding vessels & operative management
& tracheal area. for respective truamatised organ & treatment of
head injury component (If associated with).

Page 391
 Figure.1 Flowchart of Penetrating Neck injury

Investigations and s urgical referrals

History of: Stab wound

i. Gunshot wounds PenetratingPlatysma
ii. stab wounds
iii. penetrating debris e.g. glass or
shrapnel
Primary
survey:
Assess ABC

No airway Potential for

Airway compromise
compromise- airway interve ntion required:
continue with compromise: Call help and Prepare - for
primary survey Call help from surgical airway -
tracheostomy or
cricothyroidotomy
ENT/Anaesthesia
Look For: Consider OT for
i. Dysphagia Tracheal and/or airway
esophageal injury Any of the following
ii. Hoarseness Tracheal and/or 1. Vascular &/or spinal cord injury
esophageal injury (especially 2. Hypotension
recurrent laryngeal nerve) 3. Subc utaneous emphysema
iii. Oronasopharyngeal bleeding 4. Strider/resp distress
5. Haematome (explanding)
Vascular, tracheal, or
6. Active external hemorrhage from the wound site
esophageal injury 7. Bruit/thrill
iv. Neurologic deficit Vascular 8. Pulselessness/pulse deficit
v. Hypotension Nonspecific; 9. Multitrauma
may be related to the neck
injury or may indicate trauma
elsewhere Soft sign
vi. Subc utaneous emphysema Dnysphagia CT angiography
Tracheal, esophageal, or Hoarseness neck/angiography
pulmonary injury Oronasopharyngeal
bleeding
vii. Air bubbling through the
Laryngeal and/or
Supicion of airway injury
esophageal injury
Suspicion for csophageal consider
Hematoma (expa ndi ng) injury consider UGI bronchofibrescopy/DL
Vascular injury scopyor barium study or scopy
Active external hemorrhage booth

Page 392
24. BLUNT EXTERNAL LARYNGEAL TRAUMA
(FLOW CHART)

Page 393
 25.EPISTAXIS

Duration & frequency

1. Definition:
Site, Side, Type, Any medical disorder
It is defined as bleeding from inside the nose.
Drug intake
2. Types: 4.2. First aid -
2.1 Anterior Littles area compression- Pinch the nose with thumb
More common, site of bleeding is littles area, in and index finger for 2 min. & ask the pt. breath
children and young adults. orally.
4.3.1 In Anterior Epistaxisanaesthesize the bleeding
2.2 Posterior point and cauterize with bead of silver nitrate
Less common, site of bleeding is posterior superior or coagulate with electro cautery.
area, seen in adults. Anterior Nasal packing
3. Causes: 4.3.2 Posterior. Nasal Packing
4.3.3 Endoscopic cauterization
4.3.4 If above measures fails then ligation of
3.1 Local vessels.
Injuries to nose, Vascular malformation, fracture of 4.3.5 External carotid- after the origin of superior
maxilla, fracture nasal bone, nasal surgery, acute thyroid artery
sinusitis, rhinitis, nasal diphtheria, atrophic rhinitis, 4.3.6 Maxillary artery - approached through
rhinitis sicca, tuberculosis, syphilis, Rhinosporidiosis, caldwell- luc operation.
foreign body in nose like maggots, deviated nasal 4.3.7 Ethmoid artery ligation
septum.
4.4 General Measures:-
3.2 Nasopharyngeal - Sit up with back rest
Adenoids, Juvenile angiofibroma,Malingnant tumors
Record blood loss in spitting & vomiting
3.3 General causes - Reassure
hypertension, leukemia, hemophilia, aplastic anemia, Mild sedation
cirrhosis of liver, nephritis, patient with anti
coagulant therapy, influenza, chickenpox, malaria. Check vital signs
Maintain haemodynamics-blood transfusion if
4. Management: required
Intermittent oxygenation
4.1. Enquire about
Investigate & treat
Mode of onset

Page 394
 26. PREMALIGNANT LESIONS OF THE ORAL
CAVITY
1. Introduction:
Oral cavity cancer accounts for approximately 3% of
all malignancies and is a significant worldwide health
problem. Most oral malignancies occur as squamous
cell carcinomas (SCCs); Most of the oral SCCs
develop from premalignant conditions of the oral
cavity. The early detection of cancer is of critical
importance because survival rates markedly improve
when the oral lesion is identified at an early stage
(early intervention)
2. Types
2.1 Leukoplakia
White patch or plaque
2.2 Erythroplakia
A fiery red patch with a soft, velvety texture
2.3 Proliferative verrucous leukoplakia
Proliferative verrucous leukoplakia (PVL) is a unique
form of aggressive disease.
2.4 Palatal lesion of reverse smokers
The palatal lesion of reverse smokers is unique to
individuals who place the lit end of a cigarette inside
the mouth.
2.5 Oral submucousfibrosis (SMF)
It is a chronic progressive condition.In which nor mal
mucosa with blood supply is replaced by fibrous
tissue leading to narrow mouth ope ning.
2.6 Other forms:
Lichen planus, discoid lupus erythematous, and
epidermolysisbullosa.
3. Work-up and the Early
Detection of Oral Cancer:
The standard criteria for diagnosis and identification
of oral lesions is histopa thology analysis via the
procurement of a tissue sample by surgical biops y.
3.1 Oral cavity examination:
Extra oral
Inspect the head a nd neck.
Palpate cervical lymph nodes and salivary glands
Lip: Inspect and palpate inner and outer surfaces
of the upper and lower lip.
Buccal mucosa
Inspect and palpate buccal mucosa and cheek.
Inspect and palpate parotid duct to express
saliva.
Gingival and alveolar ridge: Inspect and palpate
gingival and alveolar ridge on facial and lingual
aspects.
Tongue
Inspect and palpate dorsal and ventral surfaces
with accompanying retraction of the tongue with
gauze.
Inspect and palpate lateral borders from anterior
to posterior with manual retraction.
Floor of the mouth
Inspect and palpate floor of the mouth.
Inspect and palpate submandibular ducts to
express saliva.
Hard palate: Inspect and palpate.
Soft palate and oropharynx: Depress the dorsal
surface of the tongue and inspect soft palate and
anterior oropharynx.
Salivary glands: Palpate the parotid,
submandibular, sublingual, and minor salivary
glands. Ensure clear salivary flow.
4. Investigations:
Biopsy of the lesion and histopathological
diagnosis is the gold standard investigation.
Oral cytology
Oral cytology describes a diagnostic technique used
to sample oral tissue for histopathogical analysis. To
obtain a tissue sample, the clinician applies a stiff
brush to the oral mucosa with enough pressure to
induce pinpoi nt bleeding, which ensures a full-
thickness or trans-epithelial tissue sample. These
cellular samples can then be analyzed by a variety of
unique diagnostic measures, including
cytomorphometry, DNA cytometry, and
immunoc ytoc hemical analysis.
Page 395
 27. ACUTE UPPER AIRWAY OBSTRUCTION
gagging,4 Signs of hypoxaemia
1. Introduction: andhypercarbias.a. Anxiety,confusion,lethargy
Upper airway consist of nose, nasopharynx, pharynx, and cynosis may be present as the obstruction
larynx and trachea upto carina. Different pathologies worsen.4 Powerful inspiratory efforts against an
in this area can lead to acute airway obstruction. obstruction may produce ecchymosis and
subc utaneous emphysema.
Obstruction here may be partial or complete. This is
also called as extra thoracic airway. The airway 3. Management:
collapses during inspiration and dilates during
expiration. 3.1. General measures:
1. Reverse hypoxia-100% Oxygen or as close as
2. Clinical presentation possible.
2. Iv access as soon as possible.
May be partial or complete 3. Continuous monitoring and observation.
2.1. Complete upper air way
3.2 Airway management techniques
obstruction: 3.2.1 Airway manoeuvres
1. Universal chocking sign: patient is unable to
a. Jaw thrust.
breath, speak or cough and may hold the throat
b. Oropharyngeal or nasopharyngeal airway may be
between the thumb and finger.
useful in the unconscious patient.
2. Vigorous attempts at respiration with
d. If the patient is not immediately intuba ted, t hen
intercostals and supraclavicular retraction.
give coma position i. e. Semi prone,slightly head
3. Heart rate and blood pressure raised. Patient
down.
becomes rapidly cyanosed.
4. This is followed by diminished respiratory
efforts, loss of consciousness,bradycardia,and 3.2.2 Endotracheal intubation.
hypotension.
5. Cardiac arrest Surgical airway:
6. Death is inevitable if obstruction is not relieved 1. Indicated when endotracheal intubation not
within 3-5 minutes. possible.
2. Percutaneous transtracheal jet ventilation.
2.2. Partial airway obstruction 3. Cricothyroidectomy.
1. May be stable or their may be progressive 4. Formal tracheostomy under local anaesthesia
deterioration may be tried before emergency treacheostomy.
2. Signs and symptoms may be mild but as they 5. Emergency tracheostomy rarely required.
worsen patient develops inspiratory
stridor,dysphonia,aphonia, chocking, drooling

Page 396
 28. DEAF MUTISM
1. Definition: 4. Investigation:
Deaf Mutism is the inability to acquire speech due to Brainstem Evoked Response Audiometry
profound or high degree hearing loss (congenital or (BERA) - It is of value to find out the threshold
early acquired childhood) of sensor y neural type in of hearing in infants, pa rticularly the high risk
both ear. group & in the diagnosis of retro- cochlear
pathology.
Oto acoustic emission (OAE)
2. Causes: Audiometric examination
Free field audiometry
2.1 Prenatal- Visual reinforce audiometry
i. Genetic Defect Play audiometry
ii. Maternal Infection Electro- cochleography -
iii. Drugs During Pregnancy Impedance audiometry
1. Amino glycosides
High- resolution CT scan
2. Quinine
3. Chloroquine
iv. Radiation to Mother in first trimester 5. Treatment:
v. Other factors: Nutritional deficiency, diabetes,
toxaemia& thyroid deficiency Bilateral hearing aid
Surgical interventions includi ng Coc hlear
2.2Perinatal - implant
1. Anoxia Audi tory training
2. Prematurity Language communication
3. Birth injuries
4. Neonatal Jaundice 6. Referral:
5. Ototoxic drugs
If deaf mutism is suspected after investigation, the
2.3 Post natal - child should be referred to a higher centre for
1. Genetic Cochlear implant.
2. Non-Genetic
7. Prevention:
3. Identification of Deafness:
Vaccination to child, avoidance of ototoxic drugs,
History regular antenatal checkup & care.
Responses of hearing in child by investigations

Page 397
OPHTHALMOLOGY

Page 398
 1. LID SWELLING

1. Stye (HordeolumExternum)
1.1 Definition
It is an acute suppurative inflammation of the Zeis
/Moll glands.

Figure 1.1 Stye

1.2 Etiology At night time Ciprofloxacin eye ointment for 7

days.
Bacterial- Staphylococcus Tablet Ciprofloxacin 500mg (systemic
antibiotics) twice daily and Tab. Diclofenac
1.3 Symptoms Sodium 50mg bid (anti-inflammator y) for three
Pain or four days.
Lid swelling When pus poi nts out it should be let out by
Watering pulling the affected eye lash Epilation.

1.4 Sign
A painful swelling at the lid margin.
2. HordeolumInternum
2.1 Definition
1.5 Treatment It is an acute suppurative inflammation of the
Hot fomentation 2-3 times per day. Meibomian glands.
Ciprofloxacin 0.3 % (Antibiotic) eye drops. 1-2
drops six times per day for 5 days.

Page 399
 Figure 1.2 HordeolumInternum

2.2 Symptoms The pus should be drained by incising it.

Pain, lid swelling and watering.

2.3 Sign 3. Chalazion

A painful swelling at the lid margin.
3.1 Definition
2.4 Treatment It is a chronic granulomatous inflammation of
Ciprofloxacin 0.3 % eye drops six times per day the Meibomian gland.
for 5 days
Tablet Ciprofloxacin 500mg (Systemic
antibiotics) twice daily and Tab. Diclofenac
sodium 50mg BD (anti-inflammatory) for three
days.

Figure 1.3 Chalazion

3.2 Etiology
Uncontrolled Diabetes Mellitus in adults.
Refractive errors.

Page 400
 Very rarely a malignant change may occur
(Meibomian carcinoma) especially in old age
3.3 Symptoms with a history of recurrence.
Swelling of the lid and Watering.

3.4 Sign 3.6 Treatment

Painless nodular swelling away from the lid margin. Incision and curettage under Proparacaine 0.5 %
eyedrop (local anesthesia.
3.5 Course In Marginal chalazionintralesional injection of
Spontaneous resolution. Triamcinolone 40mg/ml (Depot steroids) : 0.1 to
If secondarily infected, then it is called as 0.2 ml once may be helpful.
Internal Hordeolum. Correction of refractive errors, if any.
It may burst through the conjunctiva.

4. Blepharitis 4.1 Definition

Inflammation of the lid margin is called as
Blepharitis.

Figure 1.4 Blepharitis

4.2 Causes 4.4 Signs

SeborrhoeicBlepharitis due to dandruff at the
base of eye lashes.
Ulcerative Blepharitis because of infection by
Staph.Epidermidis / Streptococci.
4.3 Symptoms
Itching / rubbi ng of eyelids.
Edema of lid margin, dandruff /ulcer at the root of
eye lashes.
4.5 Treatment
Clean the lid margin with warm water 2-3 times
a day.
Chloramphenicol- Polymixin B combination
(Ocupol) eye oi nt. 3 times a day for 3weeks.

If a Chalazion recurs soon after removal or is rapidly growing in size or ulcerates, a biopsy must be done to rule
out any malignancy.

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 2. DACRYOCYSTITIS

1. Acute Dacryocystitis 1.1 Definition:

Acute Dacryocystitis is a suppurative infection in the
lacrimal sac caused by ablocked nasolacrimal duct.
(NLD)

Figure 2.1 Acute Dacryoc ystitis

1.2 Pathogenesis: There is also Tear Lake, fullness,

When the ope ning of NLD is blocked, tears and conjunctivalcongestion (i.e. watering and redness of
mucous will remain within sac, forming a deposit that eyes.)
gets easily infected.
1.6 Associated symptoms:
Fever, malaise.
1.3 Microorganism:
Most commonly Staphylococcal infection and
Streptococcal infection. 1.7 Treatment:
i. Tab.Ciprofloxacin 500mg twice daily initially
for 5 days.
1.4 Stages: ii. Tab. Ibuprofen 3 times a day (Non Steroidal
i. Stage of cellulitis. Anti Inflammatory Drug).
ii. Stage of lacrimal abscess. iii. Hot fomentation 3 times a day.
iii. Stage of fistula formation. iv. Ciprofloxacin 0.3% eye drop one drop four
times a da y and Ciprofloxacin eye oi ntment at
night time for 5 days.
1.5 Clinical features: v. If there is a pus point, drainage of pus is
Acute onset, painful, red, hot, firm swelling over
required.
lacrimal sac area.
In severe cases there may be a pus point, which may
NO SYRINING IS DONE IN ACUTE CASES OF
burst
DACRYOCYSTITIS

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1.8 Complications : 1.9 Referral:
Acute conjunctivitis, corneal ulcers, lid abscess, When acute attack of Dacryocystitis is subsided,
orbital cellulitis, cavernous sinus thrombosis. patient is referred to higher centre for sac surgery
(DCR) and Fistulectomy, if required.

2.2. Chronic Dacryocystitis: 2.1 Definition:

Chronic low grade inflammation of lacrimal sac is
called as Chronic Dacryoc ystitis.

Figure 2.2 ChronicDacryocystitis

2.2 Pathogenesis: 2.4 Treatment:

Stricture formed due to chronic inflammation. Topical Ciprofloxacin 0.3% eye drops four times a
day. Syringing with Ciprofloxacin 0.3% daily once
Obstruction of lower end of nasal nasolacimal duct
caused by polyp or hypertrophied inferior turbinate. for 5 days.

2.3 Clinical Picture:

Essential symptom is watering of eyes. 2.5 Complications:
Chronic intractable conjunctivitis, corneal ulcer,
There may be swelling at lacrimal sac area ectropion.
(Mucocele).
Regurgitation test (on pressure over medial
canthus of eye i.e. over sac region) is positive
2.6 Referral:
For sac surgery (Dacryoc ystor hinos tomy or
(Mucopus, pus).
Dacryocystectomy).

3. Congenital Dacryocystitis
3.1 Definition:
Non canalization of nasolacrimal duct leading to
blockage of drainagepassage may lead to congenital
Dacryoc ystitis.

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 Figure 2.3 Congenital Dacryoc ystitis

3.2 Symptoms:
Baby is brought with complaints of watering from 3.4 Treatment:
Moxifloxacin 0.5 % eye drops 4 times a day.
one/bot h eyes.
Crigglers Massage over sac region.
3.3 Signs: If the block persists for more than 6 months
Swelling at sac region,discharge on pressure over probing of nasolcrimal duct is done by
swelling. ophthalmologist under general anaesthesia.

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 3. CONJUNCTIVITIS
Infectious conjunctivitis can be bacterial or viral.
1. Defination :
Inflammation of conjunctiva is called as 2.1. Mucopurulent/purulent
conjunctivitis. (Bacterial) conjunctivitis
2.1.1 Definition:
2. Types
Acute purulent inflammation of conjunctiva.
It can be Infectious or Allergic.

Figure 3 Conjunctivitis

2.1.2 Causes:
Staphylococci ,Streptococci,Pneumococci, 2.1.5 Treatment:
Gonococci etc.
Moxifloxacin 0.5 % eye drops two hourly for 7
2.1.3 Symptoms: days.
Acute redness of eyes, grittiness of eyes with Chloramphenicol 1% eye oint. At bed time for 7
mucopurulent/ purulent discharge.
days.
2.1.4 Signs: Dark goggles.
Conjunctival congestion, mucopurulent / purulent
discharge (no diminution of vision, photophobia), 2.1.6 To prevent spread of infection:
matting of eye lashes due to discharge. Frequent hand washing.
Avoid crowded places.
Avoid sharing of handkerchief, towels, napkins,
pillows etc.

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2.2 Viral conjunctivitis 2.2.1 Definition:
Acute conjunctival inflammation caused by viruses.

Figure 3.2 Viral Conjunctivitis

2.2.2 Causative organisms :

To prevent the spread of infection
Herpes simplex, Herpes zoster, adenovirus etc.
2.2.3 Symptoms: Frequent hand washing to be done.
Avoid crowded places.
Acute redness of eyes, grittiness of eyes, watering
Avoid sharing of handkerchief, towels, napkins,
from eyes, photophobia.
pillows etc.
2.2.4 Signs: AVOID USE OF STEROIDS (BOTH TOPICAL
AND SYSTEMIC).
Local:Conjunctival congestion, follicular
hypertrophy withpreauricular
lymphadenopathy.

Systemic: Patient may have fever, Upper respiratory

tract infection.
2.2.5 Treatment:
Usually self limiting course.
Acyclovir 3% eye oint. 5 times a day for 14 days
with,
Prophylactic Moxifloxacin 0.5% eye drops four
times aday for 7 days with,
Fluromethonolone 0.02% eye drops four times a
day for 7 days.

In case of H.ZosterOphthalmicus refer to

Ophthalmologist immediately.
2.3. Allergic conjunctivitis 2.3.1 Definition:Conjunctivitis caused as allergic
reaction to pollens, dust,etc.

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 Figure 3.3 Allergic Conjunctivitis

2.3.2 Symptoms:

Recurrent attacks of redness, ropy discharge,

irritation, itching.

2.3.3 Signs:
Conjunctival congestion,mucoid discharge, papillary
hypertrophy.

2.3.4 Treatment:
If there is secondary infection, use combination Carboxymethylcellulose 1% eye
ofTobramycin 0.3%&Flurometholone 0.02% eye drops(Lubricating eye drops) one drop 4 times a
drops,One drop 4 times a day for 15 days, along day for 15 days.
with OR
Olopatidine 0.1% eye drops, One drop twice a
day for 1 week.

Prevention of spread of infection is equally important as that of treatment

Page 407
 PTERYGIUM

Figure 3.4 Pterygium

Pterygium

A Pterygium is a triangular sheet of fibro vascular

tissue which invades the cornea. Pterygia typically
develop in patients who have been living in hot
climates and may represent a response to chronic
dryness and exposure to the sun.
Signs .

The conjunctiva then overgrows the opacities

and progressively encroaches onto the cornea
in a triangular fashion.

Early cases show small, grey, corneal

opacities near the nasal limbus.

Treatment
Surgical excision is indicated either for cosmetic
reasons or in cases of progression towards the visual
axis. The excision of theconjunctival component
followed by auto grafting or amniotic membrane grafting.

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 4. CORNEALULCER
Corneal ulcer is defined as breech or discontinuation
1. Definition: of corneal epithelium with necrosis of surrounding
corneal tissue.

Figure 4.1 Hypopyon Corneal ulcer

2. Etiology Of Corneal Ulcer:

Etiology Of Corneal Ulcer
________________________________________________________________

NONINFECTIVEE

INFECTIVE

________________________________________________________

FUNGI VIRUSES
BACTERIA PROTOZOAS

Pathoge ns can inva de intact corneal epithelium & can cause ulceration.

Infective agents:
N. Gonorrhoea, C. Diptherium, N. Meningitidis.

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 NONINFECTIVE

Traumatic PostSurgical Lacrimal Lids& Lashes

Neurological Immunological Dermatologic Nutritional

Others

Figure 4.2: Etiology of Corneal ulcer

Iritis
3. Clinical features
Post. Synechia
3.1 Symptoms: Lens nor mal
Redness
IOP Normal/ Raised
Pain
Sac (Dacryocystitis)
Watering / discharge
Photophobia
Diminution of vision 4. Investigations:
Fluorescein Staining
Corneal Scrapings
3.2 Signs:
Lid Ede ma Gram Staining

Conjunctival Congestion Giemsa Staining

Ciliary Congestion KOH Mount

Corneal Ulcer Culture & Sensitivity

Hypop yon Sac syringing

Anterior Chamber Depth Shallow (Indicates Routing Investigation

Perforation)

Page 410
 Blood Pressure DiclofenacSodium 50mg BD (anti-
inflammator y) for three or four da ys.
Blood sugar
Refer the patient to Opthalmologist.
5. Treatment:
Cleanliness 6. Complications after
Fortified topical antibiotic eye drops like perforation:
Amikacin 80mg/2ml.
Adherent leucoma
Tobr amycin with a syringe, Inj 2ml of
Ant. Staphyloma
Tobramycin (40mg/ml) directly into a 5 ml
bottle of tobramycin (0.3%) eye drop. Use Corneal fistula
within 14 da ys. keep in refrigerator.
Pseudocornea
Antibiotics :Topical Moxifloxacin 0.5% eye
drops 2hrly. Spread of infection to other ocular tissues

Cycloplegics -Atropi ne sulphate 1% eye oi nt Expulsion of the lens / vitreous

twice a day. Expulsive choroidal hemorrhage
Hot fomentation. Spontaneous evisceration
Rest. Endophthalmitis / Panophthalmitis.
Systemic antibiotic Tab.Ciprofloxacin 500mg
BD for 5 days.

Page 411
 5. SCLERA
Figure 5.1 Episcleritis

1. Episclerities
Unilateral mild discomfort
It is a common, benign, self-limiting and frequently Tenderness to touch
recurrent disorder which typically affects young
adults. It is seldom associated with a systemic Watering
disorder and never progresses to a true scleritis.

4. Treatment
2. Types of Episcleritis
Mild cases
2.1 Simple Episcleritis Topical steroids, Ciprofloxacin 0.3% +
It is characterized by sectoral or rarely, diffuse dexamethasone 0.1% eye drops,one drop three
redness. It usually resolves spontaneously with times a day or topical NSAIDs, Ketorolac
1-2 weeks. Promethymene eye drops 0.5% one drop three
times a day for one week.
2.2 NodularEpiscleritis
It is localized to one area of the globe, Unresponsive recurrent cases Systemic
for ming a nodule with surroundi ng congestion. Flurbiprofen 100mg three times a day.
1. Symptoms

2. Scleritis 2.1 Defination

Page 412
 Scleritis is a granulomatous inflammation of the
sclera.

Figure 5.2 Scleritis

2.3 Types Rheumatoid Arthritis

2.2.1 Anterior scleritis Connective tissue disorders

a. Non-necrotizing diffuse or nodular. Miscellaneous conditions like relapsing

Polychondritis, Herpes Zoster.
b. Necrotizing with or without inflammation.
2.5 Treatment
2.2.2 Posterior scleritis
Oral NSAIDs Flurbiprofen 100mg three times
2.4 Symptoms a day for 5 days.
Unilateral mild discomfort Oral Prednisolone 40-80mg a day tapered
according to response.
Tenderness to touch
Combined therapy with a NSAID and low dose
Watering steroid.
2.5 Associated systemic diseases If it does not respondrefer to Opthalmologist.
About 45% of patients with scleritis have associated
systemic diseases like,

Page 413
 6.UVEITIS

1. Definition: Inflammation of Uveal tract is known as

Uveitis.

Figure 6.1 Uveitis

Keratic precipitates and aqueous cells/flare can be

2. Causes: seen on slit-lamp e xamination.
Auto immune
Infective 3.2 Intermediate uveitis
3.2.1 Symptoms:
3. Classification:
Depending on the anatomical part of Uvea involved it Decrease in vision (usually slight blurring)
is classified as Black spots in front of eyes (floaters)
1) Anterior (Irido-cyclitis)
2) Intermediate (Pars-planitis)
3) Posterior (Choroiditis) 3.2.2 Signs:
4) Panuveitis (all parts are involved) Ciliary Congestion.
Tenderness OverCiliary Body.
3.1 Acute Anterior Uveitis
3.1.1 Symptoms: Snow Banking and Vitreous haze seen on
Ophthalmoscopy.
Redness
Pain dull-aching pain , more during night
3.3 Posterior uveitis
3.3.1 Symptoms:
Watering No pain , Decrease in vision
Photophobia (intolerance to light) Black spots in front of eyes (floaters)
Decrease in vision (usually slight blurring)
3.1.2 Signs: 3.3.2 Signs:

Page 414
Vitreous haze, focal inflammatory lesions and Visual acuity.
macular ede ma detected on ophthalmoscopy. Pupillary reaction.
Slit-lamp examination for keraticprecipitates,
3.4 Panuveitis: aqueous cells and flare.
Symptoms and signs of both anterior and posterior Dilated fundus examination for vitreous haze,
uveitis are present. snow banking, chorioretinitis lesions, cystoid
macular ede ma.
4. Complications:
Complicated cataract 5.2 Investigations:
Secondary Glaucoma Depending on most likely cause in a particular case
following investigations may be required,
Cystoid macular edema
Complete Blood Count
Retinal Detachment Blood sugar levels
X-ray chest , ESR and Monteux test to rule out
Phthisis Bulbi (shrunken eye)
Tuberculosis.
VDRL / TPHA to rule out Syphilis.
5. Evaluation of a Case of ELISA for HIV.
Uveitis:
5.3 Treatment:
History
Detailed history of previous episodes, treatment Topical steroids Prednisolone Acetate 1% eye
and response to treatment. drops (1hrly initially then tapered according to
History of associated systemic conditions like response to treatment).
Tuberculosis, Syphilis, HIV infection, Cycloplegic Atropine Sulphate 1% eye drops
Rheumatoid Arthritis, AnkylosingSpondylitis, TDS.
malignancies, Diabetes Mellitus etc. Antibiotics and systemic steroids are usually not
required.
5.1 Ocular examination:

Uveitis is a vision threatening condition. Refer the patient immediately on

suspicion of Uveitis .
Long term use of steroids can cause Cataract and Glaucoma.

Page 415
 7. GLAUCOMA

1. Introduction :- 3. Classification
Second major cause of blindness. 3.1 According to aetiology
Often asymptomatic in early stage. Primary
Damage is irreversible. Secondary
Effective treatment is available. Congenital- Present at birth.
IOP Depends on the balance between production Infantile,present in first year of
and removal of aqueous hunour. life.Juvenile,pr esent in the late childhood.

2. Definition: 3.2 According To ApperanceOfThe

Chronic progressive optic neuropathy caused by Angle
a group of oc ular conditions which lead to
damage of the optic nerve with loss of visual Open angle Glaucoma
function. Closed angle Glaucoma
Combined mechanism Glaucoma
Pathogenesis

Raised IOP ( Intra Ocular pressure)-

4. Investigations :-
mechanical changes - decreased axoplasmic flow
IOP with Applanation/Schiotz Tonometer
- ganglion cell death apoptosis.
SLE (Slit Lamp Examination)
Reduced optic nerve head perfusion Ischemia.
Fundus Examintion
Gonioscopy
Visual field testing
OCT ( Optical Coherence Tomography)

Open-Angle Glaucoma

Figure 7.1 Open-Angle Glaucoma

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3.2.1 Open-angle Glaucomathe most common
form of Glaucoma, accounting for at
least 90% of all Glaucoma cases:
It is caused by the slow clogging of the drainage
canals, resulting in increased intra ocular
pressure
Has a wide and open angle between the iris and
cornea.
Develops slowly and is a lifelong condition.
Has symptoms and damage that are not noticed.
It causes SLOW damage to the optic nerve
causing gradual and irreversible loss of vision.
Open-angle means that the angle where the iris
meets the cornea is as wide and open as it should
be. Open-angle Glaucoma is also called primary
or chronic glaucoma. It is the most common type
of Glaucoma,
a. Risk Factor :
Age - 6th decade.
Sex Common in Female .
Race Common and more severe in Black.
Family Histor y and Inheritance First degree
relative of patients with POAG( Primary Ope n
angle Glaucoma ) are at increased risk of
developing the disease.
Refractive error- POAG is common in Myopia
b. Clinical features:
Generally asymptomatic headache.
Frequent changes in Presbyopic correction.
Difficulty in dark adaptation.
Scotoma (especially in inferior field).{Blindness
in particular sector}
c. Signs:
Intraocular pressure > 21 mmHg
(SchiotzTonometer).
Optic nerve head changes - C:D ratio > 0.5.
Asymmetry between two nerve heads > 0.2.
Narrowing/notching/pallor of NRR.
Disc hemorrhages.
Visual field defects.
Defects in nerve fiber layer.
d. Manage ment:
Start TimololMaleate 0.5% twice daily if patient
is not Asthmatic or not Hypertensive, according
to response.
Start Latanoprost 0.005 % /Travoprost 0.004 %
(Prostaglandi n analogues ) one Drop Once Daily
in the Eve ning if patient is Asthmatic or
Hypertensive , according to response.
Systemic Tab. Acetazolamide 250-1000 mg /day
orally.
Surgical Treatment Trabeculectomy
Refer the patient to a higher centre for evaluation
and management .
3.2.2 Primary Angle Closure Glaucoma
a. Introduction :-
Angle-closure glaucoma, a less common form of
glaucoma:
Is caused by blocked drainage canals, resulting
in a sudde n rise in intraocular pressure.
Has a closed or narrow angle between the iris
and cornea.
Develops very quickly.
Has symptoms and da mage that are usually very
noticeable.
Demands immediate medical attention.
It is also called acute glaucoma or narrow-angle
glaucoma. Unlike ope n-angle glaucoma, angle-
closure glaucoma is a result of the closure of angle
between the iris and cornea.
b. Definition:
Spectrum of conditions in which the peripheral iris
moves forward to block the openings of the
trabecular meshwork at the angle, causing a rise of
intraocular pressure.
Page 417
 Figure 7.2 Angle-Closure Glaucoma

c. Predisposing factors: Stony hard eyeball ( very high Intra Ocular

Short eye, Hypermetropia.
pressure).
Smaller corneal diameter. e. Treatment:
Shallow anterior chamber.
Relative forward positioning of lens-iris diaphr agm. Systemic - Intravenous Mannitol 20% 1-2 gm
per Kg over an hr.
d. Clinical features:
Tab. Acetazolamide , 250-1000mg per day in
Unilateral headache or brow ache. divided doses should be given if the patient is
Blurring of vision on the same side. not nauseated or vomiting and can tolerate oral
Unbroken colored halos around lights during the medication.
episode. One drop of 2% Pilocarpine placed in the eye
Gross diminution of vision. every 5 min till pupil constricts,then One drop
Red eye. QID.
Nausea, vomiting.
One drop of TimololMaleate 0.5 % twice daily.
Ciliary and conjunctival congestion, hazy cornea.
Vertically oval, mid dilated pupil.

3.2.3 Congenital Glaucoma

(Buphthalmos)

a. Definition:
Glaucoma appearing between birth and the
ages of 3-4 years.

Page 418
 Figure 7.3 Congenital Glaucoma
b. Pathogenesis: Intolerance to light.
Corneal edema.
Failure / abnormal development of the trabecular
meshwork. Watering.
Angle remains closed by persistent embryonic Blue sclera.
tissue. Iridodonesis.

c. Clinical features: d. Manage ment:

Urgent referral to higher center for Goniotomy /
Enlarged e ye. Trabeculotomy.
Hazy cornea - frosted glass appearance.

3.2.4. Lens Induced Glaucoma

Definition:
It is a type of Optic Neuropathy secondary to raised
IOP due to Cataractous lens (hypermatureCataract).

Figure 7.4Lens Induced Glaucoma

Page 419
 Complete Blood Count.
a. Classification: Blood Sugar Level estimation.
Phacolytic glaucoma. Kidney Function Test .
Phacomorphic glaucoma. Serum Electrolytes.
Phacoanaphylacticglaucoma . Serology.
b. Symptoms: B-Scan.
Diminution of vision.
Pain .
e. Aims of Manage ment:
Redness of eyes.
Headache. To relieve pain.

c. Signs: To minimize optic nerve insult secondary to

raised IOP.
Decreased visual acuity .
To remove the cause.
Conjunctival congestion.
Corneal edema. To reduce the IOP
IV Mannitol (20%) 1-2 gm/kg over 30 min.
Anterior Chamber shallow ( phacomorphic
glaucoma). IV or systemic Acetazolamide 250-1000
mg/day till IOP reduces.
Flare, cells, sterile hypop yon.
f. Surgery:
Pupil sluggishly reacting to light.
After controlling IOP.
Lens mature or hypermatureCataract.
ExtracapsularCataract Extraction with PCIOL
IOP raised. implantation.
Fundus Absent Glow. Post Operative IOP monitoring.
d. Investigations:

Visual damage in Glaucoma is irreversible hence early detection by regular screening is important.
Once diagnosed, Glaucoma is lifelong, which needs continuous lifelong treatment and follow up.
Treatment is aimed at preserving the vision.

Page 420
 8. CATARACT

A cataract is clouding of the lens of the eye, which
impedes the passage of light. Most cataracts are
related to ageing, although occasionally children may
bor n with this condition, or cataract may develop
after an injury, i nflammation or disease.
Risk factors for age-related cataract include Diabetes,
prolonged exposure to sunlight, tobacco use and
alcohol consumption. Vision Can be restored by
surgically removing the affected lens, and replacing it
by an artificial one.

Figure 8.1 Cataract

1. Definition:
Any opacity of lens or its capsule whether
congenital or acquired is known as cataract.

2. Types of cataract : 2.3 Complicated cataract

2.1 Senile cataract 2.4 Metabolic cataract
2.2 Traumatic cataract

Page 421
 Figure 8.2 SenileCataract

Figure 8.3 Traumatic Cataract

Figure 8.4 Complicated Cataract

Page 422
 Figure 8.5 Metabolic Cataract

eyedrops one drop six times a day for one week

3. Stages of Cataract: tapered every week up to six weeks & topical
Immature cataract NSAIDs, Ketorolac Promethymene eye drops
Intumescent 0.5% one drop three times a day for two week.
Mature cataract Tropicamide 1% eye drops one drop at night
Hypermature- Mor gagnian time for two weeks.
Sclerotic First follow up at end of the first week & final
follow up after 40 days for spectacle correction.
4. Clinical features:
Painless progressive diminution of vision, glare, 6.2 Complications of cataract
black spots before the eyes, distortion of objects, surgery:
polyopia.
Complications of hypermaturity like Uveitis and
Lens dislocation, Glaucoma. Early- Striate Keratitis, corneal ede ma, prolapse
of iris, Hyphema, Anterior Uveitis, delayed
formation of anterior chamber, early
5. Investigation :- Endophthalmitis, Toxic Anterior Segment
Syndrome(TASS).
V/A, IOP, Syringing. Late- Bullous Keratopathy, Cystoid Macular
Blood Pressure, Blood sugur, ECG, Urine edema, posterior capsular opacification,
routine. secondary Glaucoma, Retinal Detachment, late
A-scan. Endophthalmitis.
Xylocain sensitivity test.
Physician fitness. It is imperative for a Medical officer to recognize
late complications of cataract surgery.

6. Treatment:Surgery- 6.2.1 Bullous keratopathy

Conventional Extra Capsular Cataract Extraction
with Posterior Chamber Intra Ocular Lens
Implant (PCIOL).
Manual Small Incision Cataract Surgery (SICS)
with PCIOL.
Phacoemulsification with PCIOL
Corneal oedema due to corneal decompensation.
Managed in initial stage, by local hypertonic saline
eye drops (four times a day and eye ointment at
night) & oral tablet Acetazolamide 250mg three
times a day. If unresponsive, Keratoplasty is the
treatment of choice.

6.2.2 Posterior Capsular Opacification

It is the thick capsular opacification of posterior
6.1 Post Operative Management capsule after extra capsular cataract surgery .It can be
managed by Nd:YAGcapsulotomy.
Topical Steroid + antibiotic eye drop
Ciprofloxacin 0.3% + Dexamethasone 0.1% 6.2.3 Cystoid Macular Edema.

Page 423
Relatively uncommon in uncomplicated ConjectivalChemosis.
phacoemulsification, occurs more often after the A/C Reaction, Irits, Corneal Haze, Hypop yon,
complicated surgery. Peak incidence 6-10 weeks. Circumcorneal congestion.

6.2.4 Post OperativeEndophthalmitis d. Risk factors:

a. Definition:- Post operativeEndopthalmitis.
Refers to intraocular inflammation predominantly Environmental factors : Improper OT
involving the vitreous cavity and anterior chamber as fumigation, Improperly cleaned OT.
a result ofpost operative intraocular colonization by Improper sterilization techniques.
microor ganisms. URTI in Surgeon / staff/ patient.
Instrumentation with improperly autoclaved
b. Symptoms instruments.
Infection of Sac Blepharits.
Pain, Diminution of vision, redness and watering Open wound leak.
of eye. Poor patient hygiene .
c. Signs:- Poor compliance in putting post operative
Decrease visual acuity. medicine.
Lid swelling. Post operative rubbing of eyes/ Trauma.
Discharge.
Corneal edema.

e. Types (onset)

Immediate Delayed
Within 24-48 hrs. 48-72 Hrs.

Confection : Complete loss of eye sight if no timely
interve ntion done.
f. Treatment:
It is an acute ophthalmic emergency
- Start intrusive systemic and topical antibiotics.
- Fortifide Gentamycin eye drop every 15min.for 2
hrs. then one hourly three days.
- Moxifloxicilin 0.5% eye drops hourly.
- Cycloplegics Atropine Sulphate 1% eye
ointment, eye drops.
- Urgent referral to Ophthalmologist is required.

Page 424
 9. OPHTHALMITIS

1. Endophthalmitis:
1.1 Definition : Endophthalmitis is the clinical term used to describe
the inflammator y response of the eye to oc ular
infection.

Figure-9.1: Endopthalmitis

Acc to aetiological agents

Based on aetiological agents

Endophthalmitis

Bacterial Fungal
Fungal Viral
Parasitic

Page 425
1.2Types :

1.3 Risk Factors Contaminated IOLs, viscoelastics, poor OT

Hygiene, hospital construction activities.
1.3.1 Bacterial
Defects in sterilization of instruments.
1.4 Symptoms
Contamination of tap water. Patient presents with symptoms most commonly on
Multiple dose fluids and drugs. the second day after surgery.
1.3.2 Fungal Pain
Contaminated irrigating solutions. Red

Decreased vision. Hence, intravitreal injections are treatment of

Hazy cornea. choice.
Hypop yon. Intravitreal injections bypass the blood retinal
Post-operative endophthalmitis is the most barrier and rapidly achieve therapeutic levels at
common form. the sites of infection.
It comprises 70% of infective endophthalmitis. Large majority follow cataract surgery, most
common surgical procedure (approx prevalence
0.082%-0.1%)
1.5 Management Post-operative endophthalmitis is one of the
In established endophthalmitis, antibiotics when most dreaded complications of cataract surgery
given orally or I.V., have poor penetration into and constitutes a true emergency.
the vitreous cavity.

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Late onset Endophthalmitis
May be due to i nfection by or ganism of low virulence
or fungi. Toxic reaction to Intra Ocular Lens (IOL)
may also present as late Endopthalmitis. An urgent
referral to ophthalmologist is required.
2. Panophthalmitis
2.1 Definitions :-
Refer to the inflammation of all coats of the eye
includi ng intraocular structures. It can also extend
with the tissue surrounding the eyeball.

2.2 Symptoms of Panophthalmitis

Eye pain.
Burst opening of the eye ball.
Protruding eyeball.
Loss of Vision.

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 10. RETINAL DETACHMENT(RD)

It is one of the major ocular disease conditions Trauma

causing visual loss.
Post-cataract vitreous incarceration
Predisposing factors
Pars Planitis
High myopia.
Exudative RD
Trauma.

Family history of retinal detachment.

4. Prophylaxis
Intraoc ular Surgery-Aphakia,Pseudop hakia Indicated in retinal breaks
Inflammation. In Aphakic eyes.
Peripheral Retinal degenerations ( Lattice/ More than 1 clock hour of break.
Snailtrack).
Family history of RD.

1. Definition: Any symptomatic tear.

It is a separation of neurosensory retina from retinal
pigment epithelium due to accumulation of fluid in
the sub-retinal space through a retinal break, hole or a
tear.
2. Symptoms:
Occurrence of flashes of light (Phsotopsia) more
serious in nasal field.
Asymptomatic tears and holes can be observed.
3 Modalities of prophylaxis.
Laser Photocoagulation on slit lamp or IDO (
IndirectOphthalmoscope) with indentation.
Cryotherapy at the break to seal it.
Scleral buckling surgery for large tears(rarely).

Floaters in the vision.

5. Treatment:
Curtain/ Veil in front of eye in any portion, more
appreciated in lower field than upper. RD surgery can be done only by tertiary eye care
centres with infrastructure and trained pe rsonnel.
Sudden significant loss of vision, If macula is
involved.
A large bullous detachment. 6. Complications of long
standing RD
3. Types: Uveitis.

Rhegmatogenous RD. Complicated cataract.

Tractional RD. Glaucoma.

Diabetic Retinopathy Pthisisbulbi.

In cases of high suspicion of Retinal Detachment, patient should be refered to tertiary eye care centre
because timely treatment has better chances of saving vision.

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 11. REFRACTIVE ERRORS

a focus is not achieved, a refractive error results and

1.Introduction
Nor mally, the rays of light entering the eye are
brought to a precise focus on the retina the light
sensitive layer lining the back of the eye. When such
vision is not clear.
When parallel rays of light from a distant object are
brought to focus on the retina with the eye at rest,is
called as Emmetropia(that is not accommodating).

Figure 11.1 Emmetropia

2.Causes of Refractive Errors 3.Types of Refractive Error

The eyes ability to refract or focus light- sharpl y on Myopia.
the retina-is primarily based on three features.
Hypermetropia.
1) The overall length of the eye. Astigmatism.

2) The curvature of the cornea. Presbyopia.

3) The curvature of the lens inside the eye.

4. Myopia

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 A Diopteric condition of eye in which parallel rays of
light from infinity come to focus in front of retina
4.1. Definition: when eye is at rest.

Figure 11.2 Myopia

4.2Etiology: Best corrected vision is 6/6.

Fundus exam. Shows Myopic crescent,
Axial lengthening of eyeball (1mm=3D). Tigroidfundus and optic nerve degeneration
Curvature- abnormal curvature of cornea . with or without retinal break.

eg.Keratoconus (0.1=3D). 4.3.3Pathological Myopia:

Inde x myopi a eg. Old age, Nuclear Sclerosis. Essentially degenerative and progressive
condition , manifests in early childhood.
Acquired Myopia due to trauma.
The defect can reach up to 30D to 40D.
4.3Types: The defect has strong heredity more common in
female than male.
Developmental.
Simple. Rapid increase in Myopia during puberty.
Pathological.
Retinal evaluation is mandator y /compulsory.
4.3.1Developmental Myopia :
4.4Clinical feature:
Abnormally long eyeball Myopia 10D. Inability to see the distant object and holding the
Fundus - marked choroidal sclerosis, book close to the eye in simple Myopia.
hyperpigmantation and myopic crescent. Eye strain and headache.
Black spot in front of eye.
In pathological myopia-eye unusually prominent
Usually stationary image. with slightly dilated pupil.

4.3.2.Simple Myopia: Ophthalmoscopy reveals vitreous degeneration

Commonest , progressive from childhood to
adult, seldom exceeds 5-6D.
Generally stop progression by 21 year of age.
and opacity.
Chorio-retinal degeneration patches at posterior
Pole,choroidal sclerosis and Foster Fuchs spot at
macula, Posterior Staphyloma.

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4.5Complications : Refractive surgery like RK, PRK, ICR, LASIK

Retinal hemorrhage due to pos t vitreous 4.7 Other important aspects

detachment. Avoid contact sports where chances of blunt trauma
Lattice degeneration with retinal tear. is more

Complicated Cataract. Low vision aid- in pathological Myopia LVA is

helpful. Glasses or contact lens does not
4.5Treatment: improve the vision.
Genetic counseling.
Optical lens- concave lenses with slight under
General health-nutritional diet.
correction.
Outdoor activity.
Contact lens.
Near work in good illumination.
4.6Surgery:-

5.Hypermetropia

5.1Definition:
It is an error of refraction wherein parallel rays of
light coming from infinity are foc used be hind the
retina with accommodation at rest.

Figure 11.3 Hypermetropia

5.2Etiology: Latent .
Axial Manifest- Facultative.
-Absolute.
Curvature
Inde x
5.4Clinical feature:
Posterior dislocation of lens Low degree- no symptoms.
Aphakia High de gree-eye strain,headache.

5.3Types: Latent convergent squint in young.

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 Presbyopia develops at an early age. Optical lens- convex lens.
Predisposed to angle closure glaucoma. Contact lens.
Fundus may show features of pseudopapillitis. 5.6 Surgery -
Increased chances of acute angle closure.(Risk of Laser, Thermal Keratoplasty, LASIK, Phakic
Angle Closure Glaucoma). intraocular lenses

5.5Treatment:

6. Astigmatism
6.1. Definition:
Astigmatism is condition wherein refraction varies in
different meridian of the eye hence the point of foc us
cannot be formed on retina.

Figure 11.4 Astigmatism

ii. Irregular

6.4Clinical features :
Small Astigmatism Often asymptomatic.
Severe symptom in hyperopic astigmatism
6.2. Etiology: where accommodation brought in play to
overcome hyperopia.
Curvature Astigmatism- most common with
corneal curvature. Irregular astigmatism is caused by corneal scar,
Inde x Astigmatism- inadequacies of refractive penetrating injury to e ye, Keratoconus.
index of lens in different sector.
6.5Treatment:
6.3. Types: Cylindrical glasses.
With the rule.
Contact lens.
Against the rule.
i. Regular
6.6 Surgery :

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 LASIK, PhotoastigmaticKeratectomy, Incisional Corneal transplantation.
correction (LRI), IOL, Conductive Keratoplasty,

7. Presbyopia:
Normal aging process, when near images cant be
focused on the retina due to reduced accommodative
ability.

Figure 11.5 Presbyopia

The foc us is behind the retina as in hyperopia. If initially hyperopic :Presbyopia occurs earlier.
If initially Emmetropic: Person begins to hold Corrected with a convex lens for reading (bifocal).
reading material farther away and distance vision is
unaffected.

All refractive errors should be detected and treated in childhood by regular school health
checkups and should be fully corrected.

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 12. DIABETIC RETINOPATHY
1. Introduction :
India has become the Diabetic capital of the world.
There is a high incidence of Diabetic Retinopathy,
among patients who are suffering from Diabetes
Mellitus for more than 15-20 years duration. Early
diagnosis and intervention is crucial in dealing with
this malady. Incidence and severity is more in type I
(IDDM) than type II (NIDDM).

2.Classificaion :

Figure 12.1NPDR (Non Proliferative)

Figure 12.2 PDR (Proliferative)

2.Vitreous hemorrhage.
1. Risk Factors:
3.Traction RD.
1.Advanced Diabetic Eye disease.
4.Neovascular Glaucoma.

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 Maculopathy (Clinically Significant)

Figure 12.3 CSME

4. History
Duration of Diabetes. 6. Diagnosis
Symptoms: decreased vision, floaters .
Control of Diabetes.
On examination.
Other systemic illness.
Visual acuity.
F/H/O severe vision loss due to DR.
IOP.
Neovascularisation of iris.
5. Systemic Evaluation
Control of systemic risk factors is the Gonioscopy: Neovascularisation of the angle.
cornerstone in management of DR. Dilated fundus examination.
Glycemic control: Besides Blood Sugar Level,
HbA1c levels more than 7.0 % is a known risk 7. Fundus:
factor. Veins dilated and tortuous.

Hypertension more than 130/90mmHg. Dot and Blot hemorrhages.

Increased Triglycerides, cholesterol Decreased Hard exudates.

HDL. Cottonwool spots.
Smoking, Sedentary life style. Micro-aneurysms.

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 NPDR stage. Antioxidants.
New vessels and traction bands seen. Control of Diabetes.
PDR stage. 8.2 CSME:
Vitreous hemorrhage and traction RD
Focal/ Grid photocoagulation
complicates the picture.
Maculopathy runs as a distinct disease entity 8.3 PDR:
with maximum visual defect.
Pan Retinal photocoa gulation.
Fundus Fluorescein Examination (FFE).
Intra vitreal injection of VEGF inhibitors
Iodine based dye is injected into the i. Bevazizumab
antecubital vein and fundus pictures taken
and di gitally analysed. ii. Ranibizumab
Leaks and ischemic areas can be picked up. Vitrectomy may be needed for Vitreous
hemorrhage, Tractional RD.
Optical Coherence Tomography:
Non-invasive retinal tissue pictures 9. Prevention:
Intensive glycaemic control immediately after
diagnosis of DM leads to lessenthe
8. Treatment: complications.
8.1 NPDR : Today Telemedicine has taken sophisticated
technology to the rural masses yet the cornerstone is
Periodic observation. increasing awareness in public.

Fundus examination with dilated pupil must be done for all newly diagnosed Diabetic patients and
thereafter atleast once a year.
A tight glucose control from the beginning has more long term benefits as compared to a tight control
many years after diagnosis or after an end organ damage.

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 13. OCULAR INJURIES

Chemical.
1. Introduction :
Mechanical injuries.
Eye can get injured by chemicals, heat, radiation and
mechanical trauma. Ocular injuries are emergencies 2.1. Chemical injuries :-
and treatment in first few hours can affect the visual
prognosis. Common chemicals causing injuries are,
Alkalis lime, ammonia, sodium hydroxide, cement,
2. Type of Injuries :- detergent soaps.

Figure 13.1 Alkali burn

Acids Hydrochloric, Sulphuric, Acetic acids Distressing pain.

(vinegar), Toilet cleaners.
Watering from eyes.
2.1.1 Alkali burn:Alkalis can penetrate through
cornea causing severe inflammation. They cause Decrease /Loss of vision.
occlusion of limbal vessels causing ischemia and Inability to ope n the eye.
necrosis of ocular surface. Necrosed tissue is
sloughed off causing ulceration and healing by Signs:
granulation tissue giving rise to abnormal adhesions Severe Blepharospasm (forceful closure of
between lid and ocular surface (symblepharon), lids).
severe dry eye, vascularised opaque cornea and even
Conjunctival congestion.
phthisis bulbi.
2.1.2 Acid burn: Coagulates the ocular surface tissue Raised IOP.
but usually does not penetrate inside the eye. Acids 2.1.4Diagnosis:
can cause limbal ischemia, severe dry eye, History of the chemical causing injury should be
vascularised corneal opacities. elicited.
Examination is difficult because of severe
2.1.3 Clinical features:
a. Symptoms: Blepharospasm.

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Ocular examination should be done under surface
anaesthesia and if required sedation (especially in
children).
2.1.5 Immediate treatment:
Removal of any particulate matter.(with special
attention to lime pest/powder).
Simple treatment is WASH-WASH-WASH the
eye with water.
Continuous irrigation with one bottle of normal
saline over a period of 30 minutes.
Topical , Ciprofloxacin 0.3% + Dexamethasone
0.1% eye drops-one drop 4 times a day.
Topical Atropine sulphate 1% eye drops one
drop twice daily.
Tab Ibuprofen 400mg twice daily for pain relief.
Tablet Acetazolamide 250mg. ( carbonic
anhydrase inhibitor) one tablet four times a day.
After primary care patient should be referred to
ophthalmologist for further management.
2.1.6 Medical management at higher centre
includes
Assessment of limbal ischemia.
Topical steroids - Ciprofloxacin 0.3% +
Dexamethasone 0.1% eye drops-one drop 4
times a day first 7 days.
Topical lubricating eye drops -
Carboxymethylcellulose 1% eye drops one
drop 4 times a day for 15 days.
Prevention of symblepharon formation by
symblepharon ring.
Surgical treatment in the form of amniotic
membrane transplant, limbal stem cell
grafting or Keratoplasty.
2.1.7 Complications:
Dry eye
Corneal ulcer
Lid scarring
Symblepharon
Phthisis bulbi (shrunken eye)

Note :- Keep Limestone /Chuna And Other Sourses

Of Chemical Ocular Injuries Away from The Reach
Of Children.

Figure 13.3 Symblepharon and corneal opacity

Immediate Copious irrigation with normal saline minimizes the damage.

Use protective glasses at work place (Prevention better than cure! )

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2.2 Mechanical Injuries :
Ocular trauma classification

Mechanical eye injury

Closed globe injuies Open globe injuries

Contusion
Laceration Rupture

Superficial foreign body Perforating injry

Intraocular foreign body

Lamellar laceration

Penetrating injury

2.2.1 Superficial foreign bodies husk of seeds, wing/ mouth part of insects, caterpillar
Common extra ocular foreign bodies are particles of hair, thorns etc.
dust, coal, emery, steel, lime particle, grain of corn,

Patient gives history of foreign bod y in the eye.

Figure 13.4 foreign bodies

Forceful closure of lids.

2.2.2Symptoms:
Redness. Anaesthetize the eye with 4% xylocaine eye drops
Pain (pricking). /proparacaine eye drops (0.5%).
Watering.

Page 439
Examine the conjunctiva by everting/double everting
the upper lid.
Examine the cornea (stain with sterile fluorescein
strip if necessary) to locate the foreign body.
2.2.3Treatment:
Removal of foreign body.
Conjunctival foreign body can be removed by
cotton bud or irrigation.
Corneal foreign bod y should be removed by
cotton bud or 26 G needle (hold the needle
tangent to cornea to avoid perforation)
under surface anaesthesia of eye with 4%
xylocaine or paracaine eye drop.
Ciprofloxacin eye drop0.3 (Antibiotic) four
times a day for 5 days.
Homatropine 2% eye drops three times a day for
4 days in case of corneal foreign body.
Eye pad for 24 hrs.
Follow up to rule out infection.

If patient gives history of foreign body but it is not found on examination,

suspect intraocular foreign body and carefully examine for wound of entry.

Immediate Copious irrigation with normal saline minimizes the damage.

Take precaution by using protective glasses at work places. (Prevention
is always better than cure).

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 14. OCULAR EMERGENCIES

1. Ocular conditions requiring

emergency ophthalmological
consultation.
Trauma -Ruptured Globe
Endophthalmitis.
Lid Lacerations.
Angle Closure Glaucoma.
Chemical injuries. Severe Uveitis.
Corneal Ulceration.
Acute Vision Loss.
Optic Neuritis.
Orbital cellulitis.
Lens induced Glaucoma.

2. Common causes of sudden

diminution of vision :
Table-14.1:Common causes of sudden diminution of vision

Painful diminution of vision Painless diminution of vision

Acute congestive Glaucoma Vitreous hemorrhage

Chemical injuries Retinal Detachment
Mechanical injuries Central retinal artery occlusion
Endophthalmitis Ischemic central retinal vein occlusion
Panophthalmitis Optic Neuritis
Malingering

3. Common Causes Of Acute

Red Eye

Page 441
 Figure 14.1 Conjunctivitis

Conjunctivitis (with mucopurulent /purulent Endophthalmitis (severe pain with Diminution of

discharge)Subconjunctival hemorrhage vision).
(painless). Panophthalmitis (severe pain, proptosis,with
Corneal ulcer. painful ocular movements).
Acuteiridocylitis (dull aching pain and slight Orbital cellulitis (severe pain, proptosis,with
blurring of vision). painful ocular movements).

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 15. PAEDIATRICOCULAR PROBLEMS

Eliminating childhood blindness will lead to a

1. Introduction :-
greater reduction in the number of blind ye ars
Out of 45 million people worldwide who are blind, experienced by adults.
around 1.4 million are children under 16years of age.
The vast majority of childhood blindness happens 3. Causes of childhood
before the age of five a period when 75 per cent of
learning is through sight.
blindness :-
Refractive errors.
2. Why is childhood blindness
(For details please refer to refractive error topic).
a priority?
Corneal scarring (scarring of the outer eye
There are several reasons why stakeholders believe
because of vitamin A deficiency & trauma).
that eliminationg childhood blindness is a
priority. Cataract for ms 39 per cent of all childhood
blindness.
There are an estimated 500,000 new cases each
year of childhood blindness roughly one per Infections -
minute. Ophthalmianeonatorum.
Blindness in children is often preventable if Congenital Dacryocystitis.
communities and parents become aware of the
Blepharitis.
causes.
Squint.
Without early intervention for cataract blindness,
Ocular Trauma.
children may go bl ind pe rmanently.

Blinding conditions increase child mortality up Congenital and Developmental Cataracts .

to 50% of children who become blind die within Leukocoria.

two years.
Congenital anomalies
90% of children who are blind dont go to
school.

3.1 Ophthalmianeonatorum 3.1.1 Definition:

Conjunctivitis occurring during 1st month after birth.

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 Figure 15.1 Ophthalmianeonatorum

3.1.2 Mode of presentation, differential

diagnosis &treatment :
Table-15.1: Ophthalmianeonator um - mode of presentation, differential diagnosis and treatment

Time of onset Differential diagnosis Treatment

Within the first 48 hrs. NeisseriaGonorrhoeae Inj. Ceftriaxone IM,

Gentamycin / Moxifloxacin eye drops 1hrly

(till discharge decreases), followed by 4 times a
day for 7 days.

Bacitracin eye oint. 4 times a day for 7 days.

Chemical Wash the eyes, Erythromycin eye oint 4 times a

day for 3 days

48 hrs to 72 hrs. Other bacteria Gentamycin /Tobramycin eye dops two hourly
for 7 days.Neomycin-Bacitracin eye oint 4
times a day for 7 days.

5-7 days Herpes Simplex Virus(HSV II) Acyclovir eye oint 5 times a day for maximum
14 days.

>1 week Chlamydia Trachomatis(D-K) Erythromycin eye oint./Chloramphenicol eye

oint. 4 times a day for two weeks.

Page 444
3.2. Squint :
It is a condition where the eyes do not look in the
same direction. Whilst one eye looks forwards to
foc us on an obj ect, the other eye turns either inwards,
outwards or downwards. A child with a squint may
stop using the affected eye to see with. This can lead
to visual loss called Amblyopia, which can become
permanent unless treated early in
childhood.Treatment involves patching the good eye,
Figure 15.2 Esotropia
3.2.1 Definition:
Malalignment of visual axes is called as squint.
It can be Esotropi/Exotropia or vertical malalignment
i.e. hypertropia or hypotropia.
3.2.2 Types of Squint :-
Esotropia An eye that turns inwards.
Exotropia - An eye that turns outwards
Hypertropia - An eye that turns upwards.
Hypotropia - An eye that turns dow nwards.
Constant The squint present all the time.
Intermittent The squint comes & goes.
Manifest squint The affected eye turns when
the eyes are open and being used.
to force the use of the affected eye. Sometimes
surgery is needed to correct the appearance of a
squint. Squints are common and affect about 1 in 20
children. Most squints develop before preschool age,
usually by the time a child is three years old.
Sometimes squints develop in older children, or in
adults.
Figure 15.3 Exotropia
Latent squint The eye turns only when it is
covered or shut, but looks fine when the eye are
open.
Concomitant squint The angle (degree) of the
squint is always the same in every direction that
you look.
Incomitant squint The angle of squint can vary
according to direction
3.2.3 Symptoms:
Squint(deviation of eye), diminution of vision
3.2.4 Signs:
Squint, diminution of vision, Amblyopia (lazy eye).
3.2.5 The aims of treatment of squint are :-
Preserve or restore vision.
Straighten the eyes.
Restore binocular vision.
3.2.6 Treatment:
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 Refractive correction. Exercises and if necessary surgical correction is
done.(before 10 yrs.of age to have binocular
Amblyopia treatment. vision).

Evaluation of the squint by ophthalmologist at the earliest is must.

3.3. Leukocorea : 3.3.1 Definition:

White pupillary reflex is called as Leukocorea.

Figure 15.4 Leukocorea

3.3.2Common Causes:
Congenital Cataract.
Retinoblastoma.
Retinopathy of Prematurity.
Toxoplasma /ToxocaraEndophthalmitis.
Persistent Hyperplastic Primary Vitreous.
3.4Congenital Cataract :-
It is clouding or opacity of the normally transparent
lens inside the eye. Babies are sometimes born with
cataracts as a result of an infection, injury, or poor
development before they were born, or they may
develop during childhood.
It is very important to treat this condition as soon as
possible to get the best results. The treatment
optionsand the timing of surgery will be decided by
the ophthalmologist, based on the following factors :
Age of the child.
Density of cataract.
Whether cataract involves one eye or both eyes.
It is the cancer of the eye in children. It originates
from the retina, the light sensitive layer, in eye. It is
the commonest tumor of the eye in childhood. As the
child does not complain of any poor vision, the tumor
may remain undetected. The most common way of
presentation is a white reflex (leukocorea) behind the
pupil. It may also present as squint (crossed eye),
poor vision, painful red eye, inflammation of
thetissue surroundi ng eye, protrusion of the eye ball
(proptosis) etc.
The aim of treatment in retinoblastoma, ina order of
priority, is to save the life, eye sight and cosmesis of
the child. There are many treatment modalities for
this tumor.
3.6 Retinopathy of Prematurity :
The most important determinant of any ROP
management program is an effective screening
strategy.

3.5 Retinoblastoma : 3.6.1 Whom to screen for ROP :

Page 446
 All infants born below 1750 grams birth weight
must undergo screening and all infants between Laser Photocoagulation.
1750 grams and 2000 grams must be screened in
case of any risk factor. For advanced stages like retinal detachment
surgical treatment is required.
All infants born below 34 weeks of gestation
must undergo screening and all infants between
34-36 weeks must be screened in case of any risk 3.7 Congenital anomalies -
factor.
3.7.1 Ptosis :
Ptosis refers to drooping of an upper eyelid of one or
3.6.2 When to start screening :-
both eyes. The droop may be barely noticeable, or the
All babies must be screened not later than 30
lid can descend over the entire pupil. Surgery usually
days of life or 4 weeks after birth.
is the best treatment for drooping eyelids. Children
Babies born < 1200 grams or < 28 weeks must born with moderate or severe ptosis require treatment
be screened by the 2nd 3rd week of life. in order to get proper vision for subsequent
development of child. Failure to treat ptosis can result
in Amblyopia.
3.6.3 Treatment :-

All these are potentially vision threatening conditions which need immediate referral to ophthalmologist.
Every time the when the baby is brought for immunization look for pupillary reflex.

Page 447
 16. LOW VISION
Low vision is a reduced level of vision that cannot be
fully corrected with conventional glasses. It is not the 2. Causes
same as blindness. Unlike a person who is blind, a
person with low vision has some useful sight. Although low vision can occur at any stage in
However, low vision usually interferes with the life, most of people develop low vision because
performance of daily activities, such as reading or of eye diseases.
driving. A person with low vision may not recognize
Common causes of low vision, particularly with
images at a distance nor able to differentiate colors of
similar tones. older adults, include Macular Degeneration,
Glaucoma, and Diabetic Retinopathy.
You are legally blind when your best corrected
central acuity is less than 20/200 (perfect visual
acuity is 20/20) in your better eye, or your side vision 3. Tests and Diagnosis :
is narrowed to 20 degrees or less in your better eye.
Refraction (to assess your vision and determine
People who are legally blind may still have some
the prescription for your glasses, if glasses may
useful vision. If you are legally blind, you may
qualify for certain government benefits. It is be of any use).
estimated that approximately 17 percent of people Visual field (to assess your peripheral vision).
over the age of 65 are either blind or have low vision.

4. Treatment and Drugs

1. Symptoms
Difficulty in recognizing objects at a distance
(street signs or bus signs).
Difficulty in differentiating colors (particularly
in the green-bl ue-violet range).
Difficulty in seeing well up close (reading or
cooking).
Optical devices to help you adapt, such as
magnifiers, telephones, or closed-circuit
televisions.
Adaptive non-optical devices, such as large-
print cookboo ks and talking watches.
Occupational Therapy.

Page 448
 17. EYE BANKING
Eye bank collects, evaluates and distributes the eyes
donated by the donors. All eyes donated are
evaluated using strict medical standards.
1. Functions of eye bank:
Those donated eyes which are found unsuitable for
transplantation are used for valuable research and
medical education purpos ein the eye ba nk.
1. Availability of trained staff round the clock at Eye
donation center in all District hospitals & all Eye
bank to attend the calls.
2. Evaluate and provide quality corneas to corneal
surgeons.
3. Enable corneal research using eyes unsuitable for
grafts to find newer techniques, improve preservation
methods and train cor neal surgeons.
4. Increase public awareness about eye donation and
eye ba nking.
2. Eye donation :
2.1 Important aspects of eye
donation :
1. Eyes are to be donated only after death.
2. Eyes must be remove d within 4-6 hours after
death.
3. In case of death,nearest eye bank should be
informed immediately.
4. Eyes must be removed only by a trained doctor.
5. The eye bank team may remove eyes at home of
the deceased or at a hospital.
6. Eye removal process is simple and takes only 10
to 15 minutes.
7. Eye removal does not leads to any disfigurement
in eye.
8. Only the transparent section of the eyes called
cornea is taken out and not the complete eye
ball.
9. A small quantity of blood will be drawn to rule
out communicable diseases.
10. Anyone can pledge eyes.
11. The eyes can be pledged to any eye bank
preferably the nearest one.
12. The identities of both the donor and the recipient
remain confidential.
13. One pair of eyes gives vision to TWO corneal
blind people.
14. Eyes donated to the Eye-Bank that are not
medically suitable for transplant may be used for
medical research and education purposes.
2.2 Process of Eye donation
Pledging for eye donation procedure:
2.2.1 Eye donation can be done in either of
these two ways.
1. She/He can walk in to a nearest Eye Bank and
PLEDGE their eyes for donation. For this, a
pledge form needs to be filled, signed by a
witness (can be your relative/friend) and given
back to the eye bank. At the time of donors
death, his/her relative/friend, who was a witness
for the pledge form or any other family
member/friend who had the knowledge that the
person who passed away intended to donate the
eyes, should call the nearest eye bank. One
important aspect to be noted here that it is not
sufficient if a person pledges for donating his/her
eyes after the death, his/her relatives and friends
should be well informed and be well aware to
call the nearest eye bank, for donating the eyes
after their death.
Page 449
 2. After death, a relative or a friend of the deceased
person can infor m the eye ba nk and tell them that
they wish to donate the eyes of their bereaved
folk.
2.2.2 Donation procedure:
If there is an unfortunate death occurs of one of
your family member/close relative/close friend, pick
up the phone and dial to the nearest eye bank. Please
note that this should be done WITHIN 6 hours of the
death.
Give the eye bank officials the location of the house
along with a landmark so that they can come and
collect the eyes as quick as possible. These eyes will
give a new vision to two blind people.
2.2.3 Important points to be taken care after
a person's death, before eye donation:
After the death of a person, call the nearest eye bank within
SIX HOURS of the death of the person.
Switch off fans & keep AC on, if you have one.
Close the eye lids gently and keep a moist cloth
over the eyes.
Raise head with a pillow.
2.2.4 What happens after eye donation?
The donor's family receives a certificate of
appreciation from the eye bank.
The eyes are taken to the eye bank and evaluated
by trained staff.
Eyes are preserved in a solution of Optisol GS
and refrigerated. This solution contains
chemicals and drugs that are needed to keep the
living cells of cornea healthy and functional.
Tests are carried out and the report is sent to the
corneal surgeon
The eyes are used for a corneal transplant
operation within 72 hours, but with present day
availability of special storage media the eyes can
be stored for a longer time before being
transplanted.
The recipient is chosen from the eye ba nk's
waiting list and called for corneal transplant.
Neither the patient knows whose cornea is used
for him, nor the relatives of the donor know who
has received the cornea. This information is
strictly confidential.
Periodic follow-up of the recipient is done over
the time to ensure that the graft is successful.
Page 450
SURGERY

Page 451
 1. Abdominal Pain
Acute Abdomen is a term used synonymously for a
condition that needs immediate intervention
1. Causes of acute abdomen:
Figure 1: Acute abdomen causes
Abdominal Pain can be due to various orga ns
involve d with underlying causes & patient will
present accordingly.
2. Gastric & Duodenal ulcer:
2.1. Presentation:
Burning pain epigastric region ref. to ba ck
worsened (gastric ulcer) or relieved by intake of
food (duodenal ulcer)
Dyspepsia, nausea/vomiting, occasionally
haematemesis/malena.
Complication with aggravation/progression of
illness may cause perforation
2.2. Investigation:
Routine investigation (Hb, CBC, Urine )
X-ray abdo men standi ng - shows gas under
diaphragm in perforation
Gastroscopy
2.3. Treatment:
2.3.1 Drugs-
Ranitidine 150 mg.bd or Omeprazole 40 mg od
and alike drugs on empty stomach for 15 to 30 days
Intestinal motility regulators Domperidon 5 to 10 mg
bd after meals for 15 to 30 days
Liquid antacids
2.3.2 If perforation is diagnosed
NBM, RT aspiration
I.V. fluids RL, DNS, D 5% 1000-1500 cc in 24
hrs to stabilize the patient
Antibiotics Cefotaxime 1 gm I.V.bd , iv Genta -
80 mg/ bd,
IV Metronidazol - 400 mg / bd
Stabilize the patient & shift the patient for
surgical interve ntion within 4-6hrs
3. Biliary Tract & Pancreas:
3.1. Presentation:
Colicky pain in right upper abdomen ,
Dyspepsia, nausea/vomiting
Occasional jaundice
Page 452
3.2. Investigation: 4.1.2 Investigation:
Routine investigation Routine investigation
USG abdomen X-ray abdo men standi ng - Shows multiple
Serum amylase estimation. gas-fluid levels.

4.1.3 Treatment:
3.3. Treatment: e) NBM, RT aspiration
Analgesics Aceclofenac 50 mg / bd, f) I.V. fluids - RL DNS, D 5% 1000-1500 cc in 4 to
Dicyclomine 20 mg / bd 6 hrs to stabilize patient
Antibiotics - Cefotaxime 1 gm IV bd , IV g) Antibiotics Cefotaxime 1 gm IV bd , IV
Gentamycin 80 mg/ bd Gentamycin 80 mg/ bd,
IV Metronidazol - 400 mg / bd h) IV Metronidazole 400 mg / bd
Stabilise the patient & as diagnosed- biliary i) Stabilize the patient & shift patient for surgical
stone/ Pancreatitis patient may be referred for interve ntion within 4-6 hrs.
expert management to higher center within 12-24
hrs.
4.2. PERFORATION
4.2.1 Presentation:
3.4. Acute epididymo-orchitis / Severe pain in abdomen , vomiting
Pyocele Distension of abdo men
Acute epididymo- architis is an infection in
epididymis, testes & spermatic cord & manifests as 4.2.2 Investigation:
Acute Pain in Scrotum may be associated with fever. Routine investigation
When infection involves tunica vaginal sac at X-ray abdo men standi ng - Shows gas under
manifeds as pyocele. diaphragm

3.4.1 Symptoms - 4.2.3 Treatment:

- Pain is scrotal area. j) NBM, RT aspiration
- Erythema in local area. k) IV. fluids - RL DNS, D 5% 1000-1500 cc in 4-6
- Difficulty is walking due to pain. hrs to stabilize patient
- Fever l) Antibiotics Cefotaxime 1 gm I.V.bd , IV
Gentamycin 80 mg/ bd,
3.4.2 Investigation m) IV Metronidazole 400 mg / bd
- USG Abdomen. n) Stabilize the patient & shift patient for surgical
- CBC interve ntion within 4-6 hrs.

3.4.3 Treatment: 5. RENAL & URETERIC

a) Antibiotics
b) Inj. Cefotaxim 1 gm iv / hrly.
Inj. Metronidazole400mg iv / 8 hrly.
Inj. Diclofenac 50 mg /im 8hrly.
c) Magsulf dressing : It reduces inflammation &
pain.
d) Surgical intervention Surgical intravention is
required if conservative treatment does not give
relief. Pyocele has to be drained for relief.
COLIC
It's type of pain caused due to irritation or obstruction
by stone, in kidney or ureter itself. It is repeated
spasmodic pain of longer or shorter duration till
cause is removed i.e stone removal or expulsion.
Renal pain most of the time is located in lumbar or
back region. Ureteric pain is typical colic,

mild or severe in nature radiates from lumbar to

4. Small & Large Intestine: scrotal region.

4.1. OBSTRUCTION 5.1. Sign & symptoms

4.1.1 Presentation:
Severe pain in abdomen, vomitings Abdo minal pain from loin to groin on one side or
Distension of abdomen both sides in flank & back. Pain is associated with
burning micturation, nausea , vomiting, fever &
chills. Patient complains haematuria.

Page 453
5.2. Investigations Renal profile
X-ray abdomen (KUB)
Haemogram USG - abdomen & Pelvis
Urine- m/e, c/s
5.3. Treatment
Analgesics- Inj. Diclofenac 50 mg/im.
Antibiotics- Inj. Ampicilline 500 mg.IV./6 hrly .
Inj. Gentamycin 80 mg. IV./12 hrly. 3 to 4 days
Inj. Metronidazole 400 mg. IV./8 hrly.
IV Fluids -Ringer lactate, DNS, Dextrose 5%
Catheterization SOS
Give the treatment to stabilize the patient and / or refer the patient to higher center.

Inj. Gentamycin 80 mg.i.v./12 hrly.

6. Acute Appendicitis Inj. Metronidazole 400 mg.i.v./8 hrly.
The acute appendicitis is essentially a surgical IV Fluids -Ringer lactate, DNS, Dextrose 5%
condition & can be defined as pain of sudden onset in If patient is responding/improving, give above
right lower abdomen. treatment for 5 to 6 days

6.1. Presentation:
Pain at first starts around the umbilius or 6.3.2 Surgical Treat ment
epigastrium and later it shifts to the right iliac If during the conservative treatment there is evidence
fossa. of gangrene, perforation, generalized peritonitis or
Sudden disappearance of pain without abscess formation, operation is indicated. If patient
improvement of general condition means starts deteriorating with conservative line of
gangrene and perforation. But, pain invariably treatment then patient may be posted for emergency
returns later. appendectomy.
Nausea and Vomiting Emergency appe ndectomy is contra indicated when
Fever diagnosis is appendiculer mass.
Mucus diarrhoea
Pulse-rapid and it is proportionate to temperature 7. Obstructed Inguinal Hernia
except in cases of Gangrene, Perforation and It is due to obs truction/ retention of abdo minal
Generalized peritonitis. visceral organs in hernial sac.
Tenderness in right iliac fossa /guarding and
rigidity Patient presents with- non-reducible inguinoscrotal
swelling, pain in abdomen, distension of abdomen
6.2. Investigation: repeated vomiting . In late stages fever, septicemia.
Routine haemogram
RFT
Urine examination
X-ray abdomen, KUB 7.1. Investigations:
Abdominal Sonography
Routine heamogram
X-ray abdomen standing position -shows
6.3. Treatment: multiple gas fluid level
6.3.1 Conservative Treatment USG abdomen & pelvis
Appendicitis with signs of localization No cough impulse.
Rest in a hospital
Nothing by mouth 7.2. Treatment:
Analgesics- Inj. Diclofenac 50 mg/im 8 hourly NBM, Ryle's tube aspiration, head low position
/sos. IV Fluids - Ringer lactate, DNS, dextrose 5%
Antibiotics- Inj. Ampicilline 500 mg.i.v./6 hrly . Analgesics- Inj. Diclofenac 50 mg/im.

Page 454
 Antibiotics- Inj. Ampicilline 500 mg.i.v./6 hrly . Try to reduce the hernia if not pos sible, then
Inj. Gentamycin 80 mg.i.v./12 hrly. after stabilization of patient within 4 to 6 hours
Inj. Metronidazole 400 mg.i.v./8 hrly. shift the patient for further needful surgical
interve ntion at higher center.

Page 455
 2. WOUNDS AND ABSCESS MANAGEMENT

From the earliest times the healing of wounds has infection, to be done by secondary suturing, skin
been the central problem in surgical practice. This grafting.
applies equally to the wounds of warfare and human
assault, to the wounds of accidents, and to the 3.3.1 Suture Material:
wounds which the surgeon makes deliberately in the Non-absorbable -linen, silk, nylon, proline,
course of surgical operations. ethilone
The breach in the surface of the bod y, the skin, Absorbable- cat gut, vicryl
exposes the deeper tissues to the danger of bacterial
infection (sepsis), and this danger persists until the 3.3.2 Suture Types:
healing process has restored an intact surface. Simple - single or continues
Mattress - single or continues
1. Commonly occurring Tension sutures - when there is requirement of
forced alignment of wound edges
injuries can be open or
3.4 Supportive treatment to the
closed.
associated injury/illness as
Abrasions, bruises required- fracture site
Contusions
Lacerated wounds
stabilization etc.
Penetrating wounds
Incised 4. Abscess
Crush wounds
De-glovi ng injury- wounds with skin loss 4.1 Clinical features :
Vascular injuries An abscess is a tender mass generally surrounded by
a colored area from pink to deep red. Abscesses are
2. Observe for often easy to feel by touching. The middle of an
abscess is full of pus and debris.
2.1 Three 'B'
Painful and warm to touch, abscesses can show up
Bleeding any place on your body. The most common sites are
Breathing in your armpits (axillae), areas around your anus and
Breaks (fracture) vagina (Bartholin gland abscess), the base of your
spine (pilonidal abscess) around a tooth (Dental
2.2 Wound Contamination abscess) and in your groin. Inflammation around a
hair follicle can also lead to the formation of an
2.3 Concealed bleeding (internal) abscess, wich is called a boil (furuncle).

3. Management:
3.1 Cleaning of wounds
3.2 Debridement of dead or
devitalised tissue 4.2 Treatment
3.3 Suturing of wounds Unlike other infections, antibiotics alone will not
Wound healing may be usually cure an abscess. In general an abscess must
First intention- this is brought about by joining open and drain in order for it to improve. Sometimes
together the edges of the wounds by sutures, draining occurs on its ow n, but generally it must be
clips, adhesive materials opened by a doctor in a procedure called incision and
drainage (I&D)
Second intention- when the wound edges are not
brought together as there is- skin loss, wound

Page 456
Other risk factors for abscess include exposure to Supplementary/supportive Vit.C 500 od 3 to 4
dirty environments, exposure to persons with certain days
types of skin infections, poor hygiene, and poor
circulation. 4.4. Prevention
4.3 Self-Care at Home Maintain good personal hygiene by washing your
skin with soap and water regularly
If the abscess is small (less than 1 cm or less
than a half-inch across), applying warm Take care to avoid nicking yourself when shaving
compresses to the area for about 30 minutes 4 your underarms or pubic area
times daily can help. Seek immediate medical attention for any puncture
Do not attempt to drain the abscess by pressing wounds, especially if associated with some debris in
on it. This can push the infected material into the the wound, associated medical conditions, patient
deeper tissues. on steroids or chemotherapy
Do not stick a needle or other sharp instrument
into the abscess center because you may injure 4.5. Important points
an underlying blood vessel or cause the infection
to spread. Once treated, the abscess should heal
How long the abscess has been present Many people do not require antibiotics
Any injury to that area
Medicines being taken The pain often improves immediately and subsides
more each day
Any allergies
Fever at home Wound care include wound repacking, soaking,
washing, or bandaging for about 7 to 10 days. This
4.2. Examination and test usually depe nds on the size and severity of the
abscess
4.3.2 Drugs: After the first two days, drainage from the abscess
Antibiotics - Cap. Ampicillin 500mg qid 4 to 5 should be minimal to none. All sores should heal in
days or 10-14 days.
Tab. Ciproflox 500mg bd 4 to 5 days or Synonyms and Keywords
Tab. Cefadroxil 200mg bd 4 to 5 days Abscess, abscesses, boils carbuncles, furuncles,
hileradenitis, suppurative, pilonidal abscess, pustules,
Symptomatic treatment by analgesic, anti and whiteheads.
inflammator y dr ugs

Page 457
 3. HEAD INJURY

Head injuries comprises of injuries to skin, skull, 2.1 Intracerebral haemorrhage - in

intracranial organs with vessels, in combination or
singly.
Skull is the protective bony cage/vault for brain
though it is not a perfect fit considering weight &
vol ume of brain which may turn in to injury to the
brain by inclusive of skin & vault or singly by mere
inertia to brain & its membrane. As the brain is
suspended by superior cerebral veins from above
antero - posteriorly to the membranes and laterally by
attachments of dural process causing direct impact
injuries to site - coupi injuries or indirectly to the
opposite side of skull called counter coupe injuries.
1. Injuries can be classfied
grossly as
Concussion
Contusion
Laceration
1.1 Cerebral Concussion:
It is distortion and displacement of brain substance
minimally. Producing sudde n loss of consciousness,
motor & sensory paralysis of variable duration from
seconds to minutes. There is a complete recovery in
this injury.
1.2 Cerebral Contusion:
In this injury distortion, displacement is of severe
nature along with injury to brain matter- neural
fibers, this additional sliding movement between gray
& white matter in toto producing damage to nerves &
axons
1.3 Cerebral Laceration:
In this injury internal changes are same but the brain
surface is actually torn. Clinically causing prolonged
unconsciousness
the brain substance it is usually
associated with lacerations in
brain.
2.2 Subarachnoid- in the pre
arachnoids mesh.
2.3 Extradural Haemorrhage:
Extradural - outside the dura between dura and the
periosteum of inner table of skull.
It is a injury causing blood accumulation between
skull & dural membrane. This causes pressure effects
on brain & its functioning. It causes phase of
unconsciousness with period of apparent recovery
between two periods of unconsciousness is known as
lucid interval.
2.4 Subdural Haemorrhage:
Subdural -under the dura but outside the arachnoids
matter.
It is usually from the veins causing blood
accumulation beneath the dural membrane.
3. Signs & Symptoms &
findings:
Vomiting
Headache
Bleeding - ENT
Convulsions
Irritability, loss of consciousness, disorientation
4. Clinical Examination
Examine level of consciousness, reaction and
size of pupils
Blood pressure, pulse, respiratory rate

5. Investigations:
Routine investigations
2. Intracranial Haemorrhages: Skull X-ray
There are four anatomical types of intracranial CT-Scan
haemorrhages MRI

Page 458
6. Management:
6.4 Maintenance of air way, throat
Depends upon site, severity of injury, general
condition of patient & relevant complications. & nasal suction
6.1 Nil by mouth 6.5 Control of bleeding
6.6 Care of associated injuries
6.2 IV fluids,RL, D-10% 500-1000 6.7 Oxygen inhalation with mask,
cc SOS intubation / tracheostomy
6.3 Drugs 6.8 Management of shock
6.9 After stabilization,patient to be
IV Mannitol 100 cc/bd shifted to higher center for
IV Dexamethasone 4-8 mg/bd expert neurosurgical
Inj. Phenytoin 200-600 mg/ day or Inj.Sodium management 8-10hrs.
Valproate 400-2000 mg/ day
Inj. Cefotaxime 1gm/ bd
Inj.Gentamycin 80 mg/ bd
Inj. Aceclofenac/Dicyclomine 2 cc/im/bd

Page 459
 4. CHEST INJURY
Chest injury is common in road accident, fall from After stabilization,patient to be shifted to higher
height, stab injury center for expert management within 4-8hrs

1. Chest wall 7. Common injuries we come

Fracture ribs
Flail chest
across which need primary
Fractured sternum treatment to stabilize the
patient are:
2. Pleura:
Penumothorax 7.1. Fracture Ribs:
Tension penumothorax 7.1.1 Clinical presentation
Traumatic haemothorax May be single or multiple, simple or compound. with
or without Pneumothorax
3. Lung: Patient may present with- pain, di fficulty in breathing
Pulmonary contusion in a latter stage some times inability to take breath
Pulmonary laceration secondary to Pneumothorax,
7.1.2 Diagnosis & management
4. Mediastinal structures: patient needs to be investigated by X-ray chest
Ruptured thoracic aorta
Ruptured br onchus Analgesia
Ruptured diaphragm Breathing
Blunt injury to the heart Strapping
Haematopericardium
7.2. Flail Chest
5. Penetrationg injuries: 7.2.1 Clinical presentation
Bullet This type of injury is commonly seen in accidents
Stab wounds to the chest due to multiple rib fractures causing paradoxical
movement of chest wall. Resulting in to respiratory
6. Early Treatment: insufficiency & retention of pulmonary secretion.
Relief of pain - analgesics Inj. 7.2.1 Diagnosis & management
Aceclofenac/Dicyclomine 2 cc/im/bd
To be diagnosed by X-ray Chest
Stabilisation of the chest wall- strappi ng
Removal of pleural blood or air -Simple Patient needs following treatment.
aspiration, air tapping by needle,ICD
Propped up position
Removal of tracheo-bronchial secretions
Oxygenation by mask
Tracheostomy
Chest wall stabilization by strapping
Oxygen administration by mask
NBM Tracheostomy-SOS
IV Fluids - Ringer lactate, DNS, dextrose 5%
Antibiotics-
Inj. Ampicilline 500 mg. IV/6 hrly .
7.3. Traumatic Pneumothorax:
Inj. Gentamycin 80 mg. IV/12 hrly. 7.3.1 Clinical presentation
Inj. metronidazole 400 mg.IV/8 hrly. It is a trapped air in plural cavity due to penitrating
wounds to chest wall, pleura and or lungs. It may be
Blood t ransfusion SOS associated with hemothorax.

Page 460
7.3.1 Diagnosis & management After stabilization of the patient as and where
required as per condition of injury & patient to be
a) To be diagnosed by X-ray Chest-evidence of shifted to higher center in ALS transport vehicle.
fracture ribs, lung collapse black radiolucent chest
cavity area on injured sides. Sometimes air fluid level
in Hemo/Pneumothorax.
8. INTERCOSTAL
b) Patient needs with ICD as above
DRAINAGE
7.4. Tension pneumothorax: 1. Indications for Chest Tube
7.4.1 Clinical presentation Insertion:
Pneumothorax
A tension pneumothorax develops when there is a
one-way valvular leak of air into the pleural cavity. Hydropneumothorax
Air rapidly accumulates, compressing the lung, and
urgent treatment is required, as it is a life threatening Haemothorax
emergency. Empyema
7.4.1 Diagnosis & management
To be diagnosed and treated as above in addition 2. PREPARATION
patient needs.
a) Simple needle aspiration to release tension 2.1 Requirements for Chest Tube Insertion
b) ICD with under water seal procedure:
Chlorhexidine or povidone-iodine solution
7.5. Haemothorax: Sterile towels and drapes
7.4.1 Clinical presentation Sterile sponges
1% lidocaine without epinephrine (40 ml)
An accumulation of blood i n the pleural cavity can 10-ml syringe
occur from injury to the muscles in the chest wall, 18-, 21-, and 25-gauge needles
lung, heart or great vessels. There may also be a Mayo scissors
pneumothorax in association. Standard tissue forceps
Patient may be presented with pain, breathlessness, Towel forceps
shoc k. On examination there are signs of pleural Needle holder
collection with lack of breath sounds & dull 0-Silk suture with cutting needle
percussion note. Scalpel handle and no. 10 blade
Chest tubes (24, 28, 32, and 36 French)
7.5.2 Diagnosis & management Chest tube drainage system (filled appropriately)
2-in. adhesive tape
a) To be diagnosed by X-ray Chest
Sterile gowns and gloves, masks, caps
b) Patient needs following treatment with ICD
Blood t ransfusion SOS

Page 461
 Figure 1: Intercoastal Drainage tube
3. Pneumothorax / Haemothorax
ICD insertion procedure:
3.1 Part Preparation
Parts shaved and prepared
Consent taken
Parts painted and draped
Position: Semi recumbent (45%) on a backrest
Turn the patient's head on the opposite side
3.2 Anaesthesia: LA
3.3 Site:
2nd inter costal space, mid-clavicular line for
pneumothorax.
7th inter costal space, in the mid-axillary line for
Haemothorax.
Cut skin, Subc utanous tissue Split the muscles
with an artery forceps, till the pleura is reached.
Keep the inter costal tube ready - Malecot's
catheter or Portex ICD tube. Keep the
underwater drain and drainage tube ready.
Plunge the artery forceps into the pleura. The
ICD tube mounted on another long & blunt
artery forceps in thrust into the pleura along the
same direction.
3.4 Position the ICD tube:
all the holes of the tube should be in the pleural
cavity
3.5 Fix t he ICD tube with a skin stitch:
Air bubbles are seen coming out and a column of
fluid moving with respiration. /Blood is seen
coming out and a column of fluid moving with
respiration in Haemothorax.
Clinically, the patient improves:The
tachypnoea settle. Respiratory sounds are heard.
chest X-ray shows lung expa nsion.
3.6 Inter costal drain is re move d when the
indication is ove r:
X-ray Chest shows full expansion, Column of fluid
in the IC drain stops moving.
3.6.1 Romoval:
Cut the skin stitch, pull the IC drainage tube out
and give immediate strapping ( vaseline gugze
airtight)
Page 462
 Figure-2: Site for Lidocaine Infiltration

Figure-3: Intercostal Tube insertion

Page 463
 Figure-4: Intercostal Tube fixation
4. POST INSERTION:
4.1 X-ray chest zatch for complications:
Not draining (check for kinking)
Organ injury (lung, liver, spleen, heart,
vessel) careful insertion
Blood loss careful observation
Surgical emphysema (small hole and good
suturing)
Infection (sterile technique)
5. Safety features:
First tube connecting drain to drainage bottles
must be wide to decrease resistance
Volume capacity of this tube should exceed of
patients maximum inspiratory volume (otherwise
water may enter chest)
Volume of water in bottle should exceed of
patients maximum inspiratory volume to prevent
in drawing of air during inspiration
Drain should always stay at least 45cm below
patient (prevention of removed fluid or water
refluxing into patient)
Clamp drain when moving
Waterlevel above tube in another bottle
determines the amount of suction applied before
air drain through tube (safety suction limiting
device).
Page 464
 5. ABDOMINAL INJURIES
The abdomen has only muscle layers protecting the Cold clammy extremities
internal organs anteriorly and laterally. Restlessness
Breathlessness
1. Blunt Trauma Sweating
Occurs when the offending agent is blunt and wide Altered level of consciousness
area of contract occurs at the time of impact. Severity External injuries
of the injury depe nds on the force of the offending 3.3 Stabilize the hemodynamically
agent.
unstable patient first,
2. Penetrating trauma investigate later.
Occurs when injured by sharp instruments and the 3.4 Cardiothoracic, head and
depth and direction of the wound is more important spinal injuries get priority over
than the size of the wound.
abdominal and other skeletal
2.1. Cause:- and surface injuries.
Accidents (Traffic, industrial and disasters) Refer patient immediately for
Falls
Assaults emergency surgery & expert
In children (child abuse, bicycling, swimming, managements.
etc) 3.5 Blood transfusion SOS.
2.2. Investigation 3.6 Treatment
The history of the traumatic event is important in NBM, RT aspiration
determining the nature and severity of the intra- IV Fluids - Ringer lactate, DNS, Dextrose 5%
abdominal organ injury. Analgesics - Inj. Diclofenac 50 mg/im.
Antibiotics- Inj. Ampicilline 500 mg IV./6 hrly
3. Presentation & Management OR
3.3 Life saving measures such as Inj. Cefotaxime 1 gm/bd.

ABCDE Inj. Gentamycin 80 mg.IV /12 hrly.

Airway patency Inj. Metronidazole 400 mg. IV/8 hrly.
Bleeding control
Circulation maintenance 4. Proceed in the following
Breathlessness
Deformity (cervical stabilisation and fracture
order for haemodynamically
immobilisation) should be done first before stable patient:
transport to the hospital. Complete clinical examination
3.1 Examine head to toe thoroughly on Plain X-ray abdo men - Erect or left lateral
arrival of the trauama patient to identify position
all the injuries Categorise patient Diagnostic peritoneal tapping
immediately into hemodynamically Ultra sound abdomen (FAST)
stable or unstable. Abdominal CT
3.2 Haemodynamically unstable patient will If there is progression in illness/detected internal
have the injury, patient to be shifted for further expert
Following features treatment to higher center.

Page 465
 6. Gangrene
1. Definition:
Macroscopic death of the tissues with superadded
putrefaction.
Rest pain is an ominous symptom and usually
requires revascularization because this form of
advanced ischemia generally progresses to tissue
loss.
Patients with diabetes or renal failure are more
susceptible to the development of ischemic pedal
ulcers. Dry gangrene usually results in patients with
chronic critical limb ischemia without infection or
without any other complicating factors like diabetes,
osteomyelitis etc. It is characterized by dry shriveled
appearance, with clear line of demarcation and no
foul smell.
Wet gangrene is characterized by no clear line of
demarcation, foul smell, purulent discharge, evidence
of proximal spread in form of skip areas

Figure 1: Dry Gangrene Figure 2: Wet Gangrene

2. Treatment:
Analgesics- Inj. Diclofenac 50 mg/im.
Antibiotics- Inj. Ampicilline 500 mg. IV/6 hrly . OR
Inj.Cefotaxim 1gm. IV/12 hrly
Inj. Gentamycin 80 mg. IV/12 hrly. 3 to 4 days
Inj. Metronidazole 400 mg. IV/8 hrly.
IV fluids -Ringer lactate, DNS,dextrose 5% 1000-1500 cc

Dry gangrene: Treat the cause Requires urgent assessment and s hift the patient as
required for further surgical treatment.
Wet gangrene: Exclude Diabetes by repeated Blood Sugar
estimation.
Stabilize the patient hemodynamically.

Page 466
 Within one/two da ys, extensive gangrene of the
3. Fournier's Gangrene scrotal skin occurs resulting in sloughing of the
Idiopathic Gangrene of scrotal skin scrotal skin exposing the testicles. In few, the
gangrene can invol ve skin of the penis, anterior
Clinical features abdominal wall, medial side of thigh, perianal
Common in young apparently healthy region. In such situations, it is described as
individuals. perianeal phlegmon
Sudden appcarance of scrotal inflammation - Luckily, the testis does not get involved in
red swollen, very painful. Paitent is toxic with fourniers gangrene because of thick tunica
fever, prostration albuginea.

Treatment
Antibiotics- -Inj. Ampicilline 500 mg. IV./6 hrly OR
-Inj. Cefotaxime 1 gm/bd.
-Inj. Gentamycin 80 mg. IV/12 hrly 12-24 hrs.
-Inj. Metronidazole 400 mg. IV/8 hrly.
IV Fluids - RL , DNS 500-1000 cc
If there is no regression in ischaemic changes shift patient to higher center.

* Exclude Diabetes by blood sugar levels. When graranulations occur, skin

grafting is needed.

Page 467
 7. Burns
1. Definition/ Introduction:
A common surgical emergency. Children and females
are more vulnerable in India. Commonest are
accidental scalds due to hot water or oil in children
and stove burst or suicidal/ homicidal burns in
females.
Figure:1: Calculation of Burns percentage
3. Treatment:
3.1 Medical :
Reassure the patient. All patients having more
than 10% burns in children and >25% burns in
adults should receive intra venous fluid therapy.
Burn surface calculation using Wallace rule
of '9' and Calculate fluid requirement
2. Clinical features:
Clinically burns can be classified as follows:
Burns >10% in children and >25% in adults require
Intravenous fluid therapy. In addition certain specific
cases as shown in figure1, preferably need to be
managed i n Burn Centres.
according to Parkland Formula and administer.
Monitor strictly pa tients intake and urine
output after catheterization. If the burn surface
area exceeds 35%, consider keeping the
patient NBM and put ryles tube anticipating
paralytic ileus.
(BSA = Burn percentage)
Page 468
 Figure 2
3.2 Dressing :
3.2.1 Open
wounds to be cleaned with distilled water
and antiseptic lotion (Povidon Iodine) apply
antiseptic ointment/creams Furacin,
Silversulfadaizine+Chlorhexidine, etc.
3.2.2 Close
Deep burns need close dressing by
autoclaved bandage after completion of
procedure mentioned above or use
Tullegras(nonadhesive dressing) of
Silversulfadaizine+Chlorhexidine, Povidon-
Iodine etc.
3.3 Proper antibiotics coverage
Burn patients should be give n antibiotics
like Inj. Cefotaxin 1gm bd, I nj. Gentamycin
80 mg bd, IV Metronidazole 400 mg 8
hourly etc. for 7 to 8 days keeping in view
the condition of the pa tient.
Figure 3
3.4 Other
3.4.1 Venesection may be required in case if
peripheral lines are all collapsed. Preferably
venesection is done at the ante cubital fossa.
But if not possible due to extensive burns,
then long saphenous ve in can be canulated
for administering f luids.
3.4.2 Endotrac heal intubation SOS
Tracheostomy in patients with airway and
breathing difficulty.
3.4.3 Ischarotomy incisions may be required for
circumferential deep burns involving the
extremities or the chest. The ischarotomy
incisions are as shown in the figure.
3.4.4 daily needful dressing under aseptic
precaution
3.4.5 Adequate oral hydration
4. When to refer:
All patients requiring special burn centre care
as listed earlier.
Patients in septicaemic shock
Page 469
 8. Dressings
1. Aim of wound dressing:
In an open wound which is being allowed to heal by
secondary intention, or is being prepared for a
delayed reconstructive procedure, the requirements
are prevention of desiccation of the surface, removal
of excess wound exudates, protection from physical
damage and reduction of risk of infection
2. Types of wound dressing:
2.1 Occlusive (covered)
2.2 Non occlusive (open)
2.1 In most cases, occlusive wound dressings are
preferable since they prevent bacterial contamination,
keep the wound moist and provide a cover over the
wound allowing normal activities.
2.2 Non occlusive wound dressing may be used in
special cases of clean granulating wounds, burns, dry
Eschertic where the patient is well informed and
educated regardi ng keepi ng the wound clean and
local hygiene.
3. Indications for wound
dressing:
The primary determinant of the need for a
dressing is the depth and degree of bacterial
contamination of the wound.
Superficial clean wounds are best managed by
infrequent dressing.
Deep clean wounds are best managed by
immediate suturing and light dressing ( for
physical protection only )
Contaminated / Dirty wounds are best managed
by surgical debridement / wash followed by
regular wound dressing
All electively sutured surgical wounds DO NOT
require regular wound dressing. At most they
require a light dressing for physical wound
protection.
4. Dressing components:
4.1 Antiseptics and wound
cleaning solutions
Povidine iodine
Cetrimide
Glacial Acetic acid 10% - infected greenish
wounds (pseudomonas)
Normal saline
Hydrogen peroxide
EUSOL
4.2 Dressing material
Cotton gauze / pads / bandage
Hydrocolloid dressings
Paraffin / non adhesive gauze ( BACTIGRAS
)
Collagen granules
Adhesive strips
5. Types of wounds and
dressings:
5.1 Clean open wounds: Such wounds
require simple cleaning with normal saline
followed by a light dressing with non adherent
gauze such as Bactigras / plain paraffin gauze.
Adherent dressings such as plaincotton gauze
should be avoided as they tend to damage the
granulation tissue on dressing change.
5.2 Clean sutured wounds: Electively
sutured clean wounds require only a light
dressing of cotton gauze. The treating doctor
may or may not place a layer of antiseptic
ointment over the wound (eg: povodine iodine,
soframycin). Repeat dressings are not
required.
5.3 Contaminated sutured wounds:
Contaminated wounds require thorough
cleaning with copi ous amounts of nor mal
saline. If the de gree of contamination is high,
this should be followed by hydrogen peroxide.
The wound should then be irrigated with an
antiseptic solution and covered with cotton
gauze. Dressing change may be performed at
24 hrs and is primarily to assess the presence
of a collection or infection in the wound. The
presence of either should prompt removal of
some or all the sutures converting the wound
into an open contaminated wound. Such
Page 470
 wounds may also require systemic cover of
antibiotics depending on the degree of
contamination.
5.3 Contaminated open wounds:
Such wounds require regular (daily) dressing.
Irrigation with hydrogen peroxide should be
performed followed by normal saline to
decrease the physical contamination of the
wound. Antiseptic solution irrigation should
then be performed. Such wounds tend to
discharge, so a bulkier dressing with more
absorbent gauze may be required.
5.5 Dirty wounds: Such wounds are
characterized by presence of slough, necrotic
tissue, eschar or frank gangrene. These
wounds require initial surgical debridement for
removal of gross necrotic tissue and debris.
Debridement may have to be repeated.
Depending on the degree of slough, this may
be performed bedside or may require an OT
and anesthesia. The dressing should be
performed with hydrogen peroxide, followed
by nor mal saline and antiseptic solution. The
covering cotton gauze should be soaked in
normal saline or EUSOL. Dressing changes
need to be frequent and may have to be
repeated thrice daily. The covering material
should ideally be kept moist with saline /
EUSOL. The wounds with surrounding
cellulitis, oedema should be covered with
Magsulf. Dressings. It absorbs the fluids,
reduce oedema and pain. Large granulating
wounds should be sent for Skin grafting.
Page 471
 9. BREAST

If associated with a lump (mass)

1. Common presentations Unilateral persisting pain in postmenopausal
1.1. Lump: women
Any new discrete lump (Mass) in breast or
axillae
1.3. Nipple Discharge:
Blood stained discharge
New lump (Mass) in pre-existing modularity
Persistent single duct discharge
Asymmetrical modularity that persist after one
or two menstrual cycle 1.4. Nipple retraction or distortion /
Abscess or breast inflammation which does not nipple eczema
settle after treatment
Recurrent mass/swelling
1.5. Skin retraction of long
1.2. Pain: duration

Figure 1: signs of Breast Cancer.

With patient sitting note change contour, skin

2. Examination of breast:
some key Steps
The patient (naked to the waist) is examined in
the presence of a female attendant
tethering, nipple tethering, arms above her head
Tethering of lesion to the chest wall
Examination of axially tail with flat of hand
Lump should be assessed for size (measured by
calipers) shapes, consistency, tenderness,
mobility and fixity to the overlying skin/

Page 472
 underlying chest wall , skin changes in the for m
of oedema ( pain-d-orange)
Both axillae should be examined for palpable
lymph node s ensuring the anterior, medical
posterior and apical nodes. The size, numbers
and fixity should be recorded
Note that clinical assessment of axillary nodes
may not reflect their pathology status. For TNM
staging it is impor tant.
The supraclavicular and infraclavicular fossae
and cervical region should also be examined for
palpable lymph nodes
Any other symptomatic regions should be
examined as required for signs for metastatic
diseases
All examination findings must be recorded in
sketch or written form, as part of good clinical
practice and for medico legal reasons
Initial assessment, investigations and staging of
breast symptoms should be notified.
3. Benign Breast Conditions
Fibroadenoma
Cyst
Duct papilloma
Fibroadenosis or Fibrocystic disease of Breast.
4. Inflammatory conditions
Abscess
Fistula
5. Other conditions (Non
malignant)
5.1. Fat necrosis
Fat necrosis following trauma can occur. Small
cancer may clinically and radiologically mimic fat
necrosis. Treatment is by reassurance or excisional
biopsy.
5.2. Mastalgia : breast pain :
Can be symptom in malignancy of Breast in less
than 10%
Chest wall disease should be excluded
Intraabdominal (gall stones) intrathorac`ic
(cardiac, pleural) pain may all present as breast
pain.
Exclusion of significant breast pathology,
reassurance and non-steroidal drugs can provide
symptomatic relief.
5.3. Gynaecomastia:
Pubertal gynecomastia
Gynecomastia secondary to drugs therapy liver
disease testicular tumours hyperthyroidism renal
disease should be excluded.
6. Malignant lump (cancer) :
6.1. Definition:
the risk of developing distant metastasis increase with
tumour size. Early breast cancer is defined as the
condition in which tumour is confined to the breast,
size 2cm with obvious no metastasis.
Page 473
 Figure 2
T.N.M.: classification
6.2 T.N.M.: classification
T-primary tumor N-nodes M-metastasis
6.2.1 T Primary tumor mass
This classification is internationally accepted and
widely used to describe the extent of the tumor,
regional nodes and metastasis.
To - no demonstrable tumor
Tis - carcinoma in situ
T1-tumour diameter 2cm or less without fixation
T2-2cm to 5cm without fixation
T3-tumour greater than 5c m
T4 - Extension of a tumor of any size to skin or chest
wall.
(Pu.d.orange, skin tethering and nipple retraction
doesnt affect T classification)
6.2.2 N-regional lymph nodes.
No-No palpable homolateral axillary nodes
N1 Mobile homolateral axillary nodes
N2- fixed homolateral axillary nodes.
N3- Homolateral supraclavicular and infraclavicular
nodes and/or oedema of arm.
6.2.3 M Metastasis
Mo - No distant metastasis
M1 - Distant metastasis
6.3. Screening for breast cancer:
Beneficial in women over 40 + years age
Can detect smaller tumour with lower mass of
lymph node, metastasis
Early detection of breast cancer. By examination
and mammography reduces morbidity in
screened patients.
6.4. High Risk factors:
Strong family history of Breast or Endometrial
cancer
Carcinoma of Contralateral Breast
A history of intraductal papilloma
Childless women and those conceiving after 30
yrs of age
Breasts with dense parenchyma with prominent
duct patterns (fatty breasts with minimal
connective tissue elements are at risk)
Page 474
6.4. Diagnosis of breast cancer:

6.4.1 Physical examination of breast (self-

examination of breast fortnightly)

Figure 3

6.4.2 FNAC: fine needle aspiration cytology

Figure 4: FNAC

Page 475
6.4.3 Imaging methods/ mammography
Figure 5: Mammography
Routine mammography screening should be
avoided under 50 yrs.of age to avoid radiation
hazards.
6.5. Investigation:
Biopsy, trucut biopsy of the lesion for
histopathological evidence
Estrogen, Progestron Hor monal receptor status
MRI spine for Metastasis in the vertebras.
USG Liver for secondaries.
6.6. Treatment:
6.6.1 Aim:
To reduce morbidity and extends 5 yrs to 10 yrs
survival rate.
To conserve the breast, if possible
To achieve the control of disease.
6.6.2 Treatment options:
Surgical management
Radiotherapy
Chemotherapy
Hormonal therapy
7. Surgical management:
a) Surgical manage ment includes
Modified radical mastectomy (pateys)
Radical mastectomy (halted ) not done
commonly
Breast conservative procedure (quadrantectomy,
lumpectomy, wide local excision )
Simple mastectomy for ulcerated, foul smelling
lesion of breast (toilet mastectomy)
Breast reconstruction cosmetic surgeries-after
complete removal
b) Radiot herapy:
Pre-operative for tumor mass depletion/regression
Post operative as advi sed by Surgeon
c) Hormonal therapy : eg Tomoxifen tabs.
d) Chemot herapy
Page 476
 10. Congenital Anomalies of G.I.T
CL and CP are facial malformations that occur during
1. The most common embryonic development and they are the most
anomalies are: common congenital deformities of the head and neck.
i. Cleft Lip or Cleft Palate They may appear separately or more often together.
ii. Hernias
iii. Esophageal Atresia 1.1.1 Definitions:
iv. Anorectal malformations a) CL : is a congenital fissure in the upper lip.
b) CP: is a midline fissure of the palate that results
from failure of the two sides to fuse.
1.1 Cleft Lip (CL) or Cleft Palate
(CP)

Figure 1 Figure 2

CL and palate

Figure 3

Page 477
1.1.2 Important feature of CL/CP One or both sides.
Small notch Unilateral clefts are nine times more
Extending into the base of the nose. common than bilateral clefts.
Unilateral or bilateral. 60% to 80% of children born with cleft
CL/CP may involve the soft and hard lip and palate are male.
palate.

Figure 4

1.1.3. Diagnostic evaluations: Prenatal diagnosis after 13-14 w eeks when

Apparent at birth. the soft tissue of the fetal face can be
Examining the palate. visualized.

Figure 5

Page 478
1.1.4. Why CP more serious thanCL?
It interferes more with feeding and breathing, more
difficult to repair.
Therapeutic Management
The management of CL involves the cooperative
efforts of a multidisciplinary health care team.
7 Pediatrics
8 Plastic surgery
9 Speech/ language pathology
10 Audiology
11 Nursing and social work
1.1.5. Management is directed toward:
Closure of the clefts, Surgery can be done after 6
months of age with Hb more than 10 gms and
baby weight more than 10 kg..
Prevention of complications.
Facilitation of normal growth and development
in the child.
1.1.6. Prognosis:
Even with good anatomic closure most children
have:
Some degree of speech impairment .
Inefficient functioning of the muscles of the soft
palate and nasopharynx.
Improper tooth alignment.
Varying degree of hear loss.
Improper drainage of the middle ear.
Recurrent Otitis media with scarring of the
tympa nic membrane.
1.1.7. Nursing consideration
It is important for nurse to emphasis not only the
infants physical needs but also on the parents
emotional needs.
CL or CP reduces the infants ability to suck,
interferes with compression of the areola.
Feeding is best with the infants head in upright
position.
Large, soft nipple with large holes have been
advised and used.
Large syringe with soft rubbe r tubi ng can be
used.
With some infant spoon feeding works best
Breast pump may be useful to stimulate the let
dow n reflex.
Page 479
 Figure 6

1.1.8. Postoperative care for CL: 1.1.9. Postoperative care for CP:

Elbow restrains are used to prevent the infant Lie on the abdo men.
from rubbing or disturbing the suture line.
Feeding by bottle, breast or cup.
Older infants who roll over will require a jacket
restraint to prevent rolling on the abdo men and Oral packing, it is usually removed after 2 to 3
days.
rubbing the face on the sheet.
Elbow restrains.
Adequate analgesia is required to relieve pain.
Clear liquids are offered when the infant has Instruct the parents to keep the restrains at home
until palate is healed (2 to 6 weeks).
fully recovered from anesthesia.
Mild sedatives may be prescribed.
The suture site is carefully cleansed.
Soft food after discharging the patient as per
A thin layer of antibiotic ointment may be
applied. advice of surgeon.

Gentle aspiration of mouth and nasopharyngeal

secretions.
An upright infant position.

Page 480
1.2. Hernias The abdominal wall, or

Is a protrusion of a portion of an visceral organ The inguinal canal.

through an abnormal or normal opening. Commonly 1.2.1. Diaphragmatic Hernias
seen hernias are :
Protrusion of abdo minal organs through ope ning in
The diaphragm, diaphragm.

Figure 7 : Congenital Diaphragmatic Hernia

Figure 8 : Congenital Diaphragmatic Hernia

Page 481
a) Symptoms Resuscitation, maintain suction, oxygen.
IV fluids
Mild to severe respiratory distress Positioning head up.
Tachypnea , c yanosis, dyspnea Administer medication
Absent breath sound. Post operative:
Shoc k Carry out routine postoperative care and
observation.
b) Diagnosis:
1.2.2 Hiatus Hernia:
Symptomatic Protrusion of stomach through esophageal hiatus.
Radiographic study
a) Symptoms:
c) Treatment Dysphagia, vo miting,
Supportive treatment of respiratory distress (Use Bleeding (haematemesis)
of endo tracheal intubation, oxygenation).
Prophylactic antibiotics (Ampicillin 50 mg/kg) b) Manage ment:
Surgical reduction of hernia and repair of defect. Conservative management maintaining
posture. Surgical repair
d) Nursing care:
Preoperative:

Page 482
Figure 9 & 10 : Hiatal Hernia

Page 483
 Figure 11

1.2.3 Umbilical Hernia a) Symptoms:

Weakness in abdominal wall around umbilicus,
Noted by inspection and palpation of the
incomplete closure of abdominal wall allowing
abdomen.
intestinal contents to protrude through opening.
High incidence in premature.
b) Manage ment
Surgical repair

Page 484
 Umbilical Hernia
Figure 12
1.3 Esophageal Atresia 1.3.1. Clinical manifestation:
Excessive salivation.
The esophagus instead of being an open tube from
the throat to the stomach is closed at some point. A Coughing, choking, cyanosis,
fistula is common between the trachea and Apnea
esophagus.
Abdominal distention.

Site of attac
Figure 13 : Types of Tracheoesophagial Fistula (TEF)

Page 485
1.3.2. Nursing alert:
Any infant who has an excessive amount of frothy
saliva in the mouth or difficulty with secretions and
unexplained episodes of cyanosis should be
suspected of having an EA / TEF and referred
immediately for medical evaluation.
1.3.3.Therapeutic Management:
Maintenance of patent airway.
Prevention of pneumonia.
Surgical repair of the anomaly.
Avoid oral intake, start IV fluids.
Remova l of mouth secretion by suction.
Broad spectrum antibiotic therapy.
Gastrostomy and repair of the TEF.
1.3.4. Nursing role:
Nursing responsibility for detection of this
malformation immediately after birth.
After feeding the infant and swallows, but
sudde nly coughs and the fluid return through t he
nose or mouth, report immediately.
The infant placed in incuba tor oxygen is
administered.
Intermittent or continuous suction of nose.
Oral fluids are withheld, the fluid intake met by
IV fluids or gastrostomy.
1.3.5. Postoperative care:
The infant is returned to radiant warmer or
incuba tor.
The gastrostomy tube is connected to gravity
drainage until the infant can tolerate feeding.
Tracheal suction with extreme caution to avoid
injury to the suture line.
The initial attempt at oral feeding to make sure
that the infant can swallow without choking.
Oral feedings are begun with sterile water,
followed by frequent small feeding of formula.
Infants are usually not discharged until they are
taking oral fluids well and the gastrostomy tube
is removed.
1.2.4. Anorectal malformations
Abnormal development of genitourinary and
pelvic organs.
The rectum and urinary tract separate completely
by the seventh week of gestation.
a) Imperforate anus
Is the mos t common congenital anomaly of
GIT in newbor n.
Investigation :Invertogram- X ray.
Invertogram will tell type of anomaly Low or High.
Diagnosis:
There is no a nal ope ning.
The nurse is unable to insert the thermometer.
No passage of meconium.
Later on abdominal distention and pain occur.
Treatment :
High anomaly will require immediate colostomy
while for low anomaly Local incision and Dilatation
will be required.
Page 486
 Figure 14: Imperforate anus
Postoperative care:
The anal area should be kept dry and clean.
If a colostomy has been done the skin around the
wound must be clean and apply colostomy clean
dressing.
The excoriations of skin occurs around
Colostomy area due to digestive enzymes from
intestinal juices leaking from the side of bag. To
prevent this aluminium paint should be painted
on the skin around the Colostomy site.
Figure 15
Page 487
 11. Venous Thromboembolism
1. Introduction :
Despite increased awareness and use of prophylactic
modalities, DVT and pulmonary embolism (PE)
remain important preventable sources of morbidity
and mortality. The incidence of DVT ranges between
5 and 9 per 10,000 person-years in the general
population, and the incidence of VTE (DVT and PE
combined) is approximately 14 per 10,000 person-
years.
Figure 1
2. Clinical Evaluation
Early in the course of DVT development, venous
thrombosis is thought to begin in an area of relative
stasis, such as a soleal sinus vein or immediately
downstream of the cusps of a venous valve in the
axial calf veins. Isolated proximal DVT without tibial
vein thrombos is is unusual. Early in the course of a
DVT, there may be no or few clinical findings such
as pain or swelling. Even extensive DVT may
sometimes be present without signs or symptoms.
History and physical examination are therefore
unreliable in the diagnosis of DVT. In addition,
symptoms and signs generally associated with DVT,
such as extremity pain and/or swelling, are
nonspecific
The more common acquired risk factors
include advanced age, hospitalization and
immobilization, hormone replacement and oral
contraceptive therapy, pregnancy and the recently
postpartum state, prior VTE, malignancy, major
surgery, obe sity, nephrotic syndrome, trauma and
spinal cord injury, long-haul travel (>6 hours),
varicose veins, antiphospholipid syndrome,
myeloproliferative disorders, and polycythemia.
Heritable risk factors include factor V Leiden;
prothrombin 20210A gene variant; antithrombin,
protein C, and protein S deficiencies; and
dysfibrinogenemias.. 9
3. Investigations:
Color Doppler will confirm the diagnosis.
4. Treatment:
4.1 Antithrombotic Therapy :
Antithrombotic therapy may be initiated with IV or
SC unfractionated heparin, SC low molecular weight
heparin, or SC fondaparinux (a synthetic
pentasaccharide). This initial therapy usually is
continued for at least 5 days, while oral vitamin K
antagonists are being simultaneously administered.
The initial therapy typically is discontinued when the
international normalized ratio (INR) is 2.0 for 24
hours
Page 488
Hemorrhage is the primary complication of UFH
therapy. The rate of major hemorrhage (fatal,
intracranial, retroperitoneal, or requiring transfusion
of >2 units of packed red blood cells) is
approximately 5% in hospitalized patients
undergoing UFH therapy (1% in medical patients and
8% in surgical patients). For patients with UFH-
related bleeding complications, cessation of UFH is
required, and anticoagulation may be reversed with
protamine sulfate. Protamine sulfate binds to UFH
and forms an inactive salt compound. Each milligram
of protamine neutralizes 90 to 115 units of heparin,
and the dosage should not exceed 50 mg IV over any
10-minute period. Side effects of protamine sulfate
include hypotension, pulmonary ede ma, and
anaphylaxis.
Most patients who receive therapeutic LMWH do not
require monitoring. Patients who do require
monitoring include those with significant renal
insufficiency or failure, pediatric patients, obese
patients of >120 kg, and patients who are pregnant.
4.2 Vitamin K antagonists :
which include warfarin and other coumarin
derivatives, are the mainstay of long-term
antithrombotic therapy in patients with VTE.
Warfarin therapy usually is monitored by measuring
the INR, Vitamin K antagonist may be started on the
same day as the initial parenteral anticoagulant,
usually at doses ranging from 5 to 10 mg. Smaller
initial doses may be needed in older and
malnourished pa tients, in those with liver disease or
congestive heart failure, and in those who have
recently undergone major surgery and depends on
liver function, diet, age, and concomitant medications
Page 489
 12.VaricoseVeins

Figure 1: Varicose veins

1. Definition/ Introduction: 3. Etiology and Risk Factors

Varicose veins are dilated, tortuous and elongated
superficial ve ins of the lower limbs
Age old disease known since Hippocrates,
Mentioned in Ebers Papyrus in 1550.
Incidence - F>M , Prevalence 1023% in men
3040% in women
Skin changes 5% , Active ulcers 0.5%.
2. Clinical features:
Patient usually has Cosmetic concerns
Symptoms of tiredness & heaviness in legs and
itching and eve n leg ulcer
Heredity, Age over 40 , Prolonged standing
,Pregnancy , Obesity , Sede ntary lifestyle ,
Surgery or trauma , Use of hor monal
medications.
4. Complications
4.1 Ankle edema, Ankle flare,
Pigmentation , Venous eczema,
Venous ulcer, Profuse
Hemorrhage, Superficial
Thrombophlebitis, Equinous
deformity, Calcification.

Page 490
4.2 Deep vein thrombosis:
One of the important etiology as well as
complication of varicose veins. It presents
clinically as swollen woody calf, pain, ankle
edema and redness. Patient may have fever.
5. Investigations:
Doppler ultrasound is most ideal for complete
evaluation.
6. Treatment:
Management options at glance
Bisguards exercise Heel raises atleast
3 4 timesevery day.
Compression stockings For early
varicosities without complications. Types of
stocking are
Below/Above knee
Mid thigh
6.2 Surgical treatment
6.2.1 Flush ligation at sapheno femoral
junction with stripping of Long
saphenous Vein.
6.2.2 Perforator ligation
Subfacial.
Sclerotherapy - Ultrasound-guided
foamsclerotherapy for short segments or
recurrent varicosity.
Radiofrequency ablation (Closure),
EndoVenous Laser Ablation.
Ambulator y phlebectomy, or a .
combination of these treatments.
7. Instructions to patient:
Life style changes, Follow Bisguards exercises
daily, Use of compression stocking through the day
can be removed at night. While sleeping raise the
foot end of the bed to aid venous return.
8. Dos and Donts:
In case the varicosity starts bleeding do not panic,
immediately lie down flat on the ground a nd raise the
bleeding limb above the heart level and apply
compression.
Page 491
 13. GENITO URINARY DISORDERS

1. PARAPHIMOSIS
1.1 Clinical features :
This condi tion occurs when a tight foreskin
(phimosis) is forcibly retracted back off the glans and
cannot be pulled forwards again. The tight band
causes obs truction of ve nous returns followed by
swelling of the distal foreskin and glans. It can occur
at any age. Condition is very painful & if not taken
care may cause Ischemic/Pregangrenous changes.
Reduction of the paraphimosis is followed by a
course of antibiotics and after 8-10 days perform
Circumcision (at surgical center).
.
2. TORSION TESTIS:
It is a condition caused by the twist of suspended
testis.

2.1. Patient presents with

1.2 Treatment:
Technique of Reduction- Parts shaved & prepared Sever scrotal pain of sudden onset referred to lumbar
Patient in OT Parts painted & draped. Local region Vomiting, fever, Scrotal swelling with gross
anaesthesia 2% Xylocaine infiltrated at the root of the tenderness up to the cord
Penis.
Manual compression and reduction 2.2. Investigation:
By giving multiple needle punctures over Routine investigation
swollen & oede matous fore skin of pe nis and
squeezing it to drive out the oedema fluid USG Scrotum - Doppler study - shows decreased
followed by mechanical reduction by pulling it blood flow & also viability of the testis.
to normal position.
Dorsal slitting at 12' O clock position and 2.3 Diagnosis-
reduction. Colour Doppler study of Scrotum.
2.3. Treatment:
2.3.1 I.V. fluids - Ringer lactate, DNS, dextrose 5%
2.3.2 Analgesics- Inj. Diclofenac 50 mg/I.M.
2.3.3 Antibiot ics-Inj. Ampicillin 500 mg. I.V/6 hrly . 12 to 24 hrs.
Inj. Gentamycine 80 mg.I.V./12 hrly.
Inj. Metronidazole 400 mg. I.V./8 hrly
If not relived after stabilization of patient to be referred to surgical center.

3. EPIDIDYMO-ORCHITIS
It is a inflammatory & infective condition affecting 3.3. Treatment:
epididymis and testis 3.3.1 Analgesics tablet aceclofeanac 10-20 mg/ BD
OR Dicyclomine 50 mg/ BD
3.3.2 Antibiotics Ofloxacine 400 mg/ BD for 5 to 7
3.1. Patient present with: days OR Cefadroxine 200 mg/ BD 5 to 7
Scrotal pain days.
Testicular swelling 3.3.3 Anti inflammatory Seratiopeptidase -5 to 10
Low grade fever with chills mg/ TDS 5 to 7 days
3.3.4 Ibuprofen 200-400 mg/ TDS 5 to 7 days
3.2. Investigation: 2.3.4 Scrotal support for 2-3 weeks
Routine investigation
USG Scrotum - Doppler study

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 14. ANO-RECTAL DISORDERS

1. Hemorrhoids 1.4 Complications:-

Profuse hemorrhage
Hemorrhoids are clumps dilated veins occurring in
Fibrosis
relation to the ano-rectal junction (commonly known
as piles) Thrombosis
Infection
1.1. Classification: Pyelophlebitis
Ulceration
1.1.1. By descent Gangrene
Suppuration
Grade 1- Bleeding Portal pyemia
Grade 2- Protrusions with spontaneous reduction
Grade3- Protrusions regressing with manual 1.5 Treatment:-
reduction 1.5.1 Conservative management:
Grade4- Irreducible protrusions Dietary improvement high fiber diet
Avoid straining at defecation
1.1.2. By Location
External:-arise from inferior hemorrhoidal plexus, 1.5.2 Active Surgical Treatment
and are covered by modified squamous epithelium. Sclerotherapy
Occurs below pectinate line. Banding
Internal- arise from superior hemorrhoidal plexus, Photo coagulation
also above pectinate line.
Hemorrhoidectomy
Iterno e xternal- when both are persent.

1.2. Clinical Features

1.2.1 Symptoms:- 1.6 Postoperative care
Bleeding, bright red and painless, frequent
bleeding may led to a nemia
Prolapse
Pain on prolapse
Mucus discharge
Pruritus / itching

1.3 Investigations:-
Direct Visualisation
Digital Rectal Examination
Proctoscopy
Basic investigation (Hb, CBC, Urine )
Blood grouping and RH typing
USG Abdomen (Associated portal hypertension)
Colonoscopy

Page 493
 Table 1: Post Operative Care and Complication

Post Operative care Post Operative Complication

Watch for bleeding Early
Sitz bath twice daily in the postoperative period Pain acute retention of urine
Analgesics Reactionary Hemorrhage (24 hrs)
Stool softners and laxatives Constipation
Avoids digital rectal examination in the early Late
postoperative periods Secondary hemorrhage (24 hrs)
Anal stricture
Anal fissure
Fecal incontinence
1.7 Important note:- 2.3. Examination:-
Surgery is for failure in conservative Acute fissure Pain during per rectal examination
management or in severe cases with or without palpatory mucosal abrasion
Colonic carcinoma to be ruled out (colonoscopy)
Chronic fissure Skin tag fibrosed ano-rectal mucosa
Anemia to be corrected pre-operatively (Blood
transfusion if required) 2.4. Investigations:-
Muco-cutaneous bridges should be preserved
Basic investigation Hb, CBC, Urine
during surgery to pr event anal stenosis
Conservation treatment preferred in pregnant Colonoscopy
ladies and elder.
2.5. Treatment:-
2. Anal Fissure
2.5.1 Conservative Manage ment
2.1. Defination: Laxatives Cremaffine 30ml at bed time / stool
Anal fissure is an ulcer or a crack in the canal or anal bulking agents -
verge that may extend from mucoc utaneous junction
Ointment to relax anal sphincter and improve blood
to dentate line. Anal fissure is of particular concern if
flow like Diltiazem / Nifedipine cream / glyceryl
it is acute because the degree of patient discomfort,
trinitrate ointment
pain and disability are extremely high.
Sitz bath
The type of fissure is acute and c hronic.
High fiber diet
Acute anal fissure is a deep tear through the skin of 2.5.2 Surgery:-
the anal margin extending into the anal canal. There
is little inflammatory induration or edema of its Anal dialation under GA
edges. There is accompanying spasm of the anal
Fissurectomy
sphincter muscles.

Chronic anal fissure is characterized by inflamed 3. Pilonidal Sinus

indurated margins, and a base consisting of either
scar tissue or the lower border of the internal
sphincter muscle. Chronic anal fissure doe s not heal
with conservative measures.
2.2. Symptoms:-
Pain during the defecation and / or after defecation
Slight bleeding / streaking
3.1Clinical features :
A pilonidal sinus is a depression in the skin or small
pit that occurs at the bottom of the tailbone (coccyx)
and can become infected and filled with pus. Once
infected, the technical term is pilonidal abscess.
pilonidal abscesses look like a boil at the bottom of
the tailbone, just above the crack of the buttocks. It is
more common in men than in women. It usually
happens in young people up into the fourth decade of
life.

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3.2 Treatment : Discharge of pus from the rectum
3.2.1 Medical treatment Fatigue and general malaise
Antibiotics (Cap. Ampicillin 500 mg TDS x
Fever night sweats, and chills
5 days)
Analgesics (Tab. Diclofenac 50 mg BD x 5 Lump or nodule, swelling, redness, tenderness at
days) edge of anus
3.2.2 Surgery Painful, hardened tissue
Anal dilatation under GA.
In infants, the abscess often appears as a swollen, red,
Fissurectomy tender lump at the edge of the anus. The infant may
be fussy and irritable from discomfort, but there are
4. Anorectal abscess usually no ot her symptoms.

4.1 Defination :
Anorectal abscess is a collection of pus in the area of
the anus and rectum.
4.2 Causes
Common causes of anorectal abscess include:
Blocked glands in the anal area
Infection of an anal fissure
Sexually transmitted infection
Deep rectal abscess may be caused by intestinal
disorders such as crohn's disease or diverticulitis.
4.3. Risk factors
Anal sex
Chemotherapy drugs used to treat cancer
Diabetes
4.5 Investigations
A rectal examination may confirm an anorectal
abscess.
A proctosigmoidoscopy may be done to rule out
other diseases.
Rarely, you may need a CT scan, MRI or ultrasound
to determine where the pus collection is located
4.6. Treatment:-
4.6.1 Analgesics-
Inj. Diclofenac 50 mg/IM BD/sos
4.6.2 Antibiot ics-
Inj. Ampicillin 500 mg. I.V./6 hrly . 5 days
Inj. Gentamycine 80 mg. I.V./12 hrly.
Inj. Metronidazole 400 mg. I.V./8 hrly.
4.6.3 Treatment involves surgery, open and drain
the abscess, patient may be shifted at surgical
center.

Inflammatory bowel disease (crohn's disease and 4.6.4 Post operative care
ulcerative colitis) After surgery patient needs warm sitz baths ( sitting
Use of medications such as prednisolone. in a tub of warm water) this may help to relieve
pain, reduce swelling and make the abscess easier to
Weakened immune system (such as from drain.
HIV/AIDS)
Drained abscesses are usually left open and have no
The condition may occur in infants and toddlers who stitches.
are still in diapers and who have a history of anal
fissures. Patient should be advised to take stool softeners,
practice good hygiene and eat a soft or liquid diet
4.4. Symptoms until the abscess has healed.

4.4.1 Swelling around anus and constant 4.7. Possible complications

throbbing pain, fever are the most common
Anal fistula
symptoms. Pain with bowel move ments may be
severe. Body-wide infection (sepsis)
4.4.2 Other symptoms may include:- Continuing pain
Constipation Problem keeps coming back (recurrence)

Page 495
Scars
4.8. Prevention:-
4.8.1 Prevention or prompt treat ment of sexually
transmitted diseases may prevent this cause of
anorectal abscesses. Use condoms during
intercourse, including anal sex, to preve nt such
infections.
4.8.2 Frequent diaper change s and proper
cleaning during diaper changing will help to
preve nt both fissures and perianal abscesses in
infants and toddlers.
Page 496
 15. Tracheostomy
1. Introduction
Tracheostomy is one of the most common surgical
procedures performed in the ICU and is the airway of
choice for patients requiring mechanical ventilation
for more than 2 weeks.
2. Procedure
Patients neck is extended and the surgical field is
exposed from the chin to several inches below the
clavicle. This area is prepered and draped and
prophylactic antibiotics are administered at the
discretion of the surgeon. A vertical or horizontal
incision may be used; however, a horizontal incision
will provide a better cosmetic result. The platysma
muscle is divided in line with the incision and the
strap muscles are separated in the midline. The
thyroid isthmus is then mobilized superiorly or is
divided as needed to access the trachea. In the event
of a low-lying cricoid cartilage, dissection on the
anterior wall of the trachea helps to mobilize the
trachea out of the mediastinum, and also the use of a
cricoid hook will elevate the trachea to expose the
second or third tracheal ring. Following identification
of the second or third tracheal ring, a vertical
tracheostomy is created or a tracheal flap (Bjork flap)
is fashioned to create a fistulous tract by suturing the
tracheal mucosal flap to the skin in the incision
3. Postoperative Care
The care of a tracheostomy tube after surgery is
important. Highlighted below are some specific
issues that all intensivists need to know when caring
for patients with tracheostomies.
4. Wound and Dressing Care
Daily examinations of the stoma are important in
identifying infections or excoriations of the skin at
the tracheostomy site. In addition, keeping the wound
clean and free of blood and secretions is very
important, especially in the immediate post
tracheostomy period. Dressing changes should be
performed at least twice a day and when the dressings
are soiled. Some authors recommend cleaning the
stoma with 1:1 mixture of hydrogen peroxide and
sterile saline. When changing dressings and tapes,
special care is needed to avoid accidental dislodging
of the tracheostomy tube.
5. Inner Cannulas
The inner cannulas should be used at all times in the
ICU. They serve to extend the life of the
tracheostomy tubes by preventing the buildup
secretions within the tracheostomy. The inner
cannulas can be easily removed and either cleaned or
replaced with a sterile, disposable one. Disposable
inner cannulas have the advantage of quick and
efficient changing, a decrease in nursing time,
decrease risk of cross-contamination, and guaranteed
sterility. The obturator should be kept at the bedside
at all times in the event that reinsertion of the
tracheostomy is necessary.
6. Humidification
One of the functions of the uppe r airway is to
moisten and humidify inspired air. Since
tracheostomies bypass the upper airway, it is vital to
provide patients who have tracheostomies with warm,
humidified air. Humidification of inspired gases will
prevent complications in patients with
tracheostomies. Failure to humidify the inspired
gases can obstruct the tube by inspissated secretions,
impair mucociliary clearance, and decrease cough.
7. Suctioning
Patients with tracheostomies frequently have
increased amounts of airway secretions coupled with
decreased ability to clear them effectively. Keeping
the airways clear of excess secretions is important in
decreasing the risk of lung infection and airway
plugging. Suctioning is frequently required in
patients with poor or ineffective cough. Suction
techniques should remove the maximal amount of
secretions while causing the least amount of airway
trauma. Routine suctioning, however, is not
recommended.
8. Tracheostomy Tube
Changes
Tracheostomy tubes do not require routine changing.
In general, the tube only needs to be changed under
the following conditions: (a) there is a functional
problem with it, such as an air leak in the balloon; (b)
when the lumen is narrowed due to the buildup of
dried secretions; (c) when switching to a new type of
tube; or (d) when downsizing the tube prior to
decannulation. Ideally, a tracheos tomy tube should
not be changed until 7 to 10 days after its initial
Page 497
placement. The reason for this is to allow the tracheal Cardiorespiratory arrest (uncommon)
stoma and the tract to mature. Patients who have their Tracheo-laryngeal injury (uncommon)
tracheostomy tube changed before the tract is fully Crushed airway from dilational tracheostomy-
mature risk having the tube misplaced into the soft uncommon
tissue of the neck. If the tracheostomy tube needs to
be replaced before the tract has had time to mature,
the tube should be changed over a guide, such as a
9.2. Intermediate Complications
suction catheter or tube changer. (from day 1 to day 7)
Persistent bleeding
9. Complications of Tube displacement
Tube obs truction (mucus, blood)
Tracheostomies Major atelectasis
Wound infection/cellulitis
9.1. Immediate Complications (
24 hours) 9.3. Late Complications (>day 7)
Tube displacement Tracheoinnominate artery fistula
Arrhythmia Tracheomalacia
Hypotension Hypoxia/hypercapnia Tracheal stenosis
Loss of airway control Necrosis and loss of anterior tracheal cartilage
Pneumothorax Tracheoesophageal fistula
Pneumomediastinum Major aspiration
Acute surgical emphysema Chronic speech and swallowing deficits
Major hemorrhage Tracheocutaneous fistula
Bacteremia
Esophageal injury (uncommon)

Page 498
 16. URINERY CATHETERZATION

bedside commode or when accurate urinary output is

1. Indication: required.
Urinary catheterization is done when a person is
unable to urinate using a toilet, bedpan, urinal,

Figure 1: Diagrammatic presentation of Urinary Catheter assembly

2. Types of catheters: 2.2 A straight catheter:

2.1 A condom catheter:
consists of a soft plastic or rubber sheath, tubing,
and a collection bag for the urine. The sheath is
placed over the penis and the collection bag is
attached to the leg. Collects urine when there is
no need for catheter insertion.
3 is used when the catheter is to be inserted and
removed immediately.
2.3 An indwelling catheter:
also known as Foley catheter, is left inside the
bladder to provide continuous urine drainage.

Page 499
2.4 A suprapubic catheter:
is a type of indwelling catheter. The suprapubic
catheter is inserted into the bladder through a surgical
incision made in the abdominal wall, right above the
pubic bone.
2.5 A 3-way catheter:
for continuous bladder irrigation (CBI) is a type of
indwelling catheter. Irrigate the bladder to prevent
obstruction (i.e bleeding)

Red rubber Latex Silicon

Figure -2

Catheters

Straight Condom

Suprapubic Indwelling

Page 500
3. Sizes & Subtypes:

Figure 4

3.1 Most common sizes are 8 F to 28 6. Emptying Urine Drainage

F. Bags:
3.2 1 F is equivalent to 0.33 mm =
Urine measured at the end of each shift or every
.013" = 1/77" of diameter. 4 hourly in ward, e very hourly in ICU.
3.3 Coud" (French for elbowed) Urine drainage bags should also be emptied if
catheters have a 45 bend at the they are full.
tip to allow easier passage Leg bags need to be emptied frequently because
through an enlarged prostate they are smaller, and hold less urine.
3.4 "Councill tip" catheters have a 7. Quantity:
small hole at the tip which allows
Be sure to monitor urine output
them to be passed over a wire
Amount
5. Caring for a Person with an Characteristics (color, clarity, sediment,
Indwelling Urinary hematuria, odor)

Catheter: Less than 30 ml/hr of urine indicates a

The catheter tubing is secured loosely to the
persons body near the insertion site using a
catheter strap or adhesive tape
Securing the tubing to the persons body
prevents the catheter from being accidentally
pulled out during repositioning
The drainage bag is then secured to the bed
frame at a level lower than the persons
bladder.
problem
4. Catheter Insertion:
4.1. Equipment:
(check packages and expiry dates)
Catheter tray (with drapes, fenestrated drape,
cotton balls, swab holder, bowl)
Catheter 14-16 Fr (for wome n) 12 Fr for young
girls
16-18 Fr (for me n)
Sterile drainage tubing with collection bag
Correct size syringe (check catheter balloon)
Sterile water

Page 501
 Cleansing solution: Chlorhexidine 4%, Povidone Ide ntify meatus and assess skin integrity
Iodine 10%
Lubricant anaesthetic jelly Identify potential difficulties (i.e enlarged
Sterile gloves prostate)
Specimen container
Tape to anchor tubing 4.3. Important aspects
Arrange equipment
4.2. Assess Wash hands
Review physicians order and understand Provide privacy
purpose of inserting catheter
Raise bed, stand on left side of bed if right
Assess client (last urination, level of awareness, handed (right side if left handed)
understanding)
Water proof pad under client
Palpate bladder
Position & drape client

Figure 5 Figure 6

4.4 Position
4.4.1 Fe male: dorsal recumbent (supine with knees
flexed) or Sims position (side-lying with uppe r leg
flexed at knee and hip)

Figure 7

4.4.2 Male: supine position

With disposable gloves, wash perineal areas

Page 502
Anatomy:

Figure 8

Figure 9

Page 503
4.5 Procedure: men: over thighs and fenestrated over penis
4.5.1 Anaesthetic Lubricant jelly
4.4.2 Place sterile tray and contents between legs
4.5.2 Apply sterile drapes keep gloves sterile
4.4.3 Cleanse meatus:
women: under buttocks and fenestrated over
perineum

Cleaning of part Male Urethra Catheter in situ

Figure 10 Figure 11 Figure 12

a) Men: retract foreskin, hold penis below clean in a circular motion from meatus down to
glans, maintain position of hand, with forceps base of glans, repeat three more times

Cleaning of part Draping Catheter in situ

Figure 13 Figure 14 Figure 15

b) Women: 4.3 Insertion :

With nondominant hand, expos e meatus, maintain a) Hold end of catheter loosely coiled in
Position of hand, clean with forceps, wipe from front dominant hand, place end of catheter in tray
to back, each time take new cotton ball for each b) Insert catheter:
swipe, far labial fold, near and directly over meatus

Page 504
 Wome n: Ask client to bear down as if to void,
insert 5 to 7.5 cm or until urine flows, then
advance another 2.5 to 5 cm
Men: Hold penis perpendicular, ask client to
bear down, insert 17 to 22.5 cm or until urine
flows, then advance to bifurcation
c) Collect specimen if indicated
d) Allow bladder to empty unless policy
restricts (800 to 1000 ml) Pelvic floor blood
vessels may become engorged from the
sudden release of pressure, leading to
possible hypotensive episode. This may also
cause painful bladder spasms.
e) Inflate balloon with amount indicated (10
ml)
If client complains of pain, aspirate solution and
advance catheter further and inflate
Gently pull to feel resistance
Attach catheter to collection bag and attach to
bed frame below bladder
Anchor catheter (thigh if appropriate and coil
tubing on bed and attach to mattress)
4.6. Evaluate:
Palpate bladder
Assess comfort
Characteristics and amount of urine
4.7. Document:
Report and record type and size of catheter
Amount of fluid used to inflate balloon
Characteristics of urine, amount, reason for
catheter, specimens, clients response
8. Procedure for removal:
Deflate the bulb completely with syringe
If bulb cannot be deflated then
Cut the one way valve
Puncture the channel with needle
Go on puncturing from distal most end to most
proximal end
USG guided suprapubic needle puncturing of the
bulb
Inflate further till it gets bursted.
Page 505
 17. TRIAGE
Triage process should be completed within five
1. Introdution : minutes.
Method of quickly identifying victims who have 4.1 Important steps
immediately life threatening injuries & have the best
chance of surviving. 4.1.1 Start System:
Classification is based on
Process which place the right patient in right place at
right time to receive he right level of care. Respiration
Perfusion
Triage involve a dynamic equilibrium between needs
Mental Status
and resources
Needs= Number of wounded and types of wounds 4.1.2 Shift
Identify and remove
Resource =Infrastructure and equipment at hand &
competent personnel present Select those severely injured
The dead
2. The Triage Team The slightly injured
The uninjured
Triage team leader coordinator
4.1.3 Sort:
Clinical triage officer
Categorize the most severely injured based on:
Head nurse, matron ; chief organizer
Life-threatening conditions (ABC)
Nursing groups
Anatomic site of injury
Red Cross Wound Score
3. Triage Documentation: Treatment available in terms
3.1 General information Serious wounds: resuscitation and immediate
surgery
Name, Age, Gender, chief complaints, history of past Second priority: need surgery but can wait
illness, mechanism of injuries, past medical and Superficial wounds: ambulator y management
surgical history, allergy to food or drug and current Severe wounds: supportive treatment
medication. Date of last tetanus immunization, last
menstrual period for female age 11 to 60 years
5. Categorization:
3.2 Vital sign- temperature, Pulse,
B.P & respiration etc. 5.1Category
3.3 Level of consciousness i: Resuscitation and immediate
surgery
3.4 Visual inspection for
Patients who need urgent surgery life saving
deformities, laceration, and have a good chance of recovery. (e.g. Airway,
bruising, rashes etc. Breathing, Circulation: tracheostomy, haemothorax,
haemorrhaging abdominal injuries, peripheral blood
4. Triage Process vessels)

Gathering information at point of triage.

Perform initial assessments at point of triage.

Page 506
 Figure 1 Figure 2

5.2 Category ii: Need surgery but A large number of patients will fall into this
can wait group.( e.g. non-haemorrhaging abdo minal injuries,
wounds of limbs with fractures and/or major soft
Patients who require surgery but not on an urgent tissue wounds, penetrating head wounds GCS > 8.)
basis.

Figure 3

Page 507
Figure 4

Figure 5

Page 508
5.3 Category iii: Superficial
wounds (no surgery,
ambulatory treatment)
Figure 6
5.4 Category iv: Very severe
wounds (no surgery,
supportive treatment)
Patients with wounds requiring little or no surgery. In
practice, this is a large group, including superficial
wounds managed under local anaesthesia in the
emergency room or with simple first aid measures.
Patients with such severe injuries that they are
unlikely to survive or would have a poor quality of
survival.
The moribund or those with multiple major injuries
whose management could be considered wasteful of
scarce resources in a mass casualty situation.
Page 509
 Figure 7

Seizures
6. Hospital Triage Setting: Asthma
Doctor performs daily triage on a routine basis every Acute Bleeding or Acute Pain
day in emergency department. Depressed Level of Consciousness

6.1 Aim: 6.2.3 Urgent : Category 2 Colour Code

It is to identify those patients who have the highest
degree of compromise for the purpose of providing
rapid care to sickest patient first.
6.2 Hospital Triage System
YELLOW
Those conditions that are serious and if not treated in
timely manner are likely to become critical.Time
needed, s erious illness or injury that must be attended
to, b ut wait upto two hrs.
Example:

i. Emergent Complex long bone fractures

ii. Urgent Bleeding Controlled with a pressure dressing
iii. Non Urgent Acute psychiatry problems
iv. Deceased High fever with other vital signs stable

6.2.1 Emergent : Category 1 Colour Code 6.2.4 Not Urgent : Category 3 colour code
RED GREEN
Those patients that are life threatening but likely to
be amenable to rapid intervention. Condition that can wait without likelihood of
deterioration. Time needed, condition can wait for
Time required treatment immediately or within 15 to more than 2 hrs.
30 minutes.
Example:
Example:
Minor lacerations which requires sutures
Cardiac Arrest
Minor joint trauma requires x-ray for diagnosis
Airway Obstruction Chronic conditions that are stable such as pre
Haemorrhage with shoc k existing skin rashes.
Complicated Delivery

Page 510
iv. Category 4 colour code Black
Dead to be honoured and to be taken care as marked
in end session, if not possible by assigned agency
earlier.
7. Conclusions:
Triage is method of quickly identifying victims
who have immediately life threatening injuries
AND who have the best chance of surviving.
Key elements of the START Triage Systems are:
Respiration, Perfusion and medication.
Reverse Triage is used for mass casualty
incidents.
Page 511
ORTHOPAEDICS

Page 512
 1. INFECTIONS IN ORTHOPEDICS

Infections of bone are difficult to treat due to 1.3. Most Common Organism:
precarious blood supply. Most common is Staphylococcusaureus
Hematogenous spread.

1. Osteomyelitis 1.4. Type:

Acute, Sub-Acute&Chronic
1.1. Classification:
Based on duration and mechanism of Infection 1.5. Most Common Site:
Durat ion: Around Knee and Hip (in Paediatric cases)
1. Acute
2. Sub-Acute Diagnosis:
3. Chronic
Mechanism: 1.6. Clinical Features:
1. Exogenous Open fracture, Surgery or Pain and swelling
contagious Constitutional symptoms
2. Hematogenous
Warm to touch
Restricted movements
1.2. Factors increasing
susceptibility to Infection: 1.7. Laboratory studies:
Patient dependant factors are nutritional and
immunological status. HB, TLC, DLC&ESR
Surgeon dependant factors are skin preparation, Aspiration of fluid(>50000wbc/cu.mm.)
operation room, environment and prophylactic Gram Stain sensitivity (30%)
antibiotic therapy Culture sensitivity (90%)
Blood Culture

Fig 1.2 Xray showing Osteomylitis of tibia Fig 1.2.1 Inflammation of Skin

1.8. Imaging studies:

X-Ray
Computed Tomography (CT)
Radionuclide scanning
MRI

Page 513
1.9. Treatment: NSAIDs such as Tab.Diclofenac sodium 50mg thrice
a day along with Antacids until Inflammation
subsides and supportive treatment such as
1.9.1. Medical Therapy(Conservative)
multivitamins.
Immobilize the joint with splint for pain relief
Antibiotic therapy of Osteomylitis. 1.9.2. Surgical therapy

Treat with intravenous Antibiotics for 3 to 6 weeks Debridement

Cephalosporins and Aminoglycosides. Sequestrectomy
Saucerisation
Paediatric dosage Sinus tract excision

Inj.Cefotaxime 750mg twice a day for 3 to 6 2. Tuberculosisof Bone:

weeks.
Inj.Amikacin 250 mg/ Inj.Gentamycine 20mg IV
Bone is most common extra pulmonary site of
twice a day for 3 to 6 weeks.
Infection of Mycobacterium Tuberculosis.
Adult Dosage
2.1. Source:
Inj.Cefotaxime 1500mg IV twice a day for 3 to 6 Always secondary.
weeks.
Inj.Amikacin 500mg/Inj.Gentamycine 40mg IV 2.2. Site:
twice a day for 3 to 6 weeks. Most common site is spine followed by hip and
Knee. Commonly occurs in first three decades
Treat for atleast 3 weeks with IV Antibiotics initially of life.
and then shift to or al for another 3 weeks.
Antibiotics should be used in accordance with
Antibiotic protocol of Institute. 2.3. Agent:
Mycobacterium Tuberculosis.

Fig 2.1 Picture of Destruction of Spi ne Fig 2.2 Cross Section of Koc h Spi ne

2.4. Clinical features:

a. Mono articular.
b. History of Night cries, loss of weight,
anorexia.
c. Decreased joint movement.
d. Wasting of muscles.

Page 514
 e. Pain and Tenderness. Bed rest and Traction in acute and early stages,
f. Cold abscess. Splints and braces.
2.6.2 Operative
2.5. Investigations:
a. Capsulotomy.
b. Synovectomy.
a. HB,TLC, DLC & ESR.
c. Curettage.
b. X-rayearly De-calcification & Late Joint
d. Excision.
destruction.
c. Confirm diagnosis by biopsy or culture and
2.6.3 Abscess
start treatment.
d. MRI. Incision and dr ainage.

2.6. Principles of Treatment: 2.7Complication of Bone Infections:

a. General Support Protein rich diet.Haematinics. 1) Pathological fracture.
b. Chemotherapy-Anti-tuberculous treatment as 2) Non-union / Mal union.
per RNTCP CAT-II 3) Para-paresis in spinal tuberculosis.

2.6.1 Local Treatment

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 2. ARTHRITIS (JOINT DISEASES)

1.Osteoarthritis 1.1. Clinical Features

It is degenerative disease of joint which commonly Pain.
involves Knee, Hip and Ankle joint. Swelling.
Restricted range of movements.
Primary Osteoarthritis is degenerative process
without any precipitating factors.
Secondary Osteoarthritis is mostly due to
1.2. Investigations
X-ray ofinvolvedjoint.
Trauma,Infection and avascular necrosis.

Fig .1 X-ray Showing Severe Osteoarthritis Changes

1.3 Treatment 1.3.2 Physiotherapy

1.3.1 NSAIDS 1.3.3 Local Hydrocortisone acetate Injection 40mg

Intra articular once. Dosage can be repeated
1. Tab.Diclofenac sodium 50mg Thrice a day for 1
after 2-3 months as and when needed (under
week and SOS later Or
aseptic precautions.)
2. Tab.Indomethacin 25mg thrice a day for 1 week
and SOS later Or
3. Tab.Ibubrufen 400mg Thrice a day for 1 week 1.3.4 Surgery ( joint replacement )
and SOS Later
NSAIDs cause hyperacidity hence antacids such
as Cap. Omeprazole 20mg or Tab.Pantoprazole 2. AnkylosingSpondylitis
40mg once a day should be give n.
Local application of Diclofenac sodium Gel 4-5 Chronic progressive inflammatory disease of
times per day. sacroiliac joints and the axial skeleton, having
insidious onset affecting young patients age less than
40 years.

Page 516
2.1. Clinical Features 2.5. Treatment:
Backache. 2.5.1. Conservative Manage ment
Restricted movements of spine and hip.
Rest.
Morning stiffness, improvement with exercise,
NSAIDS.
persistence for more than 3 months. 1. Tab.Diclofenac sodium 50mg Thrice a day for 1
week and SOS later Or
2. Tab.Indomethacin 25mg thrice a day for 1 week
2.2. Extra Articular Manifestations and SOS later Or
3. Tab.Ibubrufen 400mg Thrice a day for 1 week
Acute iritis.
and SOS Later
Pericarditis. NSAIDs cause hyperacidity hence antacids such as
Aortic incompetance. Cap. Omeprazole 20mg or Tab.Pantoprazole 40mg
Subluxation of atlanto-axial joints. once a da y should be given.
Physiotherapy / back exercise.
2.3. Investigations Occupational therapy.
General preventive measures like genetic
Haemogram. counseling.
HLA B27.
2.5.2 Surgical Treatment:
X-ray, Pelvis and Spine.
Spinal Osteotomy.
Total Hip replacement.
2.4. Diagnostic Criteria Total Knee replacement.
HLA B27 positive and X-ray picture showing
bamboo spine and ankylosed SI and hip joints. Recent trends:
Tumor necrosis factor antagonist (Etanercept) is
being us

Fig 1: X- ray Showing Bamboo Spine InAnkylosing Spondylitis

Page 517

3. CONGENITAL DISORDERS

1. Congenital Torticollis
(Wryneck): 2.2. Various splints include
Von Rosen splint.
Usually due to contracted sternocleidomastoid
muscle. Pavlik harness.
Head tilted towards and chin rotated away from Triple diapers.
affected side. Craig splint.
A firm swelling at junction of mid and distal 3rd
of the muscle may be felt.
Associated with congenital anomalies in cervical
2.3. Treatment
spine. 2.3.1 Age 1 - 3 Years
Treatment includes stretching exercises, if
Initially closed reduction is tried. If it doesnt give
deformity persists for 2 yrs surgical correction
the needed result then surgical correction is opted for.
lengthening of sternocleidomastoid muscle.
Surgery is planned after a period of traction. If the
Early identification and immediate child is more than 18 months only surgical
implementation of treatment gives good results.
procedures can help.
Earlier the treatment, better are the results.

The methods are

2. CDH: Removal of the interposed soft tissue from the
Congenital Dislocation of Hip. If displacement of joint.
femoral head from its normal position within the Innominate osteotomy.
aceTab.ulum is found at birth. It is regarded as CDH Femoral osteotomy.
or Developmental Dysplasia of the Hip (DDH).
2.3.2 More than 3 Years
Preliminary traction followed by open reduction.
2.1. Clinical Features: The methods are
More common in females. Removal of limbus.
Asymmetric groin folds. Salter innominate osteotomy.
Shortening of limb. Pemberton pericapsular osteotomy of ilium.
Ortoloni and Barlow tests - Performed to test the Rotation osteotomy of femur.
vulnerability of the Hip to dislocate and relocate
within the aceTab.ulum. 2.4. Complications:
Telescopy test - Performed with Hip and Knee Avascular necrosis of femoral head.
flexed in 90 degree and axial force applied to the
Neglected cases develop painful insTab.ility of
thigh and the greater trochanter movements in
hip and degenerative arthritis in later life.
relation to the ASIS (Anterior Superior Iliac
Persistent dislocations presenting in adulthood
Spine) are seen.
with OA can be treated with total hip
X-ray shows broken shentons line.
replacement arthroplasty.
Head lying outside the aceTab.ulum.
Dysplastic aceTab.ulum / femur. Congenital Clubfoot
Early identification and immediate
implementation of treatment gives good results
3. Congenital
good p hysical examination. TalipesEquinoVarus
- Plane Radiography.
- Ultrasonography. (CTEV)

Page 518
3.1. Etiology:
Unknown but mostly attributed to mechanical causes.
Germ plasm defect and primary soft tissue
abnormalities.
Features are usually obvious at birth.
Foot is twisted and turned inwards so that it
faces posteromedially.
Foot is plantarflexed, inverted and adducted at
forefoot. The leg muscles are smaller and heel
cord is tight and associated internal tibial torsion
may be present.

Fig 1 Clinical Appearance of Bilateral Idiopathic CTEV before Treatment

3.2. Treatment: Talonavicular reduction and maintenance.

3.2.1 Conservative
Aim of treatment is to produce and maintain a Methods
painless supple plantigrade foot. Preferably should be Turco.
started within a day or two after birth. Manipulative Carroll.
correction and maintenance in cast. External fixator correction.
JESS: Less than 7 years.
Methods Ilizarov: More than 7 years upto 12 years.
French b) Bone procedures
Ponseti method produces best results which Done in case of deformity that has persisted for
comprises correction of deformity in order of more than 3 yrs.
CAVE (Cavus,Adduction,Varus&Equinus) with In addition to posteromedial release lateral
serial castings followed by column shortening and / or medial column
tendoa chillestenotomy and retention of lengthening procedures can be done.
correction in steinbeik shoes till walking age. Late / relapsed cases.

3.2.2 Surgical correction Options

Should be opted for in cases that have failed
conservative line of management.
a) Soft tissue procedure
Closed Tendo Achilles Tenotomy.
Lengthening of medial and posterior structures.
Soft tissue and bone procedures with tendon
transfers, gradual correction using Ilizarov
method.
Neglected cases can be treated by triple
arthrodesis.

Page 519


4. METABOLIC DISORDERS
1. Osteoporosis Complaints of back pain.
Increased thoracic kyphosis.
Osteoporosis is defined as abnormally porous bone
Treatment:
and its strength is less than normal for a person of
that age and sex. Physiotherapy.
Bisphosphonate
1.1. Clinical features: Alendronate 70mg once weekly give n with full
Bone pain. glass of water before breakfast (in severe cases)
for 3 months.
Fractures. Vitamin D 1000IU/ day for 3 months.
Kyphosis. Calcium - both diet and drug
Tab. Calcium carbonate 500mg twice a day for
Weakness. 2-3 months. Can be extended later
Hormone replacement therapy in selected cases.
Fatigue.
Calcitonin Nasal spray (200IU/day) once a week for
1.2. Investigations: 3 months minimum, Inj.ecTab.le calcitonin, limited
use.
X-rays.
Special investigations (if needed) includes. If and when combination of Calcium and
DEXA Scan. Vitamin D is available it should be used.

1.3. Diagnosis: 1.5. Secondary osteoporosis

SD > 2.5 below the average for premenopausal Nutritional.
women for that pop ulation group. Endoc rine.
Drug induced.
X-ray features:
Malignant disease.
Loss of trabecular definitions. Ide ntify the cause and treat it accordingly.
Thinning of cortices. Correct the nutritional deficiency.
Correction of hormonal imbalance.
1.4. Primary osteoporosis:
Physiological bone depletion that normally 1.6. Surgerys
accompanies ageing and loss of gonadal activity.
Vertebroplasty&Kyphoplasty in presence of
neurode ficit.
Post menopausal osteoporosis

Ions

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 5. REGIONAL CONDITIONS
1. PeriArthritis Shoulder
(Frozen Shoulder)
Significant restriction of both active and passive
shoulder motion.
1.1. Clinical Features:
Night pain, inability to reach overhead and reach
away from the body.
1.2. Investigations:
X-ray.
Blood - rule out meTab.olic causes.
Ultrasound (Dynamic ultra sound).
MRI (Thickness of the capsule and
synovium>4mm) to rule out other pathology.
1.3. Treatment:
Supportive - Diathermy, Ultrasound, TENS.
Medications
1) Tab..Diclofenac sodium 50mg thrice a day for 1
week and SOS later Or
2) Tab.. Indomethacin 25mg thrice a day for 1 week
and SOS later Or
3) Tab..Ibubrufen 400mg thrice a day for 1 week
and SOS Later
NSAIDs cause hyperacidity hence antacids such
as Cap. Omeprazole 20mg or Tab.. Pantoprazole
40mg once a day should be give n.
Intra- articular steroids. Inj.Hydrocortisone
acetate 40mg once every 3 months.
Physiotherapy -Streching exercises.
Manipulation under general anaesthesia (if
symptomatic > 6 months).
Surgical Release (If not response to above
treatment).
Open or Arthroscopic release at specialized
centres.
2. CubitusValgus
Outward deviation of forearm at elbow.
Normal carrying angle is 100 in male and 150 in
females.
Causes.
Nonunion fracture of lateral condyle of humerus.
Destruction of lateral condyle due to sepsis.
Tardy-ulnar nerve palsy may be present - treated
with anterior transpos ition of ulnar nerve.
Gross deformity supracondylar osteotomy.
3. CubitusVarus
Inward deviation of forearm at elbow.
Most common cause is malunion of
supracondylar fracture.
Change in arc of motion with hyper extension
and restricted flexion.
Deformity needs supracondylar osteotomy.
4. Dequervain's Disease
Chronic constrictive tenosynovitis of abductor
pollicislongus and extensor pollicisbrevis.
4.1. Clinical features:
Diffuse pain at distal end of radius laterally,
tenderness and painful movements of thumb.
Finkelstein's test positive.
4.2. Treatment:
Early - splint wrist and thumb in full extension.
Anti inflammatory drugs.
1) Tab..Diclofenac sodium 50mg thrice a day for 1
week and SOS later Or
2) Tab. Indomethacin 25mg thrice a day for 1 week
and SOS later Or
3) Tab.Ibubrufen 400mg thrice a day for 1 week
and SOS Later .
NSAIDs cause hyperacidity hence antacids such as
Cap Omeprazole 20 mg or Tab. Pantoprazole 40 mg
once a da y should be given.
Local administration of Inj.. Hydrocortisone
40mg once every 3 months.
Later soft - tissue release can be done.
5. Carpel Tunnel Syndrome
Most commonly found in IT professionals and
students.Median nerve is involved.
5.1 Clinical features:
Page 521
It is caused by entrapment of medial nerve in carpel
tunnel. Also seen in malunited lower end radius
fractures and in pregnant women. 7.2 Treatment:
Tinels sign It is reproduction of tingling sensation 7.2.1 Medical treatment
in palm and wrist by tapping over the course of 1) Tab..Diclofenac sodium 50mg thrice a day for 1
nerve. week and SOS later Or
2) Tab.. Indomethacin 25mg thrice a day for 1 week
and SOS later Or
5.2Treatment: 3) Tab.. Ibuprofen 400mg thrice a day for 1 week
5.2.1 Conservative and SOS Later
NSAIDs NSAIDs cause hyperacidity hence antacids such
1) Tab..Diclofenac sodium 50mg thrice a day for 1 as Cap. Omeprazole 20mg or Tab. Pantoprazole
week and SOS later Or 40mg once a day should be give n.
2) Tab.. Indomethacin 25mg thrice a day for 1 week
Local Steroids. Inj. Hydrocortisone acetate
and SOS later Or 40mg once every 3 months.
3) Tab..Ibubrufen 400mg thrice a day for 1 week 7.2.2Surgical release
and SOS Later.
NSAIDs cause hyperacidity hence antacids such as 8
Cap. Omeprazole 20mg or Tab. Pantoprazole 40mg 8. Avascular Necrosis of
once a da y should be given.
Or Femoral Head
5.2.2SurgicalRelease Death of bone due to gradual vascular impairment or
sudden infarction. Clinically there is pain in groin,
6. Tennis Elbow radiates to thigh and knee, local tenderness, limitation
of movements, loss of abduction and internal
6.1 Lateral epicondylitis due to repetitive stress rotation, preserved flexion.
Injury Commonly seen in housewifes and
players:
8.1. Radiological Features(X-rays):
6.2 Treatment: Stage1- Pre radiologic stage no radiologic
6.2.1 Medical treatment findi ngs.
1) Tab..Diclofenac sodium 50mg thrice a day for 1 Stage 2- Osteoporosis, sclerotic cystic areas.
week and SOS later Or Stage 3- Partial collapse, Flattening of femur
2) Tab.. Indomethacin 25mg thrice a day for 1 week head,Increased density and deformity of head.
and SOS later Or Stage 4 -Secondary deterioration of the articular
3) Tab..Ibubrufen 400mg thrice a day for 1 week cartilage.
and SOS Later.
NSAIDs cause hyperacidity hence antacids such as 8.2. Other Investigations
Cap. Omeprazole 20mg or Tab.. Pantoprazole 40mg
Radio-isotope scanning.
once a da y should be given .
MRI most sensitive to detect ischemic
necrosis.
Local Steroids. Inj.. Hydrocortisone acetate
Bone-marrow pressure measurements.
40mg once every 3 months.
Supportive splints . Intramedullary ve nography.
6.2.2 Surgical release Core biopsy of femur head.
8.3. Treatment
7. Golfers Elbow Early - Bedrest, traction, weight reduction,
withdrawal of steroid and alcohol.
7.1 Medial epicondylitis which is due to repetitive Stage 2 - Core decompression of head, muscle
stress Inj.ury commonly seen in housewifes pedicle bone grafting.
and players : Stages 3, 4 - Osteotomy and replacement
arthroplasty.

Page 522
Knee

Plantar Fasciitis
Figure 1 Bilateral Grade 4 Avascular Necrosis Of Femur Head

Tab.Diclofenac sodium 50mg thrice a day

9. Plantar Fasciitis / Calcaneal for 1 week and SOS later Or
Spur Tab. Indomethacin 25mg thrice a day for 1
week and SOS later Or
Tab. Ibuprofen 400mg thrice a day for 1
9.1. Clinical Features: week and SOS Later.
Pain bot h heels. NSAIDs cause hyperacidity hence antacids
Unable to bear weight. such as Cap. Omeprazole 20mg or Tab.
Tenderness over medial tuberosity of calcaneum Pantoprazole 40mg once a da y should be
X-ray - lateral view of calcaneum may show given.
spur.
9.2.3 Local Steroids
Investigation X-ray calcaneum lateral view to rule
Inj. Hydrocortisone acetate 40mg once
out spurBlood sugar to rule out diabetes. every 3 months.
Surgical release.
9.2. Treatment:
9.2.1 Soft sole pad in the heel 9.2.4 Ultrasound therapy
9.2.2 Medical

Page 523
 6.DISORDERS OF SPINE
s
1. Lumbar Spondylosis
1.1 Clinical Features:
Low back ache is a very common problem faced in
day to day life. Not all of them, are caused by disc
pathology. Clinical features suggestive of disc
pathology include backache associated with para
spinal spasm, stretch pain and leg pain.
1.2 Investigation:
X-rays lumbosacral spine AP.
1.3 Treatment:
Rest.
Medical management.
1) Tab.Diclofenac sodium 50mg thrice a day
for 1 week and SOS later Or
2) Tab. Indomethacin 25mg thrice a day for 1
week and SOS later Or
3) Tab. Ibuprofen 400mg thrice a day for 1
week and SOS Later.
NSAIDs cause hyperacidity hence antacids such
as Cap. Omeprazole 20mg or Tab. Pantoprazole
40mg once a day should be give n.
Local Application of Muscle relaxant gel such as
diclofenac sodium gel.
Education about proper back posture
maintenance of lumbar lardosis with erect
posture or lumbar pillow.
Physiotherapy interferential therapy, traction
Epidural steroid Injections.
1.4. Operative Indications:
CaudaEquina syndrome - especially with bowel
and bladder involvement.
Patients with persistent pain not relieved by
conservative measures for 6 - 8 weeks.
Unilateral leg pain extending below knee that has
lasted atleast 6 weeks.
Discectomy is performed usually by posterior
approach and patients will have good
postOperative pain relief.
1.5. Watch For Red Flags Signs:
Bowel-bladder involvement. a.
Hypos thesia around a nus.
If you see any of the red flags refer urgently to higher
center with surgical facility.
2. Cervical Spondylosis
2.1 It is a degenerative condition of the cervical
spine occurring over 50 yrs of age. Involves
the intervertebral discs, posterior intervertebral
joints. Commonest at C5 - C6.
2.2. Clinical Features:
Pain and s tiffness.
Radiating pain to shoulder or downwards on the
outer aspect of the forearm and hand.
Giddiness on and off.
On examination there is loss of normal cervical
lordosis and limitation in neck movements.
Tenderness over the lower cervical spine or in
the muscles of the paravertebral region.
2.3. Investigations:
X-ray cervical spine AP and Lateral.
2.4. Treatment:
Rest.
Medical management.
1)Tab.Diclofenac sodium 50mg thrice a day for
1 week and SOS later Or
2) Tab. Indomethacin 25mg thrice a day for 1
week and SOS later Or
3) Tab. Ibuprofen 400mg thrice a day for 1 week
and SOS Later.
NSAIDs cause hyperacidity hence antacids such
as Cap. Omeprazole 20mg or Tab. Pantoprazole
40mg once a day should be given Local
Application of Muscle relaxant gel such as
diclofenac sodium gel.
Education about proper Neck Posture.
Physiotherapy,interferentialtherapy,Cervical
traction.
3. Kyphosis
Is a posterior curvature of the spine.
Types
Smooth rounded kyphosis.
Scheuermanns disease.
b. Angular kyphosis.
Tuberculosis spine.
Page 524
 Traumatic.

4. Scoliosis 4.3. Investigations:

4.1. Definition: Radiography of the whole spine.
Degree of the curve is measured by the Cobbs
Scoliosis is defined as lateral curvature of the spine. angle.
Scoliosis is named according to the level and side to Skeletal maturity by the fusion of the iliac
which the main conve xity of the curve is directed. apophysis (Rissers sign) is an indicator of end
The common patterns are. of growth of spine.
a. Thoracic scoliosis.
b. Thoraco-lumbar.
4.4. Treatment:
c. Cervico-thoracic scoliosis (depending upon the Mild cases Conservative with serial custom
site of primary curve). made braces.
Moderate cases - Spinal and breathing exercise
4.2. Clinical Features: with correction by Milwaukee Brace.
Rib hump, prominence of posterior chest wall. Test Severe cases - Cobbs angle > 40 deg. Surgical
done to decide whether deformity is mobile or rigid. correction with instrumentation and Fusion
Make the patient lie in the lateral position on the carried out with cancellous bone graft.
concave side. Curvature is diminished in mobile
cases.

Fig.1 Scoliosis OfDorso - Lumbar Spine

Page 525
 7.GENERAL FRACTURE MANAGEMENT
1. Definition
Disruptions of bone tissue are called fracture, visible
disruption of articular cartilage is also called
fracture(Chondral fracture).
2. Types of fractures
Closed fracture and open fracture.
Incomplete fracture or greenstick fracture and
complete fracture.
Linear fractures - transverse, Oblique.
Spiral, Comminuted (more than two fragments).
Segmental fracture, fracture with bone loss and
Impacted fracture.
Stress fracture.
Pathological fracture.
3. Gustilo-Anderson
classification of open
fracture
Type I Open fracture with wound < 1c m Bone is
not exposed.
Type II Wound > 1cm without extensive soft
tissue da mage / skin flaps avulsion.
Type III A Ope n fracture with extensive soft
tissue damage, but with adequate soft tissue
coverage of bone. It also includes segmental
fracture, comminuted fracture with laceration <
1cm.
Type III B Extensive soft tissue loss with
periosteal stripping with bony exposure.
Type III C Open fracture with an arterial Injury
that require immediate repair regardless of size
of the wound.
4. Clinical features
Pain.
Swelling.
Inability to use the affected limb.
Deformity.
Crepitus.
Abnormal mobility.
Loss of transmitted movement.
5. Investigations
Routine X-ray AP and Lateral view.
Special views if necessary.
6. Management includes
Conservative management for closed fracture
and Type I - open fracture for which closed
manual reduction tried and patient put on
appropriate plaster of paris splint for 3 - 4 weeks.
Surgical management.
6.1. Initial management of open
Injuries:
Record vitals, start lifeline, I.V. fluids, I.V.
antibiotics, analgesics.
Immediately debride the wound of contaminated
wound, devitalized tissue look for4 Cs,
Consistency, Colour, Contractility, Circulation.
Irrigate copiously with saline Type I 3 L
saline, Type II 6 L saline, Type III 9 L saline.
Enlarge the wound if necessary for adequate
debridement.
Remove contamination in the medullary canal.
If wound can be closed, suture the surgically
created wound, put loose stitch for other wounds
over a drain if necessary. If closure is not
possible, leave the wound open.
7. Complications
7.1 Acute:
Shoc k.
ARDS.
Thrombo-embolism.
Neuro-vascular Injuries.
Crush syndrome.
DVT.
7.2 Chronic:
Delayed union, Non-union, Malunion.
Growth disturba nces.
Joint stiffness.
Volkmanns ischemic contracture.
Myositis ossificans.
Post-traumatic arthritis.
Avascular necrosis.
Page 526
7.3 Peculiar to open fractures are: osteotomy with internal or external fixation with or
without bone grafting.
Infection.
Tetanus.
Gas gangrene.
Osteomyelitis. 13. Joint stiffness
Hypovolemic shock.
Due to inappropriate fracture immobilization,
intraarticular fractures, periarticular adhesion of soft
8. Crush Syndrome tissues, capsules and muscle contractures.
Severe crush Injury of limbs and muscles results in
release of myoglobin leading to renal failure. 13.1 Treatment:
Treatment is managing acute renal failure and Physiotherapy.
Maintain hydration.
Exercises.
Manipulation under anesthesia.
9. Compartment Syndrome Surgical excision and lengthening of
It is due to ischaemic necrosis of structures of contractures.
anterior compartment of fore-arm / legs.
It is defined by the following signs (6 Ps).
a. Pain. 14. Myositis Ossificans
b. Pallor. It is a reactive lesion (ossification) occurring in
c. Paraesthesia. soft tissues and in stripped periosteum followed
d. Paralysis. by trauma and ill advised massage.
e. Pulselessness.
f. Positive Passive stretch. 14.1 Treatment:
Treatment.
a. Emergency surgical decompression by Drugs:
fasciotomy. Low dose Indomethacin (25mg TDS) for 1
month.
Mobilization and ROM excision till painfree
10. Delayed union joint range.
Union is considered delayed, when healing has not
advanced at the average rate for the location and the 15. Fractures of Necessity
type of fracture, usually 3 - 6 months. Conservative For these fracture, surgery is always necessary.
management with functional cast for addi tional 4 - 12
weeks or ORIF with appropriate implant with or Lateral humeral condyle fracture.
without bone grafting. Femoral neck fracture.
Distal tibial epiphysisfracture.
11. Non-union
16. PhysealInjuries
A diagnosis of Non-union is justified either by
clinical or X-ray findings which show healing has Salter and Harris classification of PhysealInjuries.
ceased, minimum of 9 months elapsed since Injury
Type I Epiphyseal separation through
and the fracture shows no vi sible progressive signs of
physis only with or without displacement.
union for 3 months.
TypeII Triangular metaphyseal spike
Time period attached to separated epiphysis. (Thurston
Holland sign.)
Fracture of long bone - 6 to 9 months.
TypeIII Physeal separation with fracture
Fracture of neck of femur 3 months. through the epiphysis into the joint. If there is
displacement joint incongruity occurs.
12. Malunion TypeIV Fracture through the metaphysis,
A malunited fracture is one that has healed with the physis,epiphysis.
fragments in a non - anatomical position. Corrective TypeVCompression fracture of the physis
producing growth arrest, diagnosed
retrospectively.

Page 527
 TypeVIBruise or contusion to the periphery of
the physis producing growth disturbances.

I II III IV V
Epiphyseal Fracture through Fracture through Fracture of Epiphyseal damage to the
slip on ly Epiphyseal plate with theEpiphyseal and shaft, crossing Epiphyseal plate
triangle of sheft extending into theEpiphyseal
attached Epiphyseal plate plate

Fig 1: Epiphyseal Injuries

16.1 Management: Details of splinting and transport of trauma patient

are mentioned in treatment of individual fractures.
Majority of childrens fracture are treated
conservatively. Few fractures require open reduction 2. PreparationOf Cast/Slab
and internal fixation or closed pinning. Application:
17. Open fractures In Children It is essential to prepare the patient and all necessary
material and equipment before beginning the
Frequent and vigorous debridement with irrigation processes of fracture reduction and cast application.
and adequate stabilization of fracture will reduce the
rate of non-union and secondary infection. Rarely Required materials.
after closed reduction hematogenous osteomyelitis Examination couch or Table
occurs at the fracture site.
2-4 rolls 150 mm padding.
18. SplintageAnd Transport of 8-9 plaster of Paris (POP) rolls, 150 mm wide.
Trauma Patient Bucket with cool water.
1. Guidelines: Pillows to support casted leg.
1) Immobilize one joint above and below. Aprons to protect team members and patient.
2) Usage of readily available materials such as
umbrella, plaster of paris, folded paper, wooden Paper to cover the floor.
stick.
3) Splintage should neither be too tight or too loose. Everything must be assembled and ready before
4) Do Not transfer patient unless his vitals are beginning the procedure.
stabilized.

Page 528
 Fig 2: Materials ForApplying Slab/Cast

3. Method: applied over dorsal or ventral surface with cotton

Slab is prepared by overlaying of plaster of parisrolls
of adequate length and layers to splint the fracture
along with adjacent joints in anatomical position and
padding and bandage.
Cast is cylindrical application of plaster of paris rolls
over adequate cotton padding over the fractured limb
in anatomical position.

Page 529
 8.POLYTRAUMA

1. PolytraumaIs Defined As 2.4 Golden Hour:

Injury severity score (ISS) 16 or above.
Systolic blood pressure below 80 mm Hg.
Glasgow coma score less than 15.
Higher fluid resuscitation requirements.
Chest, head, abdominal organ Injuries.
Fractures of more than one long bone.
2. Stage of Care
2.1 Acute Resuscitation Period:
(1-3 hrs)
From the first point of contact with medical
service to the control of acute life threatening
conditions.
Rapid systemic assessment to identify life
threatening conditions.
Then Airway, Breathing, Circulatory (ABC)
support should be made. This involves airway
control, thoraco-centesis, rapid control of
external bleedings, vigorous fluid and blood
replacement therapy.
Then complete diagnostic check up if there is no
acute life threatening situation.
2.2 Primary Stabilization Period:
(upto 48 hrs)
From the control of acute life threatening
situation and complete Stability of respiratory,
haemodynamic and neurologic symptoms.
Here acute management of fractures associated
with arterial Injuries and acute compartment
syndrome are managed.
Fractures are temporarily Stabilized with
external fixators and compartments.
2.3 Secondary Regeneration Period:
(2 - 10 days)
In this, general condition of the patient is
Stabilized and monitored.
Systemic inflammation and multiple organ
dysfunction syndrome are managed.
Tertiary reconstruction and rehabilitation period
(weeks to months) after trauma.
Necessary surgical procedures.
Definitive treatment of complete mid-phase
fractures.
Specialized procedures to achieve fracture
correction or joint reconstruction.
First one hour after Injury, with threefold increase in
mortality for every 30 minutes.
3. Follows ABCDE
Airway.
Breathing.
Circulation.
Disability.
Expos ure.
4. Initial Management of
patient In Shock
Direct control of obvious bleeding by direct
pressure - (preferable), tourniquet clamping of
blood vessels.
Large-bore intravenous access.
a. Ringer lactate infusion.
b. Blood replacement as indicated, by serial
haematocrit estimation and blood pressure.
Traction with Thomas Splints or extremity
splints to limit hemorrhage from unstable
fractures
Consideration of angiography or immediate
operative intervention for Hemorrhage control.
4.1HaemorrhagicShock:
Diagnosed by hypotension, tachycardia, seen in
patients with large open wounds, active bleeding,
pelvic and / femoral fractures and abdominal or
thoracic trauma.
In the absence of open hemorrhage bleeding into
voluminous space (chest, abdomen, pelvis, thigh)
must be ruled out.
This may require peritoneal lavage, angiography,
CT, MRI.
Managed by aggressive fluid replacement, blood
transfusion, Angiographic embol isation,
operative intervention, fracture Stabilization, etc.
4.2 Blood Replacement:
Fully cross matched blood is preferable.
In case of life threatening situations O-
negative blood can be used.
Warming of blood prior to administrations
prevents hypothermia.

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 Monitor coagulation factors, platelets and d. Rectal tone and sensation.
calcium levels. GCS = Eye opening score + Verbal (intubated or
non-intubated) score + Motor score.
GCS if < 13, systolic BP < 90, RR< 10 / min or
5. Indications For Immediate > 30 / min warrants Emergency trauma care.
Surgery
Hemorrhages secondary to liver, splenic renal 6. Radiographic Evalution
parenchymal Injury Laporatomy.
X-rays of Skull, pelvis, spine and Extremities.
Aortic, caval or pulmonary vessel tears Ultra sound abdomen.
Thoracotomy.
CT, MRI.
Depressed skull fracture or acute intracranial
hemorrhage Craniotomy. Assess the concomitantInjuries such as head Injuries,
Disablity (Neurologic Assessment). thoracic Injuries, genitourinaryInjuries and refer the
a. Assess level of consciousness by GCS. patient to higher centers for tertiary care
b. Pupillary response sensation. management.
c. Motor response in all extremities.
Pelvic Fracture

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 9.PELVIC INJURIES
If it is < 2.5 cm treat conservatively.
1. Introduction If it is > 2.5 cm external fixation or open
It is an emergency in orthopa edics which reduction and internal fixation.
involves multispeciality intervention. If there is unstable Fracture with vertical
Mode of Injury. displacement then treat with ORIF.
a. High energy Injuries. If haemodynamicallyunstable, then stabilize the
b. Crush Injuries. pelvis with external fixator at the casualty itself
c. Impact Injuries. without shifting the patient and follow the above
Associated with complications and other steps.
fractures.
4. Associated Complications
2. Clinical Features AndTreatment
Shoc k-blood transfusion and fluid replacement.
Pain and tenderness at affected site.
Embolisation of bleeding pelvic vessels.
Range of movements painful. (intervention radiology)
Shoc k. Urethral ruputure - diagnosed by blood in
Intra-abdominal / Urethral / Vascular Injuries. urethra, perineal hematoma, distended bladder,
managed by Urologist.
Bladder rupture-extravastation of urine-Urologist
3. Management and Surgeon.
Evaluate ABCDE and stabilize the patient. Bowel and intra-abdominal Injuries are managed
Evaluate for other associated Injuries head, by General surgeon.
chest, abdomen and spine. Thrombosis - DVT prophylaxis, vascular opinion
If haemodynamicallystable, assess radiologically must be obtained.
with X-ray pelvis AP view, inlet and outlet view. Post operatative-
If there is no or minimal displacement, treat a. Infection rate (0-25%) managed accordingly.
conservatively with strict bed rest and analgesics. b. Thrombo-embolism.
If there is displacement with anterior opening c. Pin tract infection.
type (unstable Fracture) then assess the d. Death inevitable in certain situations.
displacement.

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 10. FRACTURES OF UPPER LIMB

Bennetts Fracture.
1. Mode of Injury
Intra-articular fracture through base of first
a. Fall on Outstretch hand.
metacarpal bone in which the fractured shaft is
b. Road Traffic Accident.
displaced laterally due to unapposed pull of APL.
c. Associated Poly Trauma.
(Abductor PollicisLongus)
2. Type of Fracture a) Investigation
X- ray of hand antero posterior and oblique
2.1. Fracture of Hand: views.
a. Fracture of the base of the first metacarpal.
b) Treatment
b. Fractures of the other metacarpal bones.
c. Fractures of the phalanges. Primary Stabilization in anatomical position with
the help of available splinting material.
Closed or open reduction and internal Fixation
2.2. Fractures Around Wrist: with 'K' wire.
a. Fracture of the scaphoid bone.
b. Fractures of other carpal bones. c) Rolando Fracture
c. Dislocations of the carpal bones. It is a common extra articular fracture of base of first
d. Fracture of the lower end of the radius .(Colles' metacarpal bone.
and Smith's) d) Investigation- X-ray of hand antero posterior,
e. Galeazzi fracture dislocation. lateral and oblique views.
f. Fracture separation of the lower radial e) Treatment
epiphysis. Primary stabilization in anatomical position with
g. Fracture of the shafts of the forearm bones. the help of available splinting material.
Closed or open reduction and internal Fixation
with 'K' wire ORIF by K wire.
2.3. Fractures Around Elbow: External fixation.
a. Fracture of the head and neck of the radius.
Mini fragment T plate fixation.
b. Fracture of the uppe r end of the ulna with
dislocation of the head of the radius.(Monteggia 2.5.2 Fracture of The Other Metacarpal Bones
fracture dislocation)
a) Investigation -X-ray of hand antero posterior and
c. Fracture of the coronoid process.
oblique views .
d. Fracture of the olecranon process.
e. Fractures of the epicondyles and condyles. b) Treatment
f. Supracondylar fracture. Primary stabilization in anatomical position with
the help of available splinting material.
Conservative - cock up splint.
2.4. Fracture OfThe Humerus:
a. Fracture of the shaft. Surgical Close or open reduction and internal
fixation with K wire or mini plate.
b. Fracture of the greater tuberosity.
c. Common Fracture of Proximal Humerus/ External fixation for compound (open) fracture.
Fracture of greater tuberosity.
2.1.3Fracturesof the phalange s

2.5. Fractures OfThe Shoulder a) Symptoms - Pain & Swelling and bo ny

Girdle deformity with loss of active movements.
a. Fractures of the clavicle. b) Signs - Tenderness at Fracture sitealong
b. Fractures of the Scapula. with Crepitus and Abnor mal Mobility.
c) Investigation - X- ray of hand AP and
2.5.1 Fractures of Hand Oblique views.
Fractures of base of the first metacarpal.

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 d) Treatment-
Primary stabilization in anatomical position with
the help of available splinting material.
Fig 1: Finger Splint
e) Surgical K (Kirschner) wire or JESS
(Joshi's External stabilization System)
fixator.
2.2. Fractures Around Wrist:
2.2.1 Fracture of the scaphoid bone
It is common in young adults usually caused due to
fall on outstretch hand, often overlooked.
a) Symptoms Pain, swelling and restriction of
wrist move ment.
b) Signs Tenderness in anatomical snuff box and
impairment of wrist move ment.
c) Investigations - X-ray of wrist in AP, lateral and
two oblique projections.
d) Treatment - Primary stabilization in anatomical
(glass holding) position with the help of
available splinting material.
Conservative - Plaster immobilization usually
till 2 to 3 months.
Surgical Closed or open reduction and internal
fixation with a special compression screw.
e) Complications:
The incidence of complications is high.
Delayed or non-union.
Avascular necrosis.
Osteoarthritis.
2.2.2 Fractures of other carpal bones
These are less common serious fractures. The
treatment is conservative management with plaster
immobilization.
Conservative - Buddy strapping, POP slab,
finger splints.
2.2.3 Dislocations of the carpal bones
Complete dislocation of the wrist is very uncommon
and incomplete carpal dislocation involve one or
more of the carpal bones and are as follows:
1) Dislocation of lunate bone .
2) Perilunar dislocation of the carpus.
A. Symptoms Pain, swelling, defor mity and
restriction of move ment of the wrist joint.
B. Signs Tenderness and loss of anatomical
position of wrist and hand.
C. Investigations
X-ray of the wrist in AP, lateral and oblique
views.
CT Scan.
D. Treatment
Primary stabilization in anatomical (glass
holding) position with the help of available
splinting material.
Conservative Manipulative reduction under
anaesthesia and plaster immobilization.
Surgical operative replacement of carpal bones.
E. Complications
Avascular necrosis.
Osteoarthritis.
Injury to median nerve.
2.2.4 Fracture of the lower end of the radius:
A.Colles' fracture - It is a fracture of the lower end
Page 534
of radius at metaphyseal region which manifests in
bent fork deformity due to dorsal and radial
displacement of the distal fragment.
B. Smith's fracture It is reverse of the Colles'
fracture with ventral displacement.
C. Symptoms - Pain, swelling and bo ny de for mity of
the wrist with loss of active movements
D.Signs - Tenderness at fracture site along with or
without crepitus and abnormal mobility
E.Investigation -
X-ray of forearm with wrist AP and Oblique
views.
X-ray Wrist in Ulnar deviation.
F.Treatment
Primary stabilization in anatomical (glass
holding) position with the help of available
splinting material.
Close reduction and plaster immobilization.
Close reduction with K wire fixation.
Close reduction with K. wire fixation and
external distractor application.
Open reduction and internal fixation with
multiple K wires, plate and screws.
2.2.5 Galeazzi fracture dislocation
It is the fracture of radial diaphysis at the junction of
middle and distal third of the shaft with associated
disruption of distal radio ulnar joint.
A.Symptoms - Pain, swelling, de for mity and
shortening of the forearm.
B.Signs - Bony deformity & tenderness, crepitus &
pain aggravated by passive stretching of wrist.
C.Investigation - X- ray forearm with elbow and
wrist in AP and lateral projection.
D.Treatment
Primary stabilization in anatomical position by
appl ying gentle axial traction and splinting with
the help of available material. (moulded splints,
folded newspaper, card board or wooden plank)
Surgical - Mostly needed for prevention of
malunion.
- Open reduction and i nternal fixation with plate
and screws.
2.2.6 Fracture separation of the lower radial
epiphysis:
It is seen in children before physeal fusion in which
the epiphysis is fractured and separated from the
metaphysis and results into gross defor mity, if not
treated adequately.The clinical features and
management are same as that of fracture of lower end
of radius in adults except surgical intervention which
is rarely needed.
2.2.7 Fracture of the shafts of the forearm bones:
The forearm bones, radius and ulna get fractured
either single or both and are very common Injuries
which result into gross defor mity and functional
restriction, if not treated.
A. Symptoms Pain, swelling over forearm and
bony deformity.
B. Signs - Tenderness, crepitus, abnormal mobility
with or without signs of compartment syndrome.
C. Investigation - X-ray of the forearm with wrist
and elbow in AP and lateral projections.
D. Treatment:
1. Primary stabilization in anatomical position by
appl ying gentle axial traction and splinting with
the help of available material. (moulded splints,
folded newspaper, card board or wooden plank)
2. Splintage.
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 Fig 2:SplintageForFracture Radius /Ulna And Lower End OfHumerus
3. Conservative - Closed reduction and plaster
application under anaesthesia, mostly in children.
4.Surgical
Closed reduction and internal fixation with
elastic (in children) or rigid intramedullary nails.
Open reduction and internal fixation with plates
and screws.
External fixator application in case of open
fractures.
2.3. Fractures Around Elbow:
2.3.1Fracture of the head and neck
of the radius:
One of the commonest fractures of the upper limb in
young adults.
Symptoms : Pain and swelling on lateral aspect of
elbow and restriction of movement.
Signs : Sharp local tenderness and impaired
move ments. ( Flexion of elbow and pronation and
supination)
Investigations: X-ray of elbow joint with forearm
in AP and lateral projections.
Treatment:
1. Primary stabilization in anatomical position
(flexion at elbow and midprone position of
forearm).
2. Conservative in case of slight damage to the
radial head and neck with plaster immobilization.
3. Surgical.
Open reduction and internal fixation in case of
severe damage to the radial head and neck.
Excision of radial head in severely damaged and
displaced fractures.
2.3.2Fracture of the uppe r end of the ulna with
dislocation of the head of the radius
(Monteggia fracture dislocation)
This is uncommon Injury with characteristic
displacement the ulna is angled forwards and the
head of radius is dislocated forwards which is
obvi ously seen on clinical and X-ray examinations.
Clinical features are same as the forearm fractures.
Treatment
Accurate fracture reduction is essential. It is
seldom possible to reduce both the dislocation
and fracture by closed method.
Open reduction and internal fixation with plate
and screws is essential.
2.3.3 Fracture of the coronoid process:
The coronoid process is seldom fractured unless in
association with posterior dislocation of the elbow.
2.3.4 Fracture of the olecranon process:
The olecranon process is fractured by a fall on the
poi nt of the elbow usually in adults.
Clinical feature same as fractures above with distinct
disruption of three point bony relation of the elbow.
(It is a triangle formed by the tip of olecranon and the
two epicondyles)
The treatment depends upon the type of fracture i.e.
plaster immobilization in case of crack fracture,
internal fixation for fracture separation and excision
in case of comminuted fracture.
Page 536
2.3.5 Fractures of the condyles and epicondyles:
Condylar fractures are relatively uncommon, but
often troublesome and oc cur main in children.
A. Symptoms Pain, swelling and restriction of
movement of the elbow.
B. Signs
Marked tenderness and widening of the elbow.
Disruption of the three point bony relation.
C. Investigations - X-ray and CT Scan.
D. Treatment
Conservative - In case of simple crack fracture,
with plaster immobilization and followed by a
course of mobilizing exercises.
Surgical Displaced fractures must be treated
with closed or open reduction and internal
fixation to prevent disability.
E. Complications:
Non-union.
Deformity-Cubitus valgus with instability.
Osteoarthritis.
Epicondylar fractures occur in children and mostly
treated conservatively.
2.3.6 Supracondylar fracture:
It is one of the commonest and most important
fractures of the childhood and potentially dangerous
because of the risk of Injury to the brachial artery
near the metaphyseal region of the humerus.
A. Clinical features-Are characteristic with lower
fragment displaced and tilted backwards, but the
Fig3: SplintageOfFracture OfHumerus
three point bony relation maintained. The brachial
and radial artery pulsations should be confirmed all
the time during the treatment.
B. Treatment:
Conservative Closed reduction and plaster
immobilization.
Surgical Open reduction and internal fixation,
if closed manipulation fails.
C. Complications:
Injury to the brachial artery leading to Volkmann's
ischaemic contracture in delayed or neglected cases.
Injury to median nerve.
Malunion.
2.3.7 Inter Condylar Fracture Humerus
A. Clinical features Pain, swelling and deformity.
B. Investigation X-ray elbow, AP and lateral
views.
C. Treatment
Conservative plaster immobilization.
Surgical - Closed or open reduction and internal
fixation with K wires or cancelloussrews.
2.4. Fracture of Humerus:
2.4.1 Fracture of the shaft
A. Clinical Finding Pain and Swelling ove r arm
abnormal mobility, crepitus.
B. Investigation X-ray of arm with shoulder &
elbow AP and Lat.
C. Treatment
Splintage.
Page 537
 Surgical Closed nailing by 2.4.3 Common Fracture of Proxi mal Hume rus/ Fracture
- Rush nail of greater tuberosity
- Enders nail Children A.Clinical Finding
- Flexible nail Pain and Swelling ove r Shoulder.
- Humerus Inter locking Nail. Painful Move ments of Shoulder.
- Open reduction and internal fixation with plate & Crepitus, Tenderness.
screws.
- External fixator. B. Investigation X-ray Shoulder AP &CT Scan.
Watch for wrist drop. (radial nerve Injury pre C. Treatment
and pos t reduction) Conservative Arm to chest strapping.
Surgical Cancellous screws or plate fixation.
2.4.2 Fracture of Surgical Neck Hume rus Primary shoulder replacement.

A. Clinical Finding
Pain and Swelling ove r Shoulder.
2.5. Fractures Of The Shoulder
Painful Move ments of Shoulder. Girdle:
Crepitus, Tenderness. 2.5.1 Fracture of Clavicle
A. Clinical Finding Pain and Swelling ove r
B. InvestigationX-ray s houlder AP and shoulder.
Lateral view (special views if needed) Bony Deformity.
C. Treatment Conservative Immobilization. Crepitus, tenderness.
Surgical K wire fixation. B. Investigation X-ray Shoulder AP
Buttress plating. C. Treatment
Conservative Figure of 8 bandage. (Clavicle
brace)

Fig 4: Figure Of 8 Banda ge

Surgical - Closed reduction and K wire fixation 2.5.2 Fracture of Scapula

for fracture of lateral end and open reduction and
internal fixation with plate and screws for
midshaft fractures.
A. Clinical Pain and Swelling ove r shoulder
painfull Movements of shoulder.
B. Investigation X-ray Shoulder AP.
C. Treatment - Shoulder immobalization.

Page 538
 11. FRACTURE OF LOWER LIMB
Mode of Injury
1) Road Traffic Accident.
2) Associated Poly Trauma.
Type of Fracture
Fracture upper end femur .
i) Intra capsular.
ii) Extra capsular .
iii) Femur head fracture .
Fracture shaft femur.
Fracture Lower end femur.
i) Intra articular.
ii) Extra articular.
Fracture Patella.
Fracture Upper end tibia.
Fracture shaft tibia.
Fracture around ankle joint.
Fracture of bones of foot.
Splinting of Lower limb Injuries.

Fig 1 Step 1 Traction

Page 539
 Fig2Step 2 Limb Splinting

Fig3 Step 3 Buddy Strapping

Page 540
 Fig 4 Alternate Method Of Splinting

1.2. The aim of treatment is to achieve union of the

1. Fracture Neck of Femur fracture and a durable hip joint afterwards.
(Intra-capsular)
Introduction- Principles of management include:
Fracture neck of femur more common in old age due
to Slip and fall.
1.2.1Osteosynthesis
1.1. Classification According to the i. Screws, Moores Pins etc.
site of fracture
ii. DHS, Blade Plate.
Subcapital.
iii. Internal Fixation + Fibular Grafting.
Transcervical.
iv. Muscle pedicle Graft + Internal Fixation.
Basicervical.
1.2Osteotomy
Usually caused by trivial fall in the elderly due to
presence of osteoporosis, however metastasis from i) Pauwels valgus osteotomy.
malignancies can also lead to the pathologic
fractures. ii) Mcmurrays osteotomy.

Page 541
1.3Arthroplasty ii) Surgical
Closed reduction and internal fixation with
Hemiarthroplasty. Dynamic Hip Screw and plate (DHS).
Proximal Femoral Nail (PFN).
Total Hip Replacement. Intramedullary Hip Screw.
Dynamic Condylar Screw (DCS).
Excision Arthroplasty. For subtrochanteric fractures a DCS is the implant of
choice after closed or open reduction. Other
modalities like PFN, Angled blade plate,
2. Trochanteric Fractures Reconstruction nail or Modi fied Kuntschers nail
(Extra-Capsular Fracture may also be used as per the preference of the
surgeon.
Neck Femur)
2.1 Fracture of Greater Trochanter: 3. Fracture ShaftOfFemur
This is isolated fracture of greater trochanter due to
fall on the side of pelvis, usually minimally displaced
Fractures of the shaft of the femur are mostly due to
and managed with pelvic strippi ng and non-weight
high-energy trauma.
bearing.
2.2 Fracture of Intertrochanteric
3.1 TypesOf Femoral Shaft
Region:
Intertrochanteric hip fractures are more common in Fractures Are As Follows:
road traffic accidents in young adults and domestic
fall in elderly. Type I - Spiral or transverse. (most common)
Type II Comminuted.
2.3 Fracture of Type III Open.
Subtrochanteric:Region:
Occur between lesser trochanter and a point 5 cm
distally and are seen as independent entities or as an 3.2 Investigations:
extension of ntertrochanteric fractures. X-ray shaft femur with X-ray of pelvis and knee for
associated Injuries.

3. Classification 3.3 Treatment:

3.1 Trochanteric fractures are classified according 3.3.1 Conservative manage ment
to Boyd and Griffin classification: Conservative management of fractures in children in
spica cast or with skeletal traction.
3.2 Subtrochantericfractures are classified
according to Seinsheimers classification: 3.3.2 Surgical management
A. Clinical features:
Symptoms - Pain, swelling, br uising, shor tening
of the limb and inability to stand or walk. Kuntschers nail for isthmic fractures.
Interlocking Nailing in comminuted fractures.
Signs -
i) Severe tenderness and swelling around hip Plating for lower third fractures.
region. Plating of shaft femur fracture in children.
ii) Shortened a nd e xternally rotated lower limb.
iii) Inability to do straight leg raising. Blood transfusion if needed and correct hypovolumic
shoc k.
Investigations:
i) X-ray of pelvis with both hips in AP view and
affected hip in axial view. 4. Fracture Of Tibia/Fibula
ii) CT Scan.
4.1 Introduction:
Treatment: Mostly due to road traffic accident.
i) Conservative initial traction and
immobilization in NRB (Non Rotatory Boot) in 4.2 Signs /ymptoms:
undisplaced fracture Pain, swelling, tenderness

Page 542
4.3 Investigation: 5. Fracture Calcaneum
X-ray of Tibia along with X-ray of knee and ankle
joint. 5.1 Mode:
Fall from height.
4.4 Treatment: 5.2 Sign /Symptoms:
Swelling, oedma, pain, tenderness.
4.4.1 Conservative - In Undisplaced fracture, closed
reduction and above knee cast for 12 weeks. 5.3 Investigation:
4.4.2 Surgical Displaced fracture, Interlock nail or X-ray of heel
plating depending on fracture anatomy. CT scan for intra articular fractures.
5.4 Treatment:
Conservative (Boot Cast). Strict non-weight bearing
till fracture heals.
Intra-articular fractures of calcaneum involving sub-
talar joint should prefebaly treated with restoration of
anatomical fracture geometry is must.

Page 543
 12.DISLOCATIONS
Loss of alignment of joint surfaces which should be 1.1. Types
treated as emergency.
Anterior.
Posterior.
1. Shoulder Dislocation Inferior. (luxatioerecta)
Most common dislocation.

Fig1 - X-ray Picture Of Shoulder Dislocation

1.2. Mechanism: 1.4. Investigation:

Most commonly indirect / direct violence X-ray - AP, Scapular view, Axillary view, CT
Posterior dislocation is common in electric shock scan.
and convulsions.
1.5. Treatment:
1.3. Clinical Features: Reduction Traction Counter Traction,
1.3.1 Anterior Abduction, extension, external rotation
Patient comes with Injured s houlder in abduction reduction.
and external rotation. Stimson sedation and prone position with 5 lb
1.3.2Posterior weight.
No striking de for mity, shoulder in abduction and Surgery.
internal rotation. Irreducible dislocation.
1.3.3Luxatio erecta Displaced fracture dislocation with ORIF.
Salute position abduction forward elevation.
Severe pain, neuro vascular deficit, more with
latter two.
1.6. Complications:
Recurrent dislocation.
Axillary nerve and artery Injury.
Brachial plexus Injury.
Stiffness.

Page 544
 Occurs because of blow to the back in
2. Elbow Dislocation squatting position.
Most common: Central
Posterior Dislocationof elbow
3.1.3 Central dislocation: Occurs due to direct blow
over the trochanter
2.1 . Mechanism:
Posterior - elbow hyperextension, valgus stress, 3.2. Clinical Features:
arm abduction, fore-arm supination.
Anterior-direct force over posterior fore-arm 3.2.1 Posterior
with elbow in flexed position. Limb in flexion, adduction, internal rotation,
limb shortening
2.2. Clinical Features: Sciatic nerve Injury.
Gross instability. 3.2.2 Anterior
Swelling. Limb in flexion, abduction, external rotation,
Three point bony relation altered. limb lengthened
Associated Injuries - radial head and coronoid Injury to femoral nerve.
Fracture.

2.3. Investigation: 3.3 Investigation:

X-ray.
X-ray elbow AP and lateral. Hip AP and lateral.
Closed manual reduction under GA, followed CT, MRI.
with above elbow posterior slab 90 degree
flexion.
3.4 Management:
2.4. Operative Indications: Resuscitate, CPR attempted with in-line traction
with patient lying supine, under general
Redislocation. anesthesia.
Non-concentric reduction. Methods used are the classical Watson-jones,
Surgery: Open reduction and repair of soft Bigelow and reverse bigelow, Allis, Stimson
tissues, hinged external fixation, pinning of the gravity method.
joint. Maintain it with skeletal traction.
If irreducible, non concentric, ipsilateral neck
2.5. Complications: Fracture or acetabular Fracture then ope n
Loss of motion. reduction is done.
Neurologic compromise.
Vascular Injury. 3.5. Complications:
Compartment syndrome. Osteonecrosis.
Redislocation. Post-traumatic osteoarthritis.
Myositis ossificans. Recurrent dislocation.
Neurovascular Injury.
3. Hip dislocation Femoral head fractures.
Heterotopic ossification.
3.1. Types of dislocation: Thrombo-emblism.
3.1.1 Posterior: Posterior dislocation
Is the most common type of dislocation. Occurs 4. Knee dislocation
mainly due to dash board Injury.
Mode of Injury: high energy / low energy.
3.1.2 Anterior: Anterior dislocation Hyperextension with or without varus / valgus.

Page 545
 Fig2 - X-ray Picture Of Knee Dislocation
4.1. Clinical features:
Gross knee distortion is present.
A neurovas cular examination must be done.
4.2. Investigations:
First reduce the dislocation.
Then take X-rays AP and lateral, 45 degree
oblique, patellar sunrise views.
MRI.
Arthroscopy.
Assess the ligament Injuries.
4.3. Treatment:
Immediate closed reduction, avoid direct
pressure over the popliteal fossa after reduction,
splint at 20 - 30 degrees of flexion.
Operative indications:
Unreduced, residual soft tissue interposition
Open Injuries, ORIF with ex-fix.
Reconstrucion of ligaments at later setting.
4.4. Complications:
Limited range of movements.
Ligamentous laxity and instability.
Vascular compromise.
Nerve traction Injury.
Page 546
 13.LIGAMENTOUS INJURIES

1. Mode of Injury 4. Treatment

Indirect, Twisting Or Bending Forces On The Knee. 4.1 Initial management with brace/splint and
NSAIDs
2.Clinical Features Conservative management with bracing and
Pain, swelling, tenderness, loss of range of motion physiotherapy
and positive patellar tap. Bracing for 2 weeks followed by MRI
3. Investigations 4.2 Operative: arthroscopic ligament repair.

X-ray of associated joint and MRI.

Page 547
 14. SPINAL TRAUMA
Nor mal Motor, Sensor y, Or Autonomic Function.
1. Spinal Cord Injury (SCI)
Is An Insult To The Spinal Cord Resulting In
AChange, Either Temporary Or Permanent, In Its

Figure 1 Head to Toe Stabilization In Case Of Spinal Injury OnSpi ne Board

2.1.1 Clinical Diagnosis:

2. Optimal Diagnostic
After the ABC have been taken care of, the patient is
Criteria, Investigations, gently log rolled and whole of the spine is palpated
Treatment & Referral for tenderness or a palpable step-off deformity.
Neurogenic shock, incontinence of bowel, bladder
Criteria and penile erection indicate severe spine Injury. A
careful and detailed neurological examination is then
2.1 Rural Hospital / SDH: performed and meticulously documented.
OptimalStandards of Treatment in Situations where
technology and resources are limited.

Table 1: Assessment of motor function

Diaphragm C3-5
Shrug shoulders C4
Deltoids/elbow flexion C5
Extend wrist C6
Extension of elbow/ flexion of wrist C7
Abduct fingers C8

Page 548
 Active chest expansion T1-T12
Hip flexion L2
Knee extension L3-4
Ankle dorsiflexion L5-S1
Ankle plantar flexion S1-2

Table2: Assessment of sensory function

Deltoid area C5
Thumb C6
Middle finger C7
Little finger C8
Nipple T4
Xiphoid T8
Umblicus T10
Symphysis T12
Anterior thigh L2
Anterior knee L3
Antero-lateral ankle L4
Dorsum of great and 2nd toe L5
Lateral side of foot S1
Posterior calf S2
Perianal sensation S2-5

2.1.2 Frankels grades: 2.1.3 Investigations:

Spinal Cord Inj.ury is mos t commonly graded using
Frankels grades (A to E).
A: Complete motor and sensory loss
B: Sensation only present below lesion
C: Sensations present and motor function is
present but useless
D: Motor useful but not nor mal
E: No neurological deficit.
After the motor and sensor y examination, presence
of sacral sparing may be noted by voluntary rectal
sphincter tone and toe flexor contractions. Presence
of sacral sparing indicates a better neurological
prognosis.
Although spinal shock is ove r by 24 hours, rarely
it may be prolonged. A positive bulbocavernous
reflex or a positive anal wink indicates the end of
spinal shock. If no motor or sensory function can be
documented at this stage, a complete spinal cord
Inj.ury is present.
All patients with suspected spinal Inj.ury should have
radiographic evaluation.
a) Initial screening can be done by conventional
antero-posterior and lateral x-rays. The cervical spine
radiographs must include the C7-T1 junction to be
considered adequate
Additional Open-mouth views should be done to
evaluate odontoid Inj.ury.
Whole spine should be evaluated with a patient of
spinal Inj.ury.
b) The patient should be referred for advanced
diagnostic modalities only when the patient is
sTab.le:
i. CT
ii. MRI
2.1.4 Out Patient care
A secondary hospital is expected to provide
outpatient care to the spinal cord Inj.ury patients who
may be referred back from specialized centers after

Page 549
 definitive treatment. This may be in for m of
i. physiotherapy for passive mobilisation of all joints
and active exercises for muscles
ii. Teaching of clean intermittent cathetrisation
iii. Counselling of the patient and attendants
iv. Care of bed sores
2.1.5 Day Care
Day care might be needed for situations like
debridement of bed sores.
2.1.6 Referral criteria:
i. The pa tient should be hemodynamicallysTab.le
and fully resuscitated at the time of referral
ii. All the patients who need surgery (indications
discussed in the next section) need to be referred
to a specialized tertiary care centre.
iii. The decision of need for surgery can only be
made by an experienced spinal surgeon either
orthope dic or neuros urgeon. In absence of these
all patients with proven or suspected spine
Inj.ury should be referred to a higher center.
Fig 2 Xray view of cervical spine trauma Fig 3 MRI of spine trauma
Treatment: Standard Operating procedure
(a) On arrival in emergency room:
Once the patient with a potential spinal
2.2 At District Hospital
2.2.1 Clinical Diagnosis:
iv. As described above (in situation 1)
Investigations:
2.2.2 Radiographic evaluation of patients with
spinal Inj.ury.
i. Initial screening can be done by conventional
antero-posterior and lateral x-rays.
ii. Additional Open-mouth views should be done to
evaluate odontoid Inj.ury.
iii. Special views like swimmers view and oblique
views can be done to see junctional areas
iv. CT scan of the whole spine should be done if in
presence of clinical suspicion but fractures
cannot be demonstrated on x rays or if junctional
areas are not visualised.
v. MRI should be done to evaluate ligamentous
Inj.ury, spinal cord Inj.ury.
vi. In patients with pre-Inj.ury morbidities such as
Ankylosing
vii. stiff spi ne CT and MRI should be done to rule
out occult instability eve n if x-rays arenormal.
viii. Whole spine should be evaluated with a patient
of spinal Inj.ury
Inj.uryreaches the emergency, thepatient should be
transferred off the backboard onto a firm padded
surface while maintaining spinal alignment. A
baseline skin assessment can be performed at the
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 time of shifting the patient from spine board to be employed for logrolling during patient
hospital bed. Adequate number of personnel should repos itioning, turning and transfers.

Fig4 Log Rolling while examining and shifting of spi nal Inj.ury patient

No clinical evidence exists to definitively
recommend the use of any neuroprotective
pharmacologic agent, including steroids, in the
treatment of acute spinal cord Inj.ury to improve
functional recovery. However high dose methyl-
prednisolone may be used as per NASCIS III
recommendations (Methylprednisolone: Bolus dose
of 30 mg/kg of body weight over 15 minutes,
followed by a 45-minute pa use, and then a 23-hour
continuous infusion of mg/kg/hr,(If patient presents
between 3 and 8 hrs, give the above steroid infusion
for total of 48 hrs) if the patient presents within 8
hours of Inj.ury. The risk of complications as
infection, sepsis, respiratory complications and
gastrointestinal hemorrhage should be kept in mind
while administering steroids, It is basically a
treatment option,not standard care.
Once initial resuscitation is done, complete a
comprehensive tertiary trauma surve y in the patient
with potential or confirmed spinal cord Inj.ury.
In the patient with acute spinal cord Inj.ury,
particularly higher cervical Inj.ury, assess
frequently and early document any evidence of
traumatic brain Inj.ury (TBI) in the form of loss of
consciousness and posttraumatic amnesia .
Screen for thoracic and intra-abdominal Inj.ury in all
patients with spinal cord Inj.ury.
Perform early sTab.ilization of extraspinal fractures.
Perform this surgery as early as possible to facilitate
early rehabilitation and concomitantly with any
required spinal stabilization if the patient is
medically stable.
Surgical treatment.
(b) Out Patient
Out patient care is needed for non surgically treated
patients on ambulatory care and Surgically treated
patients. This will entail:
Prescription of appropriate orthoseshysiotherapy
servicesCounselling: social,
psychological,vocational
(c) Day Care
Referral criteria:
Surgically treated patients may be referred back to
secondary hospitals for physiotherapy, and care of
back, bladder and bowel.

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15. MANGLED EXTREMITIES (AMPUTATION)
1. Introduction 4. Standard treatment protocol
for management of mangled
Traffic is increasing day by day and so are road
traffic accidents.
extremities at RH/SDH/DH
Most of RTA involve trauma to extremities to
varying level. No Delay in receiving the patient and starting
treatment
Multi-systemic approach
2. At PHC/Sub Center level Patient should be examined according to ATLS
protocol of ABCDE
Follow ATLS guidelines of A B C D E
Look for signs of poly trauma, involvement of
After STab.ilization of patient, examine for other
head Inj.ury, spine or abdominal and pelvic
associated Injuries such as pelvis and spine
Injuries.
which are common in poly trauma
If such Injuries are present then refer the case to 4.1. Informed consent
higher center without any delay.
If absent then grade the Inj.ury according to Two surgeons should certify that the limb needs
MESS (Mangled Extremity Severity Score) amputation
which is useful for decision making regarding
Consent of the patient ( if conscious and co-
definitive surgical treatment (Salvage or
operative ) should be taken
Amputation of the limb) and refer the patient to
Consent of Relative should be taken if patient is
the higher centre.
non responsive
Detailed informed consent in their local language
3. Before referring should be taken
Wash the wound primarily with nor mal saline, 4.2. Pre operative care
iodine solution and Hydrogen Peroxide till all
visible contamination in remove d. Pain management
Stop any active bleed with help of compression Clinical assessment
banda ge or tourniquet
Decision making
Avoid Excessive handling of Inj.ured limb to
Discharge planning
avoid neurovascular complications
Record keeping
Infuse IV fluids and Blood
Inj.ect first dose of higher antibiotics 4.3. Peri operative care
Give Inj. TT. O.5 ml intra muscular
Things to be done Before Referral The scheduling of ope rations
Operation undertaken
Inform the concern center about MESS score and Antibiotic prophylaxis
expected time of arrival of patient Thromboprophylaxis
Arrange for proper transport
Make sure that patient will be 4.4. Post operative care
hemodynamicallysTab.le during entire duration
of transport. Pain management
Wound care
Rehabilitation

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 16. COMMON FRACTURES IN CHILDREN

Mode Fall on out-stretched hand Fractures of lower limb

1.6 EpiphisealInj.ury around hip and kneeClosed
1. Common fractures reduction and immobilization in splints
1.1 Lower end radius 1.7 Surgical treatment ope n reduction and
Treated by closed reduction internal fixation with multiple cancellous
1.2 Greenstick fracture both bone forearmClosed screws or mini DHS plateFractures around hip
reduction under General anesthesia Surgical treatment
1.3 Supracondylar fracture humerus Depe nding on
classification , either closed reduction or 1.8 Shaft femur
closed reduction with cross k-wire or open
Undisplaced Conservative
reduction
Displaced Shaft tibia
1.4 Fracture lateral condyle humerus
Undisplaced Conservative
Requires open reduction
Displaced Surgical in the form of closed or
1.5 Fracture clavicle ope n reduction a nd i nternal fixation with either
elastic nails or plate and screws.
Figure of 8 bandage

Page 553
 17. BONE TUMORS
Primary neoplasms of the skeleton are rare,
amounting to only 0.2% of the overall human tumour
burden. However, children are frequently affected
and the etiology is largely unknown. Significant
progress has been made in the histological and
genetic typing of bone tumours. Furthermore,
advances in combined surgical and chemotherapy
have lead to a significant increase in survival rates
even for highly malignant neoplasms, including
Osteosarcoma and Ewing sarcoma.
1.Primary bone tumors:
1.1 Benign Tumors
1.1.1 Osteoid Osteoma
True benign tumor of bone
Age group: 5 - 25yrs
Commonest site: Diaphysis of long bone. eg
tibia.
Clinical features Night pain, relieved by
salicylates.
Pathology - Consists of a nidus surrounded by
dense sclerotic bone
X-ray - Zone of sclerosis surroundi ng a nidus
Treatment - Complete excision of nidus with
sclerotic bone.
Prognosis - Good
1.1.2 Osteochondroma
Commonest benign tumor of bone, arises from
adjoining epiphysis to metaphysis
Age group - adolescents
Clinical features - painless swelling around a
joint, sessile or pedunculated
Multiple site involvement is called
Diaphysealaclasia
Complications - bursitis, neuropathy, limitations
of movement, malignant transformation
(chondrosarcoma) occur rarely
X-ray - bony growth made up of mature cortical
bone and marrow. Cartilaginous gap not visible
Treatment- excision including periosteum.
1.1.3 Fibrous Dysplasia
Normal bone is replaced by fibrous tissue.
Erodes the cortices of bone from within.
Thin layer of sub - periosteal bone forms around
the mass, so bone appears expanded. Site- upper
end of femur, tibia, ribs.
Mono-ostotic one bone is affected. Poly-ostotic
many bones are affected.
Clinical features - pain, deformity, pathologic
fractures.
X-ray - ground glass appearance.
Treatment - curettage and bo ne grafting.
1.1.4 Osteoclastoma (Giant Cell Tumor)
Common bone tumor with variable growth
potential
Age group - 20 - 40 yrs
Site - starts in epiphysis and extends into
metaphysis
Commonly lower end of femur, upper end of
tibia
Pathology
Cell of origin is uncertain
Tumor consists of undifferentiated spindle
cells with multinucleated giant cells
Clinical feature - swelling, vague pain
X-ray
Lytic expansile lesion
Eccentric location
Soap bubble appearance pathognomonic.
Page 554
Figure 1: Soap bubble appearance of giant cell tumor
Excision with reconstruction
Curettage with or without suppl ementary
procedures like chemical ablation, cryotherapy,
PMMA implantation
Amputation: aggressive tumors, recurrence
Radiation: tumor involving vertebrae.
1.2 Primary malignant bone
tumors:
1.2.1Osteogenic Sarcoma
Usually in males aged 10 to 20
Occurs most often in femur, but also in tibia and
humerus
Occasionally, in fibula, ileum, vertebra, or
mandible
Tumor arises from bone-forming osteoblast and
bone-digesting osteoclast.
Treatment
Surgery
Radical Tumor resection
Mega Voltage Radiotherapy and / or
chemotherapy or combi nation of bot h.
1.2.2 ParostealOsteogenic Sarcoma:
Usually in females ages 30 to 40.
Occurs most often in distal femur, may also be in
the humerus, tibia, and ulna.
Develops on surface of bone and progresses
slowly.
Treatment
Surgery
Tumor resection, possible amputation
Inter-scapulothoracic surgery
Hemi-pelvectomy
Chemotherapy.
1.2.3Chondrosarcoma:
Usually in males ages 30 to 50
Occurs most often in pelvis, proximal femur,
ribs, and shoulder girdle
Develops from cartilage, and grows slowly
Usually painless, locally recurrent and invasive
Hemipelvectomy
Surgical resection (ribs)
Radiation, and / or Chemotherapy.
1.2.4 Multiple Myeloma
It is the mos t common primary malignancy of bone
having short duration onset and aggressive in nature.
Page 555
Age of occurance commonly around 60yrs. 2% less
than forty.
2. Metastatic bone tumors:
The most common bony malignancies are
Clinical features: metastatic carcinomas.
Bone pain Metastatic lesions represent the most common
cause of pathology fractures due to a neoplasm.
Weakness
Usually are multiple, but can be solitary.
Weight loss
The most common primaries are breast, prostate,
Anemia
lung, kidney and thyroid, in that order.
Thrombocytopenia
Renal metastasis are quite vascular and have cold
Peripheral neuropathy
bone scans.
Hypercalcaemia
Renal failure Clinical features:
It manifests in pathological fractures commonly in Patients with known primary malignancy
spine followed by ribs and pelvis. presents with symptoms suggestive of
secondaries in bone.
Laboratory studies:
Bony pain, commonest site is spine.
Urine - Bence Jones Protein present in 30% of Pathological fractures most common in spine.
cases
Blood - Very high ESR, A/G ratio reversal Investigation:
Serum electrophoresis - Abnormal spike in X-ray - Majority are osteolytic, few are
gamma globulin region in 90% cases. osteoblastic. eg., male- prostatic secondaries,
Treatment: female breast secondaries
Blood - High ESR, elevated serum calcium,
Chemotherapy - Melphalan is the drug of choice. elevated serum acid phosphatase in prostatic
Given in combination with Vincristine, secondaries.
Prednisolone and sometimes Cyclophosphamide.
Cycles are repeated 3 - 4 weeks for 6 - 12 cycles. Treatment:
Splintage of diseased part. Symptomatic relief of pain, and prevention of
Radiotherapy- Useful in case of neurological pathologic fractures
compression. Chemotherapy
Surgical intervention in advanced tumors Radiotherapy

Page 556
ANESTHESIOLOGY

Page 557
 1. INTRODUCTION
noxious stimuli with different inhalational and
1. Definition: intrave nous drugs.
Anesthesia is the reversible state of unconsciousness
with amnesia, analgesia and unresponsive ness to

2. Types of Anesthesia
GENERAL

Types of Anaesthesia

General (GA) Regional Total Intra Monitor

Intravenous Venous Anaesthesia
Anaesthsia Regional Care
(Short GA)
Anaesthesia (MAC)
with mask (G1 A)
Stand By
or without mask

Central Nerve Block Local Localized or

Neuroaxial selective
block nerve block
With
With PNS/USG Without PNS/USG PNS/USG

Sub Arachnoid Epidural Caudal Epidural Combined Spinal

Spinal Block Blocks Block Epidural Block

Figure 1: Anesthesia General Protocol

Page 558
3. Pre-Anaesthetic Checklist
Check function of high vacuum suction
machine.
Check reserve oxygen suppl y.
Check function of breathing system.
Check vaporizer.
Check absorber if in use.
Inspect equipment for
a) Endo tracheal intubation
b) Intrave nous infusion
c) Resuscitation
4. Recommended minimum
essentials in operation
theatre
4.1 Minimum essentials required:
Continuous supply of oxygen via central pipeline
or jumbo cylinders.
Anesthesia machine with to oxygen and a nitrous
oxide input connections.
One small oxygen cylinder mounted on Boyles
other than jumbo or central line and nitrous
oxide cylinder along with cylinder valve opener
should be there.
Boyles machine should have Hypoxic and alarm
safety system.
Wor king suction machine (Foot driven and
Electric) with all connectors, tunings, and
suction round tip and e xhaust fans.
Multi-parameter (Pulse Oxymeter, NIBP, ECG,
ETCo2).
Defibrillator (adult & pediatric).
OT table with tilting facility.
Adult (Bain) & Pediatric (JR) Circuit.
Set of oral and nasal Airways sizes 00, 1, 2, 3,
4.
Silicon bag with all sizes of masks & cuffed and
plain Endo tracheal Tubes. Working
laryngoscope with 5 sizes of blades
Check gas supplies, both cylinder, pipeline &
circuit
Check oxygen suppl y failure alarm & oxygen
flush.
Check oxygen nitrous oxide ratio.
Mechanical ventilator.
Waste gas scavenging system.
Check reserved gas supply
Appl y and c heck monitoring system &
cautery, circuit and tourniquet.
Set appropriate alarm level.
Magills forceps (Adult & Pediatric), Scissors,
Ampoule cutter, Torch, Thermometer.
IV sets, Micro Sets, Blood sets, three way IV
extension tube & central line.
IV fluids crystalloids RL, DNS, D5, and Colloids
plasma expanders.
For Difficult Airways fiber optic boogie,
LMA(Classic & Pro seal), Igel, tracheostomy,
tube , percutaneous tracheostomy set, combi tube
and all size stylate(flexible & Rigid).
Disposable spinal needles 23, 24, 25, 26, 27,
Epidural set 16, 18.
Radiant warmer/blanket, heating mattress, fluid
warmer.
Postoperative recovery room with oxygen supply
and monitors.
Working BP apparatus & Stethoscope.
Vaporizers-(Goldman) Halothane & Isoflurane.
Capnography To monitor End Tidal
Carbondioxide (ETCO2) Where laparoscopic
surgeries are done.
New Born resuscitation kit weighing scale.
Paediatric resuscitation kit with all masks &
LMA & stylate.
Flexible smooth rubber cord for tourniquet to
secure IV line.
Central line (cava fix, double & triple Lumen).
Glucometer, peak flow meter, height scale &
refrigerator (for blood sample).
Page 559
4.2 Emergency medicine kit:
Chart No. 1. EMERGENCY MEDICINE KIT
Injections Metapranolol Nebulizer
Hydrocortisone Hemolock
Atropine
Dexamethaxone Butroclot
Glycopyrolate
Potassium chrolide Neloxone
Adrenaline
Calcium gluconate. ECG Lead.
Noradrenaline
Soda bicarbonate.
Dopamine. Tablets
Magnesium 25% & 50%
Dobutamine.
Mannitol Nifedepin
Mephentermine
Tranaexamic acid. Captopril
Ephedrine hydrochloride.
Dextrose 25% & 50% Sorbitrate
Phenylephrine.
Insulin. Atenolol
Vasopressin
Deriphylline
Prostaglandi n
Aminophylline
Isopr enalin
Amiodarone.
Digoxin
Xylocard 2%
Esmolol
Furosemide (lasix)
Propranolol

4.2 Doses and indication for emergency drugs:

Chart No 2. E MERGENCY DRUGS & DOSES

Drug Indication Dose

Sodium bicarbonate Acidosis 2-4 m eq/kg
Atropine Bradycardia 0.03 mg/kg
Naloxone Narcotic depression 5-10 micro gm/kg
Calcium gluconate Low perfusion 0.6 ml/kg
Epinephrine Asystole 5 Microgram/kg of 1:1000 solutions.

4.3 Various Types of anesthesia drugs:

Chart No. 3. A NAESTHESIA DRUGS

A. Premedication D. Inhalational Anasthetic Agent

1. Anticholinergics. a) Halotane.
a) Inj Glycopyrrolate b) Isoflurane.
b) Inj Atropi ne c) Sevoflurane.
2. Antacid d) Desflurance.
a) Inj Ranitidine.
b) Inj Pantaprazole
3. Antiemetic E. Reversal Agent
a) Inj Metoclopramide.
b) Inj Onda nstaron. a) Inj Neostigmine.

Page 560
 c) Inj Granisatron. F. Obstetric Drugs
4. Opiods
a) Inj Oxytocin.
a) Inj Pentazocine (Fortwin)
b) Inj Methyl ergomtrine.
b) Inj Butophanol
c) Inj Prostaglandin F2 alpha.
c) Inj Fentanyl.
d) Inj Magnesium Sulphate.
5. Benzodiazepines
a) Inj Diazepam. F. Spinal Anaethesia drugs
b) Inj Midazolam.
a) Inj Lignocaine (heavy) 5 %
b) Inj Bupivacaine (heavy) 0.5%
G. Local Anesthetics.
a) Inj Lignocaine 2%.
b) Inj Lignocaine 2% with

B. Induction Agents Adrenaline.

a) Inj Thiopentone Sodium. c) Inj Bupivacaine 0.5%

b) Inj Propofol. d) Inj Bupivacaine 0.25%
c) Inj Ketamine.
preservative free.
e) Inj Rocuronium 0.75%.
H. Other Drugs.
a) Inj Tramadol
b) Inj Diclofenac.
C. Muscles Relaxants.
c) Diclofenac Suppository.
Depolarizing Muscles Relaxants. d) Inj Buprenorphine.
e) Inj Dexmeditomidine.
a)Inj Suxamethonium. f) Inj. Clonidine.
Non- Depolarizing Muscles Relaxants g) Inj Bupivacaine 0.5% heavy.
h) Lignocaine Jelly 2%.
a) Inj Pancuronium.
b) Inj Vecuronium.
c) Inj Rocuronium.
d) Inj Atracurium.

4.6 Doses of intravenous anesthesia agents:

Chart No. 4. INTRAVENOUS AGENTS IN ANAESTHESIA

INTRAVENOUS AGENTS USED IN ANAESTHESIA

DRUG DOSE REPEAT DOSE/ INFUSION RATE
Thiope ntone 5-6 mg/kg 2 mg/kg.
Propofol 1-3 mg/kg 0.2-1 mg/kg
Ketamine 1.5-2 mg/kg 40mcg/kg/min.
Fentanyl 0.025-2 microgm/kg 4-10 mcg/kg/hr. (I)
Alfentanil 5-10 microgm/kg 05-10 mcg/kg/min. (I)
Sufentanil 0.1 microgm/kg 0.01 mcg/kg/min.) (I)

Page 561
Succinyl Choline 2mg/kg 4-10 mg/min. (I)
Pancuronium 0.08 mg/kg 0.02 mg/kg
Atracurium 0.5 mg/kg 4-12 mcg/kg/min (I)
Vecuronium 0.08-0.1 mg/kg 0.12-2 mcg/kg/min. ( I)
Rocuronium 0.6 mg/kg 9-12 mcg/kg/min. ( I)
Diazepam 0.1-0.3 mg/kg
Midazolam 0.5-0.1mg/kg
Flumazenil 0.1-0.5mg
Neostigmine 0.05 mg/kg
Adenosine 0.1 mg/kg
Digoxin 15-20 mcg/kg
Diltazen 0.15-0.35 mg/kg
Benadr yl 1 mg/kg
Furosemid 1-2 mg/kg
Mannitol 0.25-1 mg/kg
Esmolal 100-300mcg/kg/min. (I)
Dopamine 5-15mcg/kg/min. (I)
Dobutamine 7-15mcg/kg/min.(I)
NTG 1-1.5 mcg/kg/min. (I)
Amidaron 15mg/kg (loading) (I)
5mg/kg/hr. ( maint)
KCL 0.5mEq/kg/hr. (I)
Sodium 40-100mcg/min. (I)
Nitroprusside
Atropine 0.01 mg/kg
Glyco pyrolate 4 microgm/kg
Dexamethasone 0.1 mg/kg
Paracetemol 15 mg/kg
Diclofenac sodium 1.5 mg/kg
Neostigmine 0.05 mg/kg
Noradrenaline 4 mcg per mL In titrated dose
Bitartrate
Labetalol Hcl 20 mg IV push over two minute In titrated dose
40-80 over two 10 minute

I = Infusion Do not use Broom inside Operation Theatre.

Do Fogging after infected case and enter in register.
5. Operation Theatre cleaning
In between the two cases, clean O.T.
protocol
Page 562
1) Remove linen, instrument sets and used material.
2) Clean surface, wipe with Bacillocide solution.
3) Mop the floor (ideally with Lysol 3% or
Bacillocide)
6. Operation Theatre
fumigation protocol (Power
Jet and auto mist)
6.1. Fumigation agents
For O.T. fumigation 20% aqueous solution of
Hydrogen Peroxide 11 % and Silver Nitrate solution
0.01% should be used. For 1000 cu. ft. Take 400 ml
clean water and add 80 ml. of fumigant solution
Hydrogen Peroxide 11 % + Silver Nitrate 0.01 %
solution in a fogging machine. Keep the room / OT
closed for 60 min. Mop the flooring with clean floor
soaked in the same solution.
6.2. Advantages:
Solution has broad spectrum of antimicrobial activity,
effective against HIV, HBV and other pathogenic
bacteria, viruses, molds and spores. It is non toxic,
eco friendly. It liberates nascent oxygen having
strong oxidizing effect.
6.3. Procedure:
For 350 sq. ft. OT take 1000 ml (1lt) water in tank
and add solution in that.
Keep fumigation machine on floor .
Keep machine near to door so after fumigation you
can easily switch off machine.
Daily moppi ng of OT is compulsory with sol ution
Please cover all electro medicos, digital and water
resistance equipment (C arm monitor microscope
etc.) with cloth or plastic sheet.
Empty the machine tank and use balance solution.
Do not run (pow er jet) machine continuously more
than 35 minutes and total one hour in a da y; keep 4 to
6 hours of interval in between two running.
Do not operate machine in presence of patient and do
fumigation in vacant room only.

7. Grading of patients & fluid requirements:

Chart No. 5: GRADING

ASA 1 : ASA 2 : ASA 3 :

A Normal Healthy A patient with mild systemic A patient with severe systemic disease that limits
Patient with only surgical Disease (like, HTN, DM etc. activity but is not a incapacitating (Disease is not
Condition under control with treatment ) under control with treatment but not life
threatening)

Weight (kg.) Hourly Fluid Requirement

<10 4 ml/kg
11-20 40ml + 2ml/kg > 10
>20 60ml + 1ml/kg> 20
ASA Ame rican Society of Anesthesiology

Page 563
8. Fluid requirements for children:
Chart No.6: FLUID REQUIREMENT FOR CHILDREN

MONITORING STANDARDS FASTING GUIDELINES

ESSENTIALS: Ingested Minimum Fasting

1) Continuous presence of qualified material Period (h)
Anesthesiologist.
2) Oxygen suppl y failure alarm Clear Liquids 2
3) Observation of reservoir bag & chest Breast Milk 4
expa nsion.
4) Ventilator disconnect alarm. Infant for mula 6
5) Oxygen analyzer of inspired gases. Non-human Milk 6
6) Pulse oximetry.
7) Electrocardiogram. Light Meal 6
8) Non-invasive arterial blood pressure.
These recommendations apply to healthy patients
STRONGLY RECOMMENDED: of all age group who are undergoing elective
procedure.
1) Temperature. Clear liquids: water, fruits without pulp,
2) End tidal Carbon dioxide. carbonated, beverages, tea & black coffee.
3) Monitoring of neuromuscular blockade.

9. Adrenaline doses:
Chart No. 7: ADRENALINE DOSES BY AGE

Adult : Pediatric: Neonatal :

1 mg 0.01 mg/kg (0.1 ml/kg) IV or intra 0.01 mg/kg to 0.03 mg/kg (0.1-0.3
osseous ml/kg)
Repeat Q 3-5 min
Maximum does 1 mg IV/IO or 10 IV, intra osseous, or umbilical
Higher IV doses NOT
mg ET repeat Q 3-5 min
recommended. Repeat Q 3-5 min.
No Higher IV doses. ET does 0.1
ET dose 2 to 2.5 mg Higher IV doses NOT recommended
mg/kg (ten times IV dos e)
Drip 1-10 mcg/min. ET does 0.1 mg/kg (ten times IV
Strong preference for IV/IO!
dose)
Drip 0.05-1 mcg/kg/min
REACTION

Breathing Circuits
Jackson Rees circuit Use for neonate & children less than 25kg
Bain Circuit Most commonly used circuit weight more than 25 kg

Page 564
10. Airway:
Chart No.8 ORAL AIRWAYS
Formula for size of ETT
Neonate 2.5 or 3
Children < 6 years age/3 + 3.5
Children > 6 years age/4 + 4.5
Adult female ET Tube number 7 or 7.5
Adult male ET Tube number 8.5 or 9

11. Biomedical waste:

Chart No. 9: SEGREGATE MEDICAL WASTE
Red Bag Blue Bag Yellow Bag Sharp puncture proof
Container
Plastic Waste General Waste Anatomical Waste Waste Sharps
Infectious waste i.e. Pads, Plastic and rubber Appendix, Uterus, Blade
Spirit swabs, Plaster casts articles such as IV Sets, extracted teeth,
Needle
soiled with secretions catheters, venflow, urine
Placenta
bags Cut Ampoule
All Sharp objects

12. Important aspects of anesthesia:

Chart No. 10: Ten Golden rules of anesthesia

1 Do an adequate preoperative assessment.

2 Nil by mouth for six hours
3 Put patient on a tipping table
4 Check your machine and c ylinders before you start
5 Keep a suction instantly ready
6 Keep patients airway clear
7 Be ready to control patients ventilation
8 Have a vein open
9 Check patients pulse and blood pressure
10 Always have someone who can apply cricoid pressure in emergency

Page 565
13. Universal precaution for health care workers in operation
theatre
Proper hand washing before and after
CONTACT with each patient and handling
patients specimens. Do not leave sharps on bed
or beside of patient
Use of gloves, mask, gowns and protective eye-
wear
Prevent needles stick injuries with other sharp
instrument
DO NOT BEND OR RECAP NEEDLES
In case of needles stick injuries or cuts, wash the
area properly with water and soap and Contact
for post exposure prophylaxis treatment
Dispose all sharps in puncture proof container.
Avoid spills of blood & body fluids, If it occurs,
cover it with absorbent material like gauze over
which 1 % solution of sodium hypochlorite
should be poured and left for 10-15 minutes
(ideal 30min). Clean the area with a bleach mop.
Wash and dr y the mop.
Proper segregation and disposal of Bio-Medical
waste
Immunization (for Hepatitis B)
Page 566
 2. DIFFICULT AIRWAY ALGORITHM
Assess the likely hood and clinical impact of basic
management problems: In case of Difficult
Intubation and difficult Ventilation awake intubation
should be carried out. In case you ca nnot ventilate,
cannot incubate-(CVCI) Emerge ncy sur gical
airway (i.e. Crico thyrotomy) ma y be necessary
if the patient is hypoxic.

FIGURE-1: INTRODUCING LARYNGEAL MASK AIRWAY Ge

Page 567
3. PRE-ANAESTHESIA CHECK UP PROTOCOL
1. Pre Anaesthesia Checkup
(PAC)
Pre anesthetic check up should be carried on prior
day of surgery to avoid unnecessary postponement of
patients.
1.1 Following history should be
asked
1. High blood pressure, Diabetes, Asthma, Heart
Disease, Stroke, Cough and Cold in the past 2
weeks
2. History of Shortness of breath, Difficulty in
breathing on lying flat, Difficulty in breathing on
climbing stairs, Chest pain, palpitation, chronic
cough.
3. History of cardiac illness such as heart failure,
heart valve problem, high cholesterol level,
RHD, CHD or Cardiac arrest.
4. History of respiratory problems such as chronic
bronchitis, Allergic rhinitis, Snoring,
Tuberculosis, Lung cancer, Chest infection or
pneumonia.
5. History of neurological probl ems such as
epilepsy, fainting, coma, paralysis, chronic
headache, dizziness, Parkinsonism, brain tumor.
6. History of muscle or bone problems such as
Osteoporosis, Neck pain or neck stiffness,
Difficulty to open mouth, Spine problem,
congenital muscle disease.
7. History of kidney problem such as dialysis.
Gastric problem such as Heartburn, Reflux,
Jaundice.
8. History of blood or endocrine problems such as
Anemia, receipt of blood transfusion, prolonged
bleeding, Thelecemia, sickle cell anemia, thyroid
disease.
9. History of allergy.
10. History of medications such as diabetes,
hypertension, asthma, psychotropic drugs,
steroids.
11. History of smoking, alcohol, addictive drugs,
BOH.
12. History of Dentures, braces, crown, loose teeth,
implanted pacemaker, implanted cardiac
Defibrillator, Prosthetic Heart valve, orthopedic
implant, or gan recipient.
13. History of STD, Drug resistance.
14. History of anesthesia with histor y of headache
after anesthesia, Awareness during anesthesia,
transfusion reaction, admission to ICU after
surgery, any complication after anesthesia.
2. Following history should be
asked
1.1 Investigations as advice by surgeon and
anesthetist.
2.2 ASA: (American Society of Anaesthiologist)
Assessment of patient in terms of
I/II/III/IV/V/VI/E with additional risk factor.
2.3 Do prope r systemic examination of
cardiovascular system, respiratory system,
central nervous system.
2.4 Evaluate the patients airway - Thyromental
distance (If < 3finger anticipated difficult
intubations), dentition, mouth opening.
3. Consent
Info med consent of pa tient should be taken before
surgery which means consent given to a proposed
specific intervention, without any force, undue
influence, fraud, threat, mistake or misrepresentation,
and obtained after disclosing to the person giving
consent adequate infor mation includi ng risks and
benefits of, and alternatives to, the proposed
intervention in a language and manner understood by
such person with no binding to consent after being
infor med. Consent should be attested by staff nurse
of ward. There should be common consent for
surgery and anesthesia unless it is essential to take
consent for anesthesia separately.
Page 568
 4. CONDUCT OF ANAESTHESIA
1. Anesthesia can be conducted Keep glucometer and shor t acting regular insulin
ready for intra-operative use.
taking 5Ps into Assess target organ function and monitor
accordingly
consideration
They are:- 2.3 Obstetric patients
Prepare operation theatre ready for emergency
Pre operative Assessment of Patients. LSCS.
Patients Preparation. Follow anti-eclamptic regimens for patients with
Preparation of Operation Theatre. pregnancy induced hypertension.
Premedication. Verify the availability of blood.
Plan of Anesthesia. Keep the difficult intuba tion kit ready.
Take care of prophylactic measures to treat
2. Anesthesia to different aspiration (Mendelson Sydrome).
Keep the Infant resuscitation bag, smaller
groups of patients endotrachaeal tubes, laryngoscope, suction
apparatus, infant radiant warmer, oxygen hoods
2.1 Hypertensive Patients & emergency dr ugs for resuscitation.
Advise to take all anti-hypertensive drugs early
in the morning of surgery. 2.4 Trauma Patients
Avoid ACE inhibitors on the day of surgery to Stabilize the patients taking into consideration
avoid intra operative fall in BP. ABC (Air, Breathing & Circulation) of
Keep anti-hypertensive drugs like resuscitation.
Nitroglycerine, Nifedipine and Metoprolol ready. Stabilize the cervical spine (with collar for
Keep volume expanders like colloids ready. suspected C-spine injuries).
Place the inter costal drainage for chest injuries.
2.2 Diabetic Patient Splint the fractures.
Advice to skip the morning doses of insulin and Assess the GCS (Glasgow coma score).If<8,
oral hypoglycemic. intubate for airway protection.
Check fasting blood sugar, urine ketones and Transport the patient to referral centre with
serum electrolytes on the mor ning of surgery. portable ventilator, oxygen cylinder, ambu bag
on standby.
Place the diabetic patients first in the list of
surgery.
Inform the patient`s details to referral centre prior to
Specific care of the patients with autonomic or during transport.
disturbances.

Page 569
 5. COMPLICATIONS OF ANAESTHESIA
Figure-1: Complications of Anesthesia

During General Anaesthesia

CARDIOVASCULAR RESPIRATORY NEUROLOGICAL THERMAL

PERTURBATIONS
Hypertension Pulmonary Convulsions
aspiration Hypothermia&
Hypotension Delayed Recovery
Arrhythmias Hypoxia Nerve palsies Shivering
Myocardial Ischemia Hypercarbia
Cardiac arrest Bronchospasm

1. Management of common Titrate the doses of opiods. Use appropriate dose

to avoid respiratory depression. Give adequate
complications during sedation to obese and gediatric patient.
Keep Flumazenil (antidote for Benzodiazepine)
General Anaesthesia & Naloxone (antidote for Opiods) ready to
manage complications of over dosage.
1.1 Aspiration: 1.6 Nerve Palsies
Position the patient appropriately to prevent
Follow appropriate fasting guidelines.
pressure on the nerves.
Administer anti-aspiration prophylaxis like H2
blocker, Proton pump inhibitors, In prone position avoid pressure on eyes ball
Metoclopramide. Ondensatron, Granisatron. and avoid over abduction of arms to prevent
Brachial Plexus injury.
Intuba te by rapid sequence technique in full
stomach patients. In lateral decubitus position, keep axillary roll
beneath axilla to pr event Brachial Plexus injury.
1.2 Hypercarbia In lithotomy position, care must be taken to
Ventilate appropriately as hypoventilation is the avoid injury to the lateral popliteal nerve.
commonest cause.
1.7 Hypothermia and Shivering
1.3 Hypertension Increase theatre temperature (210C for adults &
Maintain good plane of anaesthesia. 280C for children).
Use opiods for adequate pain relief Use warm intravenous fluids.
1.4 Hypotension Use warm blankets and forced air warming to
Manage blood loss appropriately. combat hypothermia.
Preload the patient adequately before spinal Use IV Dexamethasone or IV Pentazocine or IV
anaesthesia. Tramadol to treat shivering.
1.5 Post Operative Apnoea:
Commonly due to over dosage or sensitivity of
Barbiturates, Opiods and inhalational agent and
inadequate reversal.

Page 570
 6. REGIONAL ANAESTHESIA
1. Indication:
For the production of local anesthesia
2. Dosage and Administration:
The dose is adjusted according to the response
of the patient and site of administration.
3. Contraindications:
Hypersensitivity knows to anaesthetics of the
amide type. Solution containing adrenaline is
contraindicated for anesthesia of fingers, toes,
tip of nose, ears and penis. Bupivacaine is
contraindicated for i.v. regional anaesthesia
4. Precautions:
Shock, heart block, known drug sensitivity,
liver disease, kidney disease, epilepsy, impaired
respiratory function.
5. Adverse Reaction:
Over dosage ma y cause CNS reaction:
Numbness of tongue, light-headedness
dizziness, and blurred vision, tremors, followed
by drowsiness, convulsions, unconsciousness
and possibly respiratory arrest. Cardiovascular
reactions of over dosage include hypotension
and myocardial depression.
Concentration dependent adverse reactions for Lignocaine
Plasma con. Mcg/ml
4 Light-headedness, tinnitus, circumoral numbness
6 Visual disturba nce
8 Muscle twitching
10 Convulsions
12 Unconsciousness
20 Respiratory arrest
24 Circulatory depression
Chart No.1 DRUG TOXICITY OF LIGNOCAINE
Methae moglobinaemia may be treated by the
intravenous administrations of 1% solution of
Methylene blue in a dose of 1mg/kg.
6. Treatment of over dosage:
Treatment of patient with toxic manifestations
consist of arresting convulsions and assuring
adequate ventilation with oxyge n, if necessary
by assisted or controlled ventilation (
respiration) if convulsions occur they must be
treated rapidly by intravenous injection of
Thiopentone 100 to 200mg. Alternatively,
Diazepam 5 to 10mg may be used and Intralipid
(1.5 mg/kg body weight.)
Once convulsions have been controlled and
adequate ventilation of the lungs e nsured, no
other treatment is generally required. If
hypotension is present. However a vasopressor,
preferably one with inotropic activity, e.g.
Ephedrine 15 to 30 mg. s hould be given
intravenously in diluted from titrated dose.
Anxiety or slight twitchng, a small intravenous
dose of Inj Diazepam,ma y be given carefully
and slowly; Oxygen s hould also be given. In
severe circulatory depression barbiturate such as
Thiopentone is contra-indicated when
convulsion has developed. Cardiovascular
collapse is treated with vasopressors & plasma
infusion, Inj intralippid
Adverse reactions
7. Local Anaesthetics:
Inj.Li gnocaine 2 % (3 to 4 mg/kg body
weight)
Inj. Lignocaine hydrochloride (2%) with
Page 571
 Adrenaline (5 to 7 mg/ kg
body weight)
Inj. Ropivacaine ( 0.75%) or Inj.
Bupivacaine (0.5 %).
8. Sedation:
Inj. Midazolam 0.05 mg/kg a nd Inj. Ketamine
0.5mg/kg and Inj. Propofol infusions in 25-
75mcg/kg/min range a nd deep sedation (50 to
100 mcg in drip for deep sedation)
9. Interscalene:
Success rate in posterior interscalene (Cervical
PVBs) approach is more than a nterior-lateral
approach
10. Spraclavicular
/Infraclavicular:
inferior-posterior quadrant of plexus for
Supraclavicular Block and Infra Clavicular
Block near posterior cord.
11. Sciatic (Infragluteal):
Infragluteal approach are more comfortable to
patients than classic Labat approaches.
12. Explanatory Footnotes on
Above Protocol:
12.1 Local Anesthetics:
For consistency, 0.75% ROPIVACAINE is
primarily used for blocks, with a dose of 20-
40ml depending on the type of block
ropivacaine results in 12-24 hrs block duration.
2% Lignocaine for 3-4 hour duration. Mixing a
short acting and long acting local anaesthetic
together appears to significantly decrease the
duration of the block.
12.2 Adjuncts:
1. De xamethasone 2-4mg and/or Clonidine
50-100ug for an average of 3-6 hour
increased duration
2. Epine phrine and Clonidine . Increase
duration of regional block .
3. Inj. De xamethasone . 4mg to 8 mg dose
as it may result in very prolonged blocks.
4. Bicarbonate . dose is 1meq/10ml. in Bier
Block.
Page 572
 7. CARDIO PULMONARY- RESUSCITATION
(CPR)
CPR consists of a series of maneuvers by which
oxygenated blood supply to brain and vital organs is
maintained during cardiopulmonary arrest (CPA) i.e.,
cessation of respiration and circulation. In children,
CPA is not sudden but end result of long period of
hypoxemia secondary to inadequate ventilation,
oxygenation or circulation. Therefore, prompt
management of these is essential to prevent CPA, the
outcome of which is poor.
1. Diagnosis of Cardiac arrest:
1. Absence of pulse in major arteries (carotid or
femoral in older children and femoral or brachial
in infants as carotid is difficult to palpate due to
short neck).
2. Absence of heart sounds on auscultation.
3. A systole / ventricular fibrillation on ECG.
2. Respiratory arrest:
Absence of respiration on looking (absent chest
movements), listening (absent air flow on bringing
ears in front of mouth) and feeling (absent air flow on
keeping hands in front of mouth or nose).
3. Levels of CPR:
There are two levels of CPR:
1. BLS (Basic life support) the elements of CPR
provided without additional equipment, skill and
speed are more essential.
2. ACLS (Advanced cardiac life support) Use of
equipment and drugs for assisting ventilation or
circulation.
3.1 Basic Life Support:
Call for help; position the victim supine on firm flat
surface with head level with the heart. As per New
AHA 2014 Guidelines ABC (Airway Breathing
Circulation) changed to CAB (Circulation - Airway
Breathing ) and chest compression and rescue breath
ratio is 30:2.
3.1.1 Circulation
Determine the absence of pulse after 2 breaths
(rescue breaths). External cardiac massage if asystole
and unresponsive to rescue breaths. In children,
perform cardiac massage if HR<60/min with signs of
poor perfusion.
3.1.2 Airway
Clear airway cleaning blood, secretions, foreign
particles (suction if available).
Prevent posterior displacement of tongue due to
muscle relaxation during CPA, by head tilt and chin
or jaw thrust (may use an airway if available). Head
tilt: Put a hand at forehead and tilt head back to
sniffing or neutral pos ition in an infant and little more
in older children and adults. (Caution: In a patient
with suspected cervical spine injury head tilt should
be avoided) Chin lift: Put finger of other hand under
bony part.
Jaw thrust: Place 2-3 fingers under each side of lower
jaw at its angle and lift jaw upward with the elbow
resting on the surface on which victim is lying.
3.1.3 Breathing
Determine the absence of breathing. Give mouth to
mouth / nose / mask / airway breath (may use bag and
mask if available). Inhale and then make a seal
around the mouth and nose together in infant and seal
mouth only in older children and adults (nose
pinched with the hand used for head tilt) to exhale
smoothly. Rate of breaths should be 20/min for
infants, 15/min in older child and 10-12/min in
adults.
Rescuer should stand or kneel at the side of the
patient so that his hips are on a level with the victims
chest.
In a newborn 2 thumbs are positioned side by side on
sternum just below the nipple line, with fingers
encircling chest and suppor ting the back and
compress sternum by 0.6 1.2 cm (120/min).
In an infant put inde x finger at the intersection of
intermammary line and sternum. Use 2 3 fingers
(index, middle and ring) to compress sternum by 1.5
2.5 cm (100/min) and do not lift the finger when
compression is released. Two thumb encircling
hands technique can also be used.
In children (1-8 years) use heel of hand on lower half
sternum with long axis of heel same as long axis of
sternum and compress 2.5 3.5 (100/min) In adults
the heel of one hand is placed on the lower sternum
and the other hand placed on top of the first. The
elbows should be locked in position with the arms
straight and the shoulders over the hands. Sternum
Page 573
should depress by 3.5 5.0 cm and the rate of
compression should be 80 to 100/min. (CAUTION:
Do not exert pressure on the ribs, costal cartilages or
xipoid)
3.1.4 Combination of ve ntilation and Cardiac
massage
If both cardiac and respiratory arrest Compression:
ventilation = 30:2 in adults and children > 8; Children
and infants 1-8 years = 5:1; Neonates =3:1.
3.2 Advanced Cardiac Life
Support (ACLS)
If ACLS facility is available, shift the patient to
ACLS as soon as possible. If this is not available then
continue cardiac massage till spontaneous HR is
more than 60-80/ min and continue Endotrachal
intubation with IPPV till adequate respiratory efforts
are present (good chest movement, no cynaosis or
shock). For ALCS proceed in the following order:
3.2.1 Procedures
I. ECG monitoring (if available)
a) If ventricular fibrillation defibrillation.
b) In adults, first shock at 200 Joules; if the first is
unsuccessful then a second shoc k at 200 -300 Joules.
If both fail, additional shocks at 300-360 Joules are
given.
In children, 2 Joules / kg and can be repeated a few
time (if does not revert to normal rhythm). Continue
cardiac, massage in the mean time.
c) All patients require oxygen (100%) because even
with best CPR, only a fraction of the cardiac output is
provided and also there are other factors causing
ventilation perfusion mismatch.
d) Establish IV line as early as possible to give drugs
and fluids and intubation of trachea should be done to
continue artificial ventilation.
3.2.2 Drugs are used in the
following order if indicated.
a) Inj. Adrenaline
Indication: A systole symptomatic bradycardia
unresponsive to ventilation. In adults: 1 mg IV every
3 5 minutes. In children : 0.1 ml/kg of 1:10,000
solution (0.01 mg/kg) IV, intra-osseous or 0.1 ml/kg
of 1:1000 solution by endotracheal tube followed by
several positive pressure breaths. Can be repeat every
5 minutes by either route. IV route is preferred and
should be used as soon as IV access is achieved
(Intracardiac route is not desirable).
b) Inj. Lignocaine
Indication: Ventricular tachycardia or fibrillation non
responsive to recurs after defibrillation. In adults:
Initials bolus dose is 1.5 mg/kg. Additional bolus of
0.5-1.5 mg/kg can be given 5-10 minutes during CPR
up to a total dose of 3mg/kg. In children: Inj. 1mg/kg
IV stat followed by infusion at 20-50 mcg/kg/min.
c) Inj.Amiodarone
Indication: Refractory shock with ventricular
fibrillation (as an alternative to or after failure of
Lignocaine). In adults : Initially 300 mg rapid
infusion in 20-30 ml saline followed by 150 ml over
10 minutes followed by 1 mg/min for up to 0.5
mg/kg/da y.
d) Inj. Atropine
Indication: Vegally mediated bradycardia during
intuba tion, HR<80 or asystole in an infant and
symptomatic bradycardia with AV block in any child.
Dose and route : 0.02 mg/kg bolus (not <0.1 mg or>
0.5 mg for a child and 1.0 mg for an adult) This dose
may be repeated after 5 minutes for a maximum total
dose of 1.0 mg for a child and 2.0 mg for an adult.
e) Inj. Naloxone
Indication: Narcotic overdose or poisoning and
newborn resuscitation (if mother has been given
Morphine or Pethidine during labour). Dose and
route 0.1 mg/kg IV.
f) Inj. Sodium Bicarbonate (NaHC03)
Not required routinely as it can cause alkalosis later
and worsen respiratory acidosis by releasing CO2 in
inadequate ventilation. Indication : Hyperkalaemia,
significant metabolic acidosis (pH<7.2) or prolonged
CPR. In adults and in children : Inj. Sodium
bicarbonate 1 mEq/kg stat and 0.5 mEq/kg every
10minutes in protracted resuscitation.
g) Inj. Calcium
Indication: Not used routinely now a days unless
there is hyperkalemia, hypocalcaemia or calcium
channel blocker toxicity. Dose and route : (in
children) 0.5 ml/kg of Calcium gluconate IV. In
adults 10 ml to be given as a slow infusion under
ECG monitoring.
h) Inj. Glucose
Indication Hypoglycaimia Dose and route : - 0.5-1
g/kg IV. Try to get ABG, serum electrolytes and
Page 574
blood suger (dextrose stick /glucometer) post
resuscitation care.
Maintain mechanical ventilation for several
hours to ensure adequate oxygenation and
ventilation.
Look for and treat seizures.
Inj. Mannitol 0.5 -1 g/kg IV if raised intracranial
tension.
Maintain temperature, fluid and electrolyte
balance and ABG.
Treat shock with fluids, dopamine, dobutamine
and adrenaline infusion as required.
Treat the underlying pa thology causing CPA.
3.2.3 Monitoring
Pulse should be palpable and chest expa nsion should
be seen during effective CPR, blood pressure, Sp02,
ET CO2 (In intubated patient and if facility
available), ABG should be monitored during and
soon after CPR.
3.2.4 Termination of CPR
If asystole persists for >10 minutes after CPR has
been performed, ventricular fibrillation eliminated,
and confirmed, adequate ventilation provided and
appropriate medications given.

3.2.5 Summery of CPR

Table 1: CPR GUIDELINES FOR HEALTH CARE PROVIDERS

(Method, compression rate, and ventilation to compression ratio)

Adult Child Infant Newborn
(<8 yr) (< 1 yr)
Lone If known asphyxia arrest, 5 5 cycles of CPR Ventilation priority,
Rescuer cycles unless sudde n compressions for HR<60,
Priority CPR witnessed collapse
Compression 1-hand 2-thumbs 2-thumbs
method Or Or 2-fingers or 2-fingers
2-hands 2-Hand If single for access to
Rescuer umbilical vein

Compression Rate 100/min 100/min 100/min 200/min

Ratio of 30:2 until intubated. 30:2 until intubated. 30:1
compressions to 8-10 breaths/min 8-10 breaths/min
ventilations After ET. After ET.
Use of AED Immediate AED Immediate AED Consider No
Consider 5 cycles 5 cycles CPR if >4-5Min Recommendation
CPR if > 4-5 min Unwitnessed Arrest. (for infant &New Born)
Unwitnessed arrest

Page 575
 PULMONARY EDEMA

Assist breathing as needed oxygen

Take blood pressure Begin working on IV line Cardiac monitor

Is arrhythmia the cause?

Due to Bradycardia? Due to tachyarrhythmia?

Bradycardia Algorithm Tachycardia Algorithm?

Sublingual Nitroglycerin 0.4 mg

Inj. furosemide 0.5-1 mg/kg IV
Propped position

Consider also:
Albuterol aerosol
positive airway pressure

Not responding?
Nitroprusside 0.1-5 mcg/kg/min
OR
Nitroglycerin 120-20 mcg/min

Consider intropic
support

Still in distress?
Consider intubation

Systolic BP>100? Systolic 70-100 or signs of shock?

Dobutamine 2-20 mcg/kg/min Dopamine 5-15 mcg/kg/min

Page 576
 8. ANAESTHESIA OBSTETRIC PROTOCOL
1. Orientation
Labour room and the operation theatre should be
connected with each other. All the anaesthetic
equipments and preparations should be ready 24/7
days apart from it. Laryngoscopes with stubby handle
and McCoy blade should be available. NICU and
prenatal ICU should be on the same floor. Emergency
drugs and plasma expanders (e.g. hetastarch &
voluven) should be present in the O.T. Blood and
blood products should be available at nearest possible
place. Aanaesthesiologist should check for
anaesthesia machines, defibrillator, Oxygen, other
equipments and the required dr ugs.
2. Labour analgesia with
epidural technique
2.1 General Aspects
i. Proper pre-operative evaluation with
counselling of the patient and the relatives.
ii. Explaining the procedure and its adva ntages
and disadvantages.
iii. Secure broad gauge I.V. cannula with starting
I.V. with crystalloid for preloading.
iv. Epidural catheter inserted with standard
technique in lateral or sitting position under
aseptic precautions at L3-L4, OR L4-L5 space.
No CSE should be performed above L1 level.
v. The catheter should not be more than 2 to 3
cms inside the epidural space. Check for any
fluid coming out of the catheter.
vi. Can give the analgesic dose of local
anaesthetic agent, preferably 0.125% of
Bupivacaine about 8 ml with 2mcg / ml of
fentanyl can be give n.
vii. The dose can be repeated as per the patients
demand. The pt. should be haemodynamically
monitored closely till the end of delivery.
viii. If interve ntion needed then continue the
epidural anaesthesia with higher conc. of
Bupivacaine i.e. 0.5% around 8 to 10ml. can
be given for LSCS.
2.2 Complications
Epidural-Bloody Tap
Patchy action or unilateral block
Subdural Block
3. Antacid Prophylaxis
All patients for elective Caesarean section must
receive oral antacid premedication. If the patient
posted for an emergency Caesarean section then
consider IV Metoclopromide 10mg, Inj. Ondensetron
4mg, IV Ranitidine 50mg, Emptying the stomach
with a large orogastric tube, keep it until patient
anaesthetised and up to e xtuba tion.
4. Regional Anaesthesia for
Caesarean Section
4.1. Advantages:
The avoidance of the hazards of aspiration of gastric
contents and failed intuba tion during general
anaesthesia. A reduction in blood loss /
thromboembolism/absence of Neonatal depression.
Postoperative analgesia may be provided using spinal
or epidural opioids.
4.2. Disadvantages:
Hypotension can occur due to aorto-caval
compression despite the use of left uterine
displacement and seemingly adequate preload.
4.3. Nausea and vomiting:
The incidence of this is often related to hypotension
and hence should be treated immediately. Nausea
following a regional block is an indication of the B.P.
fall. Consider giving 100% oxygen and legs up
position before iv Ephedrine. Use Oxytocin for
uterine contraction.
Diclofenac-
Do not administer Diclofenac to those allergic to
NSAIDs. Do not give it to unstable asthmatics. Also
avoid in those with renal dysfunction, peptic ulcer
disease and severe pre-eclampsia especially if
oliguria or thrombocytopoenia.
5. General Anaesthesia for
Caesarean Section
5.1 Pre operative assessment:
Thorough pre-operative assessment. 1. Antacid
prophylaxis. 2. NBM status. 3 informed consent
from relatives 4. Make arrangement for blood and
blood products 5. Patients should be transferred to
Page 577
 theatre in left lateral position. 6. Administer Sodium
citrate prior to pre-oxygenation. 7. IV access 14G or
16G cannula. 8. Position of the mother supine on the
table with 15 degree left lateral tilt with slight head
up. 10. Pre-oxygenate the mother using 100%
oxygen for 3 minutes unless there is severe maternal
and foetal emergency. 10. ECG,NIBP and pulse
oximeter during pre- oxygenation and ETCO2 is
switched on. 11.Perform RSI using Thiopentone 5-6
mg/kg and Suxamethonium 1.5mg/kg. Intubate after
adequate action of Suxamethonium
Ple a se re me mbe r - patie nts die from
prolonge d atte mpts to intubate le ading to
hypoxia and from unre cognise d oesophage al
int ubation and not from failure to intubate .
"If in doubt, take it out" Ensure that the ETT is
correctly placed by observing the capnograph trace
and by listening to breath sounds. Give Atracurium
when Suxamethonium action wears off.
5.2 Intubation Hints:
i. Optimise the patient's position. A smaller ETT is
often needed in obstetrics. An unexpected
invisible larynx is often due to incorrectly
applied cricoid pressure. And short stubbed
laryngoscope or polio blade. An anterior larynx
just out of reach of the ETT can usually be
cannulated with a well lubricated gum elastic
bougie.
6. Anticoagulation and
regional anaesthesia
i. The incidence of epidural haematoma is less
than 1: 100,000
ii. NSAIDS are not a contraindication to CNB.
iii. Enoxaparin 40mg sc post-operatively.
iv. If the woman is on antenatal
thromboprophylaxis. a) Enoxaparin should be
stopped 12 hours prior to performing CNB. b)
Epidural catheters should be removed 2 to 4
hours prior to administration of Enoxaparin
v. Heparin a) Heparin should be stopped 4 hours
prior to attempting neuraxial blockade or
removal of epidural catheters. b)
Unfractionated Heparins should not be
administered for 2 to 4 hours after catheter
removal.
7. Management of a Dural tap
Don't pa nic! Place you thumb against the hub of the
Touhy needle, relax and think. You have 2 options: a)
Can give 0.5% Bupivacine 2 2.5 CC intrathecally
and do LSCS under spinal anaesthesia b) Insert
epidural catheter intrathecally. Approximately 2cms
should be threaded into the subarachnoid space. c)
Remove the Touhy needle and insert at a different
level. Don't perform a CSE. Intrathecal catheter - top
up only by the anaesthetist. You can administer
either: 1ml 0.25% Bupivacaine + 15-25g of
Fentanyl as regular top up. Or 0.5 - 2ml of standard
LDM as regular top up. After delivery remove
catheter as usual. If epidural in situ treat as normal
intrathecal epidural, but each top-up to be given by
anaesthetist under strict aseptic conditions.
8. Central Neural Block
8.1. Indications:
Labour analgesia. Anticipated difficult or operative
delivery (e.g. multiple pregnancy, breech, premature
foetus). Obstetric disease (e.g. pre-eclampsia).
Maternal disease (e.g. specific cardiac, respiratory or
neuromuscular disease). Surgery during pregnancy
8.2. Contraindications:
This list contains both absolute contraindications:
Patient Objection. Local Sepsis, Coagulopathy
Relative contraindicat ions- Haemorrhage
with hypovolaemia, Raised intracranial pressure,
Some forms of anticoagulant therapy, Disease of the
nervous system, Gross spinal deformity, Systemic
sepsis, Severe foetal distress.
8.3. Central Neural Block - Special
Considerations
Low Platelet Count: A platelet count of <50000
is an absolute C/I to a regional block.
Enoxaparin /L MWH: Many patients at risk of
venous thrombos is are on daily sub cutaneous
Enoxaparin.
Unfractionated Heparin (UH): If UH has been
given, wait 4-6 hours before siting an epidural
block. Remove the epidural catheter at least 4
hours after the last dose of UH.
Aspirin: Patients on aspirin can have a regional
block. A bleeding time is not required.
Pre-eclampsia (PIH): Patients with mild to
moderate PIH should have a recent (within 24
hrs) platelet count before a regional block.
Maternal Pyrexia: Administer antibiotics.
Haematological Disorders: The most common
type of patient presenting for regional
blockade are Haemophilia Carriers and
patients with Von Willebrand's Disease.
HIV: HIV is not a Conba Indications to a
regional block nor indeed to a blood patch.
Page 578
 Standard high risk precautions should be
taken when instituting a block. Consider
double glove protection / eye protection / do
not resheath needles when performing a
block.
Prolapsed Intervertebral Disc (PIVD)
Epidural or spinal analgesia / anaesthesia are
not contraindicated.
Harrington Rods / Spinal Instrumentation
Many of these patients have severe scoliosis
with consequent cardiorespiratory
compromise. The surgical site should be
avoided. The epidural needle should be
advanced towards the convexity of the curve.
Multiple Sclerosis (MS) MS is a CNS
demyelinating disease with an incidence of
1:10,000. It is a disease of relapse and
remission.
9. Placenta Praevia
9.1. Anaesthetic management:
Ensure adequate IV access (2x 14 or 16G
cannulae)
Two anaesthetists preferable if Grade 4,
previous praevia or previous LSCS; this is
mandatory if proceeding under regional (see
below).
Manage major haemorrhage according to
guidelines.
Anaesthetic technique - considerations:
9.2. Action:
9.2.1 Ensure adequate airway / conscious level.
Give high flow oxygen.
9.2.2 At least 2 peripheral lines will be needed of
not less than 14- 16G. If the decision is made
to set up invasive monitoring, it must not
interfere with resuscitation.
9.2.3 Prevent aorto caval compression.
9.2.4 Take at least 20ml of the patient's blood for:
Blood grouping / cross matching
Full blood count
Coagulation studies (including fibrinogen /
FDP's if abruption or other cause of DIC
suspected).
9.2.5 Blood Transfusion
a) Order a minimum of 4 units of blood.
b) All patients should be given blood of their
own group as soon as possible. However for
patients with severe haemorrhage,
uncrossmatched group O, Rh negative can be
lifesaving.
c) The principles of intelligent management are:
While blood is gushing out it is useless and
wasteful to give clotting factor or platelet
replacements. Once surgical haemostasis has
been more or less achieved, continued oozing
may be due to blood clotting factor
deficiencies. Further blood samples should be
sent for coagulation screen and platelet count.
d) If there is massive blood loss the MASSIVE
TRANSFUSION PROTOCOL should be
instigated. This will ensure that FFP is
available and platelets are ordered. While FFP
can up to a point be issued "blind" as already
mentioned, the possibility of low platelets or
DIC may need different blood components for
their correction. This can only be identified by
laboratory testing.
e) A pressure bag system is essential in order to
infuse fluids rapidly.
f) Use a blood warmer as soon as possible.
g) Blood filters are NOT needed and will slow
dow n transfusion.
h) Early use of CVP monitoring and direct
arterial pressure monitoring.
i) Think ahead to order blood and blood
products in plenty of time.
j) Use the Hemocue (available in Theatre) to aid
estimation of transfusion requirements.
9.2.6 Measure the patient's temperature.
9.2.7 Additional Calcium is rarely needed and only
if there is evidence of a calcium deficiency.
10% calcium chloride is preferable to calcium
gluconate.
9.2.8 Treatment of the cause may involve delivery
of baby and placenta, repair of lacerations and
administration of oxytocics (Oxytocin
Ergometrine; 15- methyl PGF2a [Carboprost -
Hemabate]; PGE2 [Misoprostol].
9.2.9 All patients with more than moderate
continuing haemorrhage need proper
monitoring of pulse rate, CVP, blood gases,
and urinary output as well as dedicated care by
the midwifery and medical staff. Serious
consideration should be given to the potential
adva ntages of transfer to a n HDU.
Page 579
 9. SPINAL ANAESTHESIA
1. Definition:
Spinal anesthesia is produced by introducing a Hyper
local anesthetic into cerebrospinal fluid in the
subarachnoid space result in to loss of sympathetic
tone, sensation and motor function.
Sympathetic block is 2-3 segments higher than the
sensory and the motor block 2-3 segment lower than
the sensor y block.
Position 1) Sitting 2) lateral
2. Approach - Median and par
median.
2.1 Saddle block given in sitting
position by hyperbaric
anesthetic drug.
Spinal cord usually ends at the level of L2 in adult
and L3 i n children.
Important land mark is that line joining the top of the
iliac creast corresponds to L4-5
2.2 Practical implication-
While administering spinal anesthesia spinal needle
pierce 1) Skin 2) Subc utaneous fat 3) Supraspinious
& Interspinious ligament 4) Ligamentum flavum 5)
Epidural space 6) Dura 7) sub arachnoid space.
Patient is adequately prepared, with the procedure
fully explained, has reliable intravenous access, is in
a comfortable position and resuscitation equipment is
immediately available.
To be done under all aseptic precaution. Read the
label.
Patient should be well hydrated and NRM at list 6
hrs.
Strict intra operative vital parameters monitoring is
mandatory. Height of analgesia is directly
proportional to curvature of spinal column and
volume of drug, specific gravity, force and rate of
injection, barbotage technique.
Small bore needle make smaller hole in the dura i.e.
separate caudafilum and are associated with a lower
incidenc of headache than conve ntional cutting edge
needle.
Pre existing neurological deficit has to be
documented i.e. Diabetic neuropathy, Hansons
disease, Traumatic neuropathy
2.3 Drugs used for spinal anesthesia
HEAVY-
1) Inj.Lignocaine 5% solution 2)Inj.Bupivacaine
0.5% solution 3) Inj. Ropivacaine 0.75% solution
with adjuva nt-1) Inj.Clonidine 2) Inj.Buprigesic
2.4 Advantages
1) Economical 2) Minimum equipment required 3)
Control hypotension and bradycardia reduces the
bleeding at the site of surgery 4) less respiratory
infection 5) Less incidence of thromboembolic and
pulmonary complication 6) Useful in sickle disease /
trait and in Diabetic patient (Less stress related
hyperglycemia )
2.5 Contraindications
2.5.1 Absolute
Allergy to local anesthetics, Local infection at needle
insertion, Increased intracranial pressure (herniation
of brain stem)
2.5.2 Relative-
Hypovolaemia, Anticoagulation treatment, Systemic
sepsis, Neurological diseases- multiple sclerosis,
tabes dorsalis, syringomyelia, amyotrophic lateral
sclerosis, Tumors of the spine, Airway compromise,
Low back pain and peripheral neuropathies,
haemorrhagic CSF.
2.6 Complications-
2.6.2 Peri-operative
hypotension due to vasodilatation and brady-cardia
due to increased vagal tone as a result of sympathetic
blockaed, Respiratory insufficiency due to intercostal
blockde, Poor anaesthesia because of loculations of
arachnoid.
2.6.3 Post- Operative-
Page 580
Headache due lo leakage of CSF or aseptic
inflammatory reactions, Urinary retention, Backache,
Infection,- Meningism, arachnoiditis, transverse
myelitis or the cauda equine syndrome with varying
patterns of neurological impairment and sphincture
disturbances. Para-paresis and rarely paraplegia due
to the anterior spinal artery syndromei.e initially be unable to talk louder that a whisper and
prolonged vasospasm of the anterior spinal artery by
the vasoconstrictor adjutants or due to prolonged
uncorrected hypotension.
2.7 Treatment-
1 Hypotension Nausea and vomiting may be the
first sign of hypotension .Give adequate I.V.Fluid
Oxygen by mask, increasing the patients circulating
volume is by raising their legs, Vasopressors drug
one Inj. Ephedrine 30 mg (6mg/cc) Inj.
Phenylepinephirine. Inj Noradrenaline, Infusion.
(titrated)
2.7.2 Total Spinal -
Needs to be quickly recognized and treat patient will
will then stop breathing. These patients have to be
intubated and ventilated until the local anaesthetic
effect wears off and also maintain the hemodynamic
stability.
2.7.3 Headac he post dural puncture headac he
(PDPH)-
Encouraged to drink water, give intrave nous fluids to
maintain adequate hydration, strict bed rest,
Paracetamol, Aspirin or Codeine tea, coffee, epidural
blood patch, Tab. Samaritan.
Page 581
PATHOLOGY

Page 582
 1. INTRODUCTION

The Pathology department basically deals with

diagnosis of disease by means of various types of
3) Section III
tests performed on body fluids, blood and tissues. Biochemistry section:
It is divided into 4 Sections: It deals with different types of biochemical terms
to detect functions of liver, kidneys, Lungs, heart
etc.
1) Section I
Haematology section: 4) Section IV
Inwhich the blood e xamination and Urine and
Stool examination done to detect any Histopathology
abnormality like anemia,leukemia, Renal &Cytopathology:
Infection and bow el infection and infestation
In this section mainly tissue cell morphology is
studied to detect infection/tumor in body.
2) Section II
Serology section:
It deals with the Rapid terms to detect
M.P.,typhoid,V.D.,H.I.V.etc.along with
blood culture to detect typhoid etc.

Page 583
 2. HAEMATOLOGY SECTION
1. Specimen Collection:
Every specimen must be accompanied by a request
slip, which should indicate date, patients full name,
age and sex, hospital identification number, name of
referring doctor, provisional diagnosis, kind of
specimen, laboratory services and equipped, exact time
the specimen was obtained and the name of the person
who collected the specimen with signature. It is
necessary that the request slip be complete and clearly
written. Incomplete information may lead to total loss
of the report.
Specimens should be processed as early as possible.
Temporary storage in refrigerators is advisable except
for C.S.F. and specimens submitted for bacteriological
cultures. Urine and other body fluid should be
processed as early as possible (Before 2 hrs.) as delay
causes disintegration of cells and loss of morphology.
Blood is one of the most common specimens studied in
laboratories. Blood will clot within few minutes after it
is removed from the body unless an anticoagulant is
used.
1.1.1. Whole Blood:Blood with anticoagulant is called
whole blood.
1.1.2. Plasma: Fluid portion of unclotted blood is
called plasma and is obtained from anticoagulated
blood.
1.1.3. Serum: Fluid portion of clotted blood and is
obtained from clotted blood, which is collected without
any added anticoagulant.
1.2. Anticoagulant:
The anticoagulant prevents the blood from clotting.
Most of anticoagulants remove calcium. Which is one
of factor required for coagulation.

1.1. Blood:
Table 1: Various types of bulbs & its uses

Sr. Type of bulb Content(Anticoagulant) Used for

No.
1 EDTA Na and K salt of EDTA Routine Haematological work
2 Trisodium Citrate Sodium Citrate ESR
3 Heparin Heparin PCV, Osmotic Fragility test
4 Double Oxalate mixture NH4 and K Oxalate CBC, Blood Group
5 Sodium Fluoride Na Fluoride and K Oxalate Sugar

1.3. Vaccutainers:
These are plastic tubes with coloured cap with capacity
of3-5ml blood used in laboratory now a days. These
may be with or without vacuum.(The small glass
bottles can also be used for sample collections after it
is properly prepared). The colour of the cap indicates
the presence of anticoagulant present inside the tubes.
The label is attached with the tube for patients
identification. Following are the types and uses.
1.3.1. RED Cap No chemical for serum separation
(Biochemistry and Serological test)
1.3.2. GREY Cap: Sodium fluoride + Pot oxalate for
glucose estimation
1.3.3. PURPLE Cap: Potassium EDTA for CBC, Hb,
TLC, DLC, PBS (Peripheral Blood Smear),
Reticulocyte count, ESR
1.3.4. LIGHT BLUE Cap: 3.2% sodium citrate for
coagulation studies (PT, APTT, TT, FDP, D-Dimer,
Factors VIII & IX assay)

Page 584
2. Hemoglobin Estimation 2.2. Principle
When blood is added to N/10 HCL, Hb is converted to
2.1. SAHLI`S (Acid Haematin) brown coloured acid Haematin. The resulting colour
Method after dilution is compared with standard brown glass
This method used in small laboratories at PHC level. reference blocks of Sahlishaemoglobinometer.

Table 2: Haemoglobin estimation according to Sahli's method

Sr.
Test Name Methods Normal Value Interpretation
No.
1 Haemoglobin a) Sahlis Method Male 13-18gm/dl Mild Anaemia up to 10gm%
b) Hemocue Method Female 12-16.5gm/dl Mod. Anaemia up to 8 gm%
c) Cellcounter Method Pregancy 11-14gm/dl Severe Anaemia below 7gm%
Raised Hb- Polycythaemia

Table 3: WHO classification for Anaemia

Population Non Anae mia Anaemia(Haemoglobi n in grams per litre)

Mild Moderate Severe
Children 6 - 59 months of age 11 or higher 10 - 10.9 7 - 9.9 Lower than 7
Children 5 - 11 years of age 11.5 or higher 11 11.4 8 - 10.9 Lower than 8
Children 12 - 14 years of age- 12 or higher 11 11.9 8 - 10.9 Lower than 8
Non-pregnant women (15 years of 12 or higher 11 11.9 8 - 10.9 Lower than 8
age and above)

Pregnant women 11 or higher 10 10.9 7 - 9.9 Lower than 7

Men (15 years of age and above) 13 or higher 11 12.9 8 - 10.9 Lower than 8

3. Leucocyte count: 3.2. Automated Differential

3.1. Peripheral blood smear: Leucocyte Counting:
This system is able to replace manual differential
Preparation and staining of peripheral blood film is
leucocyte count to a great extent. When any abnormal
performed for doing total leucocyte count (TLC) and
cell count or abnormal morphology of cells in seen,
differential leucocyte count (DLC).
this system shows a flagging thereby suggesting a
visual count mandator y in such cases.

Page 585
 Figure 3: Various types of White blood cells

Sr.
Test Name Methods Normal Value Interpretation
No.
2 Total Leucocyte Manual by counting 4000-11000/cells mm Raised TLC in viral Bacterial -
count TLC Infections, Leukemia's
Cell counter method
Decreased TLC - Septicemia,
Enteric fever, Aplastic Anemia.
3 Differential Cell Counter Polymorphs 40-65% Raised in Acute Bacterial
Leucocyte count Infections.
(DLC) Manual by staining Lymphocytes 20-35% Raised in chronic infection like
Slides tuberculosis, leprosy
Eosinophils - 2-4% Raised in worm infestation,
allergic skin infection, Tropical
Eosinophilia -
Monoc ytes - 2-8% Raised in viral infection
Basophils - 0-1% Raised in Leukemia's

erythroc ytes in a given interval of time is the ESR

4. Estimation of erythrocyte (erythrocyte sedimentation rate).
sedimentation rate (ESR): Stages in the ESR three stages in the ESR can be
observed:-
4.1. Principle: i. In the initial 10 minutes, there is rouleaux
When well mixed anticoagulated blood is allowed to formation.
stand undisturbed in a vertical tube the erythroc ytes ii. For about 40 minutes, sedimentation occurs at a
tend to sink to the bottom. Two layers are formed the constant rate.
upper plasma layer and lower one of red blood cells. iii. Sedimentation slows in the final 10 minutes as
The length of fall of the top of the column of cells pack at the bottom of the tube.

Page 586
 Sr.
Test Name Methods Normal Value Interpretation
No.
4 ESR Wintrops Tube Method Male 0-10 mm at 1 hr. Raised in chronic infection like
Westergren tube Method Female 0-20mm at 1 hr. tuberculosis, leprosy, chronic
anemia.

4.2. Interpretation or clinical 6. Clotting time:

significance of ESR:
The whole blood clotting time is one of the simplest,
ESR is markedly elevated in monoclonal blood protein
imprecise, methods to determine the efficiency of the
disorders, such as multiple myeloma or
clotting process. Many conditions can disrupt the
macroglogulinemia, polyclonalhyperglobulinemia, due
pathways that produce a clot, including hereditary
to inflammatory disease and in hyperfibrinogenemia.
disorders, liver disease and drugs that interfere with the
Moderate elevations are seen in active inflammation
normal function of platelets and coagulation factors.
such as rheumatoid arthritis, chronic infections such as
tuberculosis, collagen diseaseand neoplastic disease.
Although ESR is a non- specific phenomenon, this an METHODS:
indicator of the presence of an active disease. If patient i. Capillary tube method
is improving ESR tends to fall. It provides an index of
ii. Lee and white method
progress of diseases such as TB, rheumatoid arthritis. It
is also a useful screening test in routine examination.
An elevated ESR occurs as an early feature in Normal Range for clotting time 5-10 minutes.
myocardial infarction.
ESR is especially low in (0-1 mm) polycythaemia, 7. Prothrombin Time:
hypofibrinogenemia, CHF, and sickle cell anaemia.
PT test is an indicator of the efficiency of common
5. Bleeding time: pathway and extrinsic coagulation pa thway, in which
This test measures the time taken for blood vessel preformed thromboplastin is added to the test plasma
constriction and platelet plug formation to occur. No in the presence of calcium and the time taken for
clot is allowed to form, so that the arrest of bleeding clotting of plasma is noted. The main factors involved
depends exclusively on blood vessel constriction and in the pathway are V, VII, X, II and I. Deficiency of
platelet action. This is one of the most important any one of them leads to prolongation of PT. The PT
preliminary test for bleeding disorders and test is used to monitor patients taking certain
preoperative investigation in patients going for medications (e.g. Control of anticoagulant therapy) as
surgery. well as sensitive to the presence of heparin in blood
The duration of bleeding from a standard puncture and to low fibrinogen levels.
wound of the skin is a measure of the function of
platelets as well as the integrity of the vessels wall.
Commonly used methods are: Dukes Method &Ivy's
Method.

Bleeding t ime is prolonge d in:

i. Thrombocytopenia (Dengue Fever) - DIC
(Disseminated Intravascular Coagulation)
ii. Acute Leukaemia - Von Willebrands disease
iii. AplasticAnaemia - Aspirin intake

Page 587
 Sr.
Test Name Methods Normal Value Interpretation
No.
5 Bleeding Time Duke's Ivy's Method 1-5 min Raised in Coagulation defect,
B.T. vasoculotoxic snake bite, rat
poisoning, Hemophilia's, ITP.
6 Clotting Time Capillary method 4-9 min
C.T.
7 Prothrombin Time Quicks method or 12-16 sec
P.T.
Semi- 12-16 sec Raised P.T. (factor no. II V, VII,&
automatedcoagulometer X)

8. Test for sickle cell anaemia

Sickle cell test is done for all ANC patients, forall Initially the patients are screened by Solubility test. If
population in tribal area & also done for all patients of Solubility test comes positive, then it is confirmed by
severe anaemia. Hb Electrophoresis.
Sr.
Test Name Methods Normal Value Interpretation
No.
8 Sickle cell Solubility test or Sickle (Hbs) Present & less than
Anemia Hemoglobi n 40% is sickle cell trait or
Electrophoresis test or
(Hbs) is carrier
HPLC method nor mally absent
Hbs more than 40% is
sickle cell disease
Laboratory Tests
1. Routine screening tests (in any haematology 8.1. Sickling test
laboratory) Na Metabisulphite is used
2. Definitive or special tests (in reference laboratory)
Cells form sickle shape under low Oxygen tension
Laboratory testing
3. Screening tests Homozygotes 1 hour at 37 C
4. Sickling test
Heterozygotes longer time
5. Solubility test

Figure 2 Sickling Test showing sickle cell

Page 588
8.2. Solubility Test Working solution : 10 ml of stock solution + 0.1g
Na dithionate just be fore use
Reagents : Phosphate Buffer (pH 7.1)
Procedure : 20 ul RBCs (washed) + 2ml working
Stoc k solution : KH2PO4 125 g solution
K2HPO4 217 g Read after 10 minutes
Saponin 2.5 g
DW gsp 1 litre

Figure 3 Solubility Test

8.3. Confirmatory Test by ii. The detection of metabolic or systemic disease

Electrophoresis
Confirmatory test for HbS after Hb electrophoresis
Reason: Sensitivity is 93% compared to HPLC
Cannot differentiate between Hb AS & HBSS
Preliminary test in remote area but confirmation
must be done by HPLC or Hb electrophoresis
URINE EXAMINATION
The urine examination is referred to as a liquid tissue
biops y of the urinary system
It is useful in -
i. Diagnosis and management of renal or urinary
diseases.
not directly related to the kidneys.
iii. Microscopic examination of the sediment may
indicate the kind of lesion present or the state of
activity of a lesion.
1. Collection of Urine:-
For routine work 15 ml or more is preferred and it
should be collected in a clean container, after properly
cleaning the external genital area to avoid vaginal
secretions and cellular debris of the urethral meatus.
2. Specimen Evaluation:
This includes proper labelling (name, date and time of
collection), proper specimen, proper receptacle, storage
condition, preservative (Thymol, formaldehyde if
added)

Page 589
3. Physical Examination: Green+
Following parameters are looked for:
Greenish Blue++
i. Quantity
Blue+++
ii. Colour.
Deep Blue++++
iii. Appearance
5. Microscopic Examination:
Character. Examination of urinary sediment the specimen
should be examined while fresh since casts begin to
iv. Odour
lyse within 1 to 3 hrs. Mix the specimen well. Take 10
v. Specific gravity ml of urine in centrifuge tube, centrifuge at 2000
rotation /min for 5 minutes. Remove the supernatant.
4. Chemical examination Place a drop of sediment of slide and put a cover slip.
i. Test for Proteins Examine under both low power & high power
ii. Reducing Substances in Urine(Urine for Sugar) Cells RBC, WBC, Epithelial cells.
iii. Ketone Bodies Cast - Hyaline, granular, epithelial, WBC cast, RBC
cast, Fatty, waxy.
iv. Bile Pigments
Crystal and amorphous chemical deposits
v. Bile Salts
Miscellaneous Mucus, spermatozoa, bacteria, yeast,
parasite
4.1 Benzidine Test (for occult blood)
Compare the urine strip results with the colour on
Results: Faint Green-Trace bottle

Table 1:Urine Examination

Finding Interpretation

A ROUTINE EXAMINATION

1 Physical examination

1.1 colour Yellow, redish Yellow in Hyperbilirubinema, red in Hematuria

1.2 appearance - clear / turbid Turbid in UTI, Nephrotic syndrome, Preeclampsia, Eclampsia.

2 Chemical Examination

2.1 Albumin - +/- UTI, Nephrotic syndrome, Preeclampsia, Eclampsia

2.2 Sugar - +/- Diabetes, Hyperglycemia

2.3 Ketone bodies - +/- Present in starvation, Diabetic ketoacidosis.

2.4 bile salts & Bile pigment - +/- Present in Hyperbilirubinema,

B Microscopic Examination

1 No of RBCS / HPF Hematuria, renal calculi, nor mal menses

Page 590
 2 No. of Pus cells/ HPF UTI

3 No. of Epithelial cells /HPF Normally present

4 Casts - Present /Absent Nephropathy

5 Crystals - Present / Absent Present in Calciurea (OxalatePhosphate,Ureate crystals)

6 Trichomonas - Present / Absent It is motile parasite

7 Spermatozoa - present /absent Present in contamination with semen

8 Bacilli - present / absent UTI

9. Detection of Malaria Parasite 2. Interpretation:

In case of positive test, band for respective kind of
byMalarial Antigen test (RDK) malaria is visible.
Malaria is serious, sometimes fatal, parasitic disease
characterized by fever, chills and anemia caused by a In case of negative test, band is absent.
parasite that is transmitted from one human to another
by the bite of infected Female Anopheles Mosquitoes. 3. Peripheral blood smear for
There are four kind of malaria that can infect humans: Malarial Parasite
Plasmodium Falciparum, Plasmodium Vivax,
Plasmodium Ovale and Plasmodium Malaria. Specimen collection by using Lancet

1. Principle:
Malaria antigen kit contain a membrane strip which is
pre-coated with one monoclonal antibody and one
polyclonal antibody as two separate lines across
attached strip. One monoclonal antibody (test line PF)
are specific to the HRP-II (Histidine Rich Protein- II,
Specific to Plasmodium Falciparum) and other
polyclonal antibody (Test Line PAN) are Pan specific
to the Lactate dehydrogenase of plasmodium species
(P. Falciparum, P. Vivax, P.Malariaeand P.Ovale).
Pierce tip of finger with sterile lancet & take one drop
of blood on clean glass slide & spread it with the help
of spreader to make thin blood smear
Fixation- Fix the blood smear by alcohol spray or spirit
Staining of smear-Staining of blood smear by field A
& B stain.
Microscopic Examination of peripheral smear:- After
applying oil on smear with the help of oil emulsion
lens screen the morphology of RBC's & any of the
following form of Malarial parasite.

Malaria Thick & thin smear Ring form Ring form - multiple small rings - Falciparum,
Detection under oil emulsion Trophozoit / schizoit single large ring - vivax
form, Gametocyte form Trophozoit / schizoit form
Commonly present Gametocyte form in
Falciparum.

Fig. 4: Different form of Malarial Parasite.

Page 591
 Plasmodium falciparum

Maurers Dots

Trophozoites

Gametocytes

Plasmodium vivax

Schuffners Dots
Trophozoites

Gametocytes
Schizonts

10. Rapid test for Leptospirosis

1. Principle:-Qualitative and differential definition
of IgG and /or IgM antibody to Leptospira in
human serum or plasma. It is only a screening
test.
2. Method:-Rapid test is solid phase
immunochromatographic assay.

Page 592
3. Sample:-Serum or plasma. 1. Collection of Sample:-
Take approximately 5-10gm of stool passed by the
4. Procedure:-Remove test device from sealed
patient at the end of de fecation, it is usually semi
pouch and place horizontally. Add 5 micro liter
solid with the half of wooden spatula (Ice cream
of plasma or serum in sample well(s) Added 4
stick) into a plastic container with cap (Urine
drops of diluents in another well provided. Read
collection cup). Morning sample is preferred and
interpretation in 20 minutes.
is transported to laboratory immediately.
5. Interpretation:-
2. Preservation of Faecal Sample:-
1) Negative only one color line at control in When sample cannot be examined immediately or
result window . it has to be transported. The sample of stool is
made into thin paste with tap water. To this an
2) Positive equal part of steaming 10% formalin and left for a
IgM positive- Two color lines at control (c) and few hours. The supernatant is discarded. It should
at Ig M (M) be noted that formalin preserved oval become in a
IgG Positive- Two color lines at control (c) & at ratio of 30:1 to stool sample. Ova can be examined
IgG for about one month.
IgM and Ig G Positive -Three color lines at 3. Examination of Stool for Ova and cyst
control (c), IgM (M) &IgG
Methods
3) Invalid Test No control line in & result
window. i. Direct Smear

- No color line in (c) & also in Ig M (M) and / or Ig G. ii. Concentration by floatation method
result window iii. Direct Centrifugal floatation.
Examination of stool for ova and cysts

Stool Examination:

Finding Interpretation
A Routine Examination
1 Physical Examination
1.1 Colour - Black, White, Red 1. Black in Occult blood in upper G.I. bleed. 2.Redish in lower G.I.
bleed, 3,white in biliary obstruction
1.2 Consistency - soft, loose, hard, Loose in Diarrhea & Dysentery , Hard in chronic constipation
semisolid
1.3 Wor ms Adult worm - AscarisLumbricoides pin worm (small sound worm)

2 Chemical Test
2.1 Reducing subs tance for Lactose intolerance in infants

2.2 Occult blood upper G.I. bleed

B Microscopic exam
1 PUS cells +/- / HPF Diarrhoea&Dysentry
2 RBCS +/- /HPF lower G.I. bleed
3 OVA & Cyst Cyst of 1.Entamoeba histolytica, Giardia Lamblia 2,Entersobins
vermicularis (Pinworm) 3,Ancylostoma duodenale ( Hook worm)
4. Taeniasolium (Tape Worm)
4 mucous +/- AmeboebicDysentery

Page 593
11. Sputum for AFB
1. Introduction:
Sputum should be obtained from the lower
respiratory tract(Bronchi of the lung) Saliva
produced by the salivary gland in the month is not
sputum, but is frequently and mistakenly sent to the
laboratory instead of sputum.
Note:-Purity of the specimen should be checked
true sputum should contain fewer than 10
squamous epithelial cells and more than 25
leucocytes/ low power filed.
2. Specimen Collection:
The patient should be instructed prope rly as to the
type of the specimen required. Specimen is
collected in the early morning. It must be coughed
up from deep down in the chest. Apply the aerosol
technique if the patient is unable to produce the
required specimen.
3. Direct Examination of Sputum
Work safely with the sputum as it is
infectious.
If possible bleach the specimen with 5%
sodium hypochlorite or bleach (1:1)
4. Acid fast staining (Ziehl-Nelson
method)
Result:
All acid fast bacilli are not pathogenic. So the
result should be reported as-
o AF organism present or positive.
o AF organism absent or negative.
Technician should examine 10 microscopic
fields under oil immersion and then repor t as
follows.
Page 594
 3. SEROLOGY SECTION
Serological tests usually done in laboratory are
broadly classified into following two groups.
Agglutination Tests: This group includes tests like
Widal test, VDRL test, RA factor test, Blood Group
test, ASO test, CRP test, HbsAg test etc.
Rapid Tests (Also known as Spot/ Line Tests) :
This group includes tests like, HbsAg test, HIV
test, Dengue test, Malaria test, Hepatitis C test
etc.
Serological Tests:
Various serological tests are done for diagnosis of
diseases. Here we are discussing common serological
tests like VDRL, HBsAg, HIV, Widal, RA factor,
dengue antibody test.
1. RPR Test for Syphilis
(VDRL)
The RPR carbon reagent is a stabilized suspension of
cholesterol crystals coated with cardiolipin. Lecithin is
added to adjust the sensitivity and charcoal particles to
improve the reading of the reaction. The reagent act as
antigen against antibodi es present in person suffering
from syphilis caused by Treponemapallidum. Reagins
are a group of antibodies against some components of
the damaged tissue from patient infected by
Treponemapallidum.
This test is rapid method for diagnosis of syphilis,
macroscopic agglutination indicate positive result.
1.1. Storage:
Kit should be stored at 2-8C and protected from light.
1.2. Patient Sample:
Fresh serum (Free of Haemolysis)
1.3. Interpretation of Result:
Medium & Large aggregates against white back
ground Reactive
Finely dispersed aggregates against white back ground
Weak Reactive
No aggregates, even grey back ground - Non Reactive
False positive results can be seen in diseases like
leprosy, SLE, infectious mononucleosis, malaria, viral
pneumonia. Any positive result must be confirmed by
other serological assay (e.g. TPHA).
2. HBsAg Test
2.1. Principle:
The HBsAg one-step Hepatitis B surface antigen test
device (serum/plasma) is a qualitative, solid phase,
two-site sandwich immunoassay for the detection of
HBsAg in serum or plasma.
2.3. Interpretation:
Double line- Positive
Single line with control - Negative
3. Rheumatoid factor test
Principle
The RF reagent is a suspe nsion of pol ystyrene latex
particle sensitized with specially prepared Human IgG.
When serum containing RF is mixed with the latex
reagent visible agglutination occurs. When serum
containing greater than 0.8mg/dl RF is mixed with the
latex reagent, visible agglutination occurs.
Result: In pos itive case agglutination occurs.
4. ASO titer
Principle
It is an immunological reaction between streptococcal
exoenzyme bound to biologically inert latex particles
and streptococcal antibodies in the test specimen.
When serum containing greater than 200 IU/ml of
ASO titre is mixed with the latex reagent, visible
agglutination occurs.
Result: In pos itive case agglutination occurs.
5. Widal test
Principle
Widal kit contains killed bacterial suspension of
salmonella which carries specific Oand H antigen.
This react with immunospecific antibodies present in
the sample resulting in agglutination.
Page 595
6. HIV Tridot spot test 3. Requirement: -
Confirmation with Elisa test
Glass slide, covers tip, pipettes, Neubauer counting
chamber, pH paper, semen diluting fluid, wide mouth
7. Dengue container for semen collection.
Spot test Elisa test
4. Specimen-
8. Urine Pregnancy Test (UPT) Freshly Collected Semen

1. Principle: - 5. Physical Examination:

Qualitative detection of human chorionic gonadotropi n
(HCG) in urine in early detection of pregnancy.
2. Method:
Pregnancy test device (Urine) is rapid chromatography
immunoassay for qualitative detection of HCG.
3. Sample:
Early morning sample for early detection of pregnancy
4. Interpretation
Negative:-
One coloured line appears in control line region and no
any coloured line appears in test region (+)
Positive:-
One coloured line in control and other coloured line in
test.
Invalid test:-
No colour line in control (c).
9. Semen Analysis/Examination.
1. Indication:
(a) To rule out male infertility
(b) Post vasectomy
2. To perform routine examination
of semen
Colour, volume, viscosity of semen.
6. Chemical Examination-
pH, Detection of fructose in semen.
7. Microscopic Examination:
Under low and high power
Study of sperm motility & its percentage
Morphology's Abnormal forms & its percentage
Pus cells, RBC or epithelial cells / HPF
Determination of sperm count with help of
Neuba uer chamber & semen diluting fluid.
Note: It is necessary to note while reporting for routine
semen examination
Abstinence- da ys
Method of sample collection
Time & place of Sample collection
Swine Flu Diagnosis / Sample collection
Principle - Detection of H1N1 (swine Flu) Virus by
polymerase chain Reaction (PCR) method.
Sample- Throat & nasal swab
Reagent- Sterile swab, Viral Transport media (VTM)
Procedure- One throat swab & nasal swab by sterile
swab should be taken & place in one VTM with
universal precaution
VTM is kept at 2 to- 8C & transported to virology lab
by maintaining temperature with icepack in thermocol
container or vaccine carrier
Detail History sheet should be provided with sample.

Page 596
Common Rapid Test:

1 Leptospirosis RDK card method Positive/Negative IgM indicates recent infection

detected for of Lepto, IgG indicates old
Leptospirosis infection of Lepto
2 Dengue RDK card method Dengue NS1, IgG&IgM Dengue NS1present in 1st 5
can be detected for days of infection,IgM
Dengue indicates recent infection of
Dengue, IgG indicates old
infection of Dengue
3 HIV RDK card method HIV I & II can be HIV I or II & HIV I & II can
detected be detect.
4 HbsAg RDK card method Positive/ Negative Hepatitis B viral infection
detected for Hepatitis B
5 Malaria RDK card method Pl Vivax& PL Pl. Vivax& Pl. Falciparum is
Falciparum can be detected
detected
6 UPT RDK card method Positive / negative Pregnancy can be detected
detected for pregnancy
7 Widal Test Rapid Agglutination Positive /Negative to Enteric /Typhoid Fever can
Method detect Enteric /Typhoid be detected
Fever
8 CRP Test Rapid Agglutination Positive/Negative to detected in infection &
Method detected infection & septicemia
septicemia
9 RA Test Rapid Agglutination Positive/Negative to detected in Rheumatoid
Method detected Rheumatoid Arthritis
Arthritis
10 VDRL Rapid Agglutination Positive/ Negative to Detected in Syphilis infection
Method detected Syphilis
infection

Page 597
 4. BIOCHEMISTRY SECTION
Biochemistry tests usually done in labor atory include 6) SGPT
following tests. These tests are done with available 7) Alkaline Phosphatase
standard biochemical kits on semi-automatic / fully 8) Serum Total Proteins
automated auto-analyzer. Procedure, method and 9) Serum Albumin
interpretation varies as per available kit. 10) Serum Na/K/Cl
11) Serum LDH
1) Blood Sugar
12) Serum Cholesterol
2) Blood Urea/ Blood Urea Nitrogen
13) Serum HDL Cholesterol
3) Serum Creatinine
14) Serum Triglycerides
4) Serum Bilirubin
5) SGOT

Page 598
 5. HISTOPATHOLOGY
1. Definition:
It is a branch of pathology which deals with the study
of disease in a tissue section.
The tissue undergoes a series of steps before it reaches
the examiners desk to be thoroughly examined
microscopically to arrive at a particular diagnosis.
To achieve this it is important that the tissue must be
prepared in such a manner that it is sufficiently thick or
thin to be examined microscopically and all the
structures in a tissue may be differentiated.
The objective of the subsequent discussions will be to
acquaint the staff with their responsibility; the basic
details of tissue handling, processing and staining.
The term histoche mistrymeans study of chemical
nature of the tissue components by histological
methods.
The cell is the single structural unit of all tissues. The
study of cell is called cytology.
A tissue is a group of cells specialized and
differentiated to perform a specialized function.
Collection of different type of cells forms an organ.
2. Type of material obtained in
laboratory:
The human tissue comes from the surgery and the
autops y room.
From surgery two types of tissue are obtained.
i. As biopsy- A small piece of lesions or tumor
which in sent for diagnosis before final removal
of the lesion or the tumor (Incisional biopsy).
ii. If the whole of the tumor or lesion is sent for
examination and diagnosis by the pathologist, it
is called excisional biopsy. Tissues from the
autopsy are sent for the study of disease and its
course, for the advancement of medicine.
3. Fixation
3.1. Definition:
It is a complex series of chemical events which brings
about changes in the various chemical constituents of
cell like hardening, however the cell morphology and
structural detail is preserved.
Unless a tissue is fixed soon after the removal from the
body, it will undergo degenerative changes due to
autol ysis and putrefaction so that the morphology of
the individual cell will be lost.
3.2. Principle of fixation:
The fixative brings about crosslinking of proteins
which produces denaturation or coagulation of proteins
so that the semifluid state is converted into semisolid
state; so that it maintains everything in vivo in relation
to each other. Thus semisolid state facilitates easy
manipulation of tissue.
3.3. Tissue Processing
The tissue processing is the heart of any tissue section
which will be cut adequately only if the tissue is
properly preserved and processed. The study of this
topic is to understand the coarse and fine details of
tissue processing so that excellent sections are
obtained.
4. Staining
The sections, as they are prepared, are colourless and
different components cannot be appreciated. Staining
them by different coloured dyes, having affinities of
specific components of tissues, makes identification
and study of their morphology possible.
Page 599
 6. CYTOLOGY STUDY
Cytology is divided into four groups fix by bio fixatives and are stained with PAP
stain.
1) Fine needle aspiration Results
cytology (FNAC) Nucleus - blue
Cytoplasm and background pink
It is done for diagnosis of any lump/mass in
body. With the help of 20 bore needle fine
aspiration from any lump or mass in the body is
3) Body fluid cytology
done. And smear is made from aspirated material It is done on CSF / Pleural fluid / Ascitic fluid /
is fixed with bio fixative and stained with Synovial fluid etc. All the body fluids are
Haematoxylin and Eosin staining(H & E). examined for physical / chemical examination.
Cell count is done on neubars chamber. The
Results smear of the deposited material is stained with
Nucleus - blue leishman stain, Gram stain and ZN stain.
Cytoplasm and background pink
4) Bronchial lavage cytology
2) Exfoliative cytology Smears are stained with H&E, Gram stain, a nd
ZN stain.
It is done in the female patients to diagnose
gynecological pathology. The cervical smears

Page 600
 7. BLOOD BANK
Blood grouping(ABO & Rh 1.3. Methods for ABO Grouping:
system) The two main methods of ABO grouping for a routine
blood bank are:
There are more than 300 blood group systems but
ABO and rhesus (Rh) systems are of impor tance from i. Slide method: The slide test is not recommended
clinical point of view. These are inherited characters as it is not reliable. It is less sensitive than the
which give rise to antigen-antibody reactions. tube test. The slide is prone to drying effect that
may be wrongly interpreted as agglutination.
1. ABO system: ii. Tube method: The tube method is recommended
It was discovered by Landsteiner in 1900. The red cells
because:
contain different types of antigens (Agglutinogen),
while plasma contains antibodies (Agglutinins). In 1.1. It allows longer incuba tion of antigen-antibody
order to determine the blood group of a subject, the red mixture without dr ying.
cells are allowed to react with a sera containing known
1.2. Tubes can be centrifuged which enhance
antibod y (Agglutinin).
antigen-antibody reactions.
1.1. Practical aspects of ABO 1.3. Both cell and serum grouping can be performed.
grouping: 1.4. Weaker antigens and antibodies can be detected.
Routine ABO grouping must include both cell and 1.5. Less reagents are required.
serum grouping as each test serves as a check on 1.6. Results can be read comfortably as there is no
the other. drying.
ABO groupi ng test should be done at room
temperature. Testing at 37 C weakens the 2. Rh blood group system:
reaction. Rh blood group system was first reported Landsteiner
and Weiner in 1940.
Tubes, slides, reagents and microplates should be
labelled properly. In contrast to ABO system, Rh antigens are present on
red blood cells only and Rh antibodies develop only in
Serum should be added before adding cells and response to a known stimulus. Rh factor is present in
examine each tube after serum has been added. 85-95% of human beings.
Tubes or slides should be clean and dry and
disposable plastic tubes may be used. 2.1. Methods of Rh Grouping:
Microscope should be used to examine reactions The two main methods of Rh groupi ng for a routine
that appe ar negative by naked e ye. blood bank are:

Results should be recorded immediately after
observation.
1.2. Blood sample
Clearly labelled samples of blood in plain tubes.
No sign of haemolysis should be there.
If serum has not completely separated or become
clear, centrifuge the blood sample at 1000-3000
rpm for 3 minutes.
Take one to two millilitres of serum in pipette and
place into a prelabeled tube for serum grouping
and other tests.
i. Slide method: The slide test is not recommended
as it is not reliable. It is less sensitive than the
tube test. The slide is prone to drying effect that
may be wrongly interpreted as agglutination.
ii. Tube method: The tube method is recommended
because:
1.1 It allows longer incuba tion of antigen-antibody
mixture without dr ying.
1.2 Tubes can be centrifuged which enhance
antigen-antibody reactions.
1.3 Both cell and serum grouping can be performed.
1.4 Weaker antigens and antibodies can be detected.

Page 601
1.5 Less reagents are required
1.6 Results can be read comfortably as there is no
drying.
2.2. Interpretation:
i. Agglutination in the tube test and in the tube
positive control and smooth suspension of
cells in the tube negative control: This is
interpreted as test cells Rh (D) positive.
ii. A smooth suspension of red cells in tubes of
test and negative controls and agglutination
in the tube labelled as positive control: This is
interpreted as test cells Rh (D) negative.
iii. Blood Donor red cells found negative should be
further tested by AHG test for weak D.
iv. If in any test negative control gives
agglutination or positive control does not give
agglutination, the results are invalid.
3. Cross Match
Major crossmatch: Recipients serum is cross
matched with donor red cells for IgM and IgG
antibodies compatibility.
Minor crossmatch: Donor serum is cross
matched with recipients red cells for IgM and
IgG antibodies compatibility. If donors serum
is tested negative for unexpected or irregular
antibodies, minor crossmatch can be avoided.
If incompatibility is not detected in cross
matching, then it is likely that the donor blood
transfused into patient will survive normally.
Finding of incompatibility indicates that
transfusion of such blood is potentially
dangerous and further steps should be taken to
identify the antibod y.
Note: It is mandatory to test the blood for the
following transfusion transmissible infections before it
is taken on stoc k and issued to the patient.
i. HIV antibod y screening by ELISA
ii. Hepatitis B surface antigen (HBsAg) by ELISA
iii. Hepatitis C antibody by ELISA
iv. Syphilis by RPR test
v. Malaria by thick and thin blood smear or
malaria antigen.
After the testing is complete, the blood bag is labelled
and then taken on stoc k and used for crossmatch and
issue to the patients.
4. Procedure of blood
TRANSFUSSION: Important aspects:
The blood bag received in the ward for transfusion to
the patient is to be maintained at room temperature for
one hour, so that it will come to the body temperature.
Pretransfusion medication to patient is done half hour
before blood transfusion.
The blood bag should not be warmed in hot water
otherwise hemol ysismay take place.
Do not transfuse the blood bag immediately after
receiving because at that time the blood bag is at 4 to 6
degree centigrade.Transfusion of cold blood may get
transfusion reaction.
Rate of blood transfusion should be such that it will
take 4 hours to transfuse the ba g. In emergency the
clinician will take decision.
During transfusion the patient is monitored for body
temperature/ pulse/blood pressure/respiratory rate and
watch for transfusion reaction.
4.1. Blood transfusion reaction:
1) Febrile
2) Pain
3) Jaundice
4) Allergic
5) Other
In case of blood transfusion reaction, BTO should be
informed immediately after stopping blood transfusion
and blood bag along with blood transfusion reaction
card duly filled should also be returned to blood bank.
4.2. Complication of blood
transfusion reactions-
i. Haemolytic transfusion reactions which could be
immediate or delayed.
ii. Allergic reactions like 1) Fever 2) Anaphylactic
reaction 3) Allergic reactions 4) Graft versus- hos t
diseases
iii. Circulatory overload leading to pulmonary
congestion and acute Heart failure,
thrombocytopenia & dilution of coagulation factors.
iv. Transmission of infections e.g. Hepatitis B & C,
malaria, HIV Infection, syphilis, infectious
mononucleosis, toxoplasmosis.
In case of blood transfusion reaction, for carrying out
investigations pre and post- blood transfusion patients
blood and urine sample is needed. Blood bag along
with blood transfusion reaction card duly filled should
also be returned to blood bank by the medical officer.
Page 602
 8. NORMAL LAB VALUES
Hematology
Hemoglobin
: 13.5-17.5 g/dl

:12.0-16.0 g/dl
Hematocrit : 39-49%

:35-45%
Red Blood Corpuscles : 4.3-5.7 (108/ul )

:3.8-5.1 (108/ul )
Platelet 150-450 103/ul

White Blood Cells (differential below) 4.5-11.0 103/ul

Neutrophils 57-67%
Lymphoc ytes 22-33%
Monoc ytes 3-7%
Eosinophils 1-3%
Basophils 0-1%
Erythroc yte Sedimentation Rate (ESR) :<15mm/hr

:<20mm/hr
Ferritin : 20-250 ng/ml

:10-120 ng/ml
Fibrinogen 150-350 mg/dl
Haptoglobin 26-185 mg/dl
Hb A1c 5.0-7.5%
Mean Corpuscular Hemoglobi n 26-34 pg
Mean Corpuscular Hemoglobi n Concentration 33-37%
Mean Corpuscular Volume 80-100fl
Prothrombin Time 10-14 sec
Activated Partial Prothrombin Time 20-40 sec
Reticulocytes 0.5-1.5%
Total Iron Binding Capacity 250-400 ug/dl
Transferrin 200-400 mg/dl
Chemistries
Sodium 135-145 mEq/l
Potassium 3.5-5.3 mEq/l

Page 603
Chloride 95-105 mEq/l
Bicarbonate 22-29 mEq/l
Blood Urea Nitrogen 10-26 mg/dl
Ceratinine 0.6-1.3 mg/dl
Glucose 70-115 mg/dl
Anion Gap 7-16 mEq/l
Osmolality 275-300 mOsm/kg
Calcium Total 8.5-10.5 mg/dl
Calcium Ionised 4.65-5.28 mg/dl
Magnasium 1.3-2.4 mEq/l
Phosphate 2.5-4.5 mg/dl
Alfa Fetoprotein <10 ng/mol
Albumin 3.5-5.5 g/dl
IgA 70-312 mg/dl
AgG 640-1350 mg/dl
IgM 56-350 mg/dl
Lactate 0.5-1.3 mEq/l
Protein (Total) 6.0-8.0 g/dl
Uric Acid : 3.0-7.4 mg/dl

:2.1-6.3 mg/dl
Zinc 55-135 ug/dl
Liver/Pancreas
SGOT/ALT 0-40 IU/l
Alkaline Phosphatase : 38-126 U/l

: 70-230 U/l

Ammonia 10-50 umol/l

AST/SGPT 7-40 IU/l
Bilirubin (Total) 0.2-1.0 mg/dl
Bilirubin (Conjugated) 0-0.2 mg/dl
Lecithin dehydrognax 90-190 U/l
Amylase 25-125 U/l
C Peptide 0.7-1.89 ng/ml
Lipase 10-140
>60yo: 10-180
Lipids

Page 604
Total Cholesterol <200 mg/dl
Low density Lipoproteins <130 mg/dl
High density Lipoproteins : >29 mg/dl

: >35 mg/dl
Triglycerides : 40-160 mg/dl

: 35-135 mg/dl
Other
Phosphokinase : 38-174 U/l

: 26-140 U/l
Phosphokinase MB <5%
Acid Phosphatase <0.8 IU/ml
B12 100-700 pg/ml
CA-125 <35 U/ml

Copper (Cu) : 70-140 ug/dl

: 80-155 ug/dl

Folate 3-15 ng/ml

Lead (Pb) <10 ug/dl

Zinc (Ionized) 70-150 ug/dl

Blood Gases
Arterial Venous
Ph 7.35-7.45 7.32-7.42
pCO2 35-45 41-51
pO2 80-100 25-40
HCO3 21-27 24-28
Oxygen Saturation 95-99%
Urine
Ph 5-9
Minimal Vol ume 0.5-1.0 mg/kg/hr
Specific Gravity 1.015-1.030
Osmolality 600-1400 mOsm/kg
Creatinine : 14-26 mg/kg/day

Page 605
 : 11-20 mg/kg/day
Creatinine Clearance : 100-150 ml/min

: 90-140 ml/min
* Rough estimate only varies with BMI
Urea Nitrogen 12-20 g/day
Calcium (Ionized) 100-300 mg/day
Potassium (Ionized) 25-125 mEq/day
Sodium (Ionized) 40-220 mEq/day
Phosphate 0.4-1.3 g/day
Uric Acid 250-750 mg/day
Albumin 10-100 mg/day
Amylase 1-17 U/hr
Glucose <0.5 g/day
Protein 10-100 mg/day
CSF
Pressure 60-180 mmH2O
White Blood Cell 0-5 /ul
Protein 15-45 mg/dl
Glucose 40-80 mg/dl
Synovial Fluid
White Blood Cell <200 /ul
Trauma, OA, SLE <3,000/ul
Gout. RA >4,000/ul
Septic >60,000/ul
Protein <3.0 g/dl
Glucose >50 mg/dl
Uric Acid <8.0 mg/dl
Endocrine
Aldosterone Supi ne: 3-10 ng/dl
Upright: 5-30
Cortisol 0800h: 6-23 g/dl
1600h: 3-15 g/dl
2200h:50% of 0800h value
Gastrin <100 pg/ml
Growth Hor mone (<60yr) : <2 ng/ml

Page 606
 : <10 ng/ml
Growth Hor mone (>60yr) : <10 ng/ml

: <14 ng/ml
Estrogen Follicular: 60-200 pg/ml
Luteal: 160-400 pg/ml
Menopa use: 130 pg/ml
Follicle stimulating Hormone Follicular: 1-9 mU/ml
Ovulation: 6-26 mU/ml
Luteal: 1-9 mU/ml
Menopause: 30-118 mU/ml
Luteinizing Hor mone Follicular: 1-12 mU/ml
Mid-Cycle: 16-104 mU/ml
Luteal: 1-12 mU/ml
Menopause: 16-66 mU/ml
Progesterone Follicular: 0.15-0.7 ng/ml
Luteal: 2.0-25 ng/ml
Prolactin <20 ng/ml
Para Thyroid Hormone 10-65 pg/ml
Sperm 20-200 million/ml
Testosterone Free 52-280 pg/ml
Total 300-1000 ng/dl
T3 Uptake 0.82-1.18
Total 100-200 ng/dl
T4 Total 5.0-12.0 g/dl
Free 0.3-2.3 ng/dl
Thyroid stimulating Hormone <10 uU/ml
>60yo : 2-7.3 uU/ml

>60yo : 2-16.8 uU/ml

Toxic Levels
Acetaminophen >200 ug/ml
Ethyl Alcohol (in a non-alcoholic patient) Intoxicated >100 mg/ml
Lethargic >200 mg/ml
Coma >300 mg/ml
Resp. Distress Death >500 mg/ml

Page 607
Ethylene Glycol >20 mg/dl
Lead >100 ug/dl
Salicylate >300 ug/ml

Differential of Cerebral Spinal Fluid

Opening
Glucose Protein
Color Pressure Cells (#mm3)
(mg/100ml) (mg/100ml)
(mmH2O)

Adult (nl) clear 70-180 45-80 0-5 lymphs 15-45

Newborn clear 70-180 2/3 serum 40-60 lymphs 20-120

Page 608
 9. LABORATORY TESTS PERFORMED
Clinical Services Rural / Sub-district District Hospitals and all
PHC
Related to: hospital 100 bedded hospitals
Viral infection Blood smear Blood smear Blood smear, serology test

Bacterial Infection Urine exam, blood smear, Urine exam, blood smear, Urine exam, blood smear,
sputum examination, Widaltest,CSF exam, Widal test, CSF exam,
Gram stain, ZN stain Gram stain , ZN stain serology , Gram stain, ZN
stain
Protozoal Urine exam, Stool, Urine exam, Stool, Urine exam, Stool,
Malarial parasite Filaria Malarial parasite, Rapid Filaria,Blood smear
Blood smear malaria test,Filaria, Blood
smear,
STD Urine exam, Blood smear Urine exam, Blood Urine exam, Blood
smear,HIV& VDRL tests smear,HIV& VDRL tests,
serology
Poisoning cases Urine exam, Blood smear Urine exam, Blood Plasma Cholinesterase,
smear, S.creatine in aluminum
phoshpmide poisoning
Animal Bites Urine exam, Blood smear Urine exam, Blood smear Urine exam, Blood smear
Environmental disorders Urine exam Urine exam, Blood Urine exam, Blood smear,
smear,
Sr Creatinine & urea
Sr Creatinine & urea
Gastro-intestinal Tract Stool exam, Blood smear Stool exam, Blood Stool exam, Blood smear
Disorder smear,Total Eosinophilic
Total Eosinophilic count
count

Respiratory disorder Sputum Gram & AFB Sputum Gram & AFB Sputum Gram & AFB stain
stain exam, Blood smear stain exam, Blood smear exam, Blood smear
Cardio-vascular Disorder Urine exam, Blood smear Urine exam, Blood Urine exam, Blood smear,
smear, SGOT Sr CMB, Troponin,
Hematological Disorder Hb %,Blood smear Hb %,Blood smear, Hb %,Blood smear,
sickling tests, BT & CT sickling tests, RBC
indices,BT, PT, APTT

Page 609
DENTISTRY

Page 610
 1. DENTAL CARIES
Dental caries is a microbial disease of the
calcified tissues of the teeth, characterized by
demineralization of the inor ganic por tion and
destruction of the organic substance of the
tooth
1. Signs and Symptoms:
Grayish black discolouration of tooth in pit
and fissure areas.
Dental Caries
Figure 1
2. Diagnosis:
2.1 Visual Examination :
For visual examination teeth should be cleaned,
dried with compressed air and illuminated under
adequate light source and observe for cavitation,
surface roughness, opacity of marginal ridge or
occlusal area, discolouration.
Figure 2OPA X-Ray Showing Radiolucent Carious lesion
Cavity formation and food lodgment.
Sensitivity if caries reaches to the dentin.
Pain and swelling in vicinity area if pulp is
involved due to caries.
Periapical abscess & draining sinus in
advancedstages
2.2 Tactile Examination:
Includes determining roughness or softness of tooth
surface / discontinuity of enamel with a sharp
explorer. Discolouration of pits and fissures may be a
universal finding in nor mal healthy adult teeth may
be mistaken for presence of caries.
2.3 Radiographic investigation:
Page 611
 Radiograph shows dental caries and its extent as
radiolucent lesion due to demineralization of
tooth structure.

Figure 4: Stages of Dental Caries

3. Treatment: 4. Prevention of Dental Caries

Avoid extreme hot and cold beverages.
Restoration of cavitated lesions if limited to
enamel and de ntin.
Endodontic therapy for pulp involvement due to
caries.
Abscess drainage followed by endodontic
therapy
Tooth extraction may be performed in advanced
cases when conservation of tooth structure is
critical.
4.1 Diet modification / Dietary
counseling:
4.2 Maintenance of oral hygiene:
4.2.1 Daily removal of plaque by tooth-
brushing/flossing/rinsing is the best measure for
preventing caries and periodontal disease.
4.2.2 Proper brushing technique
4.2.3 Flossing should be done in the interdental areas
to maintain the proximal surface clean.

Figure 5
4.2.4 Antimicrobial Agents: USE OF FLUORIDE:
a) Antimicrobial agents like chlorhexidine, a) Systemic use: systemic fluoridation can be
fluoride, antibiotics available to help prevent achieved by community water fluoridation
caries. (1ppm) in the areas of low fluoride content
b) 0.12 0.2% Chlorhexidi ne mouth rinse (below 1ppm).
prescribed for home use at bedtime as a 30- b) Topical use:
second rinse.
Self-application: Daily use of fluoridated toothpastes
4.2.5 Fluorides: and mouthwashes
To reduce caries risk primarily achieved by systemic Professional application: application on tooth
and topical fluoridation. surfaces.

Page 612
a) Use of APF gel 1.23%. Sealants mechanically fills pits and fissures with
an acid resistant resin.
b) Use of 2% sodium fluoride.
Renders pits and fissures easier to clean by tooth
brushing and mastication.
5 Pit & fissure sealants:

KEY MASSAGE:
Avoid sticky and food with rich sugar content.
Brush the teeth twice a day with prope r brushing technique.
Visit your doctor every six months for regular dental check up and get the treatment done at early
stages.

Page 613
 2. DISEASES OF DENTAL PULP AND
PERIAPICAL TISSUES
Diseases of the dental pulp initiate dental pain of
pulpal origin can be due to pulpitis, apical
periodontitis periapical abscess.
1. Pulpitis is an inflammation
of pulp may be acute or
chronic.
1.1. Acute reversible pulpitis:-
Mild to moderate inflammatory conditions of pulp
caused by noxious stimuli in which pulp is capable of
returning to the uninflamed state following removal
of the stimuli.
1.1.1 Clinical features:
Sharp momentary pain on exposure to sweet
or thermal stimuli (cold).
It does not occur spontaneously and does not
continue when the cause has been removed.
Reacts normally to percussion, palpation and
mobility and the periapical tissue is normal
on radiograph.
1.1.2 Treatment:
Removal of etiology and restoration of the
tooth.
Cap. Amoxicillin 250/500 mg 3 times a day
for 3 to 5 days.
Tab. Diclofenac 50mg 1BD for 3 days.
1.2. Acute Irreversible
pulpitis:-
A persistent inflammator y condition of pulp
symptomatic or asymptomatic caused by a noxious
stimulus.
1.2.1 Clinical features:
Sharp pain usually caused by thermal
stimuli and can occur spontaneously.
Chronic hyperplastic pulpitis
The pain persists for several minutes to
hours, lingering after removal of the
thermal stimulus.
In early stages the pain is sharp shooting,
piercing while in later stages pain is more
severe and is generally described as boring,
gnawing or throbbing and may be more
intense.
Inspection generally discloses a deep cavity
extendi ng to the pulp or decay under
filling. The pulp may be already expos ed.
1.2.2 Investigation:
Radiograph may disclose an interproximal
cavity, or may suggest involvement or
expos ure of pulp, c aries under filling.
Vitality Test.
1.2.3 Treatment:
Removal of inflamed pulp tissues with
endodo ntic therapy.
Cap. Amoxicillin 250/500mg 3 times a
day for 3 to 5 days.
Tab. Diclofenac 50mg 1BD for 3 days.
1.3. Chronic pulpitis:
1.3.1 Clinical features:
It occurs as the chronic type of pulpal
disease from its onset.
Dull pain is present which is more often
intermittent and there is a delayed response
in vitality testing.
1.3.2 Treatment:
Endodontic treatment
1.4. Chronic hyperplastic
pulpitis (Pulp polyp):
It is a productive pulp inflammation due to an
extensive carious exposure of a young pulp.
Page 614
 Figure 1
1.4.1 Clinical features
Occurs generally in children and young
adults.
Involved teeth with large, open carious
lesions.
1.4.2 Signs & Symptoms:
Chronic hyperplastic pulpitis is
symptomless, except during mastication,
when pressure of the food bolus may cause
discomfort.
Pulp appe ars as a pinkish red globule of
tissue protruding, from the pulp chamber
1.4.3 Investigation:
Radiograph shows large open cavity with
direct access to the pulp chamber.
1.4.4 Treatment:
Elimination of the polypoid tissue followed
by RCT, provided the tooth can be restored
otherwise extraction is needed.
Cap. Amoxicillin 250/500 mg 3 times a day
for 3 to 5 days.
Tab. Diclofenac 50mg 1BD for 3 days.
2. Diseases of periapical
tissues:
1. Apical periodontitis:
Apical periodontitis is a painful inflammation of the
periodontium as a result of trauma, irritation or
infection around the root apex regardless of whether
the pulp is vital or non- vital.
1.1 Clinical features:
There is pain on mastication and tooth is tender on
percussion.
Figure 2
1.2 Investigation:
Radiographic examination may show a thickened
periodontal ligament or a small area of rarefaction if
a pulpless tooth is involved and it may show normal
periradicular structures if a vital pulp is present.
1.3 Treatment:
If the inflammation is caused by occlusal trauma it
should be relieved by selective grinding. If due to
spread of pulpal infection RCT is indicated.
Cap. Amoxicillin 250/500 mg 3 times a day for
3 to 5 days.
Tab. Metronidazole 200/400 mg 1BD for 3
days.
Tab. Diclofenac 50mg 1BD for 3 days.
2. Acute alveolar abscess:
Acute alveolar abscess is a localized collection
of pus in the alveolar bone at the apex of a
tooth following death of pulp with extension of
the infection through the apical foramen into
periradicular tissue.
2.1 Clinical features:
The patient has severe throbbing pain with
swelling of the ove rlying soft tissue.
Pus may exude through tiny openings.
2.2 Treatment:
Establishing drainage and completion of RCT
after subsidence of symptom is done.
Cap. Amoxicillin 250/500 mg 3 times a day
for 3 to 5 days.
Tab. Metronidazole 200/400 mg 1BD for 3
days.
Tab. Diclofenac 50mg 1BD for 3 days.
Page 615
 3. Chronic apical periodontitis:
(periapical granuloma):
Localized mass of chronic granulation tissue formed
in response to infection.
3.1 Clinical features:
The involved tooth is non- vital and slightly tender to
percussion. Patient may complaint about mild pain on
biting. The patient feels tooth is slightly elongated in
its socket.
3.2 Radiographic examination
Periapical granuloma appears as a radiolucent area of
variable size attached to root apex.
3.3 Treatment:
Root canal treatment with or without subsequent
apicoectomy.
Cap. Amoxicillin 250/500mg 3 times a day for 3 to 5
days.
Tab. Metronidazole 200/400mg 1BD for 3 days.
Tab. Diclofenac 50mg 1BD for 3 days.
4. Radicular cyst:
It is slowly growing epithelial cyst at the apex of the
tooth. Radicular cyst presupposes physical, chemical
or bacterial injury resulting in death of pulp.
4.1 Clinical features:
The majority of cases are asymptomatic. The
associated tooth is non- vital or shows deep carious
lesion or a restoration which is seldom painful or
even sensitive to percussion.
4.2 Investigation:
Roentogenographic features:-Radiolucent area
surrounded by radiopaque border attached to root
apex.
4.3 Treatment: -
Involved tooth is extracted and periapical tissue is
carefully curetted.
5. Osteomyelitis:
Inflammation of bone and its marrow contents.
5.1 Acute suppurative osteomyelitis:
It isa serious sequel of periapical infection that often
results in a diffuse spread of infection throughout
medullary space, with subsequent necrosis of variable
amount of bone.
5.1.1 Clinical features:
Severe pain, trismus and parasthesia of lips
in case of mandibularinvolvement and
manifests an elevation of temperature with
regional lymphadenopathy.
The teeth in the area of involvement are
loose.
Pus exude from gingival margin.
In the maxilla the disease is well localized to
the area of initialinfection and in mandible
bone involvement is more diffuse &
widespread.
Radiograpically: little evidence of its
presence until the diseasehas developed for
at least one to two weeks. At this time
diffuse lytic changes in the bone, radiolucent
areas begin to appear, ill- defined margins
and have moth- eaten appearance.
5.1.2 Treatment:
General principles of management include
Debridement
Drainage and
Cap. Amoxicillin 250/500 mg 3 times a day
for 3 to 5 days.
Tab. Metronidazole 200/400 mg 1BD for 3
days.
Tab. Diclofenac 50mg 1BD for 3 days.
If sequestrum is small it gradually exfoliates through
the mucosa.If large, surgical removal may be
necessary unless proper treatment is instituted. Acute
suppurative osteomyelitis, may proceed to
development of periostitis, soft tissue abscess or
cellulitis.
5.2 Chronic Suppurative osteomyelitis:
It may develop in inadequately treated acute
osteomyelitis or may arise from dental infection
without preceding acute stage.
Page 616
 Chronic Suppurative osteomyelitis
Figure 3
Figure 3.5
5.2.1 Clinical features
Similar to acute suppurativeosteomyelitis
except all signs and symptoms are milder.The
suppuration may perforatethe bone and overlying
skin or mucosa to form fistulous tract and empty on
surface .
5.3 Chronic focal sclerosing osteomyelitis:
A reaction to mild bacterial infection entering
the bone through a carious tooth in persons who have
a high degree of tissue resistance and tissue
reactivity.
5.3.1 Clinical Features
Most commonly in children and young
adults.
Commonly invol ve mandibular first molar
Mild pain associated with an infected pulp
5.3.2 Investigation:
Radiographic features show well
circumscribed radiopaque mass of sclerotic
bone surrounding and extending below the
apex of carious tooth involving one or both
roots. Intact lamina dura. Periodontal
ligament space is widened.
5.3.3 Treatment: Extraction of carious tooth. The
sclerotic bone constituting the osteomyelitis is
not attached to the tooth and remains after the
tooth is removed. Surgical removal of sclerotic
lesion is not indicated unless symptomatic.
Cap. Amoxicillin 250/500mg 3 times a day for
3 to 5 days.
Tab. Metronidazole 200/400mg 1BD for 3
days.
Tab. Diclofenac 50mg 1BD for 3 days.
5.4 Chronic Diffuse sclerosing osteomyelitis:
It is a proliferative reaction of the bone to low-
grade infection. Portal of entry for the
infection is through diffuse periodontal
disease.
5.4.1 Clinical feature:
Occur at any age but is most common in
older person especially in edentulous areas.
Vague pain, unpleasant taste and mild
suppuration with the spontaneous for mation
of fistula when acute exacerbation of
dormant chronic infections.
5.4.2 Investigation:
Radiographic feature: - Diffuse patchy,
sclerosis of bone often described as cotton
wool appearance. Radiopaque lesion may be
extensive and is sometimes bilateral. The
border between sclerosis and normal bone is
indistinct.
5.4.3 Treatment:
Conservative treatment of acute episodes by
antibiotic administration.If the tooth is present
in one of these sclerotic areas must be
extracted.
Cap. Amoxicillin 250/500mg 3 times a day for 3
to 5 days.
Tab. Metronidazole 200/400mg 1BD for 3 days.
Tab. Diclofenac 50mg 1BD for 3 days.
5.5 Chronic osteomyelitis with proliferative
Periostitis:
There is focal gross thickening of periosteum
with peripheral reactive bone formation
resulting from mild irritation or infection.
5.5.1 Clinical feature:
Occurs exclusively in the mandible, in
children and youngadults and most cases
occur in the bicuspid and molar region.
The patient complains of toothache or pain
in the jaw and a bony hard swelling on outer
surface of jaw.
5.5.2 Radiographic features:
Page 617
 Intra oral periapical X- ray will reveal a
carious tooth.
Occlusal roentgenogram shows a focal
overgrowth of bone on the outer surface of
the cortex which may be described as
duplication of cortical layer of bone. This
mass of bone is smooth and well calcified
and may itself show a thin but definite
cortical layer.
5.5.3 Treatment:
Extraction of carious tooth
Cap. Amoxicillin 250/500mg 3 times a day for 3
to 5 days.
Tab. Metronidazole 200/400mg 1BD for 3 days.
Tab. Diclofenac 50mg 1BD for 3 days.
Page 618
 3. PERIODONTAL DISEASES

Periodontium is the anatomical structure surrounding

tooth which involves gingiva periodontal ligament,
cementum, alveolar bone.

Figure 1

Diffuse puffiness and softening of gingiva.

1. Gingivitis Redness of gingiva.Presence of exudates.
Inflammation of gingiva is called gingivitis.
Plaque usually present and calculus is often
1.1 Clinical features seen.
1.1.1 Acute gingivitis:

Figure 2: Gingivitis

Sloughing with grayish debris adhering to Soggy puffiness that pits on

eroded surface pressure.Marked softness and friability with
Vesicle formation fragmentation on exploration with probe.
1.1.2 Chronic Gingivitis Firm, Leathery consistency

1.2 Treatment: Scaling and pol ishing

Page 619
 Figure 3
2. Acute Gingival Infections:
2.1 Necrotizing Ulcerative
Gingivitis:
It is microbial disease of gingiva characterized by
death and sloughing of gingival tissue.
2.1.1 Clinical Features
Sudden onset sometime with respiratory
tract infection
Lesions are punched out crater like
depressions on crest of interdental papilla
Ulcers are covered with grey
pseudomembranous slough.
Spontaneous gingival hemorrhage and also
bleeding on slightest provocation.
Constant radiating, gnawing pain of gingiva.
Metallic foul taste.
Excessive amount of pasty salivary
secretions.
Local lymphadenopathy
In severe and acute cases high grade fever,
loss of appetite, generalized lassitude,
insomnia, constipation, headache, mental
depression may be seen.
Necrotizing ulcerative gingivitis is caused
by fusiform bacilli and spirochetes
2.1.2 Treatment of Acute Necrotizing
Ulcerative Gingivitis (ANUG)
With moist cotton and lignocaine jelly gently remove
pseudo membrane.
Antibiotic and Analgesic Cap.
Amoxycillin 500mg 8 hrly 10 days for
patient sensitive to amoxicillin.
Cap. Erythromycin 500mg x 8 hrly.
Tab.Diclofenac 50mg 1BD for five days
Rinsing with 3% H202 + Equal quantity of
water2-3 hourly. And / or 0.12%
Chlorohexidi ne mouth wash BD
After 2 days if pseudo membrane is absent
and erythematous gingiva are present,
evaluate for scaling, if sensitivity permits.
After 5 days discontinue hydrogen peroxide
gargles but continue with chlorhexidine
gargles
Vit.B complex 1 OD for ten days.
2.2 Pericoronitis:
Inflammation of the gingiva in relation to the crown
of an incompletely erupted tooth is called
pericoronitis.
2.2.1 Clinical features:
Partially erupted or impacted mandibular
third molar is common site of pericoronitis.
Pericoronitis is exacerbated by trauma, or
foreign body trapped under tissue flap.
Trismus may or may not be present
Pericoronitis presents as a red swollen
sometimes suppurating lesion with
tenderness, and pain radiating towards ear,
nose or floor of mouth.
Fever and malaise may be present.
Difficulty in swallowing may be present.
Many a times infection may spread to
different tissue spaces leading to tonsillar
abscess formation, cellulitis or Ludwigs
angina.
2.2.2 Treatment:
Area should be anesthetized.
Drainage is established by gently lifting the
soft tissue operculum.
Page 620
 Area should be irrigated by normal saline to
remove debris.
Cap. Amoxicillin 250/500 mg 3 times a day
for 3 to 5 days.
Tab. Diclofenac 50mg 1BD for 3 days.
Advice warm saline gargles every 2 hours.
Once swelling subsides, partially erupted
tooth should be treated by excision of
pericoronal flap or by extractions.
3. Gingival Enlargement:
Increase in size of gingiva is a common feature called
as gingival enlargement or gingival hyperplasia or
gingival hypertrophy.
3.1 Inflammatory Enlargements:
3.1.1 Acute Inflammatory enlargements
Clinical Features
Drug Induced Gingival Enlargement
Figure 4
3.2 Drug Induced Gingival
Enlargement
3.2.1 Clinical features
Painless bead like enlargement.
May enlarge to cover crown portions.
Enlargement is generalized.
Enlargement more in anterior teeth.
Recurs after surgical excision.
Patient gives history of taking medicines
like anticonvulsants, immunosuppressant,
and calcium channel blockers.
3.2.2 Treatment
Gingival abscess, localized, painful, sudden
onset, rapidly expanding.
Usually on marginal gingival or interdental
papilla
Appears as a red swelling with a smooth
shiny surface
Purulent exudates may be present
Tooth sensitive to percussion
3.1.2 Chronic inflammatory enlargement
Clinical Features
Ballooning of marginal gingiva and
interdental papilla or both.
Progresses slowly and painlessly
Appears like pedunculated mass on gingiva
Painful ulcerations may occur
Exposed gingival surface appears red
edematous and s hiny in mouth breathers.
3.1.3 Treatment
Scaling and root planing
If the shrinkage of fibrotic tissue doe snt
occur then surgical therapy is the treatment
of choice.
Possibility of discontinuing the drug or
changing should be assessed by consulting
the physician.
Plaque control helps to limit the
enlargement and subsequent periodontal
diseases.
If required by assessing the periodontal
status go for periodontal surgical
procedures like gingivectomy or flap as
indicated.
3.3 Gingival Enlargement
Associated with Systemic
Diseases:
Page 621
3.3.1 Pregnancy Gingivitis
Gingival enlargement may be marginal or
generalized, single or multiple tumors like
masses.
It occurs due to increased progesterone and
estrogen levels in pregnancy especially in
third trimester.
Treatment of Pregnancy Gingivitis:
Removal of local irritants in early stages of
pregnancy and emphasis should be give n on
preventing gingival diseases.
3.3.2Gingival Enlargement in Vitamin C
Deficiency (SCURVY):
Acute vitamin C deficiency itself does not
cause inflammation. But it does cause
hemorrhage, collagen de generation, oede ma
of gingival tissue.
These changes are in response to plaque.
Regular intake of vitamin C and
maintenance of oral hygiene prevents
scurvy.
3.4 Pyogenic Granuloma:
3.4.1 Clinical features:
It is a tumor like gingival swelling that is
considered as exaggerated conditioned
response to minor trauma.
It presents as a pedunculated spherical tumor
like mass.
It is red or purple.
It can be firm or friable. Sometimes surface
may be ulcerated and purulent.
3.4.2 Treatment
Excision of mass and removal of local irritating
factors.
3.5 Periodontal Abscess:
3.5.1 Clinical features
Mild to severe discomfort.
Localized red, ovoid swelling.
Periodontal pocket,Exudation.
Mobility.
Tooth elevation in socket.
Tenderness to percussion or biting
Elevated temperature,Regional
lymphadenopathy.
Radiograph shows periodontal angular bone
loss and furcation radiolucency.
3.5.2 Treatment:
Drainage through poc ket retraction or
incision.
Scaling and root planning.
Required periodontal surgery.
Systemic antibiotics
Cap. Amoxicillin 250/500 mg 3 times a day
for 3 to 5 days.
Tab. Metronidazole 200/400 mg 1BD for 3
days.
Tab. Diclofenac 50mg 1BD for 3 days.
Tooth removal if required
3.6.1 Periodontitis
3.6.1 Chronic Periodontitis
An infectious disease resulting in inflammation
within the suppor ting tissues of the teeth, leading to
progressive attachment loss and bone loss.
Clinical Features:
Supragingival and subgingival accumulation
with calculus for mation.
Gingival inflammation and pocket
for mation.
Loss of periodontal attachment and alveolar
bone.
Occasional pus discharge and poor oral
hygiene.
Moderate swelling of gingiva with pale red
to magenta colors.
Blunt or rolled gingival margins.
Bleeding on probing may be present.
Sometimes tooth may be mobile.
It may be localized or generalized.
3.6.2 Necrotizing Ulcerative Periodontitis
Necrotizing ulcerative periodontitis is an extension of
necrotizing ulcerative gingivitis. Historically it is
described as Vincents infection or trench mouth.
Clinical features
Areas of ulceration and necrosis of
interdental papilla with yellowishwhite soft
layer of pseudomembrane is present.
Lesions are painful.
Bleed without provocation.
Punched out lesions present.
Associated with malodor, localized
lymphadenopathy, fever and malaise.
Destructive progression of disease includes
destruction of periodontalattachment and
bone loss.
Deep interdental osseous craters are very
typical with necrotizing
ulcerativeperiodontisis.
Tooth mobility with untimely loss of
tooth is a common feature.
Page 622

3.6.3 Aggressive Periodontitis
a) Localized aggressive periodontitis:
(Juve nile periodontitis):
Usually first molar or incisor are
affected with interproximal bone loss.
There is lack of inflammation despite loss of
deep periodontal pocket.
Generalized Aggressive Periodontitis
Figure 5
b) Generalized Aggressive Periodontitis
Affects individuals below the age of 30.
Gives very poor response to antibiotics.
Characterized by generalized nterproximal
attachment loss affecting at least 3
permanent teeth other than first molar and
incisor.
Periods of advanced destruction is followed
by stages of quiescence of variable length
(weeks to months to years).
Quantity of amount of plaque seems
inconsistent with the amount of periodontal
destruction.
Deep poc kets and s uppuration .
Systemic manifestation may be seen such as
weightloss, mental depression and general
malaise.
c) Treatment:
Conventional periodontal therapies for
aggressive periodontitis consist of
patient education, oral hygiene
improvement, scaling and root planing
and recall maintenance.
Resective periodontal surgery can be
effective to reduce pocket depth.
Anti microbial therapy consists of Cap
Tetracycline (500 mg 1BD for 14 days
every 8 weeks).
3.7 Oral Malodor (HALITOSIS)
Rate of bone loss is four fold as compared to
chronic periodontitis.
Mobility of teeth increases fast.
Sensitivity to root surfaces.
Deep dull, radiating pain during mastication.
Usually disease starts around beginning of
puberty.
Radiological vertical bone loss is seen.
Breath odor is defined as subjective perception after
smelling someones breath. If unpleasant, the term
breath mal odor, halitosis or bad breath can be
applied.
3.7.1 Etiological factors:
Deep caries with infection, candidial
infections, pericoronitis, periodontitis, oral
ulcerations, xerostomia, tongue and tongue
coating especially in fissured tongue and
hairy tongue.
Infections like pharyngitis, sinusitis, and
chronic purulent tonsillitis,chronic
bronchitis, bronchiectasis, bronchial
carcinoma,gastric hernia, regurgitation,
esophagitis, and intestinal gas production,
chronic glomerular nephritis,diabetes.
Trimethylaminouria hereditary metabolic
disorder causes typical fishy odor.
3.7.2 Treatment:
The treatment of malodor is cause related.
Mechanical reduction of plaque and
microorganisms by cleaning dorsum of
thetongue by tongue scrapper and
interdental spaces by interdental brush and
proper cleaning of oral cavity. If required
professional periodontal treatment is to be
done.
Page 623
 Reduction of oral microbial load by mouth Masking the malodor with rinses and mouth
rinsing with Chlorhexidine0.12% sprays.
mouthwash twice a day for 15 days.

KEY MESSAGE
Maintenance of prope r oral hygiene by using correct teeth br ushing technique and rinsing the
mouth to avoid food lodgement.
Local etiological factors like accumulation of dental plaque, calculus must be eliminated in the
dental clinic.
Rule out and manage systemic disorders leading to periodontal diseases.

Page 624
 4. SPREAD OF ORAL INFECTION
Many of the fascial spaces of head and neck Dysphagia is present
communicate either directly or indirectly with each Difficulty in breathing
other, thus infection in the oral cavity spread from Midline of palate is displaced to unaffected side
one region to another through these spaces. and uvula is swollen
The spaces that get first infected are called Medial displacement of the lateral wall of the
primary spaces. pharynx.
Spaces which get infected later are called as Redness and edema of the area around the third
secondary spaces. molar.

The fascial spaces in head and neck are the potential
spaces between the various layers of the fascia
normally filled with loose connective tissue and
bounded by anatomical barrier usually bone, muscle
and fascial layer.
Differential diagnosis:
The Pterygomandibular space abscess must be
distinguished from Peritonsillar abscess. In
peritonsilllar abscess there is no dental involvement
and less trismus.

1. Important space infections 1.5 Submandibular space:

1.1 Canine space:-
Swelling of cheek and uppe r lip
Obliteration of nasolabial fold
Drooping of angle of the mouth
Edema of lower eyelid it indicates pointing of
abscess below medial corner.
Clinical features:
Firm swelling in submandibular region, below
the inferior border of mandible.
Redness of ove rlying skin, dysphagia, mode rate
trismus

1.6 Submental space

1.2 Buccal space abscess:- Clinical feature:
Space infection is dome shaped and periorbital
edema develops due to impaired venous, and Distinct, firm swelling in midline beneath the
lymphatic drainage. chin.
Swelling be gins at the lower border of the Dysphagia.
mandible and extends upwards to the level of the
zygomatic arch. 1.7 Sub lingual space
Trismus is not usually present. Clinical features:-

1.3 Submassetric space:- Swelling in the floor of the mouth

Dyspnea
Clinical features: Dysphagia
Swelling over the masseter muscle i.e. the
swelling is seen extending from lower border of 1.8 Treatment:
the mandible to zygomatic arch and anteriorly to
All space infections need antibiotics &analgesics,
anterior border of the masseter and posteriorly to
incision& drainage dependi ng upon severity.Cap.
posterior border of the mandible.
Amoxicillin 250/500mg 3 times a day for 3 to 5 days.
Pain over the region Tab. Metronidazole 200/400mg 1BD for 3 days.Tab.
Severe trismus is present Diclofenac 50mg 1BD for 3 days.
Tenderness over the angle of the mandible
Pyrexia and malaise 2. Cellulitis
1.4 Pterygomandibular space Cellulitis is a diffuse inflammation of soft
tissues, tends to spread through tissue spaces
Clinical features: and along fascial planes.
Severe trismus
Cellulitis of face and neck most commonly
Extreme radiating pain results from dental infection either as sequelaof
No evident extraoral swelling
Page 625
apical abscess or osteomyelitis or following
periodontal infection or pericoronitis
2.1 Clinical features:
Painful swelling of the soft tissues
involved that are firm and brawny.
Patient is moderately ill and has raised
temperature and leukocytosis.
If the facial cellulitis persists the infection
frequently tends to become localized and a
facial abscess may form. When this
happens the suppurative material present
seeks to point or discharge upon a free
surface. If early treatment is instituted a
resolution usually occurs without drainage
through a break in the skin.
2.2 Treatment:
Administration of antibiotics and removal of
the cause of infection. Cap. Amoxicillin +
Clavalunic acid 375/625 mg 1BD for 5 days.
Tab. Diclofenac 50mg 1BD for 5 days. To
avoid the further spread of infection or
solidification of abscess the patient should be
Figure 1
3.2 Antibiotic therapy:
Usually IV antibiotics with proper dosage and
frequency are necessary according to age and
severity.
Injection Ampicillin 250/500mg 6 hourly for 3
days
Injection Gentamycin 40/80mg 1BD for 3 days
Injection Metronidazole 50 mg ( 100ml bottle
KEY MASSAGE:
Avoid hot fomentation or application of any counter irritants locally.
Perform incision and drainage of abscess at earliest to avoid further spread of infection.
advised not to massage the affected area with
any medication.
3. LudwigsAngina:
Massive, firm, brawny cellulitis, beginning usually in
submaxillary space and secondarily involving the
sublingual and submental space bilaterally.
3.1 Clinical feature:
A rapidly developing board like swelling
of the floor of mouth and subsequent
elevation of the tongue.
Swelling is firm painful and diffuse.
Trismus, dysphagia
Difficulty in breathing
High fever, rapid pulse and fast respiration
Tongue may be raised against palate
As the disease continues, the swelling
involves the neck, and edema of the glottis
may occur. This carries the serious risk of
death by acute respiratory failure or
septicemia.
IV) TID for 3 days
Injection Diclofenac sodium 3CC for 3 days
Injection Ranitidine 2ml 1 BD for 3 days
Magnesium Sulphate dressing till the swelling
subsides
I.V fluids to maintain the electrolyte balance.
Refer to higher center for further management
immediately.
Page 626
 5. ORAL MUCOSAL LESIONS
1. Chronic cheek or lip biting
Superficial lesions produced by frequent and
repeated rubbing, sucking or chewing
movements that abrade the surface of a wide
area of lip, buccal mucosa, lateral border of
tongue without producing discrete ulceration.
1.1. Clinical feature:
It can occur at any age, common sites are buccal
mucosa at the level of occlusion, lip and lateral
border of tongue.
Traumatic Lesion involving buccal mucosa and lateral border of tongue
Figure 1
2. Oral Candidiasis:
Candidiasis is the disease caused by infection with
yeast like fungus Candida albicans. It can occur
either solely confined to the oral mucosa or as a part
of any of the several mucocutaneous candidiasis
syndromes.
2.1 Oral Thrush or
Pseudomembranous oral
candidiasis.
Candidiasis is the disease caused by infection with
yeast like fungus Candida albicans.
2.1.1 Symptom:
Burning sensation and rapid onset of bad taste.
Clinical features- Common sites are roof of the
mouth, retromolar area and mucobuccal fold.
Clinically pearly white or bluish white plaques are
present on oral mucosa. Patches are loosely adherent
to oral mucosa. Mucosa adjacent to it appears red
and moderately swollen. White patches are easily
Clinically it appear as a linear or diffuse lesion
irregular opaque white. In some cases lacerated,and
reddened area usually with patch of partly detached
surface epithelium.
It is rough on palpation as area becomes thickened
and scaled.
1.2. Treatment:
Recommendation to stop the habit, smoothening of
sharp edges of teeth .Acrylic shields can be fabricated
to cover the facial surface of teeth and there by
restricting access to buccal and labial mucosa.
Figure 2
wiped out with wet gauze leaving a bright red raw
bleeding surface. In some cases it may present as a
brightly erythematous mucosa with only scattered
white patches.
2.1.2 Treatment:
Topical treatment
Clotrimazole: One oral Troche (10 mg
tablet) dissolve in the mouth 5 times daily.
Nystatin oral pastille, 1 or 2 pastilles
dissolves slowly in the mouth 5 times a day.
Clotrimazole 1 % mouth paint topically1 to
2 times/day till lesion subsides.
Nystatin suspension 100,000 units (1 ml of
suspension held in the mouth before
swallowing)
Systemic treatment:
Nystatin -250 mg TID for 2 weeks.
Suppl imental therapy by Vit B12. Tab Vit B
Complex 1OD for 10 days.
Page 627
2.2 Denture Stomatitis: -
Denture stomatitis is a common form of oral
candidiasis that manifest as a diffuse inflammation of
the denture bearing areas and often associated with
angular cheilitis.
2.2.2 Treatment:-
Troches containing Clotrimazole and Nystatin 4-5
times should be applied on the denture after meals.
Antifungal therapy and cessation of denture wearing
till elimination of mucosal inflammation. Rinsing the
denture and applying antifungal cream before
inserting the denture.
2.3 Angular Cheilitis:-
Angular cheilitis is the term used for an infection
involving the lip commissures. The majority of cases
are candida associated and respond promptly to
antifungal therapy. Other possible etiologic cofactors
include reduced vertical dimension, nutritional
deficiency (Iron de ficiency anemia and Vit-B or Folic
acid deficiency)and rarely diabetes, neutropenia and
Figure-3: Aphthous Ulcer
3.1.1 Clinical features:
a) Sites: Occurs most commonly on buccal& labial
mucosa,buccal& lingual sulci,tongue and soft
palate.It begins with prodromal stage of tingling,
burning or itching for 1 to 2 days before the ulcer
occur.Lesions are round to oval in shape,
symmetric,single or multiple.Superficial ulcers
covered by grey membrane.It is surrounded by
localized area of erythema.
b) Minor aphthae : Minor apthae are less than 1 cm
in diameter and heal completely in 7 to 10 days
c) Major aphthae: Size of the lesion is larger than 1
cm and may reach up to 5 cm in diameter. They
interfere with speech and eating. The lesions heal
slowly and leave scars.
d)Herpetiform ulcers: Multiple small ulcers
often upto 100 in number. It is found on any
intra oral mucosal surface. It begins as small pin head
AIDS. Treatment include correction of primary
cause.
3. Ulcerative lesions of oral
cavity
Ulcerative lesions are a group of common oral
mucosal lesions. The most common causes of these
lesions are mechanical and reactive factors, infectious
diseases and neoplasms as well as autoimmune and
hematological disorders. The main clinical feature in
all these conditions is an ulcer.Ulcer consist of
margins, edges, floor and base. Site, Size, Shape of
the ulcer should be examined.
3.1. Recurrent aphthous stomatitis
(RAS)
RAS is a disorder characterized by recurring ulcers
confined to the oral mucosa in patients with no other
signs of disease.Precipitating factors are trauma,
endocrine conditions,stress, allergy, immunological
abnormalities and nutritional deficiency.
size erosion that gradually enlarge and coalesce.
Lesions are more painful. Patient get relief
immediately with 2% Tetracycline mouth wash.
3.1.2 Treatment: -
Medication prescribe should relate to the severity of
the disease.
i. Anaesthetic cream - topical protective
emollient base in mild cases with two or three
small lesions. Pain relief can be obtain with
use of topical anaesthetic agent.
ii. Topical Corticosteroid - Triamcinolone
Acitonide 3 to 4 times daily. Nutritional
suppl ementswithTab. B Complex 1 BD for 10
days.
iii. Maintenance of oral hygiene: - Chlorhexidine
0.12 % mouth wash twice a day for 10 days to
maintain oral hygiene.
Page 628
 Herpetic gingivostomatitis
Figure 4 Figure 5
4. Viral Infection
Herpetic gingivostomatitis:
Herpes simplex, an acute viral infectious disease
caused by herpes simplex virus.
4.1 Clinical features:
The disease occurring in children is frequently
primary attack and is characterized by development
of fever, irritability, headache, pain upon
swallowing,regionallymphademopathy. Within few
days mouth becomes painful and the gingiva become
intensely inflamed appe ar erythematous and
edematous. The lips, tongue, buccal mucosa, palate
may be involved. Shortly yellow fluid filled vesicles
develop. These rupture and form shallow, ragged
extremely painful ulcers cove red by an erythematous
halo. They heal spontaneously with 7 to 14 da ys and
leave no scar.
i.
4.2 Recurrent or secondary herpetic
labialis and stomatitis:-
It is usually seen in adult patients and manifest itself ii.
clinically as an attenuated form of primary disease.
The recurrent form of disease is often associated with iii.
trauma, fatigue, menstruation, pregnancy, upper
respiratory tract infection, emotional upset etc.
4.3 Clinical feature:
Recurrent herpes simplex infection may occur at
widely varying intervals, from nearly every month in
some patients to only once a year or even less in
others. Lesion may either at the site of primary
inoculation or in adjacent area supplied by the
involved ganglion. In may develop on lips (recurrent
herpes labialis) or intra-orally. The lesions are
preceded by burning or tingling sensation and a
feeling of tauntness, swelling or slight soreness at the
location in which vesicle are small 1mm or less in
diameter, tend to occur in cluster and coalesce to
for m large ulcer. These gray or gray-white vesicle
rupture quickly leaving a small red erythematous
halo.
4.4 Treatment:
Acyclovir : Acyclovir cream for lips apply 4 hourly
for 5 days.
Tab Acyclovir 200 mg 5times /day for 3 to 5 days.
Chlorhexidine 0.12% mouthwash twice a day for 10
days
Avoid stress.
Page 629
 6. PREMALIGNANT AND MALIGNANT
LESION
1. Oral leukoplakia:-
It is a whitish patch or plaque that cannot be
characterized clinically or pathologically as
any other diseases and which is not associated
with any other physical or chemical causative
agent except the use of tobacco.
1.1 Homogenous leukoplakia:
It is also called as leukoplakia simplex,
uniform raised white plaque formation,
varying in size, with regular edges.
Oral leukopl akia
Figure 1
1.3 Ulcerated leukoplakia:
It is characterized by red area, which at times
exhibit yellowish area of fibrin giving the
appearance of ulceration white patches are
present at the periphery of the lesions.
1.4 Verrucous leukoplakia:
It is also called as leukoplakia verrucosa. It is
characterized by verrucous proliferation above
the mucosal surface. These lesions
demonstrate sharp and blunt projection.
1.5 Erythroleukoplakia:
1.2 Nodular or speckled
leukoplakia:
Also called as leukoplakia erosiva. It is a
mixed red white lesion in which small
keratotic nodules are scattered over an
atrophic patch of oral mucosa. Nodules may
be pin head sized or even larger. It has got a
high malignant potential.
In some lesions of leukoplakia red component
is present. This intermixed lesions is called as
erythroleukopl akia.
1.6 Treatment:
Patient should be asked to cease tobacco
related habits immediately.
Removal of chronic irritant like sharp,
broken teeth dissimilar metal restorations
and other predispos ing factors like syphilis,
alcohol, etc should be controlled and
eliminated.
1.6.1 Conservative treatment:-
VitaminA: It is given orally, parentally or
topically. Therapeutic dose -75000-300000.
IU for 3months.
Page 630
 Antioxidant therapy: --Carotene
supplementation can be beneficial for
treatment of leukoplakia.
Vitamin B: complex: it is given as
supplement in cases of commissural and
lingual lesions.
1.6.2 Surgical management:-
Conve ntional surgery, Cryo surgery, Fulguration
(electro cautary and electro surgery), Laser treatment.
Biopsy may be carried out if there is no change in
leukoplakia after cessation of stimulus and may
require conservative or surgical treatment
1. Erythroplakia:
Erythroplakia is bright red velvety plaque or patch
which cannot be characterized clinically or
pathologically as being due to any other condition.
Erythroplakia is premalignant lesion with
frequency less than leukopl akia but more malignant
potential.
2.1 Clinical feature:
Erythroplakia occurs predominantly in older men, in
the sixth and seventh decades of life. Erythroplakia
are more commonly seen on the floor of the mouth,
the ventral tongue, soft palate and tonsillarfauces.
Although the etiology is uncertain, most cases are
Figure 3
Some times floor of mouth and gingival.
The onset of condition is insidious and is
often of 2 to 5 years of duration.
Initial symptom commonly seen as burning
sensation of oral mucosa aggravated by
spicy food followed by either hyper
salivation or dryness of mouth. Vesiculation,
ulceration, recurrent stomatitis
Late symptoms are trismus, difficulty in
tongue protrusion, swallowing.
associated with heavy smoking. Erythropl akia is
asymptomatic.
2.2 Diagnosis:
Red velvety patch with no sign of infection and
inflammation
2.3 Treatment:
Removal of cause: elimination of suspected irritant
and observation for one to two weeks. Prompt biopsy
if lesions persist.If biopsy shows dysplasia or
carcinoma total excision is indicated.
3. Oral submucous fibrosis
(OSMF):
Etiological factors are chilly and spicy food, betel
nut, tobacco & lime, nutritional deficiency, etc.
3.1 Clinical features:
It affects both sexes, majority of patients are
between 20 to 40 years, of age.
The most frequent location of OSMF is
buccal mucosa and retromolar area. It also
commonly involves soft palate, palatal
fauces, uvula, tongue and labial mucosa.
Oral submucous fibrosis
The most common and earliest sign is
blanching of mucosa.
As disease progresses the mucosa becomes
stiff and vertical fibrous bandappears. This
bands can be palpable easily.
The mobility of soft palate is restricted.
Uvula when invol ved is shrunken.
Tongue becomes smooth and its mobility is
limited.
Page 631
3.2Treatment:
The treatment of patients with OSMF depends on the
degree of clinical involvement.
3.2.1 Restriction of habit/ behavioural
therapy
The preventive measure should be in the form
of stoppage of habit, through health education.
Affected patients should be explained about
the disease and its malignant potential.
Improvement in clinical features like- gradual
increase in interincisal opening has been
observed in most of patient who discontinue
the habit.
3.2.2 Medicinal therapy
Administration of Vit.B complex and
antioxidants as supportive therapy.
Vitamin rich diet along with iron preparation
is helpful to some extent.
B-Complex preparation Intramuscular
injection starts with small doses and
continuing with larger doses (2ml ampule
daily). The course of 5 injection is repeated
after 7days.
Steroids
Oral Lichen Planus
Figure 4
4.1 Clinical feature:
It may occurs in adulthood with age range for males
35- 44 years and for females 45-54 years. It has
more predilections for females.
4.1.1 Sites:Common are buccal mucosa and to
lesser extent tongue, lips, gingiva, floor of mouth
and palate
4.1.2 Symptoms:Patients may repor t with burning
sensation of oral mucosa.
4.1.3 Clinical feature:Oral lesion is characterized
by radiating white and gray velvety thread like
Local Injection Hydrocortisone 1.5 ml (25
mg/ml) locally in the area of fibrosis
twiceaweek for four weeks or more as per
conditions.
Systemic A therapy with Hydrocortisone
25mg tablet in doses of 100mg per day for 7
days is useful in relieving burning sensation
without untoward effects.
Placental extract 2 ml biweekly or weekly
for three to four weeks locally injected
around fibrous bands.
3.2.3 Surgical treatment like Conventional
surgery ,Laser ,Cryosurgery
3.2.4 Oral Physiotherapy
This includes mouth opening and ballooning
of mouth.
3.2.5 Diathermy
4. Oral Lichen Planus:
It is a chronic immunologic inflammatory
mucocutaneous disorder that varies in appearance
from kerototic (reticular or plaque like) to
erythematous and ulcerative lichen planus
Figure 5
papules in a linear, annular or retiform arrangement
forming typical lacy, reticular patterns, rings and
streaks over the buccal mucosa to a lesser extent on
lip, tongue and palate. Tiny white elevated dots are
present at the intersection of white lines called as
Wickhams straie.
Types are reticular, papular, plaque, atrophic,
bullous, hypertrophic, annular and erosive.
4.2 Treatment:
Small and moderately sized either erosive or
ulcerative painful lesions can be treated with
triamcinolone acitonide cream base. Systemic
steroid tab. Prednisolone (5 mg tab.) in tapering
Page 632
 doses of 30 mg per day for the first of the three superadded with infections.
weeks, 15 mg per day for 2nd week and 5 mg per Radiographicallyitmayshow bone erosion.
day for 3rd and final week. 6.1 Clinical features:-
Symptomatic treatment with topical analgesic, 6.1.1 Benign Tumors:-
topical anesthetic and antihistaminic rinse.
Encapulated tumor
Psychotherapy
Base of tumor is of two types sessile and
pedunculated
5. Cyst of Jaws: Not involving the adjacent tissue
It may be epithelial or non-epithelial. Epithelial cyst Painless and slowly growing
may be odontogenic or non odontogenic. Clinically 6.1.2 Malignant Tumors:-
presenting as smooth, hard, painless Ulcero proliferative lesion
prominence.Dentigerous cyst are mainly associated Invading into adjacent structures
with impacted molars and canines. Pain, paraesthesia
Odontogenickeratocyst are seen in the lower third Trismus
molar area extending into ramus. Radiographically Bony erosion
cyst appears as well defined round or oval areas of Mobility of teeth
radiolucency circumscribed by a sharp radiopaque
Not encapsulated
margin.
Palpable Lymphnodes
Pathological Fracture of the bone
5.1 Treatment of Cyst:
Investigation:
1. Marsupialisation Lateral oblique X-ray,OPG.

2. Enucleation of cyst
6. Tumors:
Presenting as intra oral swelling may be odontogenic
or non odo ntogenic variety, may be central or
peripheral, epithelial or connective tissue origin. The
most common tumor occurring in oral cavity is
squamous cell carcinoma. Tobacco, alchohol,
smoking are the predisposing factors. The patient
may present with a swelling, ulceroprolifertive
growth with involvement of lymphnodes. Pain may
accompany if it involve the adjacent structures or
6.2 Common Cancers
Squamous cell carcinoma
A malignant epithelial neoplasm exhibiting squamous
differentiation as characterized by formation of
keratin and/or presence of intercellular bridges. The
most important task is to establish an early diagnosis
at the first stages of the disease. Risk factors include
use of tobacco in its various forms, alcohol,
ultraviolet light, chronic irritation to oral mucosa,
human papilloma virus infection.

Figure-6: Carcinoma of buccal mucosa

Page 633
6.2.1 Clinical features:- 6.2.2 Prevention: -
a) Symptoms:- Oral cancers can be prevented by /sensible
attitude towards maintenance of oral care
Ulcerative lesion in the oral cavity that does and regular checkups.
not heal. Proper education regarding the adverse
A persistent red or white patch effect of the dreaded habits
Loosening of the teeth or pain around the successful persuasion to quit the bad habits
teeth or jaw. (smoking, alcohol consumption, gutkha)
Voice changes. The presence of persistent grayish white
patches developing in people who smoke or
b) Site:- Tongue, floor of mouth, lower alveolus, chew tobacco needs to be investigated.
buccal mucosa, upper alveolar / hard palate, Maintenance of good oral hygiene.
retromolar area, lip, floor of mouth. Any faulty restoration or a sharp tooth needs
c) Signs -Clinically almost all oral cancers, to be corrected
except those in earliest stages have two
characterized feature in the form of ulceration 6.2.3 Treatment:
and indurated margin. Treatment includes surgical interve ntion,
radiation therapy and c hemotherapy.
6.2.2 Diagnosis: - 7. Tobacco Cessation Centers
History and detail clinical examination, lymph
node examination. (TCC):
It is important for early detection to decrease Setting upTCC facilities at district hospital level. At
mortality rate. the district hospital Tobacco cessation centers are
combined with dental units.

Key massege:
Any discolouration or grayish white patch in the oral cavity must be properly evaluated and managed at early
stage considering possibility of oral malignancies. Cessation of tobacco consumption and self-examination
by patients should be promoted.

Page 634
 7. OROFACIAL PAIN
An unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or
described in terms of such damage associated with
oral lesions.
1. Trigeminal Neuralgia
(TIC DOULOUREUX)
1.1 Clinical Features:
Age Middle and old age group
Episodes of intense shooting
,stabbingpainthatlastsfor a few seconds
andthen completely disappears
Quality of pain Electric shock like ,
unilateral along the course of the affected
nerve
Maxillary branch is most commonly
affected followed by the mandibular branch
and (rarely) the ophthalmic branch.
Invol ve ment of more than one branch occurs
in some cases.
Trigger zones precipitated by light touch on
a trigger zone present on the skin or
mucosa within distribution of the involved
nerve branch. Common sites for trigger
zones include nasolabial fold and the corner
of the lip
Pain aggravated by: - Shaving, showering,
eating, speaking or even exposure to wind.
Number of attacks varies from 1-2 per day
to several per minute
1.2 Treatment:-
Drug therapy
Carbamazepine: - effective therapy for greater
than 85% of newly diagnosed
cases.Tab.Carbamazepine as an initial dose,
100 mg is given twice daily until relief is
established.
Baclofen: - Patient who do not respond to
Carbamazepine alone may obtain relief from
Baclofen or by combining Carba mazepine
with Baclofen
Refer to higher centre for further management
2. Glossopharyngeal
neuralgia
(Ninth cranial nerve neuralgia)
2.1 Clinical features
Characterized by severe paroxysmal pain in
the tonsils and ear
Less intense than trigeminal neuralgia
Similar clinical features as trigeminal
neuralgia
Precipitating factors Yawning, talking,
chewing, swallowing.
Trigger zone: pain sensation following the
distribution of glossopharyngeal nerve
namely, the pharynx, posterior tongue, ear
and intraarticularretromandibular area.
2.2 Treatment:
Similar to trigeminal neuralgia.
Good response to Carbamazepine and
baclofen.
Page 635
 8. TRAUMATIC INJURIES TO TEETH
Class IX Traumatic injuries to primary teeth.
1. Classification :
Traumatic injuries are classified as 2. The various effect of
Class I Simple fracture of the crown, involving trauma to teeth are
little or no dentin. 2.1 Crown Fracture:
Class II Extensive fracture of the crown, If it involves only enamel and dentin
involving considerable dentin but not the (Uncomplicated fracture) aesthetic restoration of the
dental pulp. teeth is sufficient.
Class III Extensive fracture of the crown, 2.1.1 Enamel dentin fracture :
involving considerable dentin and Radiograph is mandatory to determine the full
expos ing the de ntal pulp. extent of the injury.
2.1.2 Fracture Crown without pulp
Class IV Traumatized tooth that become non- exposure:Objective in treating a fractured
vital, with or without a loss of crown crown without pulp e xpos ure is three fold.
structure.
Elimination of discomfort.
Class V Teeth lost as a result of trauma. Preservation of vital pulp.
Class VI Fracture of the root, with or without a Restoration of fracture crown.
loss of the crown structure.
The tooth should be tested with electric pulp tester or
with ice or ethyl chloride spray. If the pulp test is
Class VII Displacement of a tooth, without fracture vital and tooth is comfortable itshould be checked
of the crown or root. again a week, 3 weeks, 3 months, 6 months and 1
year.
Class Fracture of crown en mass and its
VIII replacement.

Figure-1: Crown fracture without pulp e xpos ure

2.1.3 Fracture with pulp involvement:

Figure-2: Crown fracture with pulp expos ure

Page 636
If there is involvement of pulp(Complicated Fracture)
vital pulp therapy canbe done for which optimal time
is first 24 hours.
In traumatic exposure after 72 hours in
immature teeth, full pulpotomy can be
considered for apexogenesis. In mature
teeth, pulpectomy should be done.
In non-vital teeth with the ope n ape x,
apexification is indicated to create an apical
stop.
2.1.3 Treatment
Crown with pulp expos ure: Following
treatments are possible :
Pulpotomy (Pulp is vital).
Apexification (Pulp is necrotic).
Endodontic treatment.
2.2 Root fracture:
In this coronal segment is reduced quickly and
functional splint is placed for 2 to 4 weeks.
When attended in time, pulp necrosis is
Figure 3: Splinting of traumatically displaced upper anterior teeth
remarkably low. It will occur only 25% of the
time and in majority of cases, necrosis will
occur only in the coronal segment and only
that is Root Canal treated.
2.2.1 Root Fracture
If at the free gingival margin Root Canal
Treatment (RCT) & Restore with pos t and
core and crown.
If at the apical 1/3 of root: Tooth should be
stabilized by splinting, RCT & may need to
resect fractured root por tion by surgery and
followed by retrofilling.
If in the middle 1/3 of root: If tooth is
restorable stabilize, RCT, Resect fracture
portion,restoration. If tooth is not restorable or
unable to stabilize extraction is needed.
2.3 Displacement injuries:
Lateral Luxation and avulsion: Lateral
Luxation, extrusion, and avulsion need
emergency splinting & later RCT if required.
Page 637
 9. DISCOLOURATION OF TEETH

1. Introduction:
Discoloration of teeth is a cosmetic problems that is
often the patients primary concern. Although
restorative procedures are available, discoloration can
often be corrected totally or partially by a more
conservative approach.

2. Etiology of Tooth Discolouration:

Extrinsic stains Intrinsic stains

Diet related Dental Fluorosis
Bacterial strains
Tetracycline staining
Medications
Tobacco related Habits Amelogenesisimperfecta
Poor oral hygiene Erythroblastosisfoetalis
Porphyria
Jaundice
Pulpal necrosis
Intrapulpalhaemorrhage due to trauma
Dentin hypercalcification

3. Treatment:
Discolouration can be minimized by oral prophylaxis,
bleaching techniques, composite resine, laminates.

Page 638
 10. MAXILLO-FACIAL INJURIES
Any injury to either a soft tissue or hard tissue of face Fractures which communicate to the exterior through
caused by an assault, road traffic accidents, sharp skin or mucous membrane
instruments, fall, sports injuries or violence can
cause loss of soft tissue and hard tissue which has to
be handled by an oral or dental surgeon meticulously
2.3. Greenstick fracture:
It occurs in immature bone where one surface is
at the time of casualty. compressed and opposing surface is stretched leads to
fracture.
1. Soft tissue injuries:
Abrasion,contusion,ecchymosis,haematoma,avulsion 2.4. Dentoalveolar fracture:
or degloving injury
Fracture of dentate alveolus may occur as a
separate clinical entity or in conjugation
2. Hard tissue injuries: with other
Fracture: External force beyond the modulus of Facial bone fractures are usually associated
elasticity of the bone with injury to teeth like fracture, subl uxation
or avulsion.
2.1. Simple fracture: Fractures of maxillary tuberosity and antral
Closed linear fractures of bone. floor are relatively common complications
which occurs during exodo ntia.
LeFort fractures
2.2. Compound fracture:

Figure 1Facial Deformity

3. Mandibular fractures angle, ramus, condylar process,

coronoid process,and alveolar
3.1 Classification: process.
Fractures of mandible are more common.
3.1.2 Mandibular fractures are
3.1.1 Mandibular fractures are classified
by the anatomicareas involved. These
areas are as follows: symphysis,body,

Page 639
 Figure 2

also classified into simple, compound, Anesthesia, Paresthesia, or Dysesthesia of the

and comminuted. Lower Lip

3.1.3 An important classification of Abnormal Mandibular MovementsMandibular

mandibular angle and body fractures fracturelimited opening and trismus,deviation on
relates to the direction of the fracture opening toward the side of a mandibular
condylar fracture, Inability to close the jaw.
line and the effect of muscle action on
the fracture fragments. Change in Facial Contour and Mandibular Arch
Form
Angle fractures may be classified as
i. Vertically favorable or unfavorable and Lacerations, Hematoma, and Ecchymosis
ii. Horizontally favorable or unfavorable. The diagnostic sign of ecchymosis in the floor of
the mouth indicates mandibular body or
symphyseal fracture.
3.1. Diagnosis of mandibular
Loose Teeth and Crepitation on Palpation
fractures
Dolor, Tumor, Rubor, and Color
The patients health history may reveal pre-existing
systemic bone disease, Tenderness on palpation
The type and direction of traumatic force can be 3.3. Radiology
extremely helpful in diagnosis. Fractures sustained in
vehicular accidents are usually far different from Panoramic radiograph
those sustained in personal alterations. Lateral oblique radiograph
Posteroanterior radiograph
3.2. Clinical Examination Occlusal view
The signs and symptoms of mandibular fractures are Periapical view
as follows. Reverse Towne's view
Temporomandibular joint, including
Change in Occlusion tomograms
Any change in occlusion is highly Computed tomography (CT) scan, CBCT
suggestive of mandibular fracture.

Page 640
Figure 3: Orthopa ntomogram (OPG) Figure 4: 3D Computed
tomography (CBCT) scan

3.4. Management of mandibular Gunning type splints

fractures
3.4.1 Closed reduction basic methods
Direct interdental wiring
Indirect interde ntal wiring
Continuous or multiple loop wiring
Arch bars
3.4.2 Open reduction with direct skeletal
fixation
Allows the bones to be directly manipulated through an
incision so that the fractured ends meet, then they can be
secured together either rigidly (with screws or plates and
screws) or non-rigidly (with transosseous wires).

Close Reductionof fracture mandibleOpen Reduction of fracture mandible

Figure 5 Figure 6

3.4.3 Post-operative care: Oral hygiene maintenance by using mouth

Soft diet and liquids rinses
Control of infection

Page 641
 10. TEMPOROMANDIBULAR
JOINT DISORDERS

1. Trismus: 1.3. Investigation:

OPG,CTscan,MRI
Restriction of normal oral opening or inability to
ope n the mouth fully. Trismus is also defined as a
condition in which muscle spasm on contracture 1.4. Management:
prevents opening of the mouth (due to infection or i. Before starting treatment reassure the patient.
other condition which alter muscle) ii. Anti-inflammatory dr ugs and a nalgesics.
iii. Antibiotics in case of infection.
1.1. Causes of trismus iv. Space infection:-antibiotics, incision and
1.1.1 Articular:- drainage.
i. Ankylosis: - Fibrous ,Bony v. Muscle relaxants and mouth gags followed by
ii. Arthritis: - Stills disease (children) ,Rheumatoid physiotherapy.
(adults) vi. Tetanus- IM Immunoglobulin followed by
iii. Pyogenic arthritis antibiotics.
iv. Osteoarthritis vii. Tetany- IV Calcium Gluconate 10mg.
v. Psoriatic viii. Splints (soft as well as anterior bite planes)
vi. Reiter Syndrome ix. Fracture: - Reduction and fixation either closed
vii. Gout or open under LA or GA.
viii. HarieStrumpell disease x. Surgical intervention.
ix. Congenital syphilis
x. Fracture Condyle
2. Dislocation, Subluxation,
1.1.2 Extra Articular Hypermobility of
i. Myositis ossificans: - following trauma to the
masticatory muscles especially masseter. Temporomandibular Joint
ii. Infection:-Orofacial infection around the TMJ
area can bring about trismus or limitation of
(TMJ):
oral opening. Odontogenic infection like
pericoronitis, Ludwigs angina, submassetric
2.1 The dislocation can be
space infection, mumps, tuberculosis unilateral or bilateral
osteomyelitis, parotid infection i. Anterior mandibular dislocation
iii. Oral Submucous fibrosis ii. Acute
iv. Systemic causes: -Tetanus,Tetany. iii. Chronic recurrent (habitual) subl uxation
v. Trauma:-Fractures involving zygomatic arch, iv. Long standing
fracture of mandible also causes trismus, pain
and tenderness or muscle spasm. The term luxation is used for complete dislocation.
vi. Malignancies of oral cavity: Either due to Subluxation or hypermobility is a partial or
infiltration or due to pain incomplete dislocation.
vii. Osteomyelitis
viii. Coronoid hyperplasia 2.2. Causes:
ix. Scarring of the temporalis Extrinsic or Iatrogenic causes:-
x. Fibrosis of pterygomandibularraphae due to
cleft palate surgery. i. Blow on the chin while mouth is ope n
ii. Injudicious use of mouth gag during general
1.2. Clinical examination: anaesthesia.
iii. Excessive pressure on mandible during dental
Detailed clinical history. Inspection, Palpation,
extraction.
Auscultation in an around thetemporomandibular
iv. Post traumatic.Intrinsic or Self-induced:
joint and muscles of mastication.

Page 642
 i. Excessive yawning,
ii. Vomiting,
iii. Opening mouth too wide for eating o
iv. Hysterical fits.
2.3. Clinical feature:
2.3.1Unilateral acute dislocation.
Difficulty in mastication and swallowing
Difficulty in speaking
Profuse drooling of saliva
Deviation of the chin toward contralateral side
Deviation produces a lateral cross and open bite
on the contralateral side
The mouth is partly open and the affected
2.4. Treatment:
condyle cannot be palpable.
Figure 1
2.4.1 Manipulation:-
Remains the same irrespective of type of anesthesia.
First of all patient should be given assurance
about procedure and asked to relax completely.
Operator has to stand infront of the patient, he
has to grasp the mandible with both the hand one
on each side.
The thumb of operator should be covered
with gauze to prevent injury during
manipulation. The thumbs are placed on occlusal
surfaces of lower molars and finger tips are
placed below the chin. Operator has to exert full
body pressure on posterior teeth to depress the
jaw and at same time the finger tips are placed
2.3.2 Bilateral acute dislocation:-
Pain, inability to close the mouth, tense
masticatory muscles.
Difficulty in speech.
Profuse drooling of saliva
Protrudi ng chin
Mandible is protruded and movements are
restricted.
Patients complains of pain in temporal region
rather than the joint.
Distinct hollowness can be felt in both
preauricular regions.
Reassuring the patient.
Tranquilizer or sedative drugs.
Pressure and massage of the area.
Manipulation with or without anesthesia.
Press his gemclar teeth
downwards at the same time
press the undermoach of his
chin upwards and backwards
below the chin to elevate it by giving upward
pressure. The downward pressure overcome
spasm of muscle, plus it brings the locked
condylar head below the level of articular
eminence and then backward pr essure is given to
push the entire mandible posteriorly.
After this reduction procedure, the mouth is
closed and patient is asked to keep the mouth
opening restricted.
Immobilization can be carried out by giving
barrel bandage for 10 to 14 days period. Patient
is kept on semisolid diet. Anti-inflammatory
analgesics prescribed for 3to 5 days.
Page 643
Long standing acute dislocation which do not
respond to above procedure can be reduced by
administering general anesthesia. If manual reduction
fails than open surgical procedure as last resort.
3. Temporomandibular
disorder (TMD):
Temporomandibular joint syndrome or
temporomandibular disorder (TMD) is the most
common cause of facial pain after toothache. TMD
can be classified broadly as TMD secondary to
myofacial pain and dysfunction (MPD) and TMD
secondary to true articular disease.
MPD form is associated with pain without apparent
destructive changes of the TMJ on x-ray. It is
frequently associated with bruxism and daytime jaw
clenching in a stressed and anxious person.
3.2. Etiology:
The etiology of TMD is multifactoral and includes
malocclusion, jaw clenching, bruxism, personality
disorders, increased pain sensitivity and stress and
anxiety.
3.3. Clinical feature:
i. Pain
ii. Muscle tenderness
iii. A clicking or popping noise in the
temporomandibular joint.
iv. Limitation of jaw motion unilaterally or
bilaterally.
3.4. Differential diagnosis:
Cluster headache, migraine headache, post herpetic
neuralgia, temporal or giant cell arteritis, trigeminal
neuralgia.
3.5. Treatment:
Counselling regarding self-care and reversal of
parafunctional habits.
Heat application to increase local circulation
which act as a sedatives and lowers muscle
tension to be given for 15 to 20 minutes 4
times a day.
Cryotherapy with Ice packs application to
the painful area 4 times a day for 20 minutes
for relief of pain followed by an acute injury
superimposed over a chronic TMD.
Mild analgesic Tab.Diclofenac 50 mg 1 BD.
Anti-anxiety agents for short duration in
acute pain like.Tab Diazepam 2 to 5 mg a
bed time for 10 days.
Physiotherapy andActive stretch exercise.
Intraoral appliances: Use of Splints,
orthopedic appliances, bite guards, night
guards or bruxing guards.
Stress management
Page 644
 11. DENTAL IMPACTION
1. Introduction:
Impaction is cessation of eruption of tooth caused by
physical barrier or ectopic positioning of tooth.
An impacted tooth is one that is erupted, partially
erupted or unerupted and will not eventually assume
nor mal arch relationship with other teeth and tissue
commonly seen with third molar and sometimes
maxillary canine teeth

Figure 1

Figure 2

2. Types of Impaction: relation to long axis of second

Soft tissue impaction. molar
Bony impaction. Mesioangular
Distoangular
3. Third molar impaction can Horizontal
Vertical
be classified by angulation in Buccoangular
Linguoangular

Page 645
4. Clinical Features:
Difficulty in ope ning the mouth and de glutition.
Localized tenderness and swelling.
Radiating pain towards ear and sometimes
headache.
Purulent discharge may be present from the site
of infection.
5. Investigations:
IOPA X-Ray, lateral oblique x-ray, OPG,
Complete haemogram
6. Treatment:
Advice antibiotics and analgesics.
Cap.Amoxicillin 500mg 1 BD for 5days.
Tab.Diclofenac 50mg 1 BD for 5days.
Surgical removal of impacted tooth.
Page 646