Clinical Surgery Notes

1
The Podmedics
Surgery Revision Notes
Podmedics 2010
Introduction
Welcome to these notes on the basics of surgery for undergraduates. Learning in an age where information, both in the clinic and the library, is so accessible, the authors have often felt a little overwhelmed. While many texts are excellent, we feel that none currently provide a good summary to get students started. Often the hardest toil in studying medicine is guring out how precisely to get started. In these notes we outline some of the common processes that are used to break down both presentation of the disease and the processes that drive it. Having done this, we then use these techniques as a schema for our notes. The notes are based upon a series of podcasts written by Jonny and Ed during early 2008 (the podcasts are available at the site). While they are clearly aimed at the level required for UK nal MBBS, they should be useful to students at any stage of their training. It is our belief that these notes, together with the supporting podcasts, make up a denitive and useful revision tool for students. A considerable amount of work has gone into preparing these notes. Please support us by telling you friends and pointing them in our general direction.
Thank you and good luck.
The Podmedics Team
Contact us
The Podmedics constantly aim to improve the quality, accuracy and consistency of their content - please do get in touch if you have any questions or comments.
Ed Wallitt: ed@podmedics.co.uk Jonny Manley: jonny@podmedics.co.uk
Please do not reproduce these notes without prior permission. All images remain the property of their original authors.
DISCLAIMER: No responsibility is taken for errors/omissions from these notes. They are written by students for students.
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Podmedics Recommended Texts/Links/Courses
Websites
www.podmedics.com Please forgive us the indulgence of being placed first.
www.onexamination.com You must answer questions from this site!
Google images Fantastic for practising presentations of just about anything you can think of.
Texts
Surgical Talk Probably the only medical book ever written that is possible to read in bed.
Lecture Notes on Surgery Harold Ellis was one of the finest surgeons and medical educators of his time. His book is great (...if you want to be a surgeon)!
Courses
The 10-week Surgery Revision Course Hosted by the MDU and the mighty Mr Barry Paraskevas
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Table of Contents
Key Principles ! Surgical Fluids and Nutrition!
Fluids! Nutrition!
8 12
12 15
Trauma Surgery!
Advanced Trauma Life Support (ATLS)! Chest Trauma! Head Trauma! Burns!
18
18 24 28 32
Peri-operative Care !
Pre-operative! Post-operative!
35
35 38
Skin Disorders! The Oesophagus !

Clinical Anatomy! Dysphagia! Oesophageal Tumours! Gastro-oesphageal reflux disease! Hiatus Hernia and other conditions!
42 47
47 48 50 52 53
The Stomach!
Clinical Anatomy! Acute Upper GI Bleed! Peptic ulcer! Perforated Peptic Ulcer! Gastric Cancer!
57
57 59 61 63 65
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Gallstone and Biliary Disease!

Clinical Anatomy! Introduction to Gallstones! Gallbladder Complications! Biliary Tree Complications! Intestinal Complications!
68
68 69 70 73 75
The Spleen!
Clinical Anatomy! Hypersplenism & Hyposplenism! Splenectomy! Splenic Trauma!
77
77 78 79 80
The Pancreas!
Clinical Anatomy! Pancreatitis! Pancreatic Tumours!
83
83 85 90
Basic Principles of the Lower Gastrointestinal Surgery !

Important Clinical Anatomy! Intestinal Obstruction!
92
92 95
Colon Cancer and Stomas!

Colorectal carcinoma! Emergency bowel operations! Stomas!
100
100 103 104
Inammatory Conditions!
Appendicitis! Diverticular Disease! Surgical Ulcerative Colitis! Crohns Disease!
105
105 107 109 111
Peri-Anal Disease!
Clinical Anatomy!
113
113
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Haemmorrhoids! Anal Fissures! Anal abscess/Anal sepsis! Anal Fistula! Rectal Prolapse! Anal Carcinoma!
114 116 117 118 119 120
Breast Disease !
Clinical Anatomy! Diagnostic Principles in Breast Disease! Benign Breast Disease! Malignant Breast Disease!
123
123 124 125 127
Neck Lumps!
Clinical Anatomy! Lymphadenopathy! Solitary Lumps in the Neck! Thyroid Surgery!
131
131 134 135 139
Hernias ! Vascular Surgery !

Clinical Anatomy! Venous Disorders! Arterial Disorders!
143 149
149 151 154
Orthopaedics!
Basic Fractures! The Hip! Important other fractures for finals! The Knee!
167
167 170 175 179
Neurosurgery!
Clinical Anatomy! Spinal Cord Compression!
183
183 184
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Neurological Tumours! Hydrocephalus!
186 187
Urology!
Clinical Anatomy! Common presentations! Kidney and Bladder! Prostate Disease! The Scrotum! Testicular Cancer!
189
189 190 197 202 206 210
Appendix!
Common abdominal scars! Common drugs!
212
212 213
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Key Principles
Here we outline some of the different common techniques that can be applied throughout the eld of surgery.
General approach to dening a disease

1. 2. 3. 4. Denition (and classication) Epidemiology (and risk factors) Aetiology Clinical features a. Symptoms/Signs (further split each into general and specic) 5. Investigations 6. Management 7. Complications
Common techniques
Aetiology When thinking about aetiology try to think in terms of... 1. Anatomy - i.e. what are the surrounding structures/associated pathologies that could be causing the given problem. Surgical sieve - what pathological processes could be occurring?
2. !
THE VINTA MEDIC SURGICAL SIEVE
Process
Sub-split Heart Blood vessels Bacterial Viral Fungal Protozoal Primary Secondary Penetrating Non-penetrating Gel and Coombs classication
Process
Sub-split
Vascular Infection
Metabolic/Nutritional Electrolytic
Anions Cations Non-charged
Neoplastic Trauma
Degenerative Iatrogenic
Drugs Interventional procedures
Autoimmune
Congenital
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Clinical features
This should be split into symptoms and signs and each of these should be sub-divided into general and specic. Have this table memorised in your head and go through it logically when you are thinking of investigations to do. Investigations
Modalities
Cultures
Tests + Findings
Blood Urine MC & S, dipstick / pregnancy test CSF Joint aspirate Pleural/peritoneal uid NB: usually justied if the patient is ill For each test you must be able to justify why you are performing it Plain X-ray e.g. chest, abdomen, bones Plain X-ray series + contrast USS CT/MRI PET/radio-isotope Specic tests for a given system that do not t into the above. e.g. ECG, lung function test, pH manometry
Bloods - ABG Bloods - Venous Imaging
Scopic/Biopsy Functional
Treatment
If an emergency you must rst talk about RESUSCITATION e.g. Airway, Breathing, Circulation etc.
Modalities CONSERVATIVE
Specics Always think about: 1. Basic things e.g. analgesia, uids, 2. Risk factor management This is surgery..but we still use drugs What techniques can be used, what do they involve and when are they indicated
MEDICAL SURGICAL
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Complications These are split into general (applicable to any surgery) and specic (applicable to the described surgery). GENERAL Think in terms of: Airway e.g. difculties with management Breathing e.g. hypoxia Circulation Drugs e.g. allergies, anaesthetic reactions Exposure to the theatre environment e.g. hypothermia, accidental injury Specic - Immediate At time of surgery e.g. primary haemorrhage, visceral damage Specic - Early 1-3 days post-surgery e.g. pyrexia, SOB, reactionary haemorrhage, urinary retention, oliguria Specic - Late 3-10 days post-surgery e.g. infection, DVT/PE, C. diff colitis
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Surgical Fluids and Nutrition

Fluids
Fluid and Electrolyte Distribution
Average 70kg man - 42L (60-70%) ! ! - INTRACELLULAR - EXTRACELLULAR (plasma, interstitial, transcellular e.g. ocular, uid, pleural)
Osmolality (280-295 mosmol/l) - should be equal between IC and EC CHARGED + UNCHARGED
(Na++K++Cl-+HCO-) + (urea+glucose) = 2(Na++K+) + urea + glucose
INPUT Oral Food Oxidative water 1.5L 1L 0.5L Urine Stool Skin Lungs TOTAL 3L
OUTPUT 1.5L 0.5L 0.5L 0.5L 3L
Total insensible = skin loss + lung loss.
Daily Requirements
Water 40ml/kg/day ~ 3 L per day Electrolytes Na+ = 100 mmol/day K+ = 60 mmol/day
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Indications for Intravenous Fluids

1. 2. 3. 4. 5. Pre-operative resuscitation Replacement of normal loss Replacement of additional loss Postoperative resuscitation Electrolyte disorders
Types of Fluids
Types CRYSTALLOIDS
- Electrolytes in water that form a true solution and pass through semi-permeable membrane.
Contents 154 mmol Na+ in 1L
Normal saline
Dextrose saline 5% dextrose Hartmanns (lactated Ringers solution) COLLOIDS

- Fluid with high molecular weight molecules that does not form a true solution and does not pass through a semi-permeable membrane.
30 mmol/l Na+ + 40g dextrose 50g dextrose in IL Anions + Cations + Ca + lactate
Natural e.g. blood, albumin
Synthetic e.g. Gelofusin, Haemaccel
Dextran compounds
Fluid Regimes
1L normal saline + 2L 5% dextrose OR 3L dextrose saline
+ 20mmol/l of K+ per bag
Important caveats: Always replace ADDITIONAL LOSSES e.g. vomiting, diarrhoea, ileostomies, 3rd space If fever (20% extra/day or 500ml/degree above 37) No potassium 24-48 hours post surgery (non-cardiac) Hartmanns is also known as LACTATED RINGERS SOLUTION and should be avoided in liver and renal failure.
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Assessment of volume status

Check uid charts and other bedside charts, quick history. Observation: awake/orientated or confused, shortness of breath. Inspect for: Cap. rell (> 3 secs) Temperature of the hands Increased skin turgor Tachycardia/tachypnoea Blood pressure (late sign) Low JVP Sunken eyes Dry mucous membranes Examine chest and peripheries for oedema
Features of JVP: Falls on inspiration Falls on standing Non-pulsatile Lies between the 2 heads of the SCM Has a double waveform
URINE OUTPUT: Should be 0.5 ml/kg/hr (= 30ml/hr for 70kg man) If no output/anuria: 1. SIMPLE STUFF e.g. check catheter & bag, ush the catheter with 50 mL saline using a bladder syringe 2. Fluid challange (250ml colloid - repeat a couple of times) 3. Senior review and consider CVP monitoring
A central venous pressure line is often used in order to gauge the response to a uid challange. If the patient is UNDERFILLED the CVP will not increase with the challange or will increase the fall again If the patient FILLED then the CVP will rise (> 10mmHg) and stay elevated
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Nutrition
Nutrition is important as it affects outcome 1. Impaired immune system 2. Delayed/poor wound healing 3. Longer rehabilitation (so increased cost, nosocomial infections, DVTs)
Assessment
HISTORY EXAMINATION
Eating habit, diet, recent changes in weight/appetite Regular weights BMI Waist circumference (>102 cm in men, > 88 cm in women) Upper arm circumference Ulnar length Grip strength Skin fold thickness Albumin Pre-albumin Phosphate Transferrin Lymphocyte count
ANTHROPOMETRIC
BLOOD TESTS
BMI = weight (kg) / height (m)2
Normal Overweight Obese Morbidly obese
18.5 - 25 25 - 30 30 - 40 > 40
Waist circumference is a better representation of omental fat + better predicts development of metabolic syndrome.
Daily Requirements
Calories:! Protein:!! Nitrogen:! 25-35 kcal/kg/2 hrs (usually ~ 2500 per day for men and ~ 2000 per day for women) 1.5 kg/24 12g per day
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Nutritional Therapy
Basic denitions:
ENTERAL - Nutrition that is delivered via the normal enteral route PARENTERAL - Nutrition that is delivered directly through the venous system.
1. Enteral Nutrition
To use this form of nutrition it is necessary for patients to have some degree of functioning bowel. There are 3 types of feed: 1. POLYMERIC Near to normal e.g. food-supplements (Nsure, Fortisip), OSMOLITE 2. DISEASE SPECIFIC Gluten-free diets in coeliac disease, liver disease feeds 3. ELEMENTAL Basic AA and saccharides e.g. chronic multiple stulae in Crohns This may be administered: 1. ORAL 2. Fine-bore NG tube (check for aspirate, CXR) [< 6 weeks] 3. Gastrostomy (surgical/PEG) 4. Jejunostomy
Complications of enteral nutrition:
Feed itself
Too much feed/too little feed Intolerance (nausea/vomiting and diarrhoea) Electrolyte + glucose imbalance Malposition of NG tube Tube obstruction Infection around gastrostomy/jejunostomy
Method of delivery
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2. Total Parenteral Nutrition
This should be avoided if at all possible. The main indication is NON-FUNCTIONING BOWEL e.g. short bowel syndrome, prolonged ileus, severe Crohns disease May be administered through: 1. Large peripheral line 2. Central line (tunnelled = Hickmann line)
Complications of parenteral nutrition:
Feed itself
Reactive hypoglycaemia Fatty liver Vitamin deciencies Complications of inserting a central line e.g. pneumothorax, bleeding Infection around site Sepsis Malposition
Method of delivery
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Trauma Surgery
Advanced Trauma Life Support (ATLS)

Trauma is the leading cause of death due to injury worldwide, and may be dened as: A body wound or shock caused by a serious and life-threatening injury.
The trimodal death distribution describes death due to injury in three peaks or periods. The rst occurs within seconds to minutes of injury and is due to severe injuries where only prevention can reduce deaths. The second occurs within minutes to hours, where the golden hour of care with rapid assessment and resuscitation can save lives. The third peak occurs after several days to weeks and is often due to sepsis and multiple organ dysfunction. When treating traumatised patients we use ATLS Principles:
1. Primary Survey/Resuscitation ABCDE 2. Secondary Survey AMPLE Top-to-toe examination 3. Denitive treatment
TRIAGE is the process of prioritising care based upon available resources and the extent of injuries sustained.
The Primary Survey

This basically is RESUSCITATION and may be remembered using the familiar mneumonic ABCDE.
Airway and C-spine
1. Airway and C-spine
Breathing
The C-spine must be secured with in-line immobilisation. Unknown trauma to this area could lead to severe spinal injury and breathing compromise. Initially this may require manual immobilisation, but eventually inline support of the C-spine needs triple immobilisation with: 1. Hard collar 2. Blocks or sandbags 3. Tape over chin and forehead
Circulation
Disability
Exposure
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The airway must be assessed and treated.
ASSESSMENT
1. If orientated and speaking...AIRWAY IS SECURE. 2. If obtunded or gurgling/stridor...AIRWAY NEEDS SECURING. 3. If complete obstruction...OPEN and SECURE. Chin lift or jaw thrust Remove foreign bodies with ngers Suction with a Yanker tube e.g. vomit, blood Secure the airway e.g. nasopharyngeal, oropharyngeal - Guedel, ET tube, surgical
TREATMENT
Types of Airway
The best person to manage the compromised airway is an anaesthetist. Airways may be divided into: NON-SURGICAL and SURGICAL and NON-DEFINITIVE and DEFINITIVE A denitive airway is an adequately secured, cuffed tube in the trachea. An ETT and tracheostomy are denitive airways. Note that an LMA is not a denite airway, as patients are still at risk of aspiration. The indications for a denitive airway are: Apnoea Inability to maintain a patent airway Risk of aspiration or obstruction GCS < 8 Inadequate oxygenation via face mask oxygenation
NON-SURGICAL AIRWAYS Nasopharyngeal Sizing - patients little nger For the conscious patient with an intact gag reex Contraindicated in basal skull fractures Sizing - from the angle of the mouth to the tragus For the unconscious patient with an absent gag reex Sizing - 6-8 mm diameter, a general rule of thumb 7 mm for an adult female and 8 mm for an adult male This is a denitive airway The correct positioning of an ETT can be conrmed with: 1. Bilateral air entry on auscultation 2. No borborygmi 3. C02 detector 4. CXR
Oropharyngeal (Guedel)
Endotracheal tube (ETT)
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NON-SURGICAL AIRWAYS SURGICAL AIRWAYS Needle cricothyroidotomy Surgical cricothyroidotomy These are required where attempted ETT has failed. A needle cricothyroidotomy is a short-term measure. It can only oxygenate the patient for 30-45 minutes, as ventilation is limited with a wide-bore cannulae. A surgical cricothyroidotomy is preferable to a tracheostomy in an emergency situation. A tracheostomy is a denitive airway.
Tracheostomy
2.
Breathing
Attach patients to a monitor for BP, HR, ECG tracing and oxygen saturations and do an ABG to assess oxygenation. All patients should have high ow oxygen through a non-rebreathing mask.
Assessment: INSPECTION Signs

Agitiation (hypoxia) Obtundation (hypercarbia) Cyanosis (peripheral/ central) Respiratory rate and oxygen saturations Breathing pattern (in cervical cord transection involving C3-5 supplying the diaphragm there will be abdominal breathing) Snoring, gurgling, stridor, hoarseness
PALPATION
Trachea for deviation Paradoxical breathing ail chest segments
PERCUSSION
Hyper-resonance (PNEUMOTHORAX) Hypo-resonance (HAEMOTHORAX)
AUSCULTATION
Air entry (absent, unilateral, bilateral)
Treat any life-threatening problems such as tension pneumothorax, massive haemothorax or ail chest. It is important to maintain adequate oxygenation to prevent cerebral hypoxaemia and ischaemia.
3. Circulation
Secure IV access (2 large bore cannulae into ante-cubital fossae) and take trauma bloods (FBC, U&Es, clotting) & CROSS-MATCH 6 units. Consider urinary catheterisation after PR to exclude a high-riding prostate, which indicates urethral injury.
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Shock can be classied into: 1. HAEMORRHAGIC 2. NON-HAEMORRHAGIC a. Cardiogenic b. Neurogenic c. Septic The most common form of shock in the context of trauma is HAEMORRHAGIC shock. Assess for hypovolaemia and SHOCK: Observation: alert and orientated, confused, or unconscious. Inspect for: Cap. rell (> 3 secs) Cold hands Tachycardia Tachypnoea Hypotension (late sign) Low JVP Low urine output
Haemorrhagic shock can be divided into four classes. The percentage blood loss parameters are easily remembered using the tennis scoring system and blood loss volume is based on a 70 kg male, where total blood volume is approximately 5 L (7 % of the circulating blood volume). Class I Blood loss (%) Blood loss (mL) HR BP PP RR UO (mL/hr) CNS status < 15 % < 750 mL < 100 Normal Normal 14 - 20 > 30 Anxious Class II 15 - 30 % 750 - 1500 mL 100 - 120 Normal Decreased 20 - 30 20 - 30 Anxious Class III 30 - 40 % 1500 - 2000 mL 120 - 140 Decreased Decreased 30 - 40 5 - 15 Confused Class IV > 40 % > 2000 mL > 140 Decreased Decreased > 35 Anuric Lethargic
Simply put, patients with Class I shock have normal parameters but maybe anxious. Class II patients are tachycardic and tachypnoeic but BP remains normal with a decreased PP. Class III patients have tachycardia, tachypnoea, hypotension and confusion, and Class IV patients have all signs of shock with a reduced GCS. All patients with signs of shock are presumed to have haemorrhagic shock, as this is the most common cause of shock in the context of trauma. 1-2 litres warm crystalloid (Hartmanns/normal saline) should be administered STAT. Blood (type-specic, crossmatched or O. negative emergency blood) may be required if the patient continues to haemorrhage. There are four main sources of HAEMORRHAGIC SHOCK which can be remembered using the mneumonic Blood on the oor x four more
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CHEST, RETROPERITONEUM, PELVIS, THIGH AND ON THE FLOOR
Response to initial uid resuscitation (2 L crystalloid) determines subsequent therapy, and response can be divided into rapid, transient and no response: Rapid Response Minimal blood loss Transient Response Ongoing blood loss or inadequate resuscitation Transient improvement but recurrence of tachycardia and hypotension 20 - 40 % High Moderate Type-specic Moderate No Response Exanguinating haemorrhage Remains shocked
Vital signs
Normal
% Blood loss Need for more crystalloid Need for blood Blood preparation Need for operative intervention
10 - 20 % Low Low Type and crossmatch Low
> 40 % High High O-negative High
4.Disability
Assess: 1. Coma scale (see head trauma) AVPU GCS 2. Limb Posture 3. Pupils! !
The Pupils Assess for size, equality and responsiveness: Appearance Bilateral fixed and dilated Cause Death, hypovolaemia, drugs (ecstasy, adrenaline)
Unilateral fixed and dilated Bilateral pinpoint
Orbital injury, oculomotor nerve compression, stroke Opioid drugs
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Bilateral constriction Irregular
Brainstem injury Trauma, post eye operation
5.Exposure
Remove all clothes & prevent hypothermia (warmed IV uids, warm resuscitation room, hot air). Look for evidence of trauma: Front Back (log-roll to protect C-spine) PR for high-riding prostate
Imaging in Trauma
There are 3 important mobile tests: 1. 2. 3. C-spine XR (must include C7-T1) Pelvis XR Chest XR
[+ ultrasound abdomen] also known as a FAST scan. Other tests may be performed but the patient should be stable rst. Beware of the donut of death!
The Secondary Survey

This has 2 important components: 1. HISTORY - AMPLE Age Medication Past medical history/pregnant Last meal Events 2. ! Top-to-toe examination
Note: if the patients state changes at any time then you must return to the beginning of the primary survey.
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Chest Trauma
There a huge number of possible chest injuries that result from trauma. Here we consider the most important: 1. 2. 3. 4. 5. Rib fractures, pulmonary contusion and ail segments Pneumothorax Haemothorax Cardiac tamponade Others: tracheobronchial tree injury, blunt cardiac injury, aortic disruption, diaphragmatic injury, oesophageal rupture
Remember the mneumonic ATOM FC memorise life threatening chest injuries: Airway obstruction Tension pneumothorax Open pneumothorax Massive haemothorax Flail chest Cardiac tamponade
1. Rib Fractures
Fractures of ribs 1 - 3 imply severe injury to the head, neck and great vessels Fractures of ribs 4 - 9 are most common and can damage adjacent viscera leading to haemopneumothorax and lung contusion Fractures of ribs 10 - 12 can damage the liver and spleen Multiple fractures can lead to Flail segment 2 consecutive ribs fractures in 2 places
This causes HYPOXIA from 1. PARADOXICAL MOVEMENT ON INSPIRATION 2. Restricted chest wall movement due to pain 3. Underlying lung contusion Treatment is with Analgesia Strapping of the segments Invasive positive pressure ventilation (if resistant hypoxia)
2. Pneumothorax Air in the pleural space.
This is due to either blunt or penetrating trauma and there are 3 types:
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a. SIMPLE - accumulation of air with no mediastinal displacement. b. TENSION - accumulation of air through a one-way valve leading to accumulation and mediastinal displacement. c. OPEN - opening in the chest wall (2/3 diameter of the trachea) resulting in a sucking chest wound.
A tension pneumothorax is a MEDICAL EMERGENCY!
INSPECTION Important signs

- Sudden cardiorespiratory compromise - SOB
PALPATION
- Reduced movement on affected side - Tracheal displacement away from affected side
PERCUSSION
Hyper-resonant
AUSCULTATION
Absent breath sounds on affected side
IMMEDIATE RX - ...large bore needle into 2nd intercostal space in mid-clavicular line. (needle thoracotomy) Initial management of an open pneumothorax is placing a sterile dressing secured on three sides in order to provide a utter-type valve effect. Denitive treatment for all pneumothoraces is the insertion of a chest drain on the affected side (draining the apex) in the 5th intercostal space, just anterior to the mid-axillary line.
3. Haemothorax Blood in the pleural space
These are due to penetration or decelerating injuries
INSPECTION Important signs

- Distress - Hypoxia - Distended neck veins
PALPATION
- Decreased movement on affected side - Tracheal deviation away from the affected side
PERCUSSION
Stony dull
AUSCULTATION
Decreased breath sounds on affected side
Treatment depends on the size Small (< 1.5L) Fluid resuscitiation Chest drain Massive (> 1.5L or draining > 200ml/hr for 2 - 4 hrs) from damage to the great vessels, hilar and heart Fluid resuscitation (including blood) Chest drain Thoracotomy
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4. Cardiac Tamponade
Blood from the great vessels/heart within the pericardial sac leading to restricted lling and contraction.
Clinical features described in BECKS TRIAD 1. 2. 3. Elevated JVP (restricted lling) Hypotension (restricted lling and contractility) Mufed heart sounds (blood in pericardial sac)
Dont forget Kussmauls sign, a rising JVP with inspiration. Investigation: Echocardiography Management: Peri-cardiocentesis with ECG monitoring (to detect myocardium) Thoracotomy
5. Others
Tracheobronchial tree injury (high mortality) Clinical features Haemoptysis Subcutaneous emphysema Tension pneumothorax with persistent air leak after tube thoracostomy Investigation Bronchoscopy Management Surgery Blunt myocardial contusion Clinical features Hypotension Dysrhythmias Wall motion abnormality on echocardiography Management Monitor for dysrrhymias
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Aortic Disruption Most common cause of death following rapid deceleration in an automobile collision or fall from a great height. Usually , there is an incomplete laceration near the ligamentum arteriosum of the aorta and a contained haematoma. Diagnosis requires a high index of suspicion. Investigation CXR - widened mediastinum CT chest Management ! Cardiothoracic surgery Diaphragmatic injury These are more common on the left side and maybe caused by blunt or penetrating trauma. Early diagnosis requires a high index of suspicion. Investigations CXR - elevation of the diaphragm Management Surgery Oesophageal rupture This maybe due to blunt or penetrating trauma. Blunt oesophageal rupture is due to the forceful expulsion of gastric contents into the oesophagus, after a severe trauma to the upper abdomen. Clinical features Pain out of proportion to the injury Left pleural effusion or pneumomediastium Particulate matter in the chest drain Investigations Oesophagosocpy Contrast studies Management Chest drain Surgery
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Head Trauma
Basic anatomy
The scalp is made up of 5 layers of tissue which can be remembered using the mneumonic SCALP: ! ! ! ! ! Skin Connective tissue Aponeurosis Loose areolar tissue Pericranium
The skull is composed of: 1. Cranial vault - divided into three regions: anterior, middle and posterior cranial fossa and is thinnest in the temporal regions (but protected by the temporalis muscle - note this is the area affected with rupture of the middle meningeal artery and development of an extradural haematoma) 2. Base - irregular in nature and prone to injury from forceful movement The meninges consists of three layers that cover the brain: 1. Dura 2. Arachnoid 3. Pia
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Classication
This is the commonest cause of trauma death. Classication of brain injury Mechanism Blunt Penetrating Severity Mild Moderate Severe Morphology Vault Basilar High or low velocity Gunshot or other penetrating injuries GCS 13 -15 GCS 9 - 12 GCS < 8 Linear or stellate, depressed or non-depressed, open or closed CSF leak or cranial nerve palsies e.g. basal skull fracture - panda eyes, rhinorrhea, Battles sign and otorrhoea Epidural, subdural, subarachnoid, intracerebral Concussion, contusion (coup and contracoup), hypoxic injury
Intracranial lesions Focal Diffuse
Severity of injury should be assessed using: 1. AVPU - a simplied version of the glasgow coma scale ! Alert ! Voice ! Pain (indicates GCS < 8) ! Unresponsive 2. GCS (see table and assess using the best motor response) ! Mild - GCS 13 -15 ! Moderate - GCS 9 - 12 ! Severe - GCS < 8 The real problem with head injury is explained using the Monroe-Kelly doctrine. It states that the total volume within the cranium must remain constant, as the cranium is a rigid, non-expansile structure. A small increase in volume can be compensated for but once the compensatory mechanism is exhausted, there is an exponential increased in the ICP. If this occurs then the pressure will rise leading eventually to BRAIN HERNIATION, also known as coning. Features of raised intracranial pressure: Headache Vomiting Seizures Drowsiness Papilloedema Features of coning: Ipsilateral pupil vasodilatation (CN III palsy) Contralateral hemiparesis Cushings response (rising BP and falling HR)
Observation Eye opening - Spontaneous - To speech - To pain - None Best verbal response - Orientated - Confused - Inappropriate words - Incomprehensible - None Best motor response - Obeys commands - Localizes to pain - Withdraws from pain - Abnormal exion - Extension - None 6 5 4 3 2 1 5 4 3 2 1 4 3 2 1
Score
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Coma
Investigations
Skull XR (lateral is the most useful) C-spine XR Head CT (see NICE guidelines for head CT) Main indications for head CT: GCS < 13 Change in GCS 2 hours following injury Focal neurological decit Open or depressed skull fracture Post-traumatic seizure Vomiting > 1 LOC and > 65 years/coagulopathy/dangerous mechanism of injury/antegrade amnesia > 30 mins
Treatment of head injury

This depends on the severity: MILD - discharge with written information and a responsible companion MODERATE - admit for neurological observations SEVERE - neurosurgical referral Modalities CONSERVATIVE Specics Airway - secure airway Breathing - oxygen Circulation - IV access, uid resuscitation Ventilation Antiepileptics for seizures Neurosurgical input
MEDICAL SURGICAL
It is important to maintain good oxygenation to avoid cerebral hypoxia and ischaemic damage, and normocapnia. Hypercapnia will cause cerebral vasoconstriction and lead to cerebral hypoxia and also increased intracranial pressure. Raised intra-cranial pressure is COMPLEX to treat.
Modalities CONSERVATIVE MEDICAL
Specics Try to correct complications e.g. hypoxia, hypercapnia, hypovolaemia Ventilation Steroids Mannitol and uid restriction Neurosurgical input is very important
SURGICAL
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Types of Cranial Bleeding

A quick revision of the different meningeal layers and blood supply in this region:
Pics from left to right
Location
Outside the dura mater
Injury
Disruption of arteries from the middle meningeal artery
Clinical Features LOC Lucid period Deterioration (coning) Death
Management
CT Lens shaped haematoma Rx: Neurosurgical drainage CT Cresenteric shaped haematoma Rx: Surgical evacuation of haematoma CT, cerebral angiography Rx: Conservative (nimodipine)/Surgery (clipping/embolisation) Surgical drainage
Extra-dural Pic: right grey lens shaped haematoma + midline shift Sub-dural Pic: left cresenteric haematoma + midline shift Subarachnoid Pic: blood in the subarachnoid basal cisterns Intra-cerebral Pic: Intracerebral and intraventricular haemorrhage
Between arachnoid Rupture of bridging vein and dura
Insidious onset (alcoholics/elderly/ epileptics/those on anticoagulants) Headache, sensory/ motor S/S
Under arachnoid
Trauma or ruptured Berry aneurysm
Sudden onset occipital headache Meningism
Within brain tissue
Damage to brain substance
Compressive and localising signs
Remember on CT acute bleeding is high attenuation = white and older bleeding is low attenuation = black/ grey. Always comment on ANY MIDLINE SHIFT!
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Burns
Burns tend to affect particular groups of people Age: Toddlers and elderly Disease states: epileptics, post-stroke, alcoholism Occupations: welders/chefs There are 4 types of burn: 1. Thermal 2. Chemical 3. Electrical 4. Friction
The severity and management of a burn depends on its thickness:
Nomenclature Supercial Partial: 1. Supercial 2. Deep Deep First degree burn
Depth Epidermis
Clinical features Erythema Painful Blistering Painful Leathery White to charred Painless
Second degree burn Third degree burn Third degree burn
Papillary dermis Reticular dermis Epidermis, dermis and subcutaneous fat
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Assessment of a burn
This is done using a special assessment tool: WALLACE RULE OF NINES
Management
Should be managed in a specialist burns unit (second/third degree burns > 10 % in children or > 20 % in adults) Requires a normal ATLS approach but with special considerations AIRWAY Laryngeal oedema following inhalation injury may complicate intubation: low threshold for intubation, surgical airways BREATHING CO poisoning (carboxyhaemoglobin) and inhalational pneumonitis - oxygen and low threshold for intubation and mechanical ventilation Escharotomy of chest wall CIRCULATION Fluid losses can be huge and must assessed and replaced, best guide to adequate uid replacement is urine output Burns calculator 4 x weight (kg) x % burn = mL crystalloid in 24h, half given in 1st 8h then 2nd half given in the following 16h or [weight (kg) x % burn]/2 = mL colloid per 4h, 4h, 4h, 6h, 6h and 12h Aim for urine output of 0.5 ml/kg/h
Additional adjuncts Partial thickness - amazine cream/clinglm/plastic bags/analgesia Escharotomy and fasciotomy Antibiotics Surgical skin grafting PPI (Curlings ulcer - stress ulcer)
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Complications
Specic - Early
Multiorgan failure Pulmonary complications e.g. atelectasis, ARDS Infection Constricting eschars Contractures Scarring Curlings ulcer Psychological e.g. PTSD
Specic - Intermediate Specic - Late
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Peri-operative Care
May be split into: - PRE-OPERATIVE - OPERATIVE - POST-OPERATIVE
Pre-operative
The main purpose is to identify RISK. Patients may be classied using the American Society of Anaesthesiologists (ASA):
ASA Grade I II III
Denition Normal Mild systemic disease No limit in activity Severe systemic disease Limits activity Not incapacitating Incapacitating systemic disease Moribund Not survive with or without surgery for > 24h
Mortality 0.05% 0.40% 4.50%
IV V
25% > 50%
Pre-Assessment of the Surgical Patient

A SCREENING PROCEDURE for disease that may compromise the conduct or complications of surgery. Can follow a basic history structure: PRESENTING COMPLAINT Review reasons for surgery and history surrounding problem. PAST HISTORY AND SYSTEMATIC ENQUIRY Medical history Surgical history (previous operation and any adverse outcomes) Modied systematic enquiry looking for:
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1) CARDIOVASCULAR DISEASE (e.g. ischaemia, hypertension, arrhythmia) 2) RESPIRATORY DISEASE (e.g. COPD, asthma, lung brosis) 3) ENDOCRINE (e.g. DM, corticosteroids, thyroids) DRUGS Allergy Current medication (steroids, anti-coagulant, contraception, immunosuppressants etc.) Anaesthetics FAMILY HISTORY History of anaesthetic problems e.g. malignant hyperthermia, sickle cell SOCIAL Habits and rehabilitation etc. Then...move onto INVESTIGATIONS for specic problems.
Preparation for Surgery

This may be split into: 1) GENERAL Consent Book theatre/anaesthetist Fasting or NBM Mark site of operation I.V. cannulation Urinary catheter
FASTING/NBM Guidelines
Fluids: none 2 hours before procedure Food: none 6 hours before procedure (usually patients are fasted from night before)
2) INVESTIGATIONS Bloods (FBC, U&Es, LFTs, clotting, G&S/CM, Hb electrophoresis) Imaging: CXR ECG MRSA swab
3) MEDICATIONS DVT prophylaxis (TEDS, LMWH) Prophylactic antibiotics e.g. abdominal surgery - cefuroxime and metronidazole, vascular surgery - coamoxiclav Bowel preparation
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Considerations for for specic conditions
CONDITIONS Type I DM
Consideration Co-existing disease e.g. renal/cardiovascular
Pre-op - First on list - Convert to sliding scale - Omit long-acting insulin - Omit oral hypoglycaemics on day of surgery - Continue steroid up until surgery - Normalise clotting - Prophylactic antibiotics
Post-op - Sliding scale until eating
Type II DM
Co-existing disease e.g. renal/cardiovascular Addisonian crisis Increased mortality: - Coagulopathy - Infections - Hepato-renal syndrome Bleeding potential
- Sliding scale post-op - Restart oral when eating - IV hydrocortisone until normal oral intake - Good hydration
Steroid use Obstructive jaundice
Anti-coagulants
- Stop/convert to heparin - FFP lower INR in an emergency - Dialyses - Desmopressin for impaired bleeding function
- Re-warfarinise once oral intake
Chronic renal failure
Hyperkalaemia/Fluids Drug clearance
- IV naloxone
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Post-operative
There are always many things to think about in the patient who has just returned from theatre:
1. Fluids (covered above in surgical uids) 2. Pain relief 3. Complications (common ones include pyrexia)
Analgesia
The management of post-operative pain has 2 stages
a. Pre-operative: effective counselling about possibility of pain and patient choice b. Post-operative: preventing and treating breakthrough pain
It is also important that pain and its perception can have effects over and above psychological distress:
Organ system Psychological Cardiovascular Respiratory Gastrointestinal Genito-urinary Musculoskeletal Endocrine Anxiety Fatigue
Effect
Increased myocardial O2 consumption Reduced coughing sputum retention Atelectasis Decreased gastric emptying Reduced gut motility Urinary retention Reduced mobility ( pressure sores and DVTs) Hyperglycaemia Protein catabolism Sodium retention
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Assessment Pain is subjective! Observer assessment is unreliable
Can be assessed by 1. Talking to patient 2. Looking at vital functions 3. Various scales Visual analogue scales Verbal numerical reporting scale Categorical rating scale
The Relief of Pain
This may be divided into: 1. NON-PHARMACOLOGICAL Basic things e.g. pre-op preparation, relaxation therapy, hypnosis, cold/heat, splinting, TENS Interventional e.g. local anaesthetic inltration of wounds, nerve blocks. 2. PHARMACOLOGICAL This uses the WHO analgesic ladder
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Consider the following Regular administration Patient-controlled analgesia
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Post-operative Pyrexia
This is exceedingly common after surgery and is associated with different complications depending on when it occurs. All these complications are more serious in
Timeframe < 24 h
Complication Systemic response to trauma Pre-operative infection
Look for Exclusion of others Tachycardia + tachypnoea Reduced air entry to bases CXR - consolidation and collapse As above + more severe As above + more severe Local erythema, discharge and dehiscence Symptoms +ve. urine dipstick
24 - 72 hours
Pulmonary atelectasis
Chest infection 3 to 10 days Chest infection Wound infection Urinary tract infection Anastomotic leak DVT/PE Intraperitoneal sepsis
Calf pain and tenderness Abdominal pain, distension and ileus
Assessment Perform a good history and examination then do basic investigations and look bedside charts. SEPTIC SCREEN Modalities Cultures Bloods - ABG Bloods - Venous Imaging Scopic/Biopsy Functional/Special ECG (? PE)
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Tests + Findings Blood Urine MC & S Yes Routine bloods (infectious markers) CXR Abdominal ultrasound/CT
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Skin Disorders
This section is basically about lumps and bumps. We have chosen to put them at the start of these notes as the principles outlined here are important for the rest of the course.
Basic Principles
Always think about lumps in terms of: ! ! ! ! ! ! ! ! SITE SIZE SHAPE (edge, surface) CONSISTENCY (transillumination, pulsation) COLOUR TENDERNESS TEMPERATURE
[+ always look for local lymph nodes]
The best way to approach lumps in an exam is to recognise what it is then real-off a modied denition. In the rest of this section we shall consider these basic denitions.
Cystic swellings
A uid lled cavity lined by epithelium.
1. Sebaceous cysts Mobile, rm swelling with a visible punctum. Fixed to skin + has a foul-smelling toothpaste-like discharge. Found in hair-bearing regions. If infected it is called an ABSCESS. Rx - excision
2. Dermoid cysts There are 2 types ! 1. Inclusion dermoids Firm cystic swelling not attached to the overlying skin that occur at sites of embryological fusion e.g. neck midline and outer angle of the orbit.
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Rx - excision 2. Implantation dermoids Firm cystic swelling not attached to the overlying skin occurring most commonly in the hands of gardeners due to penetration injury Rx - excision Ganglions Tense cystic swellings on dorsum of hand, wrist not attached to overlying skin. Lined by brous tissue originating from the synovial lining of joint/tendon sheath. Rx - excision, traditionally hit with a bible
Lipomas Soft, non-tender, uctuant lumps that have a denable edge and are not attached to the overlying skin (particularly on trunk and limbs) If multiple and painful Dercums disease Rarely calcify or undergo sarcomatous change
Keloid scarring Irregular hypertrophy of collagen forming a raised edge that extends outside the scar [cf. hypertrophic scar - does not extend outside] More common in blacks Rx - corticosteroid injections/excision
Benign and Malignant skin tumours

1. Benign Seborrhoeic keratoses Brown/yellow oval lesion with a greasy and well demarcated border Stuck-on appearance Very common in elderly patients Rx - nil
Keratoacanthoma (molloscum sebaceum) Rounded swelling with rolled edges and a central keratin plug Occurs on light-exposed skin Important differentials include BCC and SCC, however a keratoacanthoma will spontaneously regress Rx - watch and wait, or excision
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2. Malignant
Malignant cutaneous tumours are increasingly common in ageing skin exposed to prolonged UV radiation. Those of fairer skin types are at higher risk.
Basal cell carcinoma (BCC) Lesion with a pearly rolled edge, telangiectasia and central depression Known as the rodent ulcer as the tumour rarely metastasises, but local invasion can be destructive Occurs on sun exposed areas Rx - excision
Actinic or solar keratoses Flat lesions with a red/scaly surface Sun-exposed areas (face, bald scalp, forearms, dorsum of hands) that progresses to become multiple Maybe pre-malignant to SCC Cryotherapy or topical 5-FU
Bowens disease (squamous cell carcinoma in situ) Solitary patch of red, scaly skin often below the knees This is also known as Queyrats erythroplasia in the penis, or a Marjolins ulcer when a SCC develops in a chronic ulcer Maybe pre-malignant to SCC Rx - excision Squamous cell carcinoma! A keratotic lump, polypoid mass or cutaneous ulcer in a sun-exposed area Rx - excision Lentigo Maligna (Hutchinsons freckle) Flat, brown are with irregular pigmentation usually on the face Rx - biopsy Malignant melanomas These are the most dangerous of the malignant skin tumours and may occur in pre-existing moles. With the exception of lentigo maligna melanoma, they occur in a relatively younger age group than other skin cancers and incidence is rising as a result of increased sun exposure. Simplied diagnostic criteria: Asymmetry Border (iregular) Colour (non-uniform) Diameter > 7mm Elevation Look for neighbouring satellite lesions and localised lymphadenopathy.
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There are 4 types 1. Lentigo maligna melanoma - invasive nodular melanoma within a lentigo maligna 2. Supercial spreading melanoma - most common; irregularly pigmented patch with an irregular edge usually on the leg or trunk 3. Nodular melanoma - rapidly growing lump 4. Acral melanoma - rare but more common in Asian or Afro-Carribean patients; pigmented patch on the sole or palm, or subungual pigmentation Prognosis is based on Breslows thickness or Clarkes level. Rx - excision
Ulcers
Interruption in the continuity of an epithelial surface.
Necrotic material tends to accumulate as SLOUGH in the base of the ulcer.
Cause VENOUS 70 % Venous hypertension Extravasation of blood lipodermatoscleros is and poor blood supply ARTERIAL 2% 1. Large vessel disease (e.g. PVD) 2. Small vessel disease (e.g. Buergers disease) Repetitive mechanical forces of gait
Sites Medial side of the leg, above the medial malleolus (gaiters region)
Features Sloping edge
Treatment Conservative - 4 layered bandage technique (ABPI > 0.8) Surgical - Skin grafting - Treat varicosities
Pressure points 1. Ball of the heel 2. Malleoli 3. Between the toes
Punched out edge Erythematous halo Pale granulation tissue Cold skin
Treat underlying cause e.g. poor perfusion Minimise risk factors for arteriopathy e.g. smoking, HTN Remove any callus Proper shoes Metabolic control Antibiotics (pseudomonas in diabetics)
NEUROPATHIC
Plantar aspect of foot under metatarsal heads/ toes
Punched out edge Sensory loss
Neoplastic Malignant change in a pre-exisiting ulcer, with an everted/rolled edge = Marjolins ulcer
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The Oesophagus
Clinical Anatomy
The oesophagus is a muscular tube about 25 cm in length (40 cm from mouth to stomach) Important landmarks: Starts at C6 (cricoid) Passes behind thyroid and trachea. Important anterior relations: left bronchus, aortic arch, left atrium Pierces diaphragm at T8 Forms gastro-oesophageal junction at T10.
May be divided into 3 parts: 1. UPPER THIRD (striated) 2. MIDDLE THIRD (mixed) 3. LOWER THIRD (smooth)
The oesophagus is lined by squamous non-keratinising epithelium.
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Dysphagia
The 3 important swallowing symptoms: DYSPHAGIA - conscious difculty in swallowing APHAGIA - inability to swallow ODYNOPHAGIA - painful swallowing
Divide these as follows:
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ORAL
Painful
Tonsillitis Pharyngitis Ulcers Quinsy Pharyngeal pouch Epiglottitis MND GB-syndrome CVA MS MND CREST Achalasia Foreign body Food Carcinoma Stricture Retrosternal goitre Lymphadenopathy Bronchial carcinoma (left) Thoracic aortic aneurysm
Obstructive
NEUROLOGICAL
Bulbar Pseudobulbar
Local MECHANICAL In the lumen In the wall Outside the wall
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Oesophageal Tumours
Divided into: ! PRIMARY Benign e.g. polyp, lipomas, haemangiomas, leiomyomas Malignant SECONDARY (rare)
There are 2 types of: 50% squamous cell carcinoma (upper half) 50% adenocarcinoma (lower half) Adenocarcinomas are becoming more common as the incidence of GORD and Barretts oesophagus increases.
Note:
Epidemiology
10 % GORD
Men (5:1) > 50y Iran/South Africa, China Risk factors
Barretts oesophagus Adenocarcinoma
1 % Barretts
LIFESTYLE e.g. smoking, alcohol, diets rich in nitrosamines or vitamin C decient ! OTHER DISEASE e.g. Barretts (adenocarcinoma), achalasia (squamous), Plummer-Vinson (squamous)
Clinical features
GENERAL Weight loss, anorexia, malaise SPECIFIC Dysphagia (progressive, solids then liquids then saliva) Others e.g. haematemesis (bleeding), hoarseness (L. recurrent laryngeal nerve), aspiration pneumonias, perforation (rare)
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Investigations
Modalities Cultures Bloods - ABG Bloods - Venous FBC (anaemia) LFTS (mets) U&Es (nutrition/dehydration) Ca2+ (mets) G&S + CXM
Tests + Findings
Imaging
CXR Barium swallow (apple-core appearance) CT (staging) Endoscopic ultrasound or mediastinoscopy (local staging) Endoscopy & biopsy -
Metastases Local Mediastinum (trachea, aorta, pleura and lung) Lymphatic Paraoesophageal Blood Liver and lung Prognosis 5 year survival < 5%
Management
Specics Analgesia Reduce size of tumour (alcohol / lasers) Relieve obstruction (stent, dilatation) Chemoradiotherapy to shrink tumour (neo-adjuvant) Oesophagectomy + lymph node removal (approaches - thorax, abdomen or both)
MEDICAL SURGICAL Only 1/3 are operable
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Gastro-oesphageal reflux disease

Reux of acidic contents into the oesophagus Problems due to: ! ! 1. Oesophagitis ! 2. Barretts (pre-malignant transformation)
Risk factors ! ! ! LIFESTYLE e.g. alcohol, large meals, smoking (relaxes the LOS) RAISED IAP e.g. obesity, pregnancy STRUCTURAL PROBLEMS e.g. hernias
Clinical features The main feature is retrosternal, burning chest pain that is worse when bending / lying down and is made worse by meals (particularly spicy ones) and hot uids. Other features include acid and water brash, and aspiration pneumonia.
Investigations As above - most important is ENDOSCOPY + / - barium swallow. Manometry or 24h PH monitoring if endoscopy is normal.
Complications Approximately 10% develop Barretts oesophagus, which is metaplasia of squamous to columnar epithelium in the lower oesophagus. This requires regular surveillance as it is pre-malignant for adenocarcinoma.
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Hiatus Hernia and other conditions

Hernia may be dened as: Abnormal protrusion of a viscera and its coverings through a defect into a place where it should not be. (see later for more hernias)
3 types: 1. SLIDING (80%) 2. PARAOESOPHAGEAL or ROLLING (5%) 3. MIXED (15%)
Investigation Endoscopy Barium swallow Management of hiatus hernia Note: para-oesophageal hernias always require an operation due to risk of strangulation.
Modalities CONSERVATIVE MEDICAL
Specics Modify risk factors e.g. stop smoking, reduced alcohol, smaller meals, eat > 3h before bed, avoid tight clothing Antacids Alginates e.g. Gaviscon H2 antagonists e.g. ranitidine, cimetidine PPI e.g. omeprazole, lansoprazole Nissen fundoplication
SURGICAL
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Other Oesophageal Conditions
Oesophageal rupture
This is rare and has a poor prognosis. Aetiology TRAUMA (external or internal) INs/OUTs e.g. corrosives & violent emesis (Boerhaves syndrome) Clinical presentation Severe, acute chest pain and collapse, with hydropneumothorax on chest radiograph.
Treatment Fluid resuscitiation Antibiotics to prevent medastinitis Surgery
Pharyngeal pouch
This is a pulsion diverticulae that occurs due to peristalsis against resistance resulting from un-coordinated muscle spasm. The diverticulae occurs in area of weakness between the thyro-pharyngeus and crico-pharyngeus inferior constrictor muscles. This point of weakness is known as Killians dehiscence. It is more common on the left side.
Clinical features Patients present with dysphagia, regurgitation and a palpable swelling in the neck which gurgles. The patient may also complain of halitosis or present with an aspiration pneumonia.
Treatment Excise the pouch or staple it endoscopically.
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Plummer-Vinson syndrome
This is the development of a oesophageal web due to hyperkeratinisation in the upper oesophagus. This causes dysphagia and is associated with chronic iron deciency anaemia. Aetiology Middle-aged Men It is a pre-malignant condition for SCC of the oesophagus in the cricopharyngeus. Other pre-malignant conditions of the oesophagus include achalasia and Barretts oesophagus. Treatment includes ferrous sulphate tablets for iron deciency anaemia and oesophageal dilatation.
Achalasia
Degenerative of Auerbach plexus leading to loss of relaxation (lower 1/3rd) This can also occur with Chagas disease (Trypanosome cruzii). Like Barretts oesophagus and PlummerVinson syndrome, this is a pre-malignant condition for squamous cell carcinoma.
Clinical features Patients present with intermittent dysphagia.
Diagnosis is with barium swallow which shows the typical appearance of tapering birds beak or rats tail.
3 main treatments are available: 1. Endoscopic dilatation 2. Hellers cardiomyotomy 3. Botulinum injection
Note features of barium swallow: Feature Birds beak/rats tail Apple core Corkscrew/nutcracker Achalasia Oesophageal carcinoma Oesophageal spasm Pathology
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The Stomach
Clinical Anatomy
The stomach is a J-shaped organ with 2 curvatures (GREATER and LESSER) It has 4 parts: CARDIA (6) FUNDUS (2) BODY (1) PYLORIC ANTRUM (10)
Important glands of the stomach Parietal cells - secrete gastric acid and intrinsic factor; stimulated by gastrin; inhibited by somatostatin of high PH Chief cells - secrete pepsinogen and renin APUD or enteroendocrine cells - secrete gastrin, histamine, serotonin, cholecystokinin and somatostatin
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Blood supply Arterial Lesser curvature L. gastric (coeliac branch) R. gastric (R. hepatic branch) Greater curvature R. gastro-epiploic (gastroduodenal branch) L. gastro-epiploic (splenic branch) Venous Enters portal system of liver Lymphatics Perigastric Coeliac nodes Nervous supply Vagus nerve has a posterior and anterior branch. It has motor (emptying) and secretory (acid production) functions.
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Acute Upper GI Bleed

This is a MEDICAL EMERGENCY
Aetiology ULCERATION (duodenal 40%, gastric)! INFLAMMATION (gastritis, oesophagitis) OTHERS e.g. Mallory-Weiss, carcinoma, varices, angiodysplasia, HHT, Peutz-Jeghers, aortoenteric stula
Clinical features These are due to: 1. DISPLACED BLOOD leading to malaena (black/tarry) or haematemsis (coffee-ground vomit) 2. LOSS OF BLOOD leading to hypovolaemia
Management I would make sure the patient was in a safe place, attached to monitoring equipment and inform a senior colleague... ...I would then resuscitate with respect to Airway Secure Breathing High ow oxygen Circulation 2 x large bore IV cannulae Take bloods (Normal bloods + amylase + group and save and crossmatch 4 units) Assess volume status, catheterise Give uids 2L normal saline STAT Then... colloid or blood
Direct patient towards OGD with therapeutic adjuncts 1. Omeprazole 2. Antibiotics e.g. cephalosporin 3. Terlipressin (if varices are likely)
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ROCKALL SCORING SYSTEM - a prognostic indicator. It has 2 components 1. Pre-OGD (age, co-morbidity and shock) 2. At OGD (diagnosis and risk of re-bleed) [< 3 = good, > 8 = bad]
Purpose of OGD: DIAGNOSTIC THERAPEUTIC Banding Sclerotherapy Adrenaline injection
After the OGD...classify as STABLE or UNSTABLE
STABLE
UNSTABLE
= uncontrollable haemorrage/ signicant risk of re-bleed
CONSERVATIVE MEDICAL SURGICAL
Treat cause PPI H.pylori eradication
Stabilise DU - Underunning GU - Excision of gastrectomy
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Peptic ulcer
Epidemiology M > F, elderly Sites Duodenum - often in the 1st part of the duodenum, 2cm from the pylorus Stomach Oesophagus Jejunum (Zollinger-Ellison syndrome) Meckels diverticulum (in the presence of gastric mucosa)
Risk factors 1. Lifestyle: smoking, alcohol 2. Other disease: H.pylori & drugs (NSAIDS, steroids), burns (Curling ulcer), head injury (Cushings ulcer), Zollinger-Ellison Syndrome
Clinical features Patients maybe assymptomatic or present with symptoms of dyspepsia, indigestion, retrosternal pain. In a DU pain is relieved by eating (or drinking milk) and is worst at night or before meals. In PU pain is worst when eating. There are two important complications of a PU ! 1. Perforation 2. Bleeding - this usually occurs in a posterior duodenal ulcer that erodes into the gastroduodenal artery (see acute GI bleed) A PU can also lead to gastric outlet obstruction and malignancy. We will discuss a perforated PU in further detail later on.
Investigation Endoscopy and CLO test, urease test, urea breath test or serology for H.pylori.
Treatment Modalities Conservative Medical Treatment Avoid NSAIDS, steroids, alcohol and stop smoking H.pylori eradication PPI
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Modalities Surgical This is rarely required now since the success of PPIs in PU disease
Treatment Vagotomy - CN X normally stimulates gastric acid secretion and relaxation of the pyloric sphincter, therefore a highly selective vagotomy to the nerves of Latarjet can be performed. However a pyloroplasty or gastroenterostomy is required as this causes pyloric sphincter contraction and bilious vomiting. Antrectomy and vagotomy Billroth I (gastroduodenostomy) Billroth II (gastrojejunostomy) Subtotal gastrectomy and roux-en-Y formation for refractory disease or Zollinger-Ellison syndrome
Zollinger-Ellison syndrome
This is a gastrinoma of the pancreas which causes hypersecretion of gastrin, and therefore HCl from the parietal cells of the stomach. These may be sporadic or inherited (MEN) and 60 % are malignant.
Clinical features Abdominal pain Dyspepsia Diarrhoea and steatorrhoea Haematemesis
Treatment High dose PPI Excision Chemotherapy
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Perforated Peptic Ulcer

This is a MEDICAL EMERGENCY
1. Symptoms Sudden onset abdominal pain (epigastric then generalised) 2. Signs INSPECTION General Unwell patient PALPATION Rigid abdomen Generalised tenderness with guarding + rebound i.e. peritonitic PERCUSSION Tender AUSCULTATION Absent (paralytic)
Investigations Modalities Cultures Bloods - ABG Bloods - Venous Imaging Scopic/Biopsy Functional Yes As above Erect CXR (will show 70%) - free air under the diaphragm CT for location of perforation Tests + Findings
Management First RESUSCITATION If patient is very unwell and unsuitable for surgery, manage conservatively as perforation may self-seal Modalities CONSERVATIVE Analgesia IV Fluids and catheterisation NBM + NG tube Antibiotics Specics
MEDICAL
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MOST COMMON PERFORATIONS 1. Duodenal (1st part anterior) 2. Gastric 3. Ulcerative gastric cancer
Modalities SURGICAL
Specics DU - Laparotomy + washout + omental repair GU/cancer - excision or gastrectomy
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Gastric Cancer
Epidemiology M>F Common in Japan, China Risk factors ! ! Lifestyle: smoking, alcohol, diet Other diseases: Blood group A, atrophic gastritis, pernicious anaemia, previous partial gastrectomy
Pathology Most are ADENOCARCINOMAS (others - MALT, lymphoma) 2 classication systems: 1. MACROSCOPIC - Bormann Classication Fungating Excavating Ulcerating and raised Linitis plastica 2. MICROSCOPIC INTESTINAL (53%) DIFFUSE (30%) Clinical features Patients may present with general features of malignancy (weight loss, anorexia, fatigue) or specic to the stomach e.g. upper abdominal mass, haemorrhage or rarely, gastric outow obstruction
Investigations
Modalities Cultures Bloods - ABG Bloods - Venous -
Tests + Findings
FBC (anaemia due to chronic disease/blood loss) LFTs (mets) Clotting (pre-surgical & as an LFT) Barium meal CT for staging Gastroscopy + biopsy -
Imaging Scopic/Biopsy Functional
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Management
Modalities CONSERVATIVE Analgesia Antiemetics Anti-secretion e.g. hyoscine Palliative therapy Chemotherapy Only possible in early disease
Specics
MEDICAL SURGICAL
Total (proximal lesion) or partial (distal lesion) gastrectomy 2 types of partial gastrectomy 1. Billroths I - gastroduodenostomy; direct anastomosis of stomach to duodenum 2. Billroths II - gastrojejunosotmy; anastomosis of stomach to jejunum leaving a duodenal stump Lymph clearance D1 = + perigastric nodes D2 = + coeliac nodes Or palliative interventions for gastric outlet obstruction e.g bypass, resection or stenting
Complications of gastrectomy
Complication Early Haemorrhage Infection Duodenal stump leak Failure of gastric emptying and bilious vomiting D - Dumping syndrome presents with abdominal distension, ushing and sweating Early dumping syndrome: immediately after a mearl, food has an osmotic effect casuing nausea, uid shift and hypotension Late dumping syndrome: ~ 2 hours after a meal, reactive hypoglycaemia occurs due to fast transit of food through the small bowel and insulin production D - Diarrhoea D - Deciency of B12 (IF is produced by the stomach), Fe (HCl is required for the absorption of iron), vitamin D (osteomalacia) Alkaline gastritis Blind-loop syndrome - bacterial proliferation in the duodenal stump of Billroth II Recurrent ulceration Malignancy
Intermediate
Late
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Complications of Gastrectomy can be remembered using the 3 Ds.
D - Dumping syndrome D - Diarrhoea D - Deciency of vitamin B12
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Gallstone and Biliary Disease

Clinical Anatomy
Gallbladder lies between R and quadrate lobes of the liver. MCL at R. costal margin.
There are 3 parts: 1. Fundus 2. Body 3. Neck (Hartmanns pouch)
It open into CYSTIC duct (joins common hepatic to form the common bile duct) and holds around 50 ml of bile.
The blood supply is: ARTERIAL - cystic artery from R. hepatic artery VENOUS - direct to liver sinusoids The epithelium is composed of COLUMNAR CELLS + mucus glands
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Introduction to Gallstones
Stones that form within the biliary system.
There are 3 types: 1. MIXED (80%) 2. CHOLESTEROL (15%) - large stones - known as SOLITAIRES (fasceted when you cut through them) 3. PIGMENT (5%) - haemolytic states such as HS and SS
Epidemiology
5 Fs:
Incidence increasing F>M Most asymptomatic (15% over 60y) More common in blacks and Asians
Aetiology Largely unknown but common theories include 1. 2. 3. 4. BILE SUPERSATURATED WITH CHOLESTEROL (Amirands triangle) Biliary tree sepsis Lithogenic bile secretion Anatomical abnormalities
Fatty Fertile Forty Female Fair
Risk factors Traditional classication is 5 Fs - Fat, Forty, Female, Fertile, Fair.
New classication Lifestyle: e.g. high fat/cholesterol ! Other conditions e.g. haemolytic states (pigment states), loss of terminal ileum (Crohns) Drugs e.g. COC Complications depend on the site of impaction: 1. GALLBLADDER e.g. biliary colic, acute and chronic cholecystitis, mucocoele, empyema, perforation, carcinoma of the gallbladder 2. IN BILIARY TRACT e.g. obstructive jaundice, ascending cholangitis, pancreatitis 3. OUTSIDE BILIARY TRACT e.g. gallstone ileus and small bowel obstruction
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Gallbladder Complications
1. Biliary Colic Blockage in the cystic duct
Clinical features Symptoms: RUQ pain after fatty meal (radiates to epigatrium and tip of R scapula) Associated with sweating/nausea/atulent dyspepsia Signs: Mild RUQ tenderness Note: classically biliary colic IS NOT A COLIC. Pain rises to plateau and remains there for many hours!
Management FBC, LFTs, CRP are normal, however USS reveals gallstones. RESUSCITATION and exclude emergency (e.g. perforation, pancreatitis).
Specics Fluids Analgesia (pethidine 50mg/4h IM/PO) NBM
MEDICAL SURGICAL Urgent cholecystectomy Elective cholecystectomy (6-12 weeks later)
2. Acute Cholecystitis
Obstructed gallbladder + infection. This can be divided into acalculous (10%) and calculous (90%).
Clinical features - patient is more unwell Symptoms: Systemically unwell Severe, constant RUQ pain, greater radiation
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Signs: More severe RUQ tenderness Positive Murphys sign (cessation of inspiration with pressure on gallbladder - must be negative on the left) [present in 75%] Low-grade temperature
Investigations
Modalities Cultures Bloods - ABG Bloods - Venous
Tests + Findings Blood, urine dipstick (bilirubin) Lactate FBC (infection) CRP (infection) U&Es (dehydration) Amylase (exclude pancreatitis) LFTs (obstruction) Clotting (pre-surgical & as an LFT) AXR (10-15% radio-opaque) CXR (exclude perforation) USS (distended thickened gallbladder, gallstones, pericholecystic uid) -
Imaging
Management
Specics Fluids Analgesia (pethidine 50mg/4h IM/PO) NBM Cefuroxime and metronidazole Urgent cholecystectomy (< 72h and severe) Elective cholecystectomy (6-12 weeks later)
MEDICAL SURGICAL
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Complications of acute cholecystits Recurrence Gangrene leading to perforation Mucocoele Empyema (drained with cholecystostomy) Mirrizis syndrome - large gallstone compressing the bile duct causing obstructive jaundice
A cholecystectomy maybe performed open or laparoscopically. An open incision is known as a Kochers incision.
Specic complications of laparoscopic cholecystectomy
Specic Immediate
Complication Trocar related vessel or visceral damage CBD injury and bile leak Conversion to open cholecystectomy/laparotomy Stone spillage Acute pancreatitis Incisional hernia
Early Late
Laparoscopic vs. open cholecystectomy
Advantages Small incisions have better cosmesis Less post-op pain Earlier mobilisation Reduced risk of DVT and hospital acquired infection Earlier return to work
Disadvantages Special equipment and training required More difcult to control complications Loss of tactile feedback CI in bleeding disorders, shock and adhesions
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Biliary Tree Complications

There are 3 important sequelae to impaction of gallstones within the biliary tree:
1. Obstructive jaundice 2. Ascending cholangitis

3. Pancreatitis (considered later)
1. Obstructive jaundice
Small stone blocks distal biliary ducts Patient will therefore have features of an elevated conjugated bilirubin Jaundice (late) Pale stools (like houmous) Dark urine (like coca-cola) It is always important to investigate these patients for cancer e.g. pancreatic, cholangiocarcinoma. First line investigation is an ultrasound to assess for the presence of gallstones, pancreatic mass, level of obstruction, degree of dilatation of the CBD +- intrahepatic biliary tree.
2. Ascending Cholangitis
Infection upon a background of obstruction of distal biliary ducts CHARCOTs TRIAD is classical Symptoms I. FEVER (+rigors) II. PAIN III. JAUNDICE
Signs Remember Courvoisiers law: In the presence of obstructive jaundice if there is a palpable gallbladder it is unlikely to be stone.
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Investigations
As above Consider 3 SCOPIC INVESTIGATIONS:
1) Endoscopic retrograde cholangio-pancreatography (ERCP) Endoscope passed into 2nd part of duodenum and papilla is cannulated. Dye is injected an image taken of the biliary tree. Biopsies can be performed Can also be therapeutic (stone removal, stent insertion) 2) Percuaneous transhepatic cholangiography This performed 2nd line (after ERCP failure or if not possible) Percutaneous cannulation of intrahepatic bile duct and injection of dye. 3) Magnetic resonance cholangiopancreatography Non-invasive technique that does not require the use of contrast Produces images similar to ERCP
Management
Specics Fluids Analgesia (pethidine 50mg/4h IM/PO) NBM Cefuroxime and gentamicin (for pseudomonas cover) 1. EMERGENCY - remove stone and insert a T-tube (open or ERCP) 2. ELECTIVE - cholecystectomy
MEDICAL SURGICAL
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Intestinal Complications
There is only 1 important complication here and it is rare.
GALLSTONE ILEUS Occurs as large gallstone (e.g. solitaire) stulates into rst part of the duodenum then becomes stuck in the small intestine.
See later for notes on small bowel obstruction.
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The Spleen
Clinical Anatomy
Largest organ of the lymphoreticular system Situated in LUQ (9,10,11th ribs) note: spleen is not palpable in health
Important relations: Anterior: stomach Posterior: ribs, diaphragm Medial: L. kidney Lateral: splenic colonic exure
Blood supply via SPLENIC ARTERY (coeliac axis) and SPLENIC VEIN
Functions (reects pathology nicely) 1. Immunological e.g. a large lymph node 2. Haematology e.g. sequestration and removal of old cells
Clinical characteristics of the spleen Enlarges INFERO-MEDIALLY (start RIF and move toward LUQ) Dull to percussion Cannot get above it Notched Cannot ballot (cf. kidney)
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Hypersplenism & Hyposplenism
1. Splenomegaly
There are 3 types: 1. MASSIVE (> 8cm) 2. MODERATE (4-8cm) 3. TIP (<4cm)
Types MASSIVE
Causes 1. Myeloproliferative disorders e.g. CML 2. Myelobrosis 3. Tropical disease e.g. malaria, leishmaniasis, kala-azar 1. Myeloproliferative disorders 2. Inltration (Gauchers/amyloid) 1. 2. 3. 4. Myeloproliferative Congestion Excessive usage e.g. haemolytic states Infection (EBV, IE)
MODERATE TIP
MYELOPROLIFERATIVE/LYMPHOPROLIFERATIVE disorders are a cause of all of them
HYPOSPLENISM
May be either: 1. IATROGENIC (asplenism) e.g. post-trauma or surgery 1. AUTOSPLENECTOMY (hypospenism) Haemolytic e.g. sickle-cell Inammatory process e.g. SLE, coeliac, UC
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Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous Blood cultures (infection) -
Tests + Findings
FBC (leukocytosis) U&Es (dehydration, electrolyte disturbance) LFTS (liver disease) CLOTTING (liver disease) G&S + CXM (for surgery) AXR Ultrasound Abdominal CT Bone marrow biopsy (haematological disorder) Cr51 red cell scan to show ectopic splenic tissue
Imaging
Splenectomy
Indications
There are 2 important indications for splenectomy: 1) TRAUMA (see later) 2) HAEMATOLOGICAL COMPLICATIONS e.g. ITP, hereditary spherocytosis Others: part of another procedure (e.g. radical gastrectomy), primary splenic lesion (tumours, abscess, cysts, aneursyms)
Surgical Approaches Surgery may be either: 1. OPEN (emergency - laparotomy, elective - upper middle and L. subcostal incision) 2. LAPARASCOPIC
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Complications
GENERAL Specic - Early Specic - Intermediate Specic - Late
Think in terms of ABCDE L. lower lobe atelectasis Sepsis Pancreatitis Sub-phrenic abscess Encapsulated infections
ALL PATIENTS REQUIRE INFECTION PROPHYLAXIS 1. Pneumococcus (Pneumovax) 2. Meningococcus (Men C) 3. Haemophilus (Hib) + Prophylactic penicillin
Splenic Trauma
This is relatively common and an important cause of spleen removal. The key problem is vascularity of the organ that leads to large internal blood losses.
Mechanism of injury Penetration/non-penetrating trauma Iatrogenic trauma (e.g. surgery to colon/stomach) Spontaneous rupture e.g. EBV infection
Remember: small degrees of trauma may lead to SUB-CAPSULAR HAEMATOMA
Classication - based on CT scan I - Capsular Tear II - Capsular Tear + Parenchymal injury III - Tear up to the hilum IV - Complete fracture
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Clinical features There will be a history together with LUQ pain and tenderness or generalised peritonitis. Features of shock will also be present. 2 important eponymous signs: 1. Kehrs sign: L. shoulder tip pain 2. Ballances sign: new onset shifting dullness in R. ank
Management CONSERVATIVE: for Type I & II! Analgesia and uid resuscitiaion: IV uids (blood), monitoring! SURGICAL: For Type III & IV Laparotomy (suture, salvage, splenectomy - partial or total)!
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The Pancreas
Clinical Anatomy
The pancreas is a retro-peritoneal organ (level of L1 in transpyloric plane) It is contained within the C-curve of the duodenum It has 3 parts: 1. Head (+/- uncinate process) 2. Body 3. Tail
Relations POSTERIOR: IVC, aorta, mesenteric vessels, diaphragm crura ANTERIOR: stomach TAIL: splenic hilum Blood supply ARTERIAL: superior and inferior pancreatico-duodenal, splenic Corresponding VEINS (to portal system)
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Lymphatics Upper border nodes Superior mesenteric nodes
Structure/Function Pancreas has 2 broad functions 1) ENDOCRINE - insulin, glucagon, stomatostatin 2) EXOCRINE - trypsinogen (protease) and chymotrypsinogen (lipase) Microstructure is composed of alveoli of secretory cells. Formed into ductules. These then join into 2 main ductal systems: 1) Main duct (Wirsung) - joined by the common bile duct to form Ampulla of Vater. 2) Accessory duct (Santorini) - drain superior to main duct directly into D2. ISLETS OF LANGERHANS - found between alveoli (most are in the tail)
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Pancreatitis
There are 2 types of pancreatitis: 1) Acute 2) Chronic (+ acute-on-chronic)
Acute Pancreatitis
Inammatory condition of the pancreas
This should be regarded as both a local and systemic disorder.
Epidemiology Common - 1:100 general surgical admissions Middle age M=F Mortality is ~ 12%
Aetiology Gallstones (45%) Ethanol (25%) Trauma Steroids Mumps + other infections e.g. Coxsackie B Autoimmune e.g. PAN Scorpion venom Hyperlipidaemia (+ hypercalcaemia, hypotension, hypothermia) ERCP Drugs e.g. thiazides, HIV drugs IDIOPATHIC (20%)
Clinical Features Symptoms: Epigastric/perigastric pain radiating to the back Relieved by sitting forwards/Associated with vomiting Signs: General: unwell patients with fever, tachycardia, jaundice Specic: Localised/Generalised peritonitis +/- shock/ileus Cullens sign - peri-umbilical echymosses! Grey-Turners - ank echymosses
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Investigations
Tests + Findings urine dipstick (bilirubin, glucose) Yes FBC (leukocytosis and low haematocrit) U&Es (dehydration, renal function) LFTs (obstructive) Amylase Lipids (hyperlipidaemia) Serum lipase Calcium (hypo- and hypercalcaemia) Glucose Albumin Erect CXR (exclude perforation) AXR (paralytic ileus) Ultrasound (inammation around pancreas, gallstones) CT abdomen (dene anatomy + Balthazar score) ERCP -
Imaging
Notes on amylase 80% raised in acute pancreatitis within 2-12 hours (return normal within week) NON-SPECIFIC If > 1000 pancreatitis over other causes RANSON/GLASGOW (UK) CRITERIA (PANCREAS mneumonic) Predictive of severity and mortality RANSON is better for alcohol-induced and only applied after 48 hours
PaO2 < 8 kPa Age > 55 Neutrophilia > 15x109 Calcium < 2.0 mmol/l Renal function impaired Enzymes e.g. LDH > 600 IU, AST > 200 IU Albumin < 32 g/dl Sugar > 10 mmol
1 = MILD 2 = MODERATE > 3 within 48 hours = SEVERE
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Management Modalities CONSERVATIVE Specics Fluids Analgesia (pethidine and morphine) NBM + NG tube Oxygen (keep Pa02 > 8 KPa Correct abnormal metabolities e.g. calcium Insulin sliding scale if elevated glucose ? Alcohol withdrawal - chlordiazepoxide and vitamins MEDICAL SURGICAL Moderate/severe - Antibiotics (meripenem, imipenem) Indicated for severe complications e.g. necrosis, pseudocyst, abscess, failure of resolution 1. Laporotomy and debridement/lavage 2. Laparostomy (pack and leave open in ITU)
Complications
GENERAL Specic - Early
Think in terms of ABCDE ARDS Atelectasis Pleural effusion (transudate) Organ failure (cardiac, renal) DIC Infection Necrosis Pseudocyst formation Chronic pancreatities Pancreatic tumour
Specic - Intermediate
Specic - Late
Pancreatic Pseudocyst Collection of uid in lesser sac that occurs in around 20% cases.
Suspect with persistently raised amylase. If < 6cm it may resolve spontaneously If > 6cm it requires surgery e.g. percutaneous drainage, laparoscopic, laparotomy
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Chronic Pancreatitis
Repeated episodes of pancreatic inammation leading to structural damage and brosis.
Leading to complications of: 1. Exocrine dysfunction e.g. malabsorption 2. Endocrine dysfunction e.g. diabetes mellitus
Epidemiology Uncommon ~ 30/100,000 Most due to ALCOHOL Other causes are cystic brosis, congenital causes e.g. pancreas divisum, hyperlipaemia and idiopathic)
Clinical Features
Symptoms: General: weight loss, poor appetite Specic: Pain Exocrine deciency e.g. steatorrhoea Endocrine deciency e.g. polyuria, poldipsia etc. Signs: General: thin patient Specic: erythema ab igne (from hot water bottles), epigastric tenderness Investigations
Tests + Findings
FBC (leukocytosis and low haematocrit) U&Es (dehydration, renal function) LFTs (obstructive) Amylase Lipids (hyperlipidaemia) Serum lipase Calcium (hypo- and hypercalcaemia) Glucose Albumin
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Modalities Imaging
Tests + Findings AXR (speckled pancreatic calcication) CT scan (structural changes and inammation) MRCP (gallstones) MRI (structural changes) ERCP (gallstones) Pancreolauryl test (for endocrine function)
Management
Specics Analgesia (can be problematic and require strong opiods/coeliac plexus block) Treat exocrine dysfunction (Pancreatin, Creon) Treat endocrine dysfunction (insulin) Moderate/severe - Antibiotics (meripenem, imipenem) Indicated for complications e.g. uncontrolled pain 1. REMOVE OBSTRUCTION e.g. stenting, cholecystectomy 2. DRAIN DUCTS/CYSTS e.g. pancreaticojejunostomy 3. RESECT - Distal (distal pancreatectomy), Proximal (Whipples procedure = pancreatoduodenectomy)
MEDICAL SURGICAL
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Pancreatic Tumours
May be either: 1) BENIGN - uncommon. Occur as part of the MEN syndromes. 2) MALIGNANT
Pancreatic Carcinoma
Most pancreatic carcinomas are DUCTAL ADENOCARCINOMAS and occur in the HEAD. Others: ampullary tumour, insulinomas, gastrinomas, glucagonomas, VIPomas
Epidemiology Increasing incidence M>F Elderly Western Countries
Risk factors 1. 2. 3. 4. LIFESTYLE: smoking and alcohol DYE EXPOSURE: naphthylamine, benzidine DISEASE STATES: chronic pancreatities, diabetes CONGENITAL: pancreas divisum
Clinical Features Symptoms: General: anorexia, malaise, weight loss Specic: Chronic epigastric pain radiating to the back (relieved by sitting forwards), steatorrhoea i.e. disturbed exocrine function, symptoms of diabetes i.e. disturbed endocrine function. Signs: General: cachexia, lymphadenopathy, signs of chronic EtOH use, jaundice Specic: palpable gallbladder (courvoisiers law), hepatosplenomegaly, ascites Rare features are thrombophlebitis migrans and marantic endocarditis
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Investigations
Tests + Findings Urine dipstick (glucose, bilirubin) FBC (anaemia of chronic disease) U&E (illness and dehydration) LFTs (obstructive jaundice, mets) Glucose (endocrine dysfunction) CA 19.9 [sensitivity of 90%] USS abdomen (mass, dilatation and gallstones) Triple phase CT (mass and staging) MRCP ERCP + biopsy Ultrsound-guided biopsy Laparoscopy Pancreolauryl test (for endocrine function)
Imaging
Scopic/Biopsy
Functional
Management
Specics Analgesia (strong opiod or coeliac plexus block) Relieve obstruction Palliative radiotherapy 20% of tumour are resectable 1. Whipples procedure 2. Chemotherapy post-op
MEDICAL SURGICAL
The prognosis is dismal with a mean survival of around 6 months
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Basic Principles of the Lower Gastrointestinal Surgery
Important Clinical Anatomy

The Duodenum C-shaped (~ 25cm in length) 4 sections: D1-D4 Important relations: D1 - Gastroduodenal and CBD posterior D2 - Duodenal papilla receives CBD and pancreatic duct at sphincter of Oddi and accessory pancreatic duct D3 - Mesenteric vessel anteriorly 9SMA and SMV) D4 - Suspensory ligament of Treitz distinguishes this part from ileocaecal junction
Blood supply D1-D2: superior pancreaticoduodenal artery (gastroduodenal a. from coeliac axis) D3-D4: inferior pancreaticoduodenal artery (sup. mesenteric a.)
Small Intestine ~ 6.5m in length Split into 50% JEJUNUM 50% ILEUM
JEJUNUM Location Diameter Wall Arcades Umbilical Wide Thick Few
ILEUM Hypogastric/pelvic Narrow Thin Many

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Large Intestine ~ 1.5m in length Distinguished from the small bowel as it is 1. Wider 2. Taenia coli which end at the appendix 3. Haustra 4. Appendiced epiploicae Divided into: 1. Caecum 2. Vermiform appendix 3. Ascending colon 4. Hepatic exure 5. Transverse colon 6. Splenic exure 7. Descending colon 8. Sigmoid colon 9. Rectum 10. Anus Peritoneal attachments PERITONEUM: transverse and sigmoid NO PERITONEUM: ascending and descending VARIABLE: caecum, rectum Arterial Blood Supply Divide structures into: A. FOREGUT (mouth to D2) Coeliac axis (T12) B. MIDGUT (D2 to distal transverse colon) Superior mesenteric artery (L1) C. HINDGUT (distal transverse colon to anus) Inferior mesenteric artery (L3) Venous supply A. SUPERIOR MESENTERIC VEIN ( portal vein) B. INFERIOR MESENTERIC VEIN ( splenic vein)
Lymphatic drainage Corresponds with the blood supply Small nodes on bowel drain to large mesenteric nodes then to mesenteric vessel nodes then to cisterna chyli.
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Peritoneal cavity 2 layers: ! Parietal - outer ! Visceral - inner Between these layers are serous uid. The peritoneum has two main regions which is connected by the epiploic foramen (foramen of Winslow) Greater sac Lesser sac - which is further subdivided into the lesser and greater omentum The peritoneum acts to protect the organs and hold them in place. There are areas in which there are double folds of peritoneum, which are known as: 1. Mesentery contains nerves and blood vessels to supply organs. The mesentery connects organs to the posterior abdominal wall, for example mesoappendix, transverse and sigmoid mesocolon. 2. Ligaments which connect one organ with another or another part of the body. 3. Omentum which is divided into the lesser and greater omentum. The lesser omentum extends from the liver to the lesser curvature of the stomach. The greater omentum extends from the the greater curve of the stomach, descends infront of the small intestine and turns up towards the transverse colon, forming an apron. The greater omentum has a cribiform appearance, which contains adipose tissue. Sometimes a loop of intestine can become strangulated in the foramen of Winslow. Also the hepatic artery can be compressed in the foramen of Winslow if the cystic artery is damaged during cholecystectomy.
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Intestinal Obstruction
There are 3 important types of intestinal obstruction 1. SIMPLE - 1 obstructing point & no vascular compromise 2. STRANGULATED - vascular compromise 3. CLOSED LOOP - 2 obstructing points and danger of perforation LBO in the presence of a competent ileocaecal valve Caecal volvulus Sigmoid volvulous The most useful classication is based upon AETIOLOGY
1. MECHANICAL
In the lumen MECHANICAL Faeces Foreign bodies Gallstones Intussusception
In the wall CONGENITAL e.g. atresia, imperforate anus, stenosis ACQUIRED Neoplasia Inammation e.g. IBD, diverticulitis
Outside the wall ADHESIONS Hernia Volvulus
2. NON-MECHANICAL - the bowel is shock SURGICAL SHOCK e.g. post-operative, peritonitis, ischaemia MEDICAL SHOCK e.g. electrolyte aberrations, drugs e.g. anticholinergics Ogilivies syndrome: features of obstruction on AXR but no obvious obstructing point
In practice remember: Small bowel - ADHESIONS and HERNIAS Large bowel - NEOPLASIA, DIVERTICULITIS and VOLVULUS
Clinical features There are 4 cardinal symptoms: 1. PAIN (usually central - SBO, lower - LBO and colicky, if constant think of strangulation/impending perforation) 2. CONSTIPATION (absolute - no faeces or atus) 3. VOMITING (early in SBO) 4. DISTENSION (prominent in low obstruction)
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Signs
INSPECTION General Unwell patient Distended abdomen
PALPATION Tender + rebound/ guarding in strangulation/ perforation Masses
PERCUSSION Percussion tenderness if strangulation/ perforation
AUSCULTATION Small bowel Tinkling Paralytic None
Specic
Surgical scars Hernia (inguinal/ femoral)
Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous
Tests + Findings
Bloods (if septic), Urine dipstick Metabolic acidosis in ischaemia FBC (leukocytosis) U&Es (dehydration, electrolyte disturbance) Amylase (any acute abdomen) G&S + CXM Erect CXR (exclude perforation) & AXR (look for obstruction) Gastrografn enema CT -
Imaging
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Basic Interpretation of the Related Chest and Abdominal Radiograph

Erect chest radiograph
Causes of air under the diaphragm: Perforated viscus e.g. bowel/PU Iatrogenic e.g. laparotomy/scopy Gas forming bacteria Water-skiers
Abdominal radiograph The 3,6,9 rule: if SB > 3cm, LB > 6cm and caecum > 9cm, the bowel is dilated Look at the rectal area for gas - if there is no gas this is an indication for bowel obstruction
Comparison of large and small bowel obstruction features
Feature Bowel diameter (cm) Position of loops Fluid levels (erect) Bowel markings
SBO (left) 3-5 Central Many Valvulae conniventes (all the way across)
LBO (right) >5 Peripheral Few Haustra (partially across)
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Management
1. Mechanical These are mostly managed if a conservative fashion (unless there are signs of strangulation) Look for signs of resolution for around 24 hours: Reduced pain Reduced NGT aspirate Passage of atus Resolution of AXR ndings
Specics NBM & NG tube (drip and suck) Analgesia Gastrografn (oral/NG tube) Flatus tube for sigmoid volvulus There are 3 important indications: 1. Simple obstruction (neoplasms or failure of conservative approach) 2. Closed loop obstructions 3. STRANGULATION/PERFORATION
MEDICAL SURGICAL
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2. Non-Mechanical
Specics Prevention e.g reduced bowel handling, peritoneal lavage Analgesia NBM & NG tube (drip and suck) Treat cause (e.g. electrolytes) -
MEDICAL SURGICAL
As a general rule: Virgin abdomens will probably end up requiring an operation to relieve the obstruction Non-virgin abdomens will probably only require conservative management
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Colon Cancer and Stomas

Colorectal carcinoma
A malignant neoplasm of the colon or rectum.
Epidemiology 3rd commonest cancer M=F Elderly Western
Aetiology Lifestyle: Western diet (red meat, low bre), smoking Familial 1. 2. 3. 4. 5. Familial adenomatous polyposis (AD) Gardiners syndrome (AD) Hereditary non-polyposis coli Peutz-Jeghers syndrome Family history
Previous disease states: IBD - 10 % risk/10 years in those with UC Previous therapies: radiation, gastrectomy
Pathology May be classied with 2 classication systems: ! 1. MACROSCOPIC 30% recto-sigmoid junction 25% sigmoid colon L. sided tumours annular stenosing R. sided tumours sessile/polypoid 2. MICROSCOPIC (Dukes criteria) A. Conned to bowel wall B. Through bowel node but no nodal involvement C. In lymph nodes ! C1 ! C2 involved apical node D. Distant mets
! !
! !
Note that Dukes B with perforation requires adjuvant chemotherapy.
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Clinical features
Symptoms: General: weight loss, anorexia, malaise Specic R. sided tumours present late with diarrhoea and anaemia L. sided tumours commonly cause obstruction Rectal tumours obstruction/rectal symptoms (tenesmus)
Signs: General: anaemia & cachexia Specic Mass Signs of obstruction Hepatomegaly PR - mass or stulae Investigations
Modalities
Tests + Findings
FAECAL OCCULT BLOOD suggested as screening programme FBC (anaemia of chronic disease, iron deciency anaemia) U&Es (diarrhoea) LFTs (mets) CEA (better at monitoring course) Clotting G&S/CXM (pre-surgical) CXR (mets) Barium/gastrografn enema - apple core lesion CT/MRI (staging) - liver, lung and bone metastases CT for virtual colonoscopy Sigmoidoscopy + biopsy (exible sigmoidoscopy can reach the splenic exure) Colonoscopy + biopsy (colonoscopy can reach the ileocaecal valve) -
Imaging
Scopic/Biopsy
Functional
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Management
Modalities CONSERVATIVE/PALLIATIVE MEDICAL SURGICAL
Specics By-pass, diversion or decompression Adjuvant chemotherapy in Dukes C or B (perforated) or for colon tumours and neoadjuvant radiotherapy for rectal tumours RESECTION (see below)
R hemicolectomy for R sided tumours Extended R hemicolectomy for distal R sided tumour/ transverse colon tumour L hemicolectomy for left sided tumours Sigmoid colectomy for sigmoid tumours
Anterior resection for tumours > 4cm from the anal verge. The colon is anastomosed to the remaining rectal stump, and a defunctioning loop ileostomy may be performed. Abdomino-perineal resection for tumours < 4cm from the anal verge. There is complete removal of the anus and a permanent end colostomy is formed. Neoadjuvant radiotherapy maybe used to shrink the rectal tumour prior to resection. Adjuvant chemotherapy is used for types B and C colorectal carcinomas.
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Emergency bowel operations

In large bowel obstruction due to colorectal carcinoma or stricture, for example diverticulitis, a Hartmanns procedure is performed. The obstruction is removed, the rectal stump is closed and left in the pelvis whilst a temporary colostomy is formed. Often, a direct anastomosis is not undertaken as this affects healing in the presence of inammation.
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Stomas
A stoma (mouth) is a surgical created communication between the bowel and the skin.
They may either temporary or permanent
Types: 1. Colostomy 2. Ileostomy 3. Urostomy (ileal conduit)
When inspecting a stoma ask yourself: Where is it? What is in it? How is the communication created? + look for scars and ALWAYS CHECK THE PERINEUM.
Colostomy Site Bag Contents Opening L. iliac fossa (usually) Solid Flush with skin
Ileostomy R. iliac fossa (usually) Liquid Spouted
Urostomy R. iliac fossa (usually) Urine Flush with skin
Complications of stoma formation
Specic Immediate Early Haemorrhage High output stoma Hypokalaemia Retraction Ischaemia Prolapse SBO Parastomal hernia Fistulae Dermatitis
Complication
Late
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Inammatory Conditions
In this section we talk about A. B. C. D. Appendicitis Diverticular disease Crohns disease Ulcerative colitis
Appendicitis
Inammation of the vermiform appendix
Epidemiology
Very common (up to 12% of population) Can occur at any age Rare < 2 Peaks in childhood years Pathology The main processes occuring are 1. Obstruction - usually due to a feacolith 2. Lymphoid hyperplasia
The main worry is PERFORATION Localised appendix mass Systemic peritonitis
Clinical features
Symptoms: General: Pyrexia, malaise and anorexia Specic Central colicky abdominal pain (hindgut colic) Vomiting Pain localized to R. iliac fossa
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Signs: General: patient still with exed hips and knees. Pyrexia, fetor oris + coated tongue Specic Localised - garding and rebound over McBurneys point ( distance between umbilicus and ASIS) Generalised - rigid and tender over all abdomen + an ileus
Investigations
Tests + Findings Urine MC & S + dipstick + HCG FBC (neutrophil leucocytosis) CRP (infectious marker) amylase Ultrasound (exclude gynae cause, appendix inammation indicated by free uid and diameter > 6mm) CT for atypical cases Laparoscopy -
Imaging
Management
Modalities CONSERVATIVE Analgesia Fluids NBM Cefuroxime and metronidazole
Specics
MEDICAL SURGICAL
OPEN LAPAROSCOPIC - particularly good for girls
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3 important complications to be aware of:
1. PERFORATION (young and the old) 2. MASS (may resolve with antibiotics) 3. ABSCESS (may require antibiotics and drainage)
Diverticular Disease
An acquired condition of mucosal lined out-pouchings through the wall of the colon.
Epidemiology Very common F>M Risk factors Lifestyle: low bre diet and obesity Other conditions: hiatus hernia & cholelithiasis (SAINTS triad)
DIVERTICULUM DIVERTICULOSIS DIVERTICULAR DISEASE
Single out-pouching Many out-pouchings Symptomatic outpouchings
Complication Diverticulitis
Features L. sided appendicitis Sudden painless, large PR bleed Peritonitis Swinging fever and boggy rectal mass Enterocolic Colovaginal Colovesical Large bowel obstruction
Clinical features Most patients and asymptomatic ( do not have diverticular disease) Symptomatic patients may have Mild alteration in bowel habit with L. sided colic relieved on defecation A complication Investigations Will depend on the situation. For acute diverticulitis
Haemorrhage Perforation Abscess formation Fistulae
Strictures
Modalities Cultures Bloods - ABG Bloods - Venous If unwell
Tests + Findings
FBC (neutrophil leucocytosis) CRP (infectious marker) U&E (dehydration)

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Modalities Imaging
Tests + Findings Erect CXR (perforation) AXR (uid level, air in the wall) Gastrografn enema Ultrasound Angiography CT scan Sigmoidoscopy/colonoscopy -
Treatment This will depend on the severity and the specic complication. If mild symptomatic disease: Treat conservatively with! risk factor modication e.g. increase bre/uids and lose weight Antisposmodic may help e.g. mebeverine For acute diverticulitis:
Modalities CONSERVATIVE Analgesia Fluids NBM Cefuroxime and metronidazole
Specics
MEDICAL SURGICAL
This is indicated for PERFORATION, HAEMORRHAGE and OBSTRUCTION 1. Harmanns procedure 2. Elective sigmoid colectomy and anastomosis For less severe PR bleeding an angiography and embolisation can be performed
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Surgical Ulcerative Colitis

A chronic relapsing inammatory condition of the colonic mucosa
It ALWAYS starts at the rectum and spreads proximally (20% develop a PAN-COLITIS)
Epidemiology
Most common between 20 - 35 years F>M Non-smokers Clinical features
Symptoms: General: weight loss, fever, anorexia and malaise Specic Crampy abdominal pains Diarrhoea (blood/mucus) Rectal symptoms (urgency or tenesmus) Extra-intestinal manifestations e.g. uveitis, ank. spondylitis, erythema nodosum Signs: General: clubbing. Systemically unwell in acute disease Specic (if acute disease) Tender abdomen PR bleeding on glove Complications include Toxic megacolon Perforation Strictures Perianal disease Colorectal carcinoma
Investigations:
Modalities Cultures Bloods - ABG
Tests + Findings Stool (exclude infection), blood In unwell
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Modalities Bloods - Venous
Tests + Findings FBC (neutrophil leucocytosis) CRP and ESR (infectious marker) U&E (dehydration) LFT (albumin) G&S/CXM if for surgery Erect CXR (perforation) AXR (toxic megacolon, thickened walls, thumb printing, strictures) Gastrografn enema (lead-piping, loss of haustra, granular mucosa) CT scan Sigmoidoscopy/colonoscopy (no serosal involvement and crypt abscess) -
Imaging
Severity may be graded using the Truelove and Witts Criteria
Management If chronic/intermittent the MEDICAL MANAGEMENT Surgery may be reserved for chronic symptoms or high grade dysplasia. If acute SURGICAL MANAGEMENT Toxic megacolon Perforation Massive PR haemorrhage Colitis not responding to medical management
Modalities CONSERVATIVE Analgesia Fluids NBM
Specics
MEDICAL
IV hydrocortisone Rectal steroids e.g. prednisolone foam enemas Blood transfusion if Hb low If improves...prednisolone + sulphasalazine
SURGICAL
If no improvement.. Panproctocolectomy, total or subtotal colectomy with ileostomy
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Crohns Disease
An inammatory condition of unknown aetiology that can affects the entire length of the GI tract.
It is characterised by: Patchy transmural inammation Non-caseating granulomas
Epidemiology Most common between 20-35 years Smokers M=F Clinical features
Symptoms: General: weight loss, fever, malaise and anorexia Specic Diarrhoea (blood/mucus) Crampy abdominal pain Bowel obstruction Extraintestinal: anl. spond, erythema nodosum Signs: General: thin, clubbing, aphthous ulcers Specic Tender abdomen Look for RIF mass PR - perianal disease e.g. stulas, ssures, perianal abscess Investigations
Tests + Findings Stool (exclude infection), blood In unwell FBC (neutrophil leucocytosis) CRP, ESR (infectious marker) U&E (dehydration) LFT (albumin) G&S/CXM if for surgery
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Modalities Imaging
Tests + Findings Erect CXR (perforation) AXR (toxic megacolon, strictures) Gastrografn enema + FOLLOW -THROUGH (cobblestone mucosa, rosethorn ulcer, string sign) CT scan MRI (perianal disease) Colonoscopy (cobblestones appearance, ssuring, serosal involvement) -
Management
Usually this is managed medically with steroids + immunosuppressants Surgery is reserved for 2 setting: 1. 2. Emergency (complications) Elective (chronic problems)
Surgical options include Stricturoplasty Limited resections Ileo-caecal resection
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Peri-Anal Disease
Clinical Anatomy
Rectal Anatomy
The rectum is ~ 15cm and curved It starts at 3rd segment of sacrum and ends at prostate/lower of the vagina
Important relations POSTERIOR: Sacrum, midle sacral artery and coccyx ANTERIOR: Prostate, bladder, vagina Note: the muscle layer are completely fused no haustrae.
Anal Canal
The anal canal is ~ 5cm and straight It is divided into two s by the DENTATE LINE
! ! !
LOWER HALF - squamous epithelium and inferior rectal artery UPPER HALF - columnar epithelium and superior rectal artery (branch of inferior mesenteric)
Continence is maintained by two sphincters INTERNAL SPHINCTER Involuntary circular muscle of rectum EXTERNAL SPHINCTER Made up 3 striated rings (external, supercial and subcutaneous) Supplies by pudendal nerve (S 2,3,4)
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Haemmorrhoids
Dilated and disrupted vascular anal cushions
These are most commonly found at the 3,7 and 11 oclock positions
May be classied according to anatomical severity:
1st degree - never prolapse 2nd degree - prolapse on straining 3rd degree - constantly prolapsed A strangulated haemorrhoid occurs when the sphincter cuts off the blood supply
Epidemiology 50% of Western population affected Risk factors Lifestyle: low bre diet Impaired venous return e.g. pregnancy, portal hypertension and pelvic malignancy Rectal carcinoma Clinical Features
Symptoms: Fresh PR bleeding A lump Pain Itching
Signs: May be seen, ellicited or felt on PR Abdominal exam may reveal abnormality
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Management
Modalities CONSERVATIVE MEDICAL SURGICAL Increase bre and uid intake Toilet habit (limit time)
Specics
Topical steroid/anaesthetic e.g. Anusol Laxative e.g. lactulose 1. 5% phenol in almond oil 2. Endoscopic banding/cryotherapy 3. Haemorrhoidectomy (nal resort)
Note: Peri-anal haematomas These are haematomas that are caused by burst peri-anal venules. Usually due to straining Compared to haemorrhoids they appear blue. Most will resolve spontaneously but may need surgical drainage
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Anal Fissures
A tear in the anal mucocutaneous epithelium.
These are most common at the 6 and 12 oclock positions.
Aetiology is usually either hard stool or trauma. However may be associated with Crohns, syphilis and anal carcinoma.
Clinical features Symptoms: Pain on defaecation Fresh PR bleeding Signs: Pain on cheek spreading PR usually impossible May be a sentinal pile.
Treatment
Modalities CONSERVATIVE MEDICAL Increase bre and uid intake Toilet habit (limit time)
Specics
Stool softeners Reduce anal spasm e.g. 0.2% GTN cream, diltiazen cream, botulinum injection Lateral spincterotomy at 3 o'clock
SURGICAL
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Anal abscess/Anal sepsis

Anal sepsis either originated from ABOVE (e.g. pelvic abscess) or is due to a LOCAL problem (e.g. infection of the anal glands)
Common organisms include Staph. Strep. E. coli The most important compliation is the formation of a FISTULA.
Types: a. b. c. d. Perianal Ischiorectal Pelvirectal Inter-sphincteric
Clinical features Symptoms: General: Swing fevers and malaise Local Mass Throbbing pain + surround tenderness Purulent discharge Signs General: systemic infection Perianal erythema Discharge Bulging mass PR - a boggy and uctuant painful mass
Treatment
Modalities CONSERVATIVE MEDICAL SURGICAL Analgesia Flucloxacillin + penicillin If above fails Incision, drainage and packing ...leave to heal.
Specics
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Anal Fistula
An abnormal connection between the ano-rectal passage and the skin.
There are many types:
INTER-SPINCTERIC TRANS-SPINCTERIC SUPRA-SPHINCTERIC EXTRA-SPHINCTERIC
Clinical features Symptoms Pain and discharge of purulent uid/faeces Perianal irritation Signs Dot and associated discharge and skin changes PR - indurated area around the stula
Treatment
Modalities CONSERVATIVE MEDICAL SURGICAL Analgesia
Specics
Antibiotics if associated infection 1. EUA to determine extent 2. Lay open tract and heal by secondary intent
If low division of spincters Ih high...Seton suture to stimulate brosis of tract
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Rectal Prolapse
Protrusion of rectal tissue through the anal canal.
There are 2 types: a. PARTIAL - mucosa only (common in children) b. COMPLETE - full thickness of rectum
Clinical features Symptoms: Mass Associated bleeding and ulceration Incontinence of urine or faeces Signs: View the prolapse on straining PR - tone Investigations These must be investigated as there may be an underlying lesion e.g. carcinoma Imaging - endoanal ultrasound/MRI Scopic - Sigmoidoscopy Functional - anorectal manometry
Treatment
Modalities CONSERVATIVE MEDICAL SURGICAL Pelvic oor exercise Stool softeners 2 approaches
Specics
1. Delorms procedure: perineal approach to resection of excess rectal mucosa 2. Rectopexy: the rectum is xed to the sacrum
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Anal Carcinoma
Epidemiology Uncommon Most occur in male homosexuals due to associated with High Grade HPV (16, 18, 31, 33) Pathology
Can be broken down by histology 80% squamous 20% others e.g. adenocarcinoma, lymphoma, melanoma ..or location Anal margin: below the dentate line (men with a good prognosis) - spreads to pelvic nodes Anal canal: above the dentate line (women with a poor prognosis) - spread to inguinal nodes Clinical features
Symptoms: General: malaise, weight loss, anorexia Specic Rectal bleeding Pain Incontinence Signs: Mass + lymph nodes +/- stula
Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous -
Tests + Findings
FBC (anaemia of chronic disease/blood loss) LFTs (mets) Ca (mets) CT (spread) Rectal EUA + biopsy Podmedics 2010
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Treatment
Modalities CONSERVATIVE MEDICAL SURGICAL Analgsia Palliative radiotherapy
Specics
Chemo + radiotherapy (if inguinal nodes involves) Resection
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Breast Disease
Clinical Anatomy
The breast are modied sweat-glands that are located between 2-6th ribs on the anterior chest wall Underlying muscles are: PECTORALIS MAJOR SERRATUR ANTERIOR
The basic structure is composed of 1. ADIPOSE TISSUE 2.15-20 LOBULES arranged in a hierarchical duct system (TLDU, extra-lobular duct, major duct)!
Arterial Blood Supply Axillary artery Internal thoracic arteries Intercostal arteries
Lymphatic Drainage There are 3 basic lymphatic channel draining the breast and these are very important: 1. AXILLARY 2. INTERNAL MAMMARY 3. SUPRACLAICULAR The axillary nodes are split into 5 distinct groups Anterior Posterior Lateral Central Apical
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Diagnostic Principles in Breast Disease

Triple Assessment are the key words here:
Modality 1. Clinical Assessment
Specic History Particularly lumps, pain, nipple discharge PMH/FH/DH Examination Breast Nodes/back
2. Radiology
Ultrasound (if < 35 years) Mammography Oblique and cranio-caudal views 10% false negative rate
3. Biopsy
Fine needle aspiration cytology Easy to do 95% sensitivity Core biopsy/Tru-cut Histology Oestrogen receptor status
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Benign Breast Disease

These should be divided into:
a. Congenital
These are rare conditions such as amastia (absence of breast), hypoplasia and accessory nipples. Accessory nipples represent failure of the milk line to regress and can be excised if problematic.
b. Acquired You can divide these further into: 1. Hormonal/cyclical ANDI, cystic breast disease, broadenomas 2. Infective 3. Inammatory Fat necrosis, duct ectasia 4. Neoplastic Duct papilloma, lipomas, cysts
1. Hormonal/cyclical ANDI = Abnormalities of Normal Development and Involution
Benign Mammary Dysplasia/ANDI
Abnormality of cycles - Fibrocystic disease Common in pre-menopausal women (25-45) with painful and nodular lump in second half of cycle Investigation - triple assesment if lump Treatment 1st line - Analgesia/evening primrose oil 2nd line - Tamoxifen/bromocriptine 3rd line - excision Abnormality of Development - Fibroadenoma Overgrowth of single breast lobule Young women with smooth, rm, mobile mass (breast mouse) Investigate with TRIPLE ASSESSMENT If < 30 - observe, if > 30 excise
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2. Infective breast disease
They are all treated with analgesia and antibiotics (e.g. ucloxacillin)
There are 2 important types: 1. Lactational Cracked nipple from breast ffeding allows stap. entry Most important compication is breast abscess formation No need to stop breast feeding 2. Non-lactational Staph. aureus Most important complication is periductal mastitis (suggested by chronicity e.g. mastalgia, discharge and brosis that lead to nipple retraction)
3. Inammatory breast disease
1. Duct ectasia Dilated sub-areolar ducts that become lled with cellular debris periductal inamatory response Present with subareolar lump and green discharge 2. Fat necrosis Trauma (postive history in 50%) followed by brosis and calcication Increased incidence of cancer
4. Benign Neoplasms
Can be from the skin e.g. lipoma, cysts From the breast itself Duct papilloma (present with blood stained discharge and treated with microdochectomy)
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Malignant Breast Disease

Epidemiology
Very common (1:11) in the Western world. Risk increased with age Risk factors 1% occur in men Lifestyle: alcohol intake, high saturated fat diet Prolonged exposure to oestrogens: early menarche, late menopause, exogenous hormones Family history: Ca in rst degree relative. BRCA 1 & 2 1st child over 30 years
Pathology
The most important types of tumour are: 1. DUCTAL 2. LOCULAR
Both of these tumours go through an IN SITU phase (ductal is much more common). Carcinoma that has not penetrated the basement membrane Low- to high- grade Other include: Medullary - younger patients Colloid/mucinous - older patients and tend to look benign on the mammogram Papillary
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Investigation
1. Triple assessment (histological grading and oestrogen receptor status) 2. Staging CLINICAL TNM Clinical staging system
Stage 1 Stage 2 Stage 3
Early disease Tumour conned to breast Early disease Tumour spread to movable ipsilateral axillary nodes Local advanced disease Tumour spread to supercial chest wall + involvement of ipsilateral internal mammary Advanced Metastases present at distant sites e.g. liver, lungs, brain
Stage 4
TNM Staging System
0 Tumour CIS/Pagets
1 < 2cm No skin xation
2 2-5cm Skin distortion
3 5-10cm Ulceration Fixed to pectoral muscle Internal Mammary
4 > 10cm Chest wall extension
Nodes Mets
No nodes No mets
Ipsilateral Mobile Liver, bone, lung
Ipsilateral Fixed
Management
This should be in a specialist breast centre and is multi-modality e.g. surgery, radiotherapy and chemotherapy. Divide treatments into: 1. Early disease 2. Advanced disease
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1. Early disease
There are 4 aims: 1. Local treatment of the tumour Wide local excision + radiotherapy Mastectomy (large tumours or patient choice) 2. Axillary clearance Assessment with axillary sampling/Sentinal mode mapping Treatment with axillary clearance 3. Prevention of recurrence Radiotherapy after WLE Chemotherapy if young, large tumour or high risk of recurrence Hormonal e.g. Tamoxifen/Arimidex 4. Reconstruction TRAM ap Latissimus dorsi ap
Sentinal Node Mapping Involves identication of the rst node draining the tumour through injecting radioactive isotope and a dye. Sampling of this node then determines whether axillary clearance is necessary
2. Advanced disease
The rst line is usually TAMOXIFEN
Other important adjuncts include Local recurrence - re-excision, radiotherapy Metastatic disease - bisphosphonates and steroids Palliation - package of care, analgesia
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Complications of breast surgery
GENERAL Specic - Early Specic - Intermediate
Think in terms of ABCDE Pneumothorax Infection Haematoma Seroma Frozen shoulder Lymphoedema Nerve damage e.g. brachial numbness
Specic - Late
Breast Screening
This is a programme introduced after publication of the Forest Report (1988) Involves: 1. 2. Self-examination 2-view mammography every 3 years between 50-64 year old (> 64y can self-refer)
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Neck Lumps
Clinical Anatomy
The neck may be subdivided into: ANTERIOR TRIANGLE Submandibular (under chin) Submental (under chin in midline) Carotid (pulsatile) Muscular (midline)
POSTERIOR TRIANGLE
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It is important to be aware of the different lymphatic drainage areas of the neck:
1 II III IV V VI
Submental/ submandibular Jugulo-digastric Middle jugular nodes Inferior jugular nodes Posterior triangle Ant. compartment group
The Thyroid
Endocrine organ that lies in the pre-tracheal fascia over the 2-4th tracheal rings Relations: ANTERIOR: strap. muscles POSTERIOR: parathyroid glands, larynx, trachea, superior and recurrent laryngeal nerves
There are 3 parts to the gland 1. Isthmus 2. Lateral lobes 3. Pyramidal lobes (inconsistent)
Blood supply Arterial SUPERIOR THYROID A. (branch of external carotid) INFERIOR THYROID A. (branch of subclavian) Venous SUPERIOR THYROID V. (internal jugular) MIDDLE THYROID V. (internal jugular) INFERIOR THYROID V. (brachiocephalic) Lymphatic Mostly towards the middle jugular nodes
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The Salivary Glands
There are 3 sets 1. Sublingual 2. Submaxillary 3. Parotid (largest)
The Parotid Gland
This is the largest of the 3 glands Shape/Location It resembles a three-sided pyramid with the apex directed downwards. Lies over the MANDIBULAR RAMUS (anterior and inferior to the ear) Important relations ! ! FACIAL NERVE EXTERNAL CAROTID ARTERY (bifurcated beneath to form the maxillary and supercial temporal a.
Drains into Stensons duct upper 2nd molar at the parotid papilla.
The Submandibular duct
Lies above the digastric muscle Separated into SUPERFICIAL and DEEP portions by mylohyoid. Drains into Whartons duct sublingual caruncles (either side of sublingual frenulum)
The Sublingual Gland This is the smallest of the 3 glands and lies ANTERIOR to the submandibular gland. Drains via Bartholins duct to join the submandibular duct sublingual caruncles.
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Lymphadenopathy
Enlarged lymph nodes
This is the COMMONEST CAUSE of a lump in the neck.
Divide them into: LOCALISED GENERALISED
Infection LOCALISED Primary e.g. lymphadenitis Infections 1. Acute e.g. EBV 2. Chronic e.g. HIV
Neoplasia Primary e.g. lymphoma Secondary
Autoimmune
GENERALISED
Lymphoma CLL
Sarcoid
The history/examination should be fairly denitive and is the most important diagnostic tool.
Investigations
Modalities
Tests + Findings
Cultures Bloods - ABG Bloods - Venous Imaging Scopic/Biopsy Functional/Special
FBC, CRP, TFTs, LFTs, blood lm, serological test CXR FNAC, core biopsy -
Treatment Obviously directed at cause
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Solitary Lumps in the Neck

[Note: these will still usually be lymph nodes]
Divide up as follows
ANTERIOR TRIANGLE POSTERIOR TRIANGLE
Anterior Triangle lumps

This may be subdivided into 1. Pulsatile 2. Non-pulsatile 3. Submandibular
Pulsatile lumps
These occur in 3 settings: Tortuos carotid artery (normal) Carotid artery aneurysm Carotid body tumour (chemodactoma)
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Non-pulsatile lumps
Classify these according to whether they are in the midline or not
MIDLINE Thyroglossal cyst Dermoid cyst Ectopic thyroid tissue NON-MIDLINE Branchial cyst Pharyngeal pouch Laryngocele (wind instrument players) 2 important ones are:
Branchial cysts
These are embryological remnants of the 2nd pharyngeal cleft. ! Present in early adulthood with SOFT-SWELLING and transilluminated (often post-URTI) Occur at upper of anterior sternomastoid. Need aspiration shows cholesterol crystals Treatment is excision Pharyngeal pouch
This is a mucosal protrusion between the 2 parts of the inferior laryngeal constrictor Present on the left in elderly patients It is a lump that INCREASES IN SIZE ON SWALLOWING Treatment is excision + cricopharygeal myotomy.
Submandibular lumps
These are usually secondary to infection e.g. jugulo-digastric with tonsillitis. Rarely you may have Tumours Impacted salivary stones (post-parandial pain and swelling). Do a plain XR or sialogram to detect as 80% are radio-opaque.
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Posterior Triangle lumps

Common lumps here include 1. Cervical rib 2. Cystic hygroma 3. Subclavian artery aneurysm
Cervical rib Enlarged costal element from the C7 vertebra. This is fairly common (1:150) but only 10% are symptomatic Causes a variety of syndromes 1. VASCULAR - compression of subclavian Thrombosis Raynauds Arm claudication 2. NEUROLOGICAL - pressure on the brachial plexus Paraesthesia Weakness
Cystic hygroma Collection of lymphatic cysts behind the clavicle. Often notices AT BIRTH Treatment with either with injection of sclerosing hypertonic saline or excision.
Parotid Lumps
Lumps in the parotid can either be due to Swelling of the WHOLE gland e.g. mumps, bacterial infection, sarcoid (uveoparotid syndrome), chronic liver disease LOCALISED swelling (usually neoplastic) Pathology This really concerns the neoplasic processes:
PRIMARY - benign (pleiomorphic adenoma), malignant (pleiomorhic adenosarcoma, adenocarcinoma) SECONDARY - from lymphoma/mets
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Clinical Features There will be a LUMP/swelling +/- a facial palsy (LMN type) Investigations 2 investigations are important: FNA and CT scan Treatment Supercial/radical parotidectomy Radiotherapy The most important complication post-op is a FACIAL PALSY
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Thyroid Surgery
Surgeons are usually concerned about GOITRES
Any enlargement of the thyroid gland.
Causes may be divided as follows:
! ! !
1. CONGENITAL 2. ACQUIRED Simple Toxic Inammatory!
1. Congenital
2 most common are:
1. Lingual thyroids Residual tissues at the base of the tongue 2. Thyroglossal cysts Remnant thyroid tissue Midline, smooth and cystic mass that moves upwards on swallowing
2. Acquired
Smooth Simple Toxic Inammatory Simple goitre Graves disease

Acute suppurative DeQuervains Riedels Hashimotos
Nodular Multinodular goitre Toxic multinodular goitre
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1. Acute suppurative thyroditis Staph/strep infection of the thyroid 2. DeQuervains thyroiditis Viral infection. non-suppurative 3. Riedels thyroditis Woody brosis and inltration with scar tissue Associated with retro-peritoneal brosis 4. Autoimmune/Hashimotos thyroditis Lymphatic inltration of gland due to antibodies against thyroglobulin Hyperthyroidism followed by hypothyroidism Associated with LYMPHOMA
Thyroid Neoplasms
May be: Benign - follicular adenoma Malignant:
Occurrence Papillary 70%
Age Young
Associations Multi-focal and poor response to radio-iodine surgery Good response to radio-iodine MEN Type II Aggressive Possible to shrink with radiotherapy
Prognosis OK
Follicular Medullary Anaplastic
15% 10% 5%
Older Any Older
Excellent Good if no nodes V. poor
! Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous Imaging -
Tests + Findings
Thyroid function (T4, TSH, thyroid auto-antibodies) All other bloods CXR (thoracic inlet view) Ultrasound (solid vs. cystic)
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Modalities
Scopic/Biopsy
Tests + Findings
FNA & Tru-Cut Radio-isotope scan (hot vs. cold areas) Laryngoscopy pre-op (determine if laryngeal nerves involves) -
Functional/Special
Thyroid Surgery
This is indicated for 3 reasons A. Problem goitres e.g. pressure symptoms B. Relapsing hyper-function C. Malignancy e.g. medullary The operation is a subtotal thyroidectomy and involves removing of the gland via a collar incision.
Complications
GENERAL Specic - Immediate
Think in terms of ABCDE Haemorrhage (beware tension haematoma) Laryngeal oedema Nerve damage Hypocalcaemia Hypothyroidism Keloid scaring Recurrence
Specic - Early Specic - Late
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Hernias
A hernia may be dened as -
Protrusion of a viscus and its covering through a defect into an abnormal position.
It essentially has 3 components: 1. Sac (neck, body and fundus) 2. Contents (bowel, omentum) 3. Defect
There are a number of important terms used to describe them: REDUCIBLE - sac may be returned to original cavity IRREDUCIBLE - sac unable to be returned to original cavity OBSTRUCTED - contains obstructed bowel STRANGULATED - contains bowel whose blood supply has become compromised.
There are many types depending on location/defect e.g. inguinal (direct and indirect), femoral, incisional, umbilical/paraumbilical, epigastric, Spigelian, obturator, lumbar and parastomal
Inguinal Hernias
The inguinal canal is the oblique passage taken through the abdominal wall by the testis/round ligament.
It is ~ 4cm in length and moves from: INTERNAL/DEEP RING - pierces the transversalis fascia (1-2 cm above mid-inguinal point) EXTERNAL/SUPERFICIAL RING - piereces external defect in external oblique aponerosis (just above pubic tubercle)
Relations: ANTERIOR - muscle, supercial fascia and skin POSTERIOR - transversalis fascia (lateral ) and conjoint tendon (medial ) SUPERIOR - internal oblique and transversus abdominis
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INFERIOIR - inguinal ligament
In an inguinal hernia 1. SAC - peritoneum 2. CONTENTS - nothing, bowel, omentum, bladder 3. DEFECT DIRECT INGUINAL HERNIA - posterior wall INDIRECT INGUINAL HERNIA - along the canal! Epidemiology Very common (R > L) M:F = 9:1 All ages at risk Risk factors 1. Congenital e.g. patent processus vaginalis 2. Acquired Increased IAP e.g. obesity, chronic cough, straining Weakness in wall e.g. previous incision
Clinical features
Symptoms: In an emergency - pain +/- features of obstruction History of lump Dull dragging pain in the groin/scrotum Signs: Is it reducible? Can it be controlled by pressure over the internal ring?
Note: important differential for a lump in the groin: Femoral hernia Lymphadenopathy Vascular e.g. saphena varix or femoral aneurysm Psoas abscess Undescended/ectopic testes Lipoma
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Investigation
This is not usually necessary. USS, MRI and herniography may be used
Management
Specics Decrease intra-abdominal pressure e.g. loose weight, treat cough, laxatives Rarely - hernial truss 1. Open 2. Laparoscopic In this operation you must 1. Dene, inspect and excise the sac 2. Close defect and tension-free repair e.g. suture (herniorrhaphy), mest (hernioplasty)
MEDICAL SURGICAL
Complications
GENERAL Specic - Immediate Specic - Early Specic - Late
Think in terms of ABCDE Bleeding Viscus perforation Infection Haematoma Recurrence Chronic groin pain Ischaemic orchitis
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Femora Hernia
The important anatomy to be aware of here is that of the FEMORAL CANAL.
Important points here: Canal is ~ 1.5 cm Part of femoral sheath together with femoral artery and nerve Boundaries: ANTERIOR: inguinal ligament POSTERIOR: pectineal ligament MEDIAL: lacunar ligament LATERAL: femoral vein
Femoral hernias are much more common in women (female pelvis) and are commonly acquired in old age. Importantly they like to obstruct.
Aetiology ! All are acquired (same risk factors as above)!
Clinical features Symptoms Emergency - features of obstruction Non-emergency - history of lump in the groin Femoral vs. Inguinal
Femoral: INFERIOR AND LATERAL TO PUBIC TUBERCLE Inguinal: MEDIAL AND SUPERIOR TO PUBIC TUBERCLE
Management
Modalities CONSERVATIVE MEDICAL SURGICAL -
Specics
Emergency - HIGH APPROACH Elective - LOW APPROACH

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Incisional Hernias
This a hernia through a previously acquired defect.
Risk factors for their development
1. PRE-OPERATIVE e.g. high pre-op risk factor prole 2. OPERATIVE e.g. sutures used, midline incisions, skill 3. POST-OPERATIVE e.g. increased IAP due to haematoma or prolonged ileus
Clinical features There will be a history of previous injury/procedure +/- complications. On examination look for Scar Mass protruding through the scar on cough/head tilt
Management
Modalities CONSERVATIVE MEDICAL SURGICAL
Specics Reduce intra-abdominal pressure Corset Normal principles
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Umbilical/Para-umbilical
CONGENITAL Defect Abdominal wall
INFANTILE Incomplete fusion of umbilicus to abdominal wall Umbilical Afro-Caribbean Downs syndrome Congenital hypothyroidism Asymptomatic Often self-resolve Reassurance Surgical repair if not closed by 3 years
ADULT Linea alba
Types Epidemiology
Exomphalos Gastroschisis Prematurity is biggest risk factor
Paraumbilical Obesity Multiparity Middle age Above/below umbilicus Frequenctly obstructs Surgical repair (Mayo)
Features Treatment
Obvious at delivery Resuscitation Surgical repair
Rare Types of Hernia
Epigastric hernia Pea-sized swelling caused by a defect in linea alba ABOVE umbilicus Treatment is surgical Spigelian hernia Protrusion through linea semilunaris (rare cause of a mass in right lower quatrant) Usually tender Treatment is surgical. Obturator Protrusion through obturator canal (felt in femoral canal or vagina) Cause pain over the medial knee Commonly obstructs Lumbar Following loin incisions
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Vascular Surgery
Clinical Anatomy
To understand and talk about vascular disease you need a passable knowledge of vascular anatomy. Here we will basically cover: 1. Venous drainage of the lower limb 2. Arterial supply to the lower limb
1. Venous drainage of the lower limb

Blood drains from the lower limb in 2 systems: 1. 2. a. b. c. DEEP SUPERFICIAL Great/long saphenous Small/short saphenous Tributaries
The long saphenous vein Pathway: Dorsum of foot (venous arch) Anterior to medial malleolus Up medial calf and thigh Drain into sapheno-femoral junction Important peforators 3 calf-perforators 1 mid-thigh perforator (Hunterian)
The short saphenous vein Pathway: Dorsum of foot Posterior to malleolus Up back of calf Drain inconsistently into deep veins at politeal fossa
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The sapheno-femoral junction Landmark: 4cm lateral and below the pubic tubercle.
2. Arterial supply to the lower limb

The basic arterial tree is shown below
abdominal aorta
L2
internal iliac external iliac 5cm distal to inguinal ligament common femoral
deep femoral supercial femoral
posterior tibial anterior tibial
lateral plantar dorsalis pedis medial plantar
Anterior tibial artery anterior compartment Peroneal artery lateral compartment Posterior tibial artery posterior 2 compartments
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Venous Disorders
The basic conditions to cover here are: 1. Varcose veins 2. Lymphoedema
Varicose veins
Long, tortuous and dilated veins of the supercial venous system
Most common site is LOWER LIMB (may also occur in abdominal wall, anus, vulva and pampiniform plexus)
Epidemiology Very common F>M Aetiology This may be divided into 3 sets of risk factors:
Specic Proximal venous obstruction Abdominal/pelvic malignancy Ascites Pregnancy Thrombosis Overactive muscle pump AV malformation e.g. Kippel-Trenaunay
Destruction of valves Increased ow
The most common sites of incompetence are Sapheno-femoral junction Mid-thigh perforators Sapheno-popliteal junction Calf perforators
Varicose veins must be described in terms of their distribution e.g. long saphenous, short saphenous, medial calf, mixed
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Clinical Features Patients most often complain about cosmetic problem. Some get mild pain and ankle swelling. Important skin changes most commonly occur in the GAITER REGION (lower medial of leg) Lipodermatosclerosis (induration and thickening) Eczema Haemosiderosis Ulceration
Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous Imaging -
Tests + Findings
Pre-surgical set (FBC, U&E) Colour duplex scanning (shows valvular and perforator incompetence) Venography (obstructions) Ultrasound (demonstrates reux into supercial veins) Cough test Tredelenburg/Tourniquet test
Scopic/Biopsy Functional/Special
Management
Surgery is required for patients with sapheno-femoral incompetence or major perforator damage.
Specics Treat underlying cause e.g. relieve constipation, lose weight Graded support stockings Injection sclerotherapy (small veins as an outpatient) 1. Ligation operation (long saphenous Trendelenburg procedure, short saphenous, perforators) 2. Stripping 3. Multiple avulsion 4. Endoscopic divison (SEPS)
MEDICAL SURGICAL
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Complications of varicose vein surgery
Most are performed as DAY CASE SURGERY.
Think in terms of ABCDE Haematoma Infection Nerve damage e.g. saphenous in stripping Recurrence
Lymphoedema
This may be split into: ! ! PRIMARY (congenital < 1y, praecox < 35y, tarda > 35y) SECONDARY Previous surgery e.g. axillary clearance Malignant obstructing disease Radiotherapy Infection (parasites/multiple previous episodes of cellulitis)
There is usually as history of limb swelling that is worse on standing. The oedema is NON-PITTING and usually unilateral. Consider primary type if bilateral. Associated skin changes: secondary infection, ssuring, hyperkeratosis.
Aims of management are: a. Allow function e.g. skin care, physiotherapy, prevention of infection b. Decrease swelling e.g. compression, debulking operations, bypass operations !
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Arterial Disorders
In this section we shall cover: 1. 2. 3. 4. 5. 6. Limb ischaemia Carotid artery disease Aneursyms Aortic dissection AV stulas Vasospastic conditions
Limb Ischaemia
A spectrum of ischaemic changes resulting from atherosclerotic process.
These changes may lead to: 1. Narrowing CHRONIC ISCHAEMIA 2. Thrombosis secondary to rupture ACUTE ISCHAEMIA/ACUTE-ON-CHRONIC ISCHAEMIA STAGE Stage 1 Stage 2 Stage 2: Intermittent claudication Stage 3 Stage 4 Symptoms Asymptomatic Intermittent claudication Ischaemic rest pain Ulceration/ gangrene
This changes are formally classied using the Fontaine Classication
Symptoms: This is a muscular, cramp-like pain experienced on walking and relieved by rest.
There also be rest pain at night that is relieved by walking or hanging the leg. Site Calf (femoral disease) Buttock (iliac disease) Signs: INSPECTION Signs
Loss of hair Pale, discoloured skin Muscle wasting Venous guttering ULCERS Necrotic toes Nail changes
Special
Vascular angle/ Buergers angle Buergers test/venous lling time
PALPATION
Temperature Capillary rell Pulses
AUSCULTATION
Bruits in: - aorta - iliac - adductor canal
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Note: Ulcers are typically described as punched out with pale granulation tissue and an erythematous halo. Inspect all pressure areas (heel, malleoli, in between toes) Dorsalis pedis is non-palpable in 10% people. Walk test = treadmill for 5 mins and stop when maximal claudication. Mearure ABPI ( > 20% drop signicant)
Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous Imaging
Tests + Findings
Urine dipstick (renal disease) FBC (baseline), U&Es (renal function), clotting, lipids, G&S Dopplex (triphasic vs. biphasic vs. monophasic) ABPI MRA / spiral CT Angiography (advance guide wire to aorta then inject to visualise arterial tree) - look for 1. Level of blockage 2. Collateral blood supply ECG
Management Modalities CONSERVATIVE MEDICAL SURGICAL Treat underlying risk factors Aspirin 75mg O.D. (clopiodgrel if contra-indicated) 1. ENDOVASCULAR e.g. PTA - best for iliac and supercial femorals, stents and PTFE/Dacron grafts 2. BYPASS SURGERY (autologous veins below inguinal ligament or synthetic above) Types 1. Anatomical e.g. fem-pop 2. Extra-anatomical e.g. axiloofemoral 3. Endarterectomy 4. Amputation 5. Sympathectomy (chronic pain in small vessel disease) Specics
Amputations is indicated for 1. Lethal limb (ischaemia, tumour) 2. Dead limb (PVD, extensive loss) 3. Useless limb (xed exion deformity, vestigial ngers)
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Acute Limb Ischaemic

This is a SURGICAL EMERGENCY
Aetiology Thrombosis 60% e.g. previously stenosed vessel Embolism 30% e.g. from LA thrombus, air, cholesterol Others e.g. trauma, vasospastic disorders, aortic dissection, popliteal aneurysm It is important to tell the difference between thrombosis and embolism
Thrombotic Hx of claudication/rest pain Onset over hours Signs of chronic vascular insufciency Hard arteries. No bruits
Embolic Recent MI, atrial brillation, aneurysm Onset over seconds No evidence of previous disease Soft artery. Bruits
Clinical features The 6 Ps
1. 2. 3. 4. 5. 6.
Pallor (marble white mottled with branching mottled and non-blanching xed staining) Pain Pulselessness Perishing with cold Paraesthesia (severe sign) Paralysis (severe sign)
Management
First...Resuscitate the patient
Modalities CONSERVATIVE Analgesia Fluids NBM
Specics
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Modalities MEDICAL
Specics Antibiotics Heparinisation Thrombolysis (tPA or streptkinase) 1. Endovascular e.g. angioplasty, stenting, embolectomy 2. Emergency reconstruction + fasciotomy 3. Amputation
SURGICAL
The precise rst line guidelines depend on whether the event is EMBOLIC or THROMBOTIC.
1. Thrombotic Thrombolysis 2. Embolic
Embolectomy with Fogarty catheter Then..thrombolysis (in unsuccessful)!
Post-operative care
All patients require heparin for 48 hours then long-term anticoagulation.
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Carotid Artery Disease

Patients with signicant carotid stenosis are at increased risk of
1) Stroke - Sudden neurological decit of vascular origin > 24h. ! 2) Transient Ischaemic Attack (TIA) - Sudden neurological decit of vascular origin < 24h.
Clinical Features Most are asymptomatic and picked up on cardiovascular examination (bruit or thrill) If they do present with a neurological event it will be of the ANTERIOR CIRCULATION (unilateral weakness, dysphasia/dysarthria, visual defects)
Investigations Duplex doppler scan is most important Others - intravenous/arterial DSA, MRA
Management Based upon trial data from NASCET and ECST.
Specics Control risk factors for all patients Aspirin (clopidogrel) for all patients ENDARTERECTOMY if stenosis > 70% Transluminal angioplasty is alternative
Note Risk of stroke with stenosis > 70% = 5% per year Never operate if < 30% stenosis
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Aneurysmal Disease
An aneurysm is an abnormal dilatation of a blood vessel.
It may be classed as: a. TRUE aneurysm - involves ALL layers and > 50% diameter. b. FALSE aneurysm - dilated blood vessel representing a haematoma around an area of damage. c. DISSECTING aneurysm - blood tracking into layers of vessel wall.
Process CONGENITAL ACQUIRED Degenerative Infective Mycotic Inammatory Traumatic Connective tissue disease
Examples Berry aneurysms in Circle of Willis Atheroscerotic (infrarenal AAA) Syphilis (thoracic) Bacterial endocarditis
Trauma Ehlers-Danlos Marfans Pseudoxanthoma elasticum
Specic types covered here include 1. AAA 2. Others e.g. thoracic, popliteal, femoral 3. Dissecting aneurysms
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Abdominal aortic aneurysms

These are the most common type of aneurysms and occur just below the renal arteries. Epidemiology Elderly Male > female Clinical features Symptoms: 75% are asymptomatic Patients may complain of Bloating Pulse/mass in abdomen Emergency presentation Epigastri/umbilical pain radiating to the back, ank or into the groin Acute limb ischaemia Blue-toe syndome Aortointestinal stula Signs: This obviously depends on the situation General: patient may have known vasculopathy. Present hypotensive and shocked Specic Abdominal tenderness Left midline expansile and pulsatile mass Bruits over aneurysm Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous Imaging If unwell
Tests + Findings
If unwell: EMERGENCY e.g. FBC, U&Es, clotting, LFTs, CXM - 10 units CT scan/MRI Ultrasound Plain abdominal xray (poor but may be signs of calcication) Arteriography may be used to describe relations of vessel ECG
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Management
Obviously in the case of rupture this is an EMERGENCY with a very poor survival. Aim to keep systolic less than 80 mmHg
Specics < 5cm should have serial ultrasounds/CT Treat co-exisiting risk factors This may be either to PREVENT complications or deal with rupture 1. Conventional grafts (aorta clamped above and below then disease portion replaced with dacron graft). Mortality ~ 5% 2. Endovascular repair (EVAR) - endoprosthesis introduce through a femoral arteriotomy
Guideline for surgery based upon UK small aneurysm trial. Indications include 1. Symptomatic 2. Asymptomatic > 5.5cm in diameter Expanding > 1cm per year Complicated e.g. emboli
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Aortic Dissection
Split of the intima and internal media such that blood is able to enter and track up and down the vessel wall.
Leading to 1. Double lumen formation that may occlude vital branches e.g. coronaries, carotids, renal 2. Haemorrhage 3. Undermining of attachments e.g. aortic valve aortic incompetence
Classication There are 2 types:! ! ! ! Type A (70%): ascending aorta and arch Type B (30%): discending aorta affected distal to left subclavian
Clinical features Symptoms Sudden severe chest pain that is tearing in nature and radiaed to back Features of hypotension due to haemorhage Features of other vessel involvement e.g. hemiplegia (carotids), paraplegia (spinal arteries), renal (anuria and haematuria) Signs General: shocked patient Specic: differening BP between each arm Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous Imaging If unwell
Tests + Findings
If unwell: EMERGENCY e.g. FBC, U&Es, clotting, LFTs, CXM - 10 units CXR (mediastinal widening + L. pleural effusion) Echo (aortic regurgitation) CT scan - investigation of choice but patient must be stable
Scopic/Biopsy Functional/Special ECG (signs of infarct)
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Management
This is a SURGICAL EMERGENCY and the patient may very well require resuscitation.
Ultimately management will depend on the type of dissection:
Type A: require surgical management e.g. replacement of aortic root.
! Type B: Conservative treatment e.g. -blockers to prevent further extension. + revascularisation of secondary ischeamia
Other types of aneurysm
Locations Ascending thoracic aorta 1. 2. 3. 4. Arch of aorta
Presentation
Treatment
Chest pain SVC obstruction Aortic regurgitation Obstruction to R main bronchus
Classically caused by syphilis - now atherosclerosis and Marfanss 1. 2. 3. 4. Hoarse voice Compression of trachea Ulceration into trachea Compression of L bronchus
Descending thoracic aorta
1. Back pain 2. Compression of oesophagus 3. Erosion into oesophagus ACUTE LIMB ISCHAEMIA ACUTEL LIMB ISCHAEMIA Saphenous vein bypasss graft
Popliteal Femoral
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AV stulae
An abnormal connection between the arterial and the venous system. They may be either large (macrostulae) or small (microstulae)
Aetiology 1. Congenital - rare Localised e.g. in head and neck Multiple e.g. Kippel-Trenaunay syndrome 2. Acquired Trauma Renal stula
Clinical features/Investigations
1. Supercial These are palpable as soft, pulsatile swelling that have a machinery bruit on auscultation. 2. Deep Detected on CT/angiography.
Management
Modalities CONSERVATIVE MEDICAL SURGICAL Left to resolve spontaneously
Specics
Embolisation Occlusion of feeding vessel and excison
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Vasospastic disorders
A group of conditions that affect the small arteries of the distal extremities.
1. Raynauds disease - idiopathic disease and normal arterioles. A bilateral process (usually of women) that involves episodes of vasospasm leading to colour changes in the digits 1. Digital pallor (vasoconstriction) 2. Cyanosis (arterioles have relaxed but no venules) 3. Reactive hyperaemia (complete reversal)
2. Raynauds phenomenon - underlying disease of the arterioles. Associated with Vibrating tools Connective tissue disease (SLE, RA, scleroderma) Haematological conditions - polycythaemia, cryoglobulinaemia Cervical rib Drugs e.g. beta blockers and ergot alkaloids
Management
Modalities CONSERVATIVE Remove cause Heated gloves/socks Avoidance of cold Nifedipine 5HT antagonists
Specics
MEDICAL SURGICAL
Sympathectomy (symptoms usually return within 6 months)
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Orthopaedics
Basic Fractures
Denition and Classications
A fracture is a break in the continuity of the bone.
Further classied as: 1. Simple fracture - skin is intact 2. Open/compound fracture - skin broken with bone out 3. Complicated fracture - neurovascular compromise
When talking about a fracture talk about:
1. FRACTURE LINE e.g. transverse, oblique, spiral, crush, comminuted, greenstick, avulsion
2. SHIFT or DISPLACEMENT e.g. lateral, medial 3. TILT or ANGULATION e.g. degree of lateral or medial 4. TWIST or ROATIONS
Fracture Aetiology There are 3 important mechanisms 1. Trauma (direct, indirect, avulsion) 2. Stress e.g. continual pressure on 1 area 3. Pathological i.e. low energy that normal would not fracture bone. Indicated underlying pathology e.g. osteoporosis, malignancy
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Clinical Features
These are fairly obvious but it is important to always do a NEURO-VASCULAR examination.
Investigations Most of the time this is an X-ray. But Obtain 2 views (lateral and AP) Joint above and below If pathological fracture or scaphoid you may need CT or bone scan.
Management First RESUSCITATE THE PATIENT (see ATLS chapter)
1. REDUCE
Alignment is more important than opposition 1. Manipulation e.g. Colles 2. Traction (skin or skeletal) 3. Open (if intra-articular or complicated)
2. FIX
CONSERVATIVE e.g. slings/plaster/collar&cuff SURGICAL 1. Internal xation 2. External xation
3. WAIT FOR UNION
This depends on good bone healing 1. 2. 3. 4. 5. Haematoma formation Organisation of haematoma and broblastic inltration Callus formation Consolidation of lamellar bone Remodeling
4. REHABILITATE
Basically involves graded-exercise therapy and physio.
Rules of thumb for bone healing Upper limb: 6-8 weeks Lower limb: 12 weeks Children: the time
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Complication of fractures
GENERAL
Blood loss Fat embolus Visceral damage e.g. rib fractures Nerve damage Vascular damage Infection Compartment syndrome - always suspect with pain on passive stretching or if poor perfusion Rx - remove bandaging or fasciotomy If not treated may result in Volkmanns ischaemic contracture
Specic - Immediate
Specic - Early
Specic - Late
Joint stiffness and later osteo-arthritis Problems with union e.g. mal-union, delayed union, non-union Avascular necrosis e.g. NOF, scaphoid, talus Reex sympathetic dystrophy/Sudeks atrophy Myositis ossicans (elbow)
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The Hip
SI joint Iliac crest
ASIS Superior pubic rami
Obturator foramen
Pubic tubercle
Inferior pubic rami Pubic symphysis
Greater trochanter
Lesser trochanter
Muscles acting on the hip
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Type FLEXORS
Muscles Psoas major Rectus femoris Sartorius Pectineus Gluteus maximus Hamstrings Gluteus medius Gluteus minimus Adductor longus Adductor brevis Adductor magnus Gluteus maximus assisted by obturators Anterior bres of gluteus medius and minimus
EXTENSORS ABDUCTORS ADDUCTORS
LATERAL ROTATORS MEDIAL ROTATORS
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Fractured Neck of Femur

Very common fracture - particularly in elderly, osteoporotic individuals. Mortality is approx. 30% in 6 months following a fracture.
Classication These may be 1. INTRACAPSULAR Subcapital Trans-cervical 1. EXTRACAPSULAR Basicervical Inter-trochanteric Sub-trochanteric
The intracapsular fractures are then further classied using GARDENS CLASSIFICATION
II
III
IV
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Clinical features
Symptoms Hip pain Unable to weight bear Signs Shortened (pulled up by ileo-psoas) Externally rotated (gluteus maximus) Remember to consider cause and effect of the fall Cause e.g. UTI, pneumonia, MI, arrhythmias Effects e.g. aspiration, dehydration, head injury
Investigations
Tests + Findings
FBC (infection) U&E (electrolytes disturbance, dehydration) G&S/CXM - 2 units AP pelvic xray + lateral of affected side CXR (cause) ECG (signs of infarct)
Imaging
Management
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Specics Analgesia (consider 5lb skin traction) Fluids NBM Post-operative - physiotherapy + OT assessment
MEDICAL SURGICAL
Treat cause 1. INTRACAPSULAR I, II - screw, III, IV - Austin-Moore I/II - Cannulated screw or dynamic III/IV - Hemiarthroplasty (Austin-Moore - uncemented, Thompson cemented) 2. EXTRACAPSULAR Dynamic hip screw
Complications
Think in terms of ABCDE Deep vein thrombosis Infection Avascular necrosis Mal-union Acetabular wear from hemiarthroplasty (so THR if severe OA)
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Important other fractures for finals

Fractures at the Wrist
1. Colles fracture Fracture of distal radius with shortening, dorsal displacement and angulation of the distal fragment. M.O.A. - fall on outstreched hand Rx: Closed reduction followed by immobilisation in forearm cast for 6 weeks Check position with XRay 1 week after.
2. Smiths fracture Fracture of distal radius with shortening, anterior displacement and angulation of the distal fragment Rx Try closed reduction Often requires open reduction and xation with a butress plate.
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3 uncommen intra-articular fractures are: Bartons fracture: fracture subluxation of the distal radius Galeazzi fracture: distal radial fracture + dislocation of the radio-ulnar joint Monteggia fracture: proximal ulnar fracture with dislocattion of the radial head
3. Scaphoid fracture Fracture of scaphoid bone M.O.A. - fall on outstretched hand Clinical features: Pain and swelling in the wrist + tenderness in the anatomical snuffbox/telescoping of the tumb. Most important complication: avascular necrosis of proximal portion Investigations: AP and lateral X-rays of wrist. Diagnosis often uncertain repeat after 10 days. Rx Immobilise in scaphoid plaster (if displaced/non-union internal xation with a Herbet screw)
4. Bennetts fracture Intra-articular fracture dislocation of the rst metacarpal bone Very common thumb injury Rx Usually requires xation with K-wire/screw
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Upper limb fractures/dislocations
1. Shoulder dislocation Most common is an anterior and inferior dislocation. Posterior dislocations in association with epileptic t/electric shock Clinical features of pain and decreased movement, together with a loss of deltoid contour and the arm being held internally rotated and abducted Most important complications - axillary nerve damage Investigation: AP and axial (Y-view) X-rays Treatment Reduction e.g. modied Kochers method Immobilize with broad sling
2. Proximal humeral fracture Often occurs in elderly M.O.A - RTA, fall from standing height Treatment is usually CONSERVATIVE - collar-and-cuff + physiotherapy If comminuted then needs ORIF
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Lower limb fractures
Tibial Plateau Fracture Often complex fractures caused by high-impact injuries May be classied using the Schatzker system (Type I-IV) Requires ORIF due to possible articular consequences
Tibial Fracture
High energy fractures that are associated with large amounts of soft tissue injury. The most important complications are: COMPARTMENT SYNDROME Common peroneal injury (proximal)! Test sensation to rst toe web space and dorsiexion movement of the great toe.
Treatment is with: Plaster Intramedullary nail External xation e.g. Ilizarov frame
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The Knee
The structures that are most often affected by pathology in the knee are: BONES e.g. arthritis! KNEE CAP e.g. recurrent dislocation MENISCI e.g. meniscal injuries CRUCIATE LIGAMENTS e.g. ACL and PCL injuries
Osteoarthritis of the Knee

Epidemiology Very common Older people May be related to trauma Clinical features
Symptoms: Pain, stiffness and swelling made worse by use of the joint. Joint locking + painful give-way due to loose bodies. Signs LOOK: varus/valgus deformity, swelling FEEL: effusion, tenderness over joint lines, crepitus MOVE: movement-xed exion deformity Management
Specics Weight loss Analgesia Walking stick + foam heel wedges Physiotherapy Variety of procedures possible 1. Arthroscopy (determine extent + wash-out - may provide up to 1 year of relief) 2. Osteotomy (particularly good for younger patients where medial only side is affected - last 8-10 years) 3. Total knee replacement
MEDICAL SURGICAL
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Recurrent patellar dislocations

Patella is a mobile sesamoid bone within the quadriceps tendon
There are 2 types: 1.! Full dislocation: always lateral following direct trauma to medial side. Knee locked in 30-40 degree exion + pain + swelling 2.! Subluxation: patella felt to pop out turning. Momentary pain and swelling 24h later
Important to due a SKYLINE x-ray to reveal a OSTEOCHONDRAL fracture.
Meniscal injuries
These occur when the meniscus becomes trapped between joint surfaces.
The distribution is: Medial meniscus 70% (less mobile than lateral) Lateral meniscus 25% Both 5% Clinical features Symptoms: History of twisting injury Pop/click or tearing sensation Swelling Signs LOOK: swelling, wasted quadriceps FEEL: effusion, tenderness at joint line MOVE: springy feel in a locked knee. McMurrays test Management Modalities CONSERVATIVE MEDICAL SURGICAL Specics Analgesia/anti-inammatories (creams etc) Physiotherapy Indicated for failure of conservative 1. Arthroscopy (diagnostic and therapeutic to excise the tear)
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Cruciate Ligament Injury

1. ACL Injury
Common. Occur following twisting and valgus strain e.g. men - football, women - skiing. There is often co-existant damage to medial collateral ligament and medial meniscus Clinical features Only diagnoses 70% Management
Modalities CONSERVATIVE MEDICAL SURGICAL Intensive rehabilitation Brace -
Specics
Arthroscopy (diagnosis and reconstruction) 1. Extra-articular strengthening - strength lateral side of knee with fascia 2. Intra-articular strengthening - ACL replaced with variety of materials e.g. bovine collagen, autologous patellar
2. PCL Injury
Not common. Usually occurs in RTA when tibia is forced posteriorly on femoral condyles.
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Neurosurgery
In this section we shall be looking at: a. Spinal cord compression b. Neurological tumours c. Hydrocephalus For information on intracranial bleeds please see trauma section
Clinical Anatomy
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Spinal Cord Compression

THIS IS A MEDICAL EMERGENCY Compression of the spinal cord
Clinical features Structure Symptoms Sudden onset back pain Neurological phenomena: 1. Leg weakness 2. Sensory loss 3. Painless urinary retention Vertebral disc Spinal cord Blood vessels Vertebral body Pathology Malignancy (primary/secondary) Osteoporosis Abscess e.g. Potts Acute intervertebral disc rupture Chronic degenerative disease Tumour Haematoma (e.g. warfarin therapy)
Signs This will usually be an upper motor neurone pattern. Increased tone Weakness in a pyramidal distribution Hyper-reexia Up-going plantars
+ a SENSORY LEVEL. Note: with sudden onset spinal compression there may be spinal shock (LMN pattern)
Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous Imaging Scopic/Biopsy Functional/Special Urine dipstick (? BJP) -
Tests + Findings
FBC (anaemia), U&Es, clotting (coagulopathy), Calcium (malignancy) MRI (to look at presence/degree of spinal compression) CT for bone injuries -
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Management
The management depends on the cause. The key is EARLY INTERVENTION - this offers the best chance of recovery.
Modalities CONSERVATIVE Neurological observations Analgesia Fluids NBM if for surgery
Specics
MEDICAL SURGICAL
Metastases - steroids, bisphosphonates, radiotherapy Abscess - antibiotics 1. Disc prolapse - decompression 2. Abscess - drainage 3. Metastases - surgical decompression
Cauda Equina Syndrome

This is a particular form of compression where the problem is with the cauda equina. As the cauda equina is made up of nerves that have come from the spinal cord the signs may be different: LMN signs e.g. weakness with absent reexes Bladder and bowel dysfunction Treatment is as for above.
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Neurological Tumours
There are lots of different tumours that affect the brain and spinal cord. They are rare but may be divided into: 1. PRIMARY Benign Malignant 2. SECONDARY (most common)
Table of the most common tumours and their features
Origin Glioma Primary from glial cells 1. 2. 3. 4. Meningioma Astrocytomas Medulloblastomas Ependymomas Oligodendromas
Characteristics
Treatment Surgery where possible Palliation
Primary from arachnoid cells
Benign and slow growing
Surgery where possible Palliation
Acoustic Neuroma
Primary from schwann cells of CN VIII. Note: usually unilateral. Bilateral if with NF
Press on 1. 8th nerve (deafness) 2. 5th/7th nerve (facial numbness and weakness) 1. Endocrine abnormalities e.g. hypopituitarism, Cushings syndrome 2. Visual abnormalities e.g. biltemporal hemianopia
Surgery but risk of nerve damage.
Pituitary Tumours
Adenomas
Medical hormonal manipulation Surgical - removal
Lymphoma
B cell T cell Breast, lung, kidney and malignant melanoma
Association with AIDS
Radiotherapy Poor survival
Metastases
V. common
Palliative e.g. steroids
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Hydrocephalus
Raised CSF pressure within the ventricular system that is characterised by dilated cerebral ventricles.
Note: the intraventricular pressure may either be NORMAL or RAISED
Types: 1. Communicating hydrocephalus Obstruction within subarachnoid space dilatation in entire system e.g. meningitis, subarachnoid haemorrhage, congenital abnormality in arachnoid villi. 2. Non-communicating hydrocephalus Obstruction within the ventricular system E.g. aqueduct stenosis, intraventricular tumours.
Acute hydrocephalus present with features of a raised ICP e.g. headache, visual disturbance Signs would be Loss of physiological cupping Blurring of disc margins Engorged pulsatile veins Chronic hydrocephalus present with characteristic features Enlarging head circumference Sun-set eyes Tense fontanelle Cranial nerve palsies
Investigation The most important study here is MRI
Management
Established hydrocephalus required drainage. This may be 1. Temporary e.g. to an extraventricular dran 2. Permanent e.g. peritoneum, right atrium, pleural cavity
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Urology
Clinical Anatomy
The Kidney These are retroperitoneal organs Contains a hilum into which goes the renal artery, renal vein, pelvis of ureter, nerves and lymphatics. Contains adrenal glands on superior aspect. Structure: 1. Pelvis 2. Major calyces 3. Minor calyces (collecting ducts discharge here) Blood supply Renal artery from aorta Renal vein into IVC Para-aortic lymph nodes The Ureter 25 cm in length and split into 3 parts: 1. Abdominal 2. Pelvic 3. Intravesical Blood supply: Segmental blood supply from all arteries along its course There are 3 important sites of narrowing 1. Pelvis of kidney (PUJ) 2. Pelvic brim 3. Ureteric orice (VUJ)
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The testicles/scotum
Common presentations
Renal tract stones
Also known as nephrolithiasis/renal calculi
Epidemiology Very common to see Any age M:F = 2:1 Aetiology
Can form anywhere in the system (kidney to urethra) Aetiology can be linked to 3 basic factors:
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1. Increased solute concentration
Hypercalcaemia Hyperoxaluria (tea, spinach, rhubarb) Hyperuricaemia Cystinuria Thiazides decreasing calcium excretion
2. Increased urine concentration
Dehydration Increased dietary protein Diuretics
3. Stasis
UTIs Congenital tract abnormalities e.g. pelvic-ureteric junction obstruction/ horse-shoe kidney
Types of stone
1. 2. 3. 4. 5.
Calcium oxalate (75%) - spikey and radio-opaque [metabolic/idiopathic] Triple phosphate (17%) - large, radio-opaque may form staghorn calculus [proteus UTIs] Uric acid (5%) - smooth, brown, radio-lucent [hyperuricaemia] Hydroxyapatite (1%) Cysteine (1%) - yellow, crystalline, semi-opaqe [renal tubular defects, cystinuria]
Clinical Features
NOTE: a febrile patient with renal obstructed is a SURGICAL EMERGENCY
Symptoms: Asymptomatic Ureteric colic: severe pain from loin to groin Associated with pyrexia, vomiting, rigors +/- blood in urine Features of infection: polyuria, dysuria Signs: General: moving around on the bed, febrile, Specic: loin tenderness is a feature of infection above the stone
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Investigations
Modalities
Tests + Findings
Urine: MC & S, dipstick (haematuria, infection), 24h collection for ions FBC (leucocystosis) U&Es (dehydration) Specic levels of Ca2+, Mg2+, urate, phoshate Plain KUB (85% are radio-opaque) IVU (control, immediate, 20 min -
Management Denitive management will depend on the size of the stone If stone < 5mm in lower then will pass - send pt. home If stone > 5mm - operative intervention
Specics Analgesia (e.g. diclofenac/pethidine/morphine) Encourage oral intake/I.V. uids Home if pain resolved and stone < 5mm If infection - cefuroxime and metronidazole If stone > 5mm or pain not resolved 1. Kidney - ESWL, percutaneous nephrolithotomy, open removal 2. Ureter - Ureteroscopic removal, ultrasound/laser 3. Bladder - lithotripsy or open
MEDICAL INTERVENTIONAL
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Haematuria
The passage of blood in the urine.
2 types: Microscopic Macroscopic
Or may be divided according to aetiology:
1. FALSE e.g. beetroot, rifampicin, porphyria, PV/PR bleed
2. TRUE 1. General Coagulopathy, HSP, anticoagulants 2. Kidney Stones, tumours, infections 3. Ureter Stones, tumours, infections 4. Bladder Stones, tumours, infections 5. Prostate Stones, tumours, BPH 6. Urethra Stones, tumours, infections, trauma
Clinical features It is important to determine the following in the history 1. 2. 3. 4. 5. Timing (beginning, end or throughout) Painful vs. painful Clots? Other obstructive symptoms Drug history and clotting defects
Investigations
Modalities
Cultures Bloods - ABG
Tests + Findings
Urine: MC & S, dipstick, urine cytology -
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Modalities
Bloods - Venous FBC (leucocytosis) U&Es (renal function) Clotting (? coagulopathy) IVU Renal USS
Tests + Findings
Flexible cystoscopy and biopsy CT scan -
Management
Treat the cause
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Acute Urinary Retention

This is a common - particularly in the post-operative setting.
The aetiology may be: 1. ACUTE 2. CHRONIC 3. Acute-on chronic
IN THE LUMEN
Stones Cots (with clot retention) Tumours (bladder, prostate, urethra) Infection Trauma Constipation Fibroids Cauda equina syndrome Drugs (e.g. EtOH, anticholinergics)
IN THE WALL
Clinical Features OUTSIDE THE WALL Symptoms: Progressive reduction in ability to pass water Suprapubic pain Signs: General: patient agitated and in pain Specic: Palpable bladder that may extend up to umbilicus Always do a PR for constipation, prostate and rectal tone Neurological examination as well. SYSTEMIC
Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous Urine MC & S, dipstick If unwell FBC (leukocytosis) U&E (renal function) G&S PSA
Tests + Findings
CXR & KUB (? stones) USS (residual volume, size of bladder and hydronephrosis) ECG
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Management
Modalities CONSERVATIVE Mobilise + run tap Treat underlying cause IV uids for secondary diuresis
Specics
Catheterise (+ shot of gentamicin) TWOC only > 24 hrs 1. Suprapubic catheter 2. Emergency TURP
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Kidney and Bladder

Topics covered here 1. Renal transplantation 2. Renal cell carcinoma 3. Bladder carcinoma
Renal Transplantation
Kidneys may be obtained from: 1. Live related donor 2. Cadaveric donor (brainstem death or non-heart beating donor)
The most important indication is END STAGE RENAL FAILURE (GFR < 10ml/min).
Suitable candidates should be Young Fit for anaesthesia Suitable anatomy Compliant with post-op immunosuppression Suitable anatomy
Recipient Normal pre-op Specic bloods - ABO screen, HLA matching (A, B, DR), cross-match with donor lymphocytes Normal pre-op
Donor
Specic bloods - ABO screen, HLA matching (A, B, DR), cross-match Infectious screen - HIV, CMV, HTLV-1, hepatitis, syphilis Imaging - IVU, USS, MRA
Imaging - USS, KUB,
Procedure The operation occurs in 2 parts. 1. Remove donor kindey 2. Anatastomosis in recipient with: Renal vein external iliac vein Renal artery external iliac artery Note: may be palpated in the abdomen.
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There will be 2 scars: 1. Loin scar for a nephrectomy 2. Rutherford-Morrison incision for anastamosis
Post-operatively Immunosupression using steroids, azothioprine and cyclosporine.
GENERAL Specic - Immediate Specic - Early Specic - Late
Think in terms of ABCDE Hyperacute rejection Accelerated rejection Acute rejection - u-like symptoms and graft tenderness. Chronic rejection Tumours (skin cancers/lymphomas) Complications of immunosuppressive treatment (steroids, infection and malignancy) UTIs
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Renal Tumours
Renal tumours may be: a. BENIGN (e.g. cysts) b. MALIGNANT
Epidemiology They are uncommon Present late middle age M>F = 2:1 Aetiology Carcinogens TCC Stones SCC Hypernephroma in Von Hippel-Lindau Syndrome
LOCATION PELVIS
TYPES Transitional cell carcinoma Squamous cell carcinoma Papilloma
CHARACTERISTICS Associated with carcinogens Highly malignant Associated with chronic stones
KIDNEY
Hypernephroma (Grawitz tumour)
Most common types (80%) Adenocarcinoma Large & aggressive Large tumours in children
Nephroblastoma (Wilms tumour)
Clinical features
Symptoms: General: weight loss, PUO Specic Microscopic haematuria Rarely - loin pain, loin mass and haematuria Metastatic symptoms Signs: General: anaemia Specic Mass in loin
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Varicocele (tumour spreads along renal vein obstructing left testicular vein) Hypertension Polycythaemia Hypercalcaemia
Investigations
Modalities
Cultures Bloods - ABG Bloods - Venous Urine dipstick (haematuria) If unwell
Tests + Findings
FBC (anaemia of chronic disease, polycythaemia) U&Es (renal function) LFTs (mets) Ca2+ Clotting CXR (mets - cannonball) IVU (lling defect, hydronephrosis, renal mass) Renal USS (demonstrate mass and look at IVC) CT (staging) ECG
Imaging
Management
Modalities CONSERVATIVE MEDICAL INTERVENTIONAL
Specics Palliation with radiotherapy and chemotherapy Radio/chemo are never curative 2 operations 1. Nephro-uretectomy (TCC - removal of entire 1 side, one scar in loin and second in groin) 2. Nephrectomy (other tumours - may require chest apporach!)
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Bladder Carcinoma
Epidemiology Common in middle aged and elderly M:F = 4:1 Aetiology Important predisposing factors are smoking, dye exposure and chronic irritation say with schistosomiasis.
Pathology 1. 2. 3. 4. Transitional cell carcinoma (90%) - solid or papillary Squamous (7%) - associated with chronic irritation Adenocarcinoma (2%) Sarcoma
There is a detailed staging system that it is not necessary to know - most are pT1 (invasion of sub-epithelial tussie) or pT2 (involvement of supercial muscle) They may also be classied according to differentiation eg. G1 (well), G2 (intermediate), G3 (poor)
Clinical features
Symptoms: General: Weight loss, anorexia Specic Painless haematuria Urinary retention (clots or bladder neck obstruction) Uraemic symptoms Signs: Usually there are NONE. General: anaemia Specic: Bladder mass Lymphadenopathy Features of metastases e.g. papable liver, abnormal chest examination
Management This depends on the stage 1. Trans Urethral Resection of Bladder Tumour (TURBT) - Tis, T1, T2 Adjuvants - Intravesical chemotherapy, immunotherapy using Montreal strain of BCG 2. Cystectomy with re-implantation of ureters through an ileal conduits Adjuvants - Radiotherapy
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Prostate Disease
In this section we shall talk about 1. Prostatitis 2. Benign Prostatic Hyperplasia 3. Carcinoma of the prostate
Prostatitis
Infection and inammation of the prostate.
May be ACUTE or CHRONIC
Most common organisms are Strep. feacalis E. coli Chlamydia
Clinical features Symptoms: General: malaise, fever/rigors Specic Pain (prostadynia) Haetospermia Retention Features of urinary tract infection e.g. dysuria, discharge Signs General: pyrexia Specic Tender prostate on PR Tender testicles in epididymo-orchitis Investigation as you might expect e.g. FBC, CRP and MSU
Denitive treatment is antibiotics e.g. ciprooxacin
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Benign Prostatic Hyperplasia (BPH)#

Benign and profuse nodular proliferation of the musculobrous and glandular layers of the prostate
Epidemiology Very common and get worse with advancing years Aetiology
There are 2 theories behind its development a. HORMONE THEORY - reduced testosterone and proportional increase in oestrogen hyperplasia b. NEOPLASTIC THEORY - benign neoplastic enlargement
Clinical features
Symptoms: Obstructive symptoms e.g. poor stream, hesitancy, post micturation dribbling Symptoms due to bladder retention e.g. frequency, nocturia, overow incontinence, infection, stones Signs: Smoothly enlarged prostate with denable median sulcus. Invesigations
Modalities Cultures Bloods - ABG Bloods - Venous Urine dipstick & MC & S FBC (Hb low if uraemia) U&E (renal function) PSA
Tests + Findings
Imaging
KUB & IVU USS of kidneys and bladder (residual volume, hydronephrosis) Transrectal ultrasound Urodynamics (pressure/ow cystometry)
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Management
Modalities CONSERVATIVE MEDICAL Address drinking habits
Specics
1. Alpha blockers e.g. Tamsulosin 1c 2. 5 reductase inhibitors e.g. Finasteride Indicated if severely affecting QOL. 1. Trans Urethral Resection of Prostate (excise lateral and middle lobes with diathermy cutting loop) Send chipping to histology 2. Trans Urethral Incision of Prostate - youger patients 3. Trans Urethral ElectroVaporisation of Prostate 4. Laser Prostatectomy (Nd: YAG - lower risk of impotence and retrograde ejaculation) 5. Open - if very large 6. Transurethral Microwave Thermotherapy
INTERVENTIONAL
Carcinoma of Prostate
Epidemiology Most common cancer in men 60% over 80 have it at autopsy Aetiology Involves age-dependent alteration in oestrogen and androgens
Pathology These are always ADENOCARCINOMAS and affect the outer zone of the gland. ! ! Note: malignant spread causes osteosclerotic lesions on XR)
It is staged using the GLEASON SYSTEM (based upon two worsed affected areas)
Clinical features Many pts. are asymptomatic Symptoms: General: many Specic:
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Obstructive symptoms Sympoms of spread e.g. back pain, SOB, pathlogical fracture Signs: Prominent nodule on PR Investigations Modalities Cultures Bloods - ABG Bloods - Venous Urine dipstick & MC & S FBC (anaemia of chronic disease) U&E (renal function) Alk phosphate PSA CXR, spine/skull/pelvic radiographs USS of prostate/liver CT scan Bone scan Transrectal biopsy Tests + Findings
Imaging
Quick notes on the PSA A proteolytic enzyme that is part of the ejaculate Values increased with: age, infection (UTI, prostatitis), TURP, post-ejaculation Treatment
Specics Watch and wait stategy (PSA & PR) For palliation DXT used
MEDICAL
1. LHRH analogue e.g. Goserelin (Zoladex) 2. Anti-androgens e.g. cyproterone acetate 3. Radiotherapy for spinal mets 1. TURP 2. Radical prostatecctomy and lymph clearance 3. Brachytherapy
INTERVENTIONAL
Note: old treatment is bilateral or orchidectomy
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The Scrotum
In this section we look at: a. Torison of the testicle b. Undescended testicles c. Lumps in the scrotum
Testicular Torsion
A twisting of the spermatic cord that cuts off the blood supply to the testicle and surrounding structures within the scrotum.
This is a SURGICAL EMERGENCY! 4-6 hours window in which testicle is salvageable
Usually affects affects children and young adults.
Aetiology Trauma Lack of a bare area attaching testicle to scrotum predisposed to torsion. This is know as a CLAPPER BELL TESTICLE
Clincal features Symptoms: Extreme pain in scrotum (unilateral) Lower abdominal pain (T10 innervation_ Signs: Hot and swollen testicle Extreme tenderness HIGH RIDING and TRANSVERS in lie Managment Direct patient to theater ASAP (do not perform US) Procedures i. Untwisting of testicle with salvage ii. Orchidectomy
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Undescended Testicles
The testicles should normally be present in scrotum at birth
Epidemiology 3% are undescended at birth 1% after 1 year Prematurity increases the risk hugely. There are a number of possible results
1. Crytoorchidism - complete lack of testicles from the scrotum ! 2. Retractile testes - norma genitalia but overactive cremasteric reex. Testes may be persuaded in scrotum with warm hand No treatment except reassurance 3. Maldescended testes - testicles stopped descending down normal path. Scrotum is underdeveloped and at Testicle will be small There will a patent processus vaginalisis (+/- a hernia) Always require repair
4. Ectopic testicles - testes in an abnormal site. Common sites: abdomen, supercial inguinal pouch, root of penis Complications Infertility Prone to trauma/torsion (supercial site) Hernias Malignancy (replacing it does not help this)
Management
ORCHIDOPLEXY (< 2y) - Dantos pouch procedure
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Lumps in the Scrotum
This is v. common for exams.
Always ask yourself 4 questions:
a. Can you get above it? If not then it must be from above inguinal hernia b. Is the testis separate from the lump? What structure is it from? - testis or epididymis/cord c. Is the lump tender? Epidido-orchitis is most common ! d. Does the lump transilluminate? Cystic things transulluminate e.g. hydrocele/varicole Tumours/spermatoceles/haematocele do not
Brief notes on each conditions
Hydrocele A collection of serous uid within the tunica vaginalis. May be PRIMARY (congenital and associated with patent processus, large) or SECONDARY (reaction to other pathology in testis, small) Rx Infants - leave until 1y as most will resolve spontaneously Adults - should resolve spontaneously if not aspirate and send for cytology Drainage and excision in theatre Varicocele Dilated veins of the pampiniform plexus. May be PRIMARY (idiopathic) or SECONDARY (left sided renal tumour). Present with bag of worms scrotum and a dull ache (L > R) Rx Conservative Surgical Clip the testicular vein
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Haematocele Blood within the tunica vaginalis Rx Conservative Surgical - drain Epididimo-orchitis Infection and inammation of the testis and surrounding structures. Occurs in association with Mumps (usually 1 week post-parotitis) Ascending infection e.g. UTI, prostatitis STD e.g. Chluamydia Present in a similar fashion to testicular tumours: Importat differences are systemic features (fever, unwell), features of UTI/STD, secondary hydrocele Denitive treatment Analgiesia, bed rest, scrotal support Ciprooxacin Sperm granuloma Painful lump post-vasectomy Epididymal cyst Tender cystic lump coomon in middle-aged and elderly. May be bilateral
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Testicular Cancer
Epidemiology Tumour of young men Aetiology Increased risk with undescended testicles and infertility
Pathology
Teratomas for Troops (young), Seminomas for Sergeants (older)
1. Seminomas Solid and slow growing tumours Radiosensitive 2. Teratomas Solid or cystic Secrete -fetoprotein Rare types Choriocarcinomas (HCG producing) Leydig cell tumours (secrete androgen) Sertoli adenomas (secrete oestrogens) Lymphomas (elderly with poor prognosis)
Clinical features Symptoms: Asymptomatic Lump Signs: Heavy, irregular lump Non-tender
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Investigations
Staging is via the Royal Marsden Classication
Tests + Findings
FBC (anaemia of chronic disease) U&E (renal function) 2 tumour markers 1. -fetoprotein 2. -HCG CXR (mets) USS scrotum CT abdomen (staging) Never perform a percutaneous biopsy (seeding) -
Imaging
Treatment
Specics Important adjuncts - Conservation of other testicle for fertility - Cryopreservation of semen - Prosthesis Chemotherapy and radio-therapy may be offered to para-aortic nodes 1. Inguinal orchidectomy +/- lymph node dissection
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Appendix
Common abdominal scars
+ Roof-top = Mercedes-benz
Roof-top Roof-top Loin Roof-top Midline Loin
Subcostal/ Kochers
R. paramedian
Loin
Lanz
L. paramedian
Grid-iron
Pfannenstiel
Inguinal
+ always look for lapaoscopy scars!
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Common drugs
Drug ANALGESIA Paracetamol Aspirin Diclofenac Codeine phosphate Morphine Tramadol Pethidine
Dose
Drug HYPNOTICS
Dose
1g Q.D.S. 300mg Q.D.S. 50mg T.D.S. 30mg Q.D.S. 5-10mg / 4h 50mg / 4h 50mg / 4h
Zopiclone Temazepam
3.75-7mg nocte 10-20mg nocte
ANTI-HISTAMINES Chlorphenamine Cetirizine 10mg IV/4mg PO 5-10mg/24h PO
ANTI-ACIDS ANTI-EMETICS Cyclizine Metaclopramide Ondansetron 50mg T.D.S. 10mg T.D.S. 4mg T.D.S. Cimetidine Ranitidine Omeprazole Lansoprazole 800mg nocte 300mg nocte 20mg 30mg
ANTIBIOTICS Amoxicillin Flucloxacillin Erythromycin Ciprooxacin Cefuroxime Metronidazole 500mg T.D.S. 500mg Q.D.S. 500mg Q.D.S. 500mg B.D. 1.5 g I.V. 500mg I.V.
ANTI-DIARRHOEALS Loperamide Codeine phosphate 4mg stat then 2mg with each motion 30mg Q.D.S.
ANTI-COAGULANTS Unfractionated heparin Enoxaparin 5000U B.D. s.c. DVT prophylaxis 20-40mg/24 s.c.
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Podmedics 2010

Clinical Surgery Notes

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Surgery Revision Notes

Thank you and good luck.

The Podmedics Team

Ed Wallitt: ed@podmedics.co.uk Jonny Manley: jonny@podmedics.co.uk

Podmedics Recommended Texts/Links/Courses

www.onexamination.com You must answer questions from this site!

Skin Disorders! The Oesophagus !

Gallstone and Biliary Disease!

Basic Principles of the Lower Gastrointestinal Surgery !

Colon Cancer and Stomas!

114 116 117 118 119 120

Hernias ! Vascular Surgery !

Neurological Tumours! Hydrocephalus!

General approach to dening a disease

THE VINTA MEDIC SURGICAL SIEVE

Bloods - ABG Bloods - Venous Imaging

Surgical Fluids and Nutrition

Osmolality (280-295 mosmol/l) - should be equal between IC and EC CHARGED + UNCHARGED

(Na++K++Cl-+HCO-) + (urea+glucose) = 2(Na++K+) + urea + glucose

OUTPUT 1.5L 0.5L 0.5L 0.5L 3L

Total insensible = skin loss + lung loss.

Indications for Intravenous Fluids

Contents 154 mmol Na+ in 1L

Dextrose saline 5% dextrose Hartmanns (lactated Ringers solution) COLLOIDS

30 mmol/l Na+ + 40g dextrose 50g dextrose in IL Anions + Cations + Ca + lactate

Natural e.g. blood, albumin

Synthetic e.g. Gelofusin, Haemaccel

+ 20mmol/l of K+ per bag

Assessment of volume status

BMI = weight (kg) / height (m)2

Normal Overweight Obese Morbidly obese

Complications of enteral nutrition:

2. Total Parenteral Nutrition

Complications of parenteral nutrition:

Advanced Trauma Life Support (ATLS)

The Primary Survey

1. Airway and C-spine

The airway must be assessed and treated.

Endotracheal tube (ETT)

Assessment: INSPECTION Signs

CHEST, RETROPERITONEUM, PELVIS, THIGH AND ON THE FLOOR

10 - 20 % Low Low Type and crossmatch Low

> 40 % High High O-negative High

Unilateral fixed and dilated Bilateral pinpoint

Orbital injury, oculomotor nerve compression, stroke Opioid drugs

Bilateral constriction Irregular

Brainstem injury Trauma, post eye operation

The Secondary Survey

2. Pneumothorax Air in the pleural space.

A tension pneumothorax is a MEDICAL EMERGENCY!

INSPECTION Important signs

3. Haemothorax Blood in the pleural space

These are due to penetration or decelerating injuries

INSPECTION Important signs

Intracranial lesions Focal Diffuse

Treatment of head injury

Modalities CONSERVATIVE MEDICAL

Types of Cranial Bleeding

Pics from left to right

Clinical Features LOC Lucid period Deterioration (coning) Death

Between arachnoid Rupture of bridging vein and dura

Insidious onset (alcoholics/elderly/ epileptics/those on anticoagulants) Headache, sensory/ motor S/S