PEDIA Ear and Throat

EAR AND THROAT DISORDERS
I. OTITIS MEDIA
A. Incidence 1. Most common bacterially-caused condition in childhood 2. Common in children because their Eustachian tube is shorter, wider and straighter B. Signs and symptoms 1. Generally follows as a respiratory infection (colds/rhinitis) or low-grade fever 2. Sudden increase in temperature 3. Sharp constant pain in one or both ears due to pressure of accumulating fluid in the ear 3.1 Infant extremely irritable and pulls or tugs at affected ear to attempt relief 3.2 Older child verbalizes presence of popping noises and difficulty of hearing
I. OTITIS MEDIA
C. Management
1. Medications 1.1 Antibiotics give full length of treatment (usually 10 days) to prevent recurrence 1.2 Decongestant nose drops to open the Eustachian tubes and allow air to enter the middle ear 1.3 Analgesic ear drops when instilling ear drops, position with affected ear up to allow eardrops to run onto the eardrum
I. OTITIS MEDIA
2. Facilitate drainage of infected ear discharges 2.1 Position with affected ear down 2.2 Apply local heat (hot water bottle or bag 38.9 degrees Fahrenheit) with the childs affected ear on top of it 2.3 Myringotomy if no spontaneous perforation of the tympanic membrane occurs, surgical incision will have to be done to relieve pain and allow eardrum to heal. 3. Observe for complications, e.g., mastoiditis, meningitis or chronic otitis media with perforation of tympanic membrane 4. Examine effectiveness of treatment 4.1 For children below 3 years of age pull the ear down and back 4.2 For children above 3 years of age pull the ear up and back
II. TONSILITIS AND ADENOIDITIS
A. General information: Tonsils and adenoids are lymphoid tissues circling the pharynx and form part of the Waldeyers Ring. This ring is believed to filter and protect the respiratory and gastrointestinal tracts against invasion by pathogenic microorganisms. It is also known to have a role in antibody formation. Up to 5 years of age, the childs susceptibility to infection is great. But as the childs immunity increases through immunization and exposures, the protective role of the Waldeyers Ring decreases.

B. Signs and symptoms 1. Persistent sore throat 2. Offensive breath odor 3. Dysphasia; mouth breathing 4. Cervical lymphadenopathy 5. Impairment of taste, smell and hearing
C. Indication of tonsillectomy and adenoidectomy (T & A): chronic peritonsilar and retrotonsilar abscesses (enlarged tonsils are not indications for surgery). Surgery can be done 2-3 weeks after infection has subsided to prevent spread of the organisms to other parts of the body
D. Nursing management 1. Preoperative nursing care 1.1 Parents should inform the child about the operation prior to hospital admission 1.2 Laboratory tests (bleeding time, clotting time, platelet smear; CBC), as well as PE and routine urinalysis are done 1.3 Withhold solid foods after supper the night before surgery and liquid breakfast early on the day of the operation 1.4 Atropine sulfate given preoperatively reduces formation of respiratory secretion. Side effects: 1.4.1 Dilated pupils 1.4.2 Dryness of nasopharynx; thirst 1.4.3 Flushed face; warm skin
2. Postoperative nursing care important: hemorrhage is the most common complication 2.1 Immediate post-op 2.1.1 Position on prone/semi-prone to facilitate drainage of secretions (Remember: suctioning is never done in T & A) 2.1.2 Observe for signs of hemorrhage - Restlessness; pallor; cool skin - Decreased BP; increased PR and RR - Frequent swallowing

2.2 When alert or awake
2.2.1 Allow child to sit upright 2.2.2 Chipped ice or ice cream is given in an hour or two cold causes vasoconstriction thus reduces edema in the postop site 2.2.3 Ice collar applied to relieve sore throat, reduce swelling and discomfort in the operative site 2.2.4 Encourage small servings of soft food (chewing increases circulation and thus promote healing)

3. Discharge instructions
3.1 Restrict activities for 2 weeks more 3.2 Eat soft, cool, easily swallowed foods for several days 3.3 Plenty of fluids 3.4 No coughing, gargling or clearing of the throat only rinsing of the mouth is allowed
Sample Question
Jimmy had a tonsillectomy performed earlier in the day. He is now 4 hours postop. Which of the following is an abnormal finding and cause for concern? A. An emesis of dried blood B. Increased swallowing C. Pink-tinged mucus D. Jimmys complaints of a very sore throat
Answer: B. Increased swallowing

Increased swallowing could be a sign of hemorrhage from the surgical site. Vomiting of dried blood, pinktinged mucus, and complaints of a very sore throat would be expected following a tonsillectomy.
Which
of the following signs is most characteristic of a child with croup? A. Barking cough Fever Low heart rate Respiratory distress
RENAL DISORDERS
RENAL DISORDERS
I. WILMS TUMOR
A. Description 1. A tumor involving the kidneys 2. Once diagnosed, a sign should be posted at the bedside, No abdominal palpation
B. Signs and symptoms 1. Abdominal mass 2. Abdominal pain especially in older children 3. Late manifestations 3.1 Weight loss and anemia 3.2 Fever a sign of tissue necrosis 3.4 Hematuria means poor prognosis
RENAL DISORDERS
I. WILMS TUMOR
C. Management sequence depends on the stage of disease at the time of diagnosis 1. If without metastasis 1.1 Surgery nephrectomy 1.2 Chemotherapy actinomycin D;Vincristine 1.3 Ionizing radiation cobalt/ deep X-ray for 24 exposure days 2. If with metastasis 2.1 Radiation to both lung fields 2.2 Chemotherapy Actinomycin 2.3 Surgery thoracotomy
RENAL DISORDERS
I. WILMS TUMOR
D. Prognosis
1. The younger the patient, the better the outlook 2. No metastasis is better; but even with metastasis, as long as it is not in the bones or the bone marrow, prognosis is still fair 3. A two-year period free of the disease is considered a cure
RENAL DISORDERS
II. ACUTE GLOMERULONEPHRITIS (AGN)
A. Definition: Hypersensitivity reaction of the kidneys to Group A Beta hemolytic streptococci B. Strep infection associated with AGN 1. Tonsillitis 2. Otitis media
3. Impetigo
4. Pyoderma
RENAL DISORDERS
C. Signs and symptoms due to release of histamines by damaged cells 1. Hematuria and periorbital edema presenting complaints 2. Scanty, smoky, reddish or brownish urine 3. Pallor 4. Mild to moderate hypertension first felt as severe headaches 5. Shortness of breath; malaise; fatigue; anorexia; with occasional vomiting; lethargy
RENAL DISORDERS
D. Laboratory data 1. Increased anti-streptolysin O (ASO) titer normal is 250 U 2. RBC, leukocytes, epithelial cells and casts in the urine 3. +3 or +4 urine proteins 4. Increased BUN and creatinine levels 5. Decreased Hgb and Hct transient anemia 6. X-ray reveals cardiac enlargement and pulmonary congestion
RENAL DISORDERS
E. Management largely supportive 1. Complete bed rest most important aspect of treatment 2. Diet: low sodium (because of edema), low protein (if with high BUN), limited potassium (because of oliguria) 3. Medications 3.1 Antihypetensiveness 3.2 Magnesium sulphate 3.3 Digitalis if in failure 3.4 Penicillin, the drug of choice exerts a bacteriostatic effect by suppressing the formation of bacterial cell wall
RENAL DISORDERS
4. Weigh daily 5. Elevate head to relieve periorbital edema 6. Renal biopsy position on prone for 12 hours after biopsy to prevent hemorrhage (the most common complication of renal biopsy)
RENAL DISORDERS
F. Complications
1. Hypertensive encephalopathy 2. Acute cardiac failure 3. Acute renal failure
RENAL DISORDERS
G. Prognosis 1. Generally benign in young children 2. Not excellent in older children because it can progress on to chronic renal disease and eventually lead to renal failure 2.1 Initial symptom: lethargy 2.2 Cause: destruction of nephrons 2.3 Indication of progress: hypertension 2.4 Treatment: dialysis
RENAL DISORDERS
III. NEPHROTIC SYNDROME/ NEPHROSIS
A. Cause: unknown B. Pathogenesis: increased glomerular membrane permeability to large molecules causes considerable quantities of plasma proteins to escape into the urine. Albumin, because of its high plasma concentration and relatively low molecular weight, is lost in greater quantity.
RENAL DISORDERS
C. Diagnosis James Schema 1. Proteinuria 3.5 Gms/24 hours or more 2. Hypoalbuminemia 3 Gms or less 3. Hyperlipidemia (300 mg % or more) the change in serum albumin-globulin ratio, wherein because of loss of albumin, globulin, specially the cholesterol fraction, increases (may also termed hypercholesterolemia) 4. Edema due to decreased osmotic pressure of blood; develops first in periorbital tissues. If absent, means poor prognosis
RENAL DISORDERS
D. Signs and Symptoms 1. Extracellular fluid collection in cavities, legs and external genitalia
2. Abdominal skin is stretched shiny, with prominent veins

3. Respiratory embarrassment 4. Waxy pallor
RENAL DISORDERS
5. Decreased frequency of urination; urine is foamy or frothy because of high amounts of proteins; maybe tea-colored. 6. Progressive wasting of skeletal muscles due to negative nitrogen balance stick-like extremities 7. Tires easily; poor appetite
8. Normal, or even slightly lower blood pressure
RENAL DISORDERS
E. Management since the cause is unknown, many treatment modalities are used 1. Ambulation is advised; bed rest observed only when acutely ill and rapid diuresis is occurring. 2. Elevate the head to reduce discomfort due to edema (semi-upright position) 3. Diet: High protein, extra potassium, moderate sodium restriction
RENAL DISORDERS
4. Skin care edema fluid is a good medium for bacteria
4.1 4.2 4.3 4.4 Never apply heat; no adhesives nor plasters Frequent position changes Binders for scrotal edema Careful washing and drying of skin fold with mild soap and water; put cotton between skin surfaces to prevent intertrigo
RENAL DISORDERS
5. Drug of choice: Prednisone 5.1 Effect: dieresis begins in 8-14 days after onset of treatment 5.2 Untoward side effects 5.2.1 Immunosuppression children receiving steroids should be protected against sources of infection (reverse isolation) 5.2.2 Weigh again due to fluid retention and increased appetite 5.2.3 Hypertension monitor BP 5.2.4 Striation; acne 5.2.5 Growth arrest
RENAL DISORDERS
5.2.6 Emotional disturbances; psychosis 5.2.7 Gastric ulcer 5.2.8 Delayed healing 5.2.9 Activation of healed TPB 5.2.10 Cushings syndrome moonface; muscle weakness, facial, hirsutism, osteoporosis 5.3 Precaution: steroids should be discontinued in tapered doses to prevent extreme exhaustion and hypoglycemia due to adrenal insufficiency.
RENAL DISORDERS
F. Complications 1. Infection 2. Diarrhea 3. Ascites 4. Respiratory distress 5. Pneumococcal pneumonitis
G. Prognosis 1. Exacerbations are precipitated by acute infections 2. Forerunner of chronic glomerulonephritis
Sample Question
Tyrone, age 4 years, has just been diagnosed as having nephrotic syndrome. His potential for impairment of skin integrity is related to A. Joint inflammation B. Drug therapy C. Edema D. Generalized body rash
Answer: C. Edema
A child with nephrotic syndrome will have massive edema. A child with edema is prone to skin breakdown. Drug therapy is usually steroids and diuretics, neither of which is related to impairment of skin integrity.
INTEGUMENTARY DISORDERS
I. ATOPIC DERMATITIS/INFANTILE ECZEMA
A. General Considerations 1. Earliest manifestation of an allergic tendency in childhood; frontrunner of asthma 2. Hereditary predisposition is usual 3. Usually appears by the 4th month when solid foods are being introduced and clears spontaneously by the 4th year 4. Most often seen in well-nourished, well -cared for, healthy infants
B. Most common allergens 1. Cows milk 2. Wheat cereals 3. Egg white - yolk as source of iron is needed, not egg white; should not be given to infants below 1 year, especially if with family history of allergy 4. Vitamin C rich fruits C. Complication: bacterial infection of lesions
D. Signs and symptoms 1. Pruritus, erythema and edema, then papules and vesicles first evident on the cheeks, then spreading to the forehead, scalp and extremities 2. Generalized lymphadenopathy; splenomegaly 3. Low-grade fever 4. Child is uncomfortable, fretful and irritable 5. Increased eosinophil count (eosinophils engulf bacteria and contribute to body defense) 6. Scarring may occur due to secondary infection. Over the years, skin thickens and darkens in color, called lichenification, the hallmark of chronic eczema
E. Management
1. Accurate history to identify allergens that is why the first principle in the introduction of solid foods is: Introduce one new food at a time. 2. Clove- hitch restraint to prevent the child from scratching 3. Cleanse skin with mineral oil, plain water or NSS 4. Burrows solution wet compresses for bacteriostatic, antipruritic and drying effects
II. IMPETIGO
A. Definition: Infectious disease of the superficial layers of the skin B. Etiologic agents: streptococci, staphylococci or pneumoccoci C. Incidence 1. In children of poor hygiene who live in overcrowded settings and who are malnourished 2. Maybe primary or a complication of chickenpox, mosquito bites, etc.
II. IMPETIGO
D. Manifestations lesions commonly found on the face about the mouth and nose
1. Small, reddish macules filled with serum and rapidly becoming cloudy 2. Skin blisters 3. Pustules which rupture, discharging serous and purulent fluid 4. Brown, thick crusts
II. IMPETIGO
E. Management 1. Meticulous hygiene daily baths with hexachlorophene scrub to the scabs 2. Penicillin F. Complications: Acute glomerulonephritis or Rheumatic Heart Disease if due to Group A betahemolytic streptococci
Sample Question
When teaching parents about known antecedent infections in acute glomerulonephritis, which of the following should the nurse cover? A. Herpes simplex B. Scabies C. Varicella D. Impetigo
Answer: D. Impetigo
Impetigo, a bacterial infection of the skin, may be caused by streptococcus and may precede acute glomerulonephritis. Although most streptococcal infections do not cause acute glomerulonephritis, when they do, a latent period of 10 to 14 days occurs between the infection, usually of the skin (impetigo) or upper respiratory tract, the onset of clinical manifestations.
III. BURNS
A. General considerations 1. It is the most severe form of trauma to the integumentary system 2. Burn wounds are three-dimensional 2.1 Extent usually expressed as percentage of total body surface area burned (TBSA). The Rule of 9 is widely used but is not an adequate clinical method for children. The Lund and Browder allows for the changes in percentage during different stages of development.
III. BURNS
2.2 Depth traditionally classified as: 2.2.1 First-degree involves only the epidermis: is superficial, with tender slightly swollen redness; with edema formation; is painful; 3-5 days healing time; no scarring. Eg, sunburn 2.2.2 Second-degree involves the epidermis and the dermis; characterized by blister formation or reddened discoloured region with moist weeping surface; is extremely painful because nerve endings for pain are exposed; very edematous; 21-28 days healing time
III. BURNS
2.2.3 Third-degree involves the entire dermis plus portions of the subcutaneous tissue; brown leathery appearance with little surface moisture; painless to touch because nerve endings for pain have been also burned; marked edema; scar formation (therefore, grafting is needed) 2.2.4 Fourth-degree subcutaneous tissue + fascia + muscles + perhaps bone 2.3 Volume amount of fluid found in the interstitial spaces causes edema 2.3.1 Abnormal capillary permeability which allows proteins to escape into tissue spaces 2.3.2 Increased capillary hydrostatic pressure which causes water and electrolytes shifts.
III. BURNS
Lund and Browder Method
III. BURNS
B. Bodys responses to burns 1. Destroy the evaporative water barrier, thus increasing insensible water loss from 4-15 times the normal. In children, the ratio of body surface area to body weight is greatly increased and 70% of the body is made up of water; insensible water loss is thus severe. 2. Decrease the efficiency of the temperature control mechanism of the body 3. Destruction of skin causes loss of the first line of defense against infection and produces an excellent medium for bacteria, specifically pseudomonas. For this reason, tetanus immunization is given 4. Response of the cardiovascular system to burn shock 4.1 Signs and symptoms 4.1.1 Thirst 4.1.2 Pale, clammy skin
III. BURNS
4.2 Effects 4.2.1 Decrease in cardiac output 4.2.2 Decreased vascular permeability results in free loss of plasma proteins from the blood vessels into the extracellular spaces edema 4.2.3 Hematocrit is higher because of the release of plasma into the tissues at the burn sites 4.2.4 Sodium and calcium deficit; potassium excess during the first 48 hours
III. BURNS
5. The reaction of the pulmonary system is a major cause of mortality and morbidity in burns
5.1 Pneumonia; atelectasis

5.2 Inhalation injury
III. BURNS
5.3 Upper airway problem because of edema and consequent obstruction of the upper airway, or bronchospasms due to chemical irritation from toxic products of combustion (Implication: In children whose upper half of the body has been burned, a tracheostomy set should always be at the bedside for emergency purposes). 5.4 Because of the loss of bicarbonate ions, metabolic acidosis occurs. In an effort of the body to rid itself of the excess carbonic acid, respirations become deep and rapid: Kussmaul breathing
III. BURNS
6. The response of the renal system to burns is renal insufficiency due to hypovolemic shock. Because of diminished cardiac output, renal blood flow is drastically reduced, causing impaired renal functioning and decreased effectiveness of the kidneys. (Implications: because of immature renal functioning in young children, they are no more susceptible to impaired kidney function, leading to renal damage.)
III. BURNS
7. Gastrointestinal complications 7.1 Acute ulcerations of stomach or duodenum (Curlings ulcers) the most frequent life threatening situation 7.2 Paralytic ileus this is the main reason why burn victims are put on NPO with an NGT inserted; to remove gastic contents, thus prevent vomiting and aspiration 7.3 Acute gastric dilatation first sign of invasive sepsis 7.4 Hemorrhagic gastritis bleeding from congested capillaries in the gastric mucosa
III. BURNS
8. Metabolic responses 8.1 Weight loss 8.2 Negative nitrogen balance 8.3 Increased basal metabolic rate 8.4 Markedly increased energy requirements
III. BURNS
9. Neuromusculoskeletal changes are all due to infection, immobilization and metabolic changes
9.1 9.2 9.3 9.4 9.5
Contractures Tendon dislocation Joint dislocation Limb amputations Weakness due to neuropathy
III. BURNS
C. Management 1. First-aid treatment in the home: apply cold water 2. In the hospital 2.1 Replacement of fluids most important goal of initial therapy 2.1.1 Solution: Ringers Lactate is the choice because it most closely resembles the composition of the extracellular fluid compartment 2.1.2 Dosage: 3-4 ml/KBW/%TBSA 2.1.3 Schedule total quantity to be given in 24 hours - One-half during the first 8 hours - The other half during the next 16 hours
III. BURNS
3.
adherent material by gentle iodine-based solution or and water, then thoroughly
Remove foreign washing with hexachlorophene rinsing with NSS
4. Shave hair from burned area and area immediately surrounding it 5. Excision of fragments of dead and devitalized tissues
III. BURNS
6. Application of topical agents

6.1 0.5% silver nitrate unknown action; not very popular because it stains the skin 6.2 Gentamicin cream 6.3 Mafylon/Sulfamylon or silver sulfadiazine (Silvadene) the burn butter 6.3.1 Purpose: to prevent bacterial invasion
III. BURNS
6.3.2 Method of application: applied evenly 1/8 inch in thickness 6.3.3 Side effects - Reduces buffering capacities of the blood because it increases bicarbonate excretion (when bicarbonates are broken down, they provide a heavy acid load). Remember: Monitor pH level of blood - Causes burning sensation for 20 minutes after application
III. BURNS
7. Dressings may (closed method) or may not (open method) be used. If closed method is used, dressings are changed everyday. 8. Wound debridement is done with each dressing change to prevent eschar (a tough coagulum of necrotic tissues). Necrotic tissues are not only good media for bacteria, but also promote growth of granulation tissues. 9. Daily removal of dried cream by soaking in whirlpool bathtub prior to debridement 10. Morphine sulphate, gr. to relieve pain of seconddegree burns 11. Use of Bradford frame for ease of turning and maintenance of good body alignment.
III. BURNS
12. Position flat on bed with legs extended specia;;y during the first 24-48 hours in order to:
12.1 Avoid postural shock because of fluid loss, circulation to the head may become inadequate 12.2 Support healing of burn wounds 12.3 Prevent hip contractures 12.3.1 Proper splinting 12.3.2 Active and passive range of motion exercises
III. BURNS
13. Grafting is done to minimize growth of granulation tissues which results in contractures and ugly scars 13.1 Xenograft from animals 13.2 Homograft from other individuals 13.3 Autograft oneself
NEUROLOGIC DISORDERS
I. SPINA BIFIDA
congenital problem in which there is a defective closure of the spinal column.
A. Classification 1. Occulta L5 and S1 are affected, with no protrusion of spinal contents. Skin over the defect may reveal a dimple, a small fatty mass or a tuft of hair. 2. Cystica 2.1 Meningocoele contains fluid - penetrated by fluorescent bulb 2.2 Myelomeningocoele congenital failure of the arches of one or more vertebrae to unite at the center of the back, so that the bony wall normally surrounding the spinal canal at that place is missing. There is external protrusion, through a transparent sac, containing spinal fluid, meninges, spinal cord and/or nerve roots. It is the most severe of the spinal deformities.
I. SPINA BIFIDA
B. Associated clinical problems depend on the location; all body parts below the lesion are affected. 1. Motor function 1.1 Feet maybe deformed 1.2 Joints of ankles, knees or hips may be immobile 1.3 Variable degrees of weakness in the lower extremities 1.4 Spontaneous and induced movement are decreased or absent
I. SPINA BIFIDA
2. Sensory function 2.1 Sensations usually absent below the level of the defects 2.2 Ulcerations of the skin are common 2.3 Impaired functioning of the autonomic nervous system 2.3.1 Skin is dry and cool 2.3.2 Sweating ability is impaired
I. SPINA BIFIDA
2.4 Urinary and bowel problems
2.4.1 Inefficient bladder causes constant urinary dribbling 2.4.2 Stasis of urine causes UTI 2.4.3 Possible renal destruction 2.4.4 Fecal incontinence or retention due to poor innervation of the anal sphincter and bowel musculature. 2.5 Hydrocephalus occurs in 65% of children; usually develops within the first 6 weeks of life.
I. SPINA BIFIDA
C. Preoperative management/conservative treatment 1. Careful handling to avoid rupture, pressure, irritation or leakage from the protruding mass by putting the child on prone position, with the hips abducted 2. Meticulous skin hygiene to prevent irritation; sterile donut ring over the lesion 3. Watch for signs of increased intracranial pressure 3.1 Anterior fontanel for tenseness, fullness, pressure 3.2 Shrill, high-pitched cry 3.3 Increased head circumference 3.4 Vomiting; irritability 3.5 Increasing BP, decreasing PR and RR and widening pulse pressure
I. SPINA BIFIDA
D. Surgical correction 1. Early excision of the sac if it is small and then primary closure is done 2. If base of the defect is too large for epithelization to take place and then closure is done at a later time. E. Postoperative care 1. Keep on prone position 2. Monitor urine output bladder injury is a high possibility in operations involving the spinal column 3. Measure head circumference daily 4. Monitor movement of lower extremities; passive range of motion (ROM) exercise to impaired lower extremities
I. SPINA BIFIDA
F. Complications 1. Meningitis 2. Severe neurologic deficits 3. Hydrocephalus 3.1 Types 3.1.1 Noncommunicating blockage within the ventricles which prevents CSF from entering the subarachnoid space. 3.1.2 Communicating obstruction in the subarachnoid cistern at the base of the brain and or within the subarachnoid space.
I. SPINA BIFIDA
3.2 Management 3.2.1 1.5-2 grams Mannitol 20%/KBW for 10-15 minutes since Mannitol is a diuretic, an indwelling castheter should be inserted for accurate recording of intake and output 3.2.2 Ventriculoperitoneal / ventriculoatrial shunt to bring the CSF to an area from where it can be excreted from the body. After the procedure, the child should be positioned on the side where the shunt is to prevent sudden decrease in intracranial pressure.
Sample Question
The nurse is caring for an infant with hydrocephalus. She has a shunt inserted. Which of the followinf signs indicates that the shunt is functioning properly? A. The sunset sign B. A bulging anterior fontanel C. Decreasing daily head circumference D. Widened suture lines
Answer: C. Decreasing daily head circumference

With improved drainage of the CSF, the head circumference should become smaller. All the other signs indicate an increased ICP.
II. CEREBRAL PALSY
A. Definition: Disorders created by damage to the motor centers of the brain, specifically the pyramidal tracts of the CNS. There is difficulty in controlling the voluntary muscles due to brain injury (which is not progressive, through). Since it involves voluntary muscles, therefore, it can not be diagnosed early in life, not until the child has started to move about.
B.
Incidence: Occurs most frequently among preemies and those who were in occipitoposterior positions while in utero.
II. CEREBRAL PALSY
C. Etiology 1. Prenatal causes 1.1 Hereditary factors 1.2 Irradiation of lower abdominal area especially during the first trimester 1.3 Infections. Eg., rubella, meascles, mumps, chickenpox, etc. 1.4 Anoxia due to placenta previa, abruption placenta, maternal blood loss, allergy to analgesics, reaction to anesthesia 1.5 Cord anomalies 1.6 Fetal cerebral hemorrhage 1.7 Prematurity 1.8 Maternal history of abortion, diabetes or toxemia
II. CEREBRAL PALSY
2. Natal causes 2.1 Abnormal delivery situations, e.g., prolonged labor, forceps delivery, CS, precipitate delivery 2.2 Use of analgesics and anesthetics 2.3 Placental abnormalities 2.4 Poor natal care 2.5 Fetal anoxia 2.5.1 Mechanical respiratory obstruction 2.5.2 Ateslectasis; RDS 2.5.3 Neonatal infections 2.5.4 Kernicterus; hemolytic disease 2.5.5 Blood incompatibility
II. CEREBRAL PALSY
3. Postnatal causes
3.1 Traumatic head injuries, e.g., falls, wounds, skull fracture 3.2 Infections. E.g., TB, meningitis, encephalitis 3.3 Encephalopathy due to carbon monoxide poisoning or internal hydrocephalus
II. CEREBRAL PALSY
D. Manifestations vary according to the portion of the brain that has been damaged 1. Weakness 2. Paralysis and incoordination of voluntary movements of the muscles 3. Seizures 4. Visual and hearing difficulties
II. CEREBRAL PALSY
5. Emotional disorders 5.1 Irritability 5.2 Overactivity 5.3 Impulsiveness 5.4 Short attention span 5.5 Mood swings
6. Speech problems 7. Mental retardation not always present
II. CEREBRAL PALSY
E. Classification based on brain areas involved and resulting patterns of movement 1. Spastic muscles are hyperactive, hypertonic, hyperirritable, hyperelastic, react readily to stimuli; exaggerated stretch reflex 2. Flaccid (+) deep tendon reflexes and (+) plantar response 3. Athetosis abnormal amount and type of involuntary motion; unpredictable, snake-like, worm-like movement; disappeares when asleep and relaxed 4. Rigid lead-pipe tonicity 5. Ataxic primary incoordination 6. Tremor uncontrollable, involuntary motions of a rhythmic, alternating, pendular patter 7. Atonic lack of tone; no response of muscles to volitional stimulation 8. Mixed
II. CEREBRAL PALSY
F. Management: the overall aim of treatment is muscle re-education. Maximize assets and minimize liabilities. 1. Physiotheraphy provide a period of quiet relaxation before starting sessions 2. Drugs - muscle relaxants; anticonvulsants 3. Maintain safe environment seizure precautions and use of safe toys 4. Prevent accidental falls because of scissoring and toe-pointing gait which results from tension on hip adductors, hip internal rotators and calf muscles (for this same reason, it is advisable to carry CP children astride the hips).
II. CEREBRAL PALSY
5. Encourage independence while providing adequate nutrition 5.1 Cut food into small pieces 5.2 Serve foods that stick to the spoon 5.3 Position properly; do not feed when child is tired or excited 5.4 Disregard messy eating 5.5 Allow child to hold spoon, guiding it to his mouth. To establish a hand-to-mouth pattern to serve as a basis for beginning self-feeding 5.5.1 Encourage finger foods 5.5.2 Play games that call for pointing out mouth, nose, eyes, etc. 5.5.3 Practice raising an empty glass to the mouth and setting it down again 5.5.4 Place food at the back of the tongue because CP children have a tendency to push their tongue forward 6. Discipline is necessary for the child to feel loved and secure do not overprotect
Sample Question
Which of the following is the most common permanently disability in childhood? A. Developmental dysplasia of the hip B. Cerebral palsy C. Muscular dystrophy D. Scoliosis
Answer: B. Cerebral palsy

CP is a group of disabilities caused by injury or insult to the brain either before or during birth, or in early infancy. Developmental dysplasia of the hip and scoliosis should not cause permanent disability.
Sample Question
Which of the following statements made by the mother of a 4-month-old would indicate that the child may have cerebral palsy? A. I am very worried because my baby has not rolled all the way over yet. B. my babys left hip tilts when I pull him to a standing position. C. My baby wont lift her head up and look at me; she is so floppy. D. he holds his leg so stiff that I have a hard time putting on his diapers. .
Answer: C. My baby wont lift her head up and look at me; she is so floppy.
Hypotonia or floppy infant is an early manifestation of CP. Typically, the infant lifts his head to a 90 degree angle by 4 months with only a partial head lag by 2 months. Rolling completely over usually does not occur until the infant is 6 months old. Tilting of the hip and limitation in one leg suggest developmental dysplasia of the hip.
III. MENINGITIS
A. Definitions: Inflammation of the meninges
B. Causes
1. Bacteria H. Influenza and pneumococcus, meningococcus (most severe type), staphylococcus and E. coli, streptococcus
2. Viruses rubella, mumps, herpes, chickenpox
III. MENINGITIS
C. Signs and symptoms
1. Early or prodromal signs
1.1 1.2 1.3 1.4
Irritability Anorexia Fever chill Headache
III. MENINGITIS
2. Specific signs 2.1 Nuchal rigidity chief sign 2.2 Stupor; convulsions 2.3 (+) Kernigs - pain on extending leg after it has been flexed on the abdomen 2.4 (+) Brudzinskis sign as head is elevated, passive flexion of the neck causes flexion of things at the hips and flexion of ankles and knees 2.5 Opisthotonous (head and legs are drawn backwards together) the position characteristically assumed by children seriously ill with meningitis 3. Signs of increased intracranial pressure 3.1 Vomiting every 8-10 minutes an early sign of increased ICP in children 3.2 Increased BP; decreased PR and RR and widening pulse pressure 3.3 Increasing head circumference 3.4 Bulging, tense anterior fontanel (in children below 18 months of age)
III. MENINGITIS
D. Diagnosis
1. Based on signs and symptoms 2. Lumbar puncture/spinal tap reveals 2.1 Increased ICP, unless CSF has just been obtained prior to the tap 2.2 Cloudy, if bacterial, and bacteria can be isolated in culture and nasopharyngeal secretions 2.3 High in protein, low in glucose a reversal on values means improvement in condition
III. MENINGITIS
E. Management 1. Provide rest and quiet minimal handling in darkened, non-stimulating environment to prevent convulsions 2. Phenobarb and Valium to control restlessness and prevent convulsions 3. Keep close watch over the 4 major components of neurological status 3.1 Level of consciousness (LOC) indicates highest degree of cerebral activity; take note of alertness and orientation to time, person and place confused, conscious, comatose, etc. 3.2 Pupillary response pupils are normally equal, round, reactive to light and accommodation (PERRLA). Remember, pupils constrict in the light and dilate in the dark. 3.3. Vital signs 3.4 Motor activity let child move all 4 extremities or grasp examiners hand
III. MENINGITIS
4. Prevent transient increase in ICP 4.1 When with IV, the danger of increasing the ICP is very real, so monitor fluid volume very closely 4.2 Non-constipating diet to prevent valsalva maneuver, crying, sneezing, coughing or vomiting should be avoided 4.3 Do not burp on upright sitting position because pressure on the jugular veins will increase ICP; just turn to side and rub the back 4.4. Move as little as possible; sitting and head movement cause increased ICP 4.5 Use straw when giving liquids
III. MENINGITIS
5. Position properly
5.1 Flat on bed if with nuchal rigidity 5.2 Side-lying if opisthotonic 6. Isolation masks are used to prevent the spread by direct contact or indirect droplet or inhalation. Cardinal rule in the use of isolation masks: discard when wet
III. MENINGITIS
F. Complications 1. Hydrocephalus common 2. Peripheral circulatory collapse/Waterhouse Friderichsen syndrome most serious complication due to bilateral adrenal hemorrhage leading to acute adrenocortical insufficiency 2.1 Profound shock 2.2 Petechiae; ecchymotic lesions 2.3 Vomiting 2.4 Prostration 2.5 Hypotension G. Prognosis: Good, if treated early, but with complications and long-term effects
Sample Question
To meet the sensory need of a child with viral meningitis, nursing strategies should include A. Minimizing bright lights and noise B. Promoting active range of motion C. Increasing environmental stimuli D. Avoiding physical contact with family members
Answer: A. Minimizing bright lights and noise

Photophobia and hypersensitivity to environmental stimuli are common clinical manifestations of meningeal irritation and infection. Comfort measures include providing an environment that that is quiet and has minimal stressful stimuli. Promoting active ROM at this time would not be beneficial. Viral meningitis is not contagious, so contact with family members is not contraindicated.
IV. ENCEPHALITIS
A. Definition: Inflammation of brain tissue due to bacteria, viruses, protozoa or fungi B. Signs and symptoms : same as meningitis C. Management and prognosis: same as meningitis
V. BRAIN TUMORS
A. General considerations 1. Occur most commonly in the 5-7 years age group 2. Vomiting in the morning is the initial symptom; signs of increased intracranial pressure occur early 3. Uncommon for children to have metastatic tumors B. Types depends on the location in the brain 1. Astrocytoma in the cerebellum 1.1 Course: insidious onset with a slow course 1.2 Signs and symptoms 1.2.1 Increased ICP 1.2.2 Hypotonia; diminished reflexes 1.2.3 Papilledema; blindness; nystagmus
V. BRAIN TUMORS
2. Medulloblastoma in the cerebellum
2.1 Course: highly malignant, rapidly growing (death occurs in one year) 2.2 Signs and symptoms 2.2.1 Unsteady walk; ataxia 2.2.2 Anorexia; vomiting 2.2.3 Early morning headache 2.2.4 Papilledema; drowsiness; nystagmus
V. BRAIN TUMORS
3. Gliomas in the brain stem; most common type in children
3.1 Course: slow 3.2 Signs and symptoms 3.2.1 Palsies, ataxia, sensory loss 3.2.2 Signs of increased ICP 3.2.3 Headache
V. BRAIN TUMORS
4. Ependymona in the first, second and fourth ventricles of the brain. Signs and symptoms:
4.1 Increased ICP; headache 4.2 Nausea and vomiting
4.3 Unsteady gait
V. BRAIN TUMORS
5. Craniopharyngioma near the pituitary gland
5.1 Signs and symptoms like disbetes insipidus 5.1.1 Stimulated growth 5.1.2 Myxedema 5.1.3 Delayed puberty 5.1.4 Visual defects 5.1.5 Alterations in personality and memory 5.1.6 Increased ICP
V. BRAIN TUMORS
C. Diagnostic procedures
1. 2. 3. 4. 5. EEG Pneumoencephalogram Skull series; brain scans Ventriculograms; arteriograms Lumbar tap
V. BRAIN TUMORS
D. Nursing Care successful treatment is uncertain in many instances because the location of the tumor renders surgical removal difficult and sometimes impossible. 1. Preoperative management 1.1 Enema not given because of possibility of increased ICP 1.2 Monitor neurologic and vital signs 1.3 Observe seizure precautions 1.4 Diet and fluids as tolerated 1.5 Consider body image in shaving the headexplain its necessity and allow child to verbalize his feelings
V. BRAIN TUMORS
2. Postoperative care 2.1 Assess ICP; level of consciousness 2.2 Observe for hemorrhage and edema. Mark stain or spot on head dressings in order to determine any increase in size 2.3 Position: head elevated, with body turned on the unoperated side. 2.4 When changing position, support the head and the neck and turn the child in one piece (logrolling)
Sample Question
Jack is 10 years old and is receiving cranial irradiation for a brain tumor. He has developed alopecia. Which of the following is an appropriate nursing intervention? A. Have Jack identify famous movie stars and sports heroes who are bald. B. Assure Jack that his hair will grow in before he leaves the hospital. C. Wrap a bandage around his head. D. Help him select a variety of hats.
Answer: D. Help him select a variety of hats.

Selecting hats to cover his head will help Jack deal with the change in body image. The other suggestions are all inappropriate.
VI. EPILEPSY
A. Definition: A disease diagnosed primarily from a history of seizure episodes because of increased basal level of excitability of the CNS. B. Classification and their description 1. Grand Mal 1.1 Abrupt onset preceded by an aura (any peculiar feeling, sight, sound, taste, smell or twitching and spasm of small muscle group) 1.2 Child falls to the ground, becomes pale, pupils dilate, with upward rolling of the eyeballs. Head is thrown backward or to one side; chest and abdominal muscles are rigid; limbs are rigid and contracted the tonic phase
VI. EPILEPSY
1.3 As air is forced out of a closed glottis by sudden contraction of the diaphragm, the child lets out a short, startling cry; the tongue may be bitten 1.4 Involuntary urination and defecation will follow 1.5 The 20-40 second tonic phase is followed by clonic activity involving spasms of the entire body 1.6 The child sleeps after the episodes; on awakening, he appears drowsy, stuporous and accomplishes routine tasks in an automatic fashion 1.7 When seizures are so frequent that they appear to be constant, it is termed status epilepticus, a medical emergency which may result in brain damage because of decreased oxygen supply to the cerebrum
VI. EPILEPSY
2. Petit Mal seen mainly in children 2.1 Transients losses of consciousness 2.2 Eye-rolling; drooping of fluttering of eyelids; drooping of the head; quivering of limb or trunk muscles 2.3 On completion of the seizure, the child immediately resumes activity without knowledge of what happened 2.4 Can be precipitated by hyperventilation or induced by blinking light 3. Jacksonian convulsion starts with one muscle or group of muscles and then spreads to other parts of the body
VI. EPILEPSY
C. Management 1. During seizures in Grand Mal, ease child on to the floor and loosen clothes around the neck and the abdomen, remove mall chairs, tables and other objects that can harm the child. Keep the head on the side or put his abdomen with the head on one side to prevent the tongue from falling against or obstructing the airway. 2. May participate actively in sports, but not in hazardous activities unless accompanied by a responsible adult. 3. Ketogenic (high fat) diet believed to decrease incidence of seizures
VI. EPILEPSY
4. Mainstays of treatment anticonvulsant drugs 4.1 Important information 4.1.1 Purpose: to allow the child to function as normally as possible 4.1.2 Choice of drug depends on the type of seizure and the severity of the symptoms 4.1.3 Drug alterations are done infrequently since it takes 1-2 weeks before they exert their maximal effects
VI. EPILEPSY
4.1.4 When patient has been seizure-free, medications must still be continued on a regular basis for at least 4-5 years after the last seizure 4.1.5 Drug should not be discontinued suddenly (just like steroids) especially during puberty when incidence of seizures is again on the rise 4.1.6 Dosage and drug are re-evaluated during early adolescence because they may need some changing
VI. EPILEPSY
4.2 For Grand Mal
4.2.1 Phenobarb initial drug of choice; safe to use 4.2.2 Dilantin causes stomatitis and hypertrophy of the gums (Implication: Meticulous oral hygiene is a must). Folic acid and Vitamin B12 are given to prevent megaloblastic anemia.
VI. EPILEPSY
4.3 For Petit Mal 4.3.1 Zarontin blood dyscrasias are less common 4.3.2 Trimethadione (Tridione) decreases the excitability of the motor area of the cerebral cortex; less hypnotic effect than Zarontin but has toxic effects: blood dyscrasias; insomnia; fatigue; photophobia; skin rashes
Sample Question
Henry, a 13-year-old who has been diagnosed as having epilepsy. A positive sign that Henry is taking his Dilantin properly is A. Hair growth on his upper lip B. Absence of seizures C. Lowered hemoglobin and hematocrit D. Drowsiness
Answer:
Dilantin is an antiepileptic drug that controls seizures. All the other signs and symptoms are side effects of the medications.
VII. MENTAL RETARDATION (DOWNS SYNDROME/TRISOMY 21)
A. Definition: Condition characterized by subnormal mental, physical and physiological capacity from early in life and during the growth period, which is shown by lack of maturation and ability to learn and manifested by poor adaptive behavior. B. Psychological classification 1. IQ of 50-70 mildly retarded or educable 2. IQ of 30-50 moderately retarded or trainable 3. IQ below 30 severely retarded or of the custodial type
C. Possible causes (other than Downs syndrome) 1. Micro-/hydrocephaly 2. Craniosynostosis premature closure of the fontanel 3. Rubella; sexually-transmitted disease; blood incompatibility 4. Kernicterus 5. Meningitis; encephalitis 6. Poisoning 7. Brain tumors 8. Deprivation; malnutrition
D. Characteristics 1. Lateral upward slant of the eyes 2. Flattened occiput 3. Short nose with flat bridge 4. Protruding fissured tongue 5. Single transverse palmar crease simian crease 6. increased spaces between first and second fingers and toes
7. Broad and square hands and feet 8. Congenital heart defect is common 9. Abnormally aligned teeth 10. Prone to respiratory tract infections 11. Less sensitive to heat , cold and pain 12. Poorly developed genitalia and delay in the development of secondary sex characteristics
E. Management behavior modification 1. Factors that affect rehabilitation program 1.1 Parental acceptance and degree of cooperation 1.2 Childs motivation 2. Consider functional/developmental level, not the chronological age 3. Help the child achieve his maximum potential; the ultimate dignity as an individual is to be considered
Sample Question
Jeffrey, age 17, has Downs syndrome. He4 is 57 inches tall and weighs 155 lbs. In planning his care, it is most important for the nurse to take into consideration A. His mental age B. His chronological age C. His bone age D. Growth chart percentiles.
Answer: A. His mental age

All Downs syndrome children are retarded and care must be geared to their mental age.
Sample Question
Downs syndrome is caused by A. An autosimal recessive defect B. An extra chromosome. C. A sex-linked defect D. A dominant gene
Answer: B. An extra chromosome.

In Downs syndrome there is an extra chromosome on the 21st pair , which is why the disease is also called trisomy 21.
Sample Question
Louise was born with a meningomyelocele with accompanying hydrocephalus. She has had a shunt procedure to alleviate the hydrocephalus. Louse should be placed in which of the following positions? A. Trendelenburgs B. On her back C. With her legs abducted D. On her abdomen
Answer: D. On her abdomen

Pressure must be kept off the spinal sac. As there is paralysis of the lower extremities, the legs should be abducted. Trendelenburg position is contraindicated in hydrocephalus.
Sample Question
Jennifer Pine, 3 years old, is admitted with a diagnosis of viral meningitis. During an initial assessment of Jennifer, the nurse would expect to find A. Headache, fever, and petechiae B. Seizures, lethargy, and hypothermia C. Pallor, anorexia, and bulging fontanels D. Fever, irritability, and nuchal rigidity
Answer: D. Fever, irritability, and nuchal rigidity

The clinical symptoms of viral meningitis (aseptic meningitis) include fever, irritability, and nuchal rigidity. Other symptoms include headache, seizures, and lethargy. Bulging fontanels are a sign of hydrocephalus.
MUSCULOSKELETAL DISORDERS
I. ERB-DUCHENNE PARALYSIS/BRACHIAL PLEXUS INJURY
A. Definition: A kind of paralysis caused by traumatic injury to the upper brachial plexus. It occurs most commonly in childbirth from forcible traction during delivery, with injury to one or more cervical nerve roots. B. Causes 1. Lateral traction exerted on head and neck during delivery of the shoulder in vertex presentation 2. Excessive traction on the shoulders during breech presentation, especially when arms are exerted over the head
C. Signs and symptoms 1. Loss of sensation in the arm 2. Paralysis and atrophy of the deltoid, the biceps and the brachialis muscles. 3. The arm on the affected side hangs loosely with the elbow extended and the forearm pronated. 4. Inability to abduct arm from the shoulder, to rotate the arm externally or to supinate forearm. 5. Absent Moro reflex on affected arm 6. Some sensory impairment in outer aspect of affected arm
D. Treatment 1. Initially, the arm and shoulder should be immobilized to allow swelling and inflammation of the associated neuritis to resolve. 2. Abduct the affected arm in externally rotated position with the elbow flexed. 3. Physical therapy and splinting may be necessary to improve function of the muscles and to prevent flexion contracture of the elbow.
II. CONGENITAL HIP DYSPLACIA (CDH)
A. Incidence 1. Appears at the rate of 1.5 cases per 1000 live births. 2. Affects females eight times more frequently than males. 3. Approximately one third of the degenerative hip joint disease cases found in adults is caused by residual effects of CDH. May be treated by total hip arthroplasty.
B. Types 1. Teratological develops in utero and is commonly associated with other orthopedic problems 2. Typical 2.1 Occurs just before, during or shortly after birth. 2.2 Probably caused by the softening effects of the maternal hormone relax in on the infants ligaments and the stress of labor and birth. 2.3 Classification 2.3.1 Dislocation or luxation the femoral head is completely displaced from socket or acetabulum.
2.3.2 Subluxation or partial displacement more common, occurring in approximately 1 in 60 births. A subluxated hip may become completely dislocated during an infants care unless certain types of maneuver are avoided. - Infants should never be lifted by their feet for diapering - Their legs should never be pulled, nor should their hips be completely extended when wrapped in a blanket. - Since this problems may be overlooked on the initial examination, these precautions should apply to the care of all infants. - Barring complications, 88% of newborns with subluxation becomes normal by 2 months of age.
C. Signs and symptoms 1. On supine, there is resistance when legs are flexed on abdomen and abducted 2. Ortolanis sign on supine, put thumbs on groin while abducting the legs; a click is felt 3. On prone, baby has unequal gluteral folds
D. Treatment 1. Goal: Immediate return of the femoral head to the acetabulum since the hip socket becomes progressively more distorted if reduction is delayed. Early treatment can reduce therapy to approximately 3 months duration. 2. Specific measures 2.1 When on supine, put a pillow between the thighs to abduct the affected hip 2.2 Carry the child astride the hip
2.3 Apply 2 diapers instead of one 2.4 Traction 2.5 Hip spica cast when child is around 6 months old, before he learns how to walk, the cast is applied from the waist to below the knee of the affected leg and above the knee of the unaffected leg. 2.6 Pavlic harness allows flexion and abduction but prevents extention or adduction. E. Prognosis: If the childs x-ray film indicates normal location of the hip at years of age, the condition may be considered cured.
III. SCOLIOSIS
A. Definition: Lateral curvature of the spine B. Age group at risk: schoolage C. Types 1. Postural/functional can be corrected by correct posture and exercises 2. Structural can be corrected only by surgery
III. SCOLIOSIS
D. Screening test to differentiate one type from the older have the child bend forward over at the waist and inspect equality of shoulders, hips and scapula E. Clues to diagnosis 1. Uneven hemline 2. One hip is more prominent than the older 3. One shoulder blade is higher than the other
III. SCOLIOSIS
Screening Procedure for Scoliosis
III. SCOLIOSIS
F. Management 1. Conservative 1.1 Exercises 1.1.1 Pelvic tilt to increase muscle strength of the body so as to counteract effects of splinting 1.1.2 Swimming is known to be therapeutic 1.3 No contact sports or violent gymnastics 1.4 Avoid obesity
III. SCOLIOSIS
2. Corrective 2.1 Surgical spinal fusion with or without Harrington rods. Postoperatively: 2.1.1 Do logrolling changing position of the child in one piece 2.1.2 Use firm mattress 2.1.3 Monitor intake and output, emphasizing urine output damage of nerves that control the bladder is a possible complication in surgeries involving the spinal column.
III. SCOLIOSIS
2.2 Immobilization in Milwaukee brace to provide longitudinal traction and lateral pressure 2.2.1 Worn for as long as growth is occurring (20-25 years of age) 2.2.2 Used 24 hours of the day, except when taking a bath 2.2.3 Avoid strong deodorants which can cause rashes
III. SCOLIOSIS
2.2.4 Skin care to prevent sore areas at contact points 2.2.5 Wear T-shirt underneath the brace to prevent skin irritations 2.2.6 Wear loose clothing over the brace to protect body image
G. Prognosis: better when curvature begins at an older age when less growth remains and when curve is mild at the time of initial diagnosis and treatment.
III. SCOLIOSIS
Pelvic Tilt
Sample Question
A routine physical examination on 2day old Melissa Baylon uncovered evidence of congenital dislocation of the right hip. When assessing Melissa, a sign of one-sided hip dislocation is A. An usually narrow perineum B. Pain where her leg is abducted C. Symmetrical skin folds near her buttocks and thighs D. Asymmetrical skin folds over the buttocks and thighs
Answer: D. Asymmetrical skin folds over the buttocks and thighs

Displacement of the hip on one side causes asymmetry of skin folds.
Sample Question
An infant is being treated for congenital hip dislocation with a Pavlik harness. The babys mother asks if she can remove the harness if it becomes soiled. The best response for the nurse to make is A. No, the harness may not be removed. B. No, she will only be wearing it a few days. C. Yes, just long enough to clean the area. D. Yes, just overnight while she is sleeping.
Answer: A. No, the harness may not be removed.

The harness is not to be removed until the hip is stable within 90 degrees of flexion and x-ray confirmation. This usually occurs after about 3 weeks of in a Pavlik harness.
TETRALOGY OF FALLOT
TETRALOGY OF FALLOT
- is a congenital heart defect which is classically understood to involve four anatomical abnormalities (although only three of them are always present). It is the most common cyanotic heart defect, representing 55-70%, and the most common cause of blue baby syndrome. It was described in 1672 by Niels Stensen, in 1673 by Edward Sandifort, and in 1888 by the French physician tienne-Louis Arthur Fallot, for whom it is named.
TETRALOGY OF FALLOT
Anatomic morphology
TETRALOGY OF FALLOT
As classically described, tetralogy of Fallot involves four heart malformations which present together: 1. A ventricular septal defect (VSD): a hole between the two bottom chambers (ventricles) of the heart. The defect is centered around the most superior aspect of the ventricular septum (the outlet septum), and in the majority of cases is single and large. In some cases thickening of the septum (septal hypertrophy) can narrow the margins of the defect.
TETRALOGY OF FALLOT
2. Pulmonary stenosis: a narrowing of the right ventricular outflow tract and can occur at the pulmonary valve (valvular stenosis) or just below the pulmonary valve (infundibular stenosis). Infundibular pulmonic stenosis is mostly caused by overgrowth of the heart muscle wall (hypertrophy of the septoparietal trabeculae), however the events leading to the formation of the overriding aorta are also believed to be a cause. The pulmonic stenosis is the major cause of the malformations, with the other associated malformations acting as compensatory mechanisms to the pulmonic stenosis. The degree of stenosis varies between individuals with TOF, and is the primary determinant of symptoms and severity. This malformation is infrequently described as sub-pulmonary stenosis or subpulmonary obstruction.
TETRALOGY OF FALLOT
3. Overriding aorta: An aortic valve with biventricular connection, that is, it is situated above the ventricular septal defect and connected to both the right and the left ventricle. The degree to which the aorta is attached to the right ventricle is referred to as its degree of "override." The aortic root can be displaced toward the front (anteriorly) or directly above the septal defect, but it is always abnormally located to the right of the root of the pulmonary artery. The degree of override is quite variable, with 5-95% of the valve being connected to the right ventricle.
TETRALOGY OF FALLOT
4. Right ventricular hypertrophy: The right ventricle is more muscular than normal, causing a characteristic boot-shaped appearance as seen by chest X-ray. Due to the misarrangement of the external ventricular septum, the right ventricular wall increases in size to deal with the increased obstruction to the right outflow tract. This feature is now generally agreed to be a secondary anomaly, as the level of hypertrophy generally increases with age.
TETRALOGY OF FALLOT
Other variations
There is anatomic variation between the hearts of individuals with tetralogy of Fallot. Primarily, the degree of right ventricular outflow tract obstruction varies between patients and generally determines clinical symptoms and disease progression. In addition, tetralogy of Fallot may present with other anatomical anomalies, including:
TETRALOGY OF FALLOT
Other variations 1. stenosis of the left pulmonary artery, in 40% of patients 2. a bicuspid pulmonary valve, in 40% of patients 3. right-sided aortic arch, in 25% of patients 4. coronary artery anomalies, in 10% of patients 5. an atrial septal defect, in which case the syndrome is sometimes called a pentalogy of Fallot 6. an atrioventricular septal defect 7. partially or totally anomalous pulmonary venous return 8. forked ribs and scoliosis
TETRALOGY OF FALLOT
Tetralogy of Fallot with pulmonary atresia (pseudotruncus arteriosus) is a severe variant in which there is complete obstruction (atresia) of the right ventricular outflow tract, causing an absence of the pulmonary trunk during embryonic development. In these individuals, blood shunts completely from the right ventricle to the left where it is pumped only through the aorta. The lungs are perfused via extensive collaterals from the systemic arteries, and sometimes also via the ductus arteriosus.
TETRALOGY OF FALLOT
Epidemiology and etiology Tetralogy of Fallot occurs in approximately 3 to 6 per 10,000 births and represents 5-7% of congenital heart defects. Its cause is thought to be due to environmental or genetic factors or a combination. It is associated with chromosome 22 deletions and diGeorge syndrome. It occurs slightly more often in males than in females. Embryology studies show that it is a result of anterior malalignment of the conal septum, resulting in the clinical combination of a VSD, pulmonary stenosis, and an overriding aorta. Right ventricular hypertrophy results from this combination, which causes resistance to blood flow from the right ventricle.
TETRALOGY OF FALLOT
Pathophysiology and Symptoms Tetralogy of Fallot results in low oxygenation of blood due to the mixing of oxygenated and deoxygenated blood in the left ventricle via the VSD and preferential flow of the mixed blood from both ventricles through the aorta because of the obstruction to flow through the pulmonary valve. This is known as a right-to-left shunt. The primary symptom is low blood oxygen saturation with or without cyanosis from birth or developing in the first year of life. If the baby is not cyanotic then it is sometimes referred to as a "pink tet".
TETRALOGY OF FALLOT
Pathophysiology and Symptoms Other symptoms include a heart murmur which may range from almost imperceptible to very loud, difficulty in feeding, failure to gain weight, retarded growth and physical development, dyspnea on exertion, clubbing of the fingers and toes, and polycythemia.
TETRALOGY OF FALLOT
Pathophysiology and Symptoms Children with tetralogy of Fallot may develop "tet spells". The precise mechanism of these episodes is in doubt, but presumably results from a transient increase in resistance to blood flow to the lungs with increased preferential flow of desaturated blood to the body. Tet spells are characterized by a sudden, marked increase in cyanosis followed by syncope, and may result in hypoxic brain injury and death. Older children will often squat during a tet spell, which cuts off circulation to the legs and therefore improves blood flow to the brain and vital organs.
TETRALOGY OF FALLOT
Diagnosis The abnormal boot-like appearance of a heart with tetralogy of Fallot is easily visible via chest x-ray, and before more sophisticated techniques became available, this was the definitive method of diagnosis. Congenital heart defects are now diagnosed with echocardiography, which is quick, involves no radiation, is very specific, and can be done prenatally.
TETRALOGY OF FALLOT
Treatment Emergency management of tet spells Prior to corrective surgery, children with tetralogy of Fallot may be prone to consequential acute hypoxia (tet spells), characterized by sudden cyanosis and syncope. These may be treated with beta-blockers such as propranolol, but acute episodes may require rapid intervention with morphine to reduce ventilatory drive and phenylephrine to increase blood pressure. Oxygen is ineffective in treating hypoxic spells because the underlying problem is lack of blood flow through the lungs and not oxygenation within the lungs. There are also simple procedures such as squatting in the knee-chest position which increases aortic wave reflection, increasing pressure on the left side of the heart, decreasing the right to left shunt thus decreasing the amount of deoxygenated blood entering the systemic circulation.
TETRALOGY OF FALLOT
Treatment
Palliative surgery The condition was initially thought untreatable until surgeon Alfred Blalock, cardiologist Helen B. Taussig, and lab assistant Vivien Thomas at Johns Hopkins University developed a palliative surgical procedure, which involved forming an anastomosis between the subclavian artery and the pulmonary artery (See movie "Something the Lord Made"). It was actually Helen Taussig who convinced Alfred Blalock that the shunt was going to work. This redirected a large portion of the partially oxygenated blood leaving the heart for the body into the lungs, increasing flow through the pulmonary circuit, and greatly relieving symptoms in patients. The first Blalock-Thomas-Taussig shunt surgery was performed on 15-month old Eileen Saxon on November 29, 1944 with dramatic results. The Pott shunt and the Waterson procedure are other shunt procedures which were developed for the same purpose. Currently, Blalock-Thomas-Taussig shunts are not normally performed on infants with TOF except for severe variants such as TOF with pulmonary atresia (pseudotruncus arteriosus).
TETRALOGY OF FALLOT
Treatment Total surgical repair The Blalock-Taussig procedure was the only surgical treatment until the first total surgical repair was performed in 1954. Between 1944 and when total repair became available at major surgical centers in the early 1960s, many infants and children were treated palliatively with Blalock-Taussig procedures. This first total repair was performed by C. Walton Lillehei at the University of Minnesota in 1954 on a 10-month boy. Total repair initially carried a high mortality risk which has consistently improved over the years. Surgery is now often carried out in infants 1 year of age or younger with a <5% perioperative mortality. The surgery generally involves making incisions into the heart muscle, relieving the right ventricular outflow tract stenosis by careful resection of muscle, and repairing the VSD using a Gore-Tex patch or a homograft. Additional reparative or reconstructive work may be done on patients as required by their particular anatomy.
TETRALOGY OF FALLOT
Prognosis Untreated, tetralogy of Fallot rapidly results in progressive right ventricular hypertrophy due to the increased resistance on the right ventricle. This progresses to heart failure (dilated cardiomyopathy) which begins in the right heart and often leads to left heart failure. Actuarial survival for untreated tetralogy of Fallot is approximately 75% after the first year of life, 60% by four years, 30% by ten years, and 5% by forty years. Patients who have undergone total surgical repair of tetralogy of Fallot have improved hemodynamics and often have good to excellent cardiac function after the operation with some to no exercise intolerance (New York Heart Association Class I-II). Surgical success and long-term outcome greatly depends on the particular anatomy of the patient and the surgeon's skill and experience with this type of repair.
TETRALOGY OF FALLOT
Prognosis Ninety percent of patients with total repair as infants develop a progressively leaky pulmonary valve as the heart grows to its adult size but the valve does not. Patients also often have damage to the electrical system of the heart from surgical incisions, causing abnormalities as detected by EKG and/or arrhythmias. Long-term follow up studies show that patients with total repair of TOF are at risk for sudden cardiac death and for heart failure. Therefore, lifetime follow-up care by an adult congenital cardiologist is recommended to monitor these risks and to recommend treatment, such as interventional procedures or reoperation, if it becomes necessary. Antibiotic prophylaxis is indicated during dental treatment in order to prevent infective endocarditis.

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EAR AND THROAT DISORDERS

EAR AND THROAT DISORDERS

EAR AND THROAT DISORDERS

EAR AND THROAT DISORDERS

II. TONSILITIS AND ADENOIDITIS

EAR AND THROAT DISORDERS

II. TONSILITIS AND ADENOIDITIS

EAR AND THROAT DISORDERS

II. TONSILITIS AND ADENOIDITIS

EAR AND THROAT DISORDERS

II. TONSILITIS AND ADENOIDITIS

EAR AND THROAT DISORDERS

II. TONSILITIS AND ADENOIDITIS

EAR AND THROAT DISORDERS

II. TONSILITIS AND ADENOIDITIS

EAR AND THROAT DISORDERS

Answer: B. Increased swallowing

2. Abdominal skin is stretched shiny, with prominent veins

G. Prognosis 1. Exacerbations are precipitated by acute infections 2. Forerunner of chronic glomerulonephritis

Lund and Browder Method

5.1 Pneumonia; atelectasis

9.1 9.2 9.3 9.4 9.5

Remove foreign washing with hexachlorophene rinsing with NSS

6. Application of topical agents

Answer: C. Decreasing daily head circumference

Answer: B. Cerebral palsy

1.1 1.2 1.3 1.4

Irritability Anorexia Fever chill Headache

Answer: A. Minimizing bright lights and noise

4.3 Unsteady gait

Answer: D. Help him select a variety of hats.

Answer: A. His mental age

Answer: B. An extra chromosome.

Answer: D. On her abdomen

Answer: D. Fever, irritability, and nuchal rigidity

Screening Procedure for Scoliosis

Answer: D. Asymmetrical skin folds over the buttocks and thighs

Answer: A. No, the harness may not be removed.

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