pedia ear and throat

8/22/2019 PEDIA Ear and Throat

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EAR AND THROAT

DISORDERS



A. Incidence1. Most common bacterially-caused condition in childhood2. Common in children because their Eustachian tube is

shorter, wider and straighterB. Signs and symptoms1. Generally follows as a respiratory infection

(colds/rhinitis) or low-grade fever2. Sudden increase in temperature

3. Sharp constant pain in one or both ears – due topressure of accumulating fluid in the ear3.1 Infant extremely irritable and pulls or tugs at

affected ear to attempt relief3.2 Older child verbalizes presence of “popping noises”

and difficulty of hearing

EAR AND THROATDISORDERS

I. OTITIS MEDIA



C. Management

1. Medications1.1 Antibiotics – give full length of treatment

(usually 10 days) to prevent recurrence1.2 Decongestant nose drops – to open the

Eustachian tubes and allow air to enter the

middle ear1.3 Analgesic ear drops – when instilling ear

drops, position with affected ear up to alloweardrops to run onto the eardrum


I. OTITIS MEDIA



2. Facilitate drainage of infected ear discharges2.1 Position with affected ear down2.2 Apply local heat – (hot water bottle or bag – 38.9

degrees Fahrenheit) with the child’s affected ear on

top of it2.3 Myringotomy – if no spontaneous perforation of thetympanic membrane occurs, surgical incision will haveto 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 tympanicmembrane4. Examine effectiveness of treatment

4.1 For children below 3 years of age – pull the eardown and back

4.2 For children above 3 years of age – pull the ear upand back


I. OTITIS MEDIA



A. General information: Tonsils and adenoids arelymphoid tissues circling the pharynx and formpart of the Waldeyer’s Ring. This ring is believedto filter and protect the respiratory andgastrointestinal tracts against invasion bypathogenic microorganisms. It is also known tohave a role in antibody formation. Up to 5 years of

age, the child’s susceptibility to infection is great.But as the child’s immunity increases throughimmunization and exposures, the protective role ofthe Waldeyer’s Ring decreases.


II. TONSILITIS AND ADENOIDITIS



B. Signs and symptoms1. Persistent sore throat2. Offensive breath odor

3. Dysphasia; mouth breathing4. Cervical lymphadenopathy5. 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 management1. Preoperative nursing care

1.1 Parents should inform the child about the operationprior to hospital admission

1.2 Laboratory tests (bleeding time, clotting time,platelet smear; CBC), as well as PE and routineurinalysis are done

1.3 Withhold solid foods after supper the night beforesurgery and liquid breakfast early on the day of the

operation1.4 Atropine sulfate given preoperatively – reducesformation of respiratory secretion. Side effects:1.4.1 Dilated pupils1.4.2 Dryness of nasopharynx; thirst

1.4.3 Flushed face; warm skin





2. Postoperative nursing care – important: hemorrhage isthe most common complication

2.1 Immediate post-op2.1.1 Position on prone/semi-prone to facilitate

drainage of secretions (Remember: suctioningis 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 houror two – cold causes vasoconstriction thusreduces edema in the postop site

2.2.3 Ice collar applied to relieve sore throat,

reduce swelling and discomfort in theoperative site2.2.4 Encourage small servings of soft food

(chewing increases circulation and thuspromote healing)





3. Discharge instructions

3.1 Restrict activities for 2 weeks more3.2 Eat soft, cool, easily swallowed foods for several

days3.3 Plenty of fluids

3.4 No coughing, gargling or clearing of thethroat – only rinsing of the mouth is allowed





Sample Question

Jimmy had a tonsillectomy performedearlier in the day. He is now 4 hourspostop. Which of the following is an

abnormal finding and cause for concern?A. An emesis of dried bloodB. Increased swallowing

C. Pink-tinged mucusD. Jimmy’s complaints of a very sorethroat



Answer: B. Increased

swallowing

Increased swallowing could be asign of hemorrhage from the surgicalsite. Vomiting of dried blood, pink-tinged mucus, and complaints of avery sore throat would be expectedfollowing a tonsillectomy.



Which of the following signs is mostcharacteristic of a child with croup?

A. Barking coughFeverLow heart rate

Respiratory distress



RENAL DISORDERS



A. Description1. A tumor involving the kidneys 2. Once diagnosed, a sign should be posted at the

bedside, “No abdominal palpation”

B. Signs and symptoms1. Abdominal mass2. Abdominal pain – especially in older children

3. Late manifestations3.1 Weight loss and anemia3.2 Fever – a sign of tissue necrosis3.4 Hematuria – means poor prognosis

RENAL DISORDERS

I. WILM’S TUMOR



C. Management – sequence depends on the stageof disease at the time of diagnosis1. If without metastasis

1.1 Surgery – nephrectomy1.2 Chemotherapy – actinomycin D;Vincristine1.3 Ionizing radiation – cobalt/ deep X-ray

for 24 exposure days2. If with metastasis

2.1 Radiation to both lung fields2.2 Chemotherapy – Actinomycin2.3 Surgery – thoracotomy

I. WILM’S TUMOR

RENAL DISORDERS



D. Prognosis

1. The younger the patient, the better the outlook2. No metastasis is better; but even with metastasis,as long as it is not in the bones or the bonemarrow, prognosis is still fair

3. A two-year period free of the disease isconsidered a cure

I. WILM’S TUMOR

RENAL DISORDERS



A. Definition: Hypersensitivity reaction of thekidneys to Group A Beta hemolytic streptococci

B. Strep infection associated with AGN1. Tonsillitis

2. Otitis media

3. Impetigo

4. Pyoderma

II. ACUTE GLOMERULONEPHRITIS (AGN)

RENAL DISORDERS



C. Signs and symptoms – due to release ofhistamines by damaged cells

1. Hematuria and periorbital edema – presenting complaints2. Scanty, smoky, reddish or brownish urine3. Pallor4. Mild to moderate hypertension – first felt as

severe headaches5. 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 U2. RBC, leukocytes, epithelial cells and casts in theurine

3. +3 or +4 urine proteins4. Increased BUN and creatinine levels5. Decreased Hgb and Hct – transient anemia6. X-ray reveals cardiac enlargement and pulmonary

congestion


RENAL DISORDERS



E. Management – largely supportive1. Complete bed rest – most important aspect of

treatment2. Diet: low sodium (because of edema), low protein

(if with high BUN), limited potassium (because ofoliguria)3. Medications

3.1 Antihypetensiveness3.2 Magnesium sulphate

3.3 Digitalis – if in failure

3.4 Penicillin, the drug of choice – exerts abacteriostatic effect by suppressing the formationof bacterial cell wall


RENAL DISORDERS



4. Weigh daily

5. Elevate head to relieve periorbital edema

6. Renal biopsy – position on prone for 12 hoursafter 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 canprogress on to chronic renal disease andeventually lead to renal failure

2.1 Initial symptom: lethargy 2.2 Cause: destruction of nephrons2.3 Indication of progress: hypertension2.4 Treatment: dialysis


RENAL DISORDERS



A. Cause: unknown

B. Pathogenesis: increased glomerular membranepermeability to large molecules causesconsiderable quantities of plasma proteins toescape into the urine. Albumin, because of itshigh plasma concentration and relatively lowmolecular weight, is lost in greater quantity.

III. NEPHROTIC SYNDROME/ NEPHROSIS

RENAL DISORDERS



C. Diagnosis – James’ Schema1. Proteinuria – 3.5 Gms/24 hours or more2. Hypoalbuminemia – 3 Gms or less

3. Hyperlipidemia (300 mg % or more) the change inserum albumin-globulin ratio, wherein because ofloss of albumin, globulin, specially the cholesterolfraction, increases (may also termedhypercholesterolemia)

4. Edema – due to decreased osmotic pressure ofblood; develops first in periorbital tissues. If absent,means poor prognosis


RENAL DISORDERS



D. Signs and Symptoms

1. Extracellular fluid collection in cavities, legs andexternal genitalia

2. Abdominal skin is stretched shiny, withprominent veins

3. Respiratory embarrassment

4. Waxy pallor


RENAL DISORDERS



5. Decreased frequency of urination; urine is foamyor frothy because of high amounts of proteins;maybe tea-colored.

6. Progressive wasting of skeletal muscles due tonegative nitrogen balance – stick-likeextremities

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 onlywhen acutely ill and rapid diuresis is occurring.

2. Elevate the head to reduce discomfort due toedema (semi-upright position)

3. Diet: High protein, extra potassium, moderatesodium restriction


RENAL DISORDERS

SO S



4. Skin care – edema fluid is a good medium forbacteria

4.1 Never apply heat; no adhesives nor plasters4.2 Frequent position changes4.3 Binders for scrotal edema4.4 Careful washing and drying of skin fold with

mild soap and water; put cotton between skinsurfaces to prevent intertrigo


RENAL DISORDERS

RENAL DISORDERS



5. Drug of choice: Prednisone5.1 Effect: dieresis begins in 8-14 days after onset of

treatment5.2 Untoward side effects

5.2.1 Immunosuppression – children receivingsteroids should be protected against sources ofinfection (reverse isolation)

5.2.2 Weigh again – due to fluid retention andincreased appetite

5.2.3 Hypertension – monitor BP5.2.4 Striation; acne5.2.5 Growth arrest


RENAL DISORDERS

RENAL DISORDERS



5.2.6 Emotional disturbances; psychosis5.2.7 Gastric ulcer5.2.8 Delayed healing

5.2.9 Activation of healed TPB5.2.10 Cushing’s syndrome – moonface;

muscle weakness, facial, hirsutism,osteoporosis

5.3 Precaution: steroids should be discontinued intapered doses to prevent extreme exhaustion andhypoglycemia due to adrenal insufficiency.


RENAL DISORDERS

RENAL DISORDERS



F. Complications1. Infection2. Diarrhea

3. Ascites4. Respiratory distress5. Pneumococcal pneumonitis

G. Prognosis1. Exacerbations are precipitated by acute infection

2. Forerunner of chronic glomerulonephritis


RENAL DISORDERS



Sample Question

Tyrone, age 4 years, has just beendiagnosed as having nephrotic syndrome.His potential for impairment of skin

integrity is related toA. Joint inflammationB. Drug therapy

C. EdemaD. Generalized body rash



Answer: C. Edema

A child with nephroticsyndrome will have massive edema.A child with edema is prone to skin

breakdown. Drug therapy is usuallysteroids and diuretics, neither ofwhich is related to impairment of

skin integrity.



INTEGUMENTARY

DISORDERS

INTEGUMENTARY



A. General Considerations1. Earliest manifestation of an allergic tendency in

childhood; frontrunner of asthma2. Hereditary predisposition is usual3. Usually appears by the 4th month when solid

foods are being introduced and clearsspontaneously by the 4th year

4. Most often seen in well-nourished, well -cared for,healthy infants

I. ATOPIC DERMATITIS/INFANTILE ECZEMA

INTEGUMENTARYDISORDERS

INTEGUMENTARY



B. Most common allergens1. Cow’s milk

2. Wheat cereals3. Egg white - yolk as source of iron is needed, notegg white; should not be given to infants below 1year, especially if with family history of allergy

4. Vitamin C – rich fruits

C. Complication: bacterial infection of lesions



INTEGUMENTARY



D. Signs and symptoms1. Pruritus, erythema and edema, then papules and

vesicles – first evident on the cheeks, then

spreading to the forehead, scalp and extremities2. Generalized lymphadenopathy; splenomegaly3. Low-grade fever4. Child is uncomfortable, fretful and irritable

5. Increased eosinophil count (eosinophils engulfbacteria and contribute to body defense)

6. Scarring may occur due to secondary infection. Overthe years, skin thickens and darkens in color, called

lichenification, the hallmark of chronic eczema



INTEGUMENTARY



E. Management

1. Accurate history to identify allergens – that iswhy the first principle in the introduction of solidfoods is: “Introduce one new food at a time”.

2. Clove- hitch restraint – to prevent the child fromscratching

3. Cleanse skin with mineral oil, plain water or NSS4. Burrow’s solution – wet compresses for

bacteriostatic, antipruritic and drying effects



INTEGUMENTARY



A. Definition: Infectious disease of the superficiallayers of the skin

B. Etiologic agents: streptococci, staphylococci orpneumoccoci

C. Incidence1. In children of poor hygiene who live in

overcrowded settings and who are

malnourished2. Maybe primary or a complication of chickenpox,

mosquito bites, etc.

II. IMPETIGO


INTEGUMENTARY



D. Manifestations – lesions commonly found on theface about the mouth and nose

1. Small, reddish macules filled with serum andrapidly becoming cloudy

2. Skin blisters3. Pustules which rupture, discharging serous and

purulent fluid4. Brown, thick crusts

II. IMPETIGO


INTEGUMENTARY



E. Management1. Meticulous hygiene – daily baths with

hexachlorophene scrub to the scabs2. Penicillin

F. Complications: Acute glomerulonephritis orRheumatic Heart Disease if due to Group A beta-hemolytic streptococci

II. IMPETIGO




Sample Question

When teaching parents aboutknown antecedent infections in acuteglomerulonephritis, which of the

following should the nurse cover?A. Herpes simplexB. Scabies

C. VaricellaD. Impetigo



Answer: D. Impetigo

Impetigo, a bacterial infection of theskin, may be caused by streptococcus andmay precede acute glomerulonephritis.

Although most streptococcal infections donot cause acute glomerulonephritis, whenthey do, a latent period of 10 to 14 daysoccurs between the infection, usually of

the skin (impetigo) or upper respiratorytract, the onset of clinical manifestations.

INTEGUMENTARY



A. General considerations1. It is the most severe form of trauma to the

integumentary system2. Burn wounds are three-dimensional2.1 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. TheLund and Browder allows for the changes inpercentage during different stages ofdevelopment.

III. BURNS


INTEGUMENTARY



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 dayshealing time; no scarring. Eg, sunburn2.2.2 Second-degree – involves the epidermis and

the dermis; characterized by blister formation orreddened discoloured region with moist weeping

surface; is extremely painful because nerveendings for pain are exposed; very edematous;21-28 days healing time

III. BURNS


INTEGUMENTARY



2.2.3 Third-degree – involves the entire dermis plusportions of the subcutaneous tissue; brownleathery appearance with little surface moisture;painless to touch because nerve endings for pain

have been also burned; marked edema; scarformation (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 edema2.3.1 Abnormal capillary permeability which allows

proteins to escape into tissue spaces2.3.2 Increased capillary hydrostatic pressure which

causes water and electrolytes shifts.

III. BURNS


INTEGUMENTARY



Lund and Browder Method

III. BURNS


INTEGUMENTARY



B. Body’s responses to burns1. Destroy the evaporative water barrier, thus increasing

insensible water loss from 4-15 times the normal. Inchildren, the ratio of body surface area to body weightis greatly increased and 70% of the body is made up ofwater; insensible water loss is thus severe.

2. Decrease the efficiency of the temperature controlmechanism of the body

3. Destruction of skin causes loss of the first line ofdefense against infection and produces an excellent

medium for bacteria, specifically pseudomonas. For thisreason, tetanus immunization is given4. Response of the cardiovascular system to burn shock

4.1 Signs and symptoms4.1.1 Thirst

4.1.2 Pale, clammy skin

III. BURNS


INTEGUMENTARY



4.2 Effects4.2.1 Decrease in cardiac output

4.2.2 Decreased vascular permeability results infree loss of plasma proteins from the bloodvessels into the extracellular spaces – edema

4.2.3 Hematocrit is higher because of the release

of plasma into the tissues at the burn sites4.2.4 Sodium and calcium deficit; potassium

excess during the first 48 hours

III. BURNS


INTEGUMENTARY



5. The reaction of the pulmonary system is amajor cause of mortality and morbidity in burns

5.1 Pneumonia; atelectasis

5.2 Inhalation injury

III. BURNS


INTEGUMENTARY



5.3 Upper airway problem because of edema andconsequent obstruction of the upper airway, orbronchospasms due to chemical irritation from

toxic products of combustion (Implication: Inchildren whose upper half of the body has beenburned, a tracheostomy set should always be atthe bedside for emergency purposes).

5.4 Because of the loss of bicarbonate ions, metabolicacidosis occurs. In an effort of the body to riditself of the excess carbonic acid, respirationsbecome deep and rapid: Kussmaul breathing

III. BURNS


INTEGUMENTARY



6. The response of the renal system to burns is renalinsufficiency due to hypovolemic shock. Because of

diminished cardiac output, renal blood flow isdrastically reduced, causing impaired renalfunctioning and decreased effectiveness of thekidneys. (Implications: because of immature renalfunctioning in young children, they are no more

susceptible to impaired kidney function, leading torenal damage.)

III. BURNS


INTEGUMENTARY



7. Gastrointestinal complications7.1 Acute ulcerations of stomach or duodenum

(Curling’s ulcers) – the most frequent life

threatening situation7.2 Paralytic ileus – this is the main reason why burnvictims are put on NPO with an NGT inserted; toremove gastic contents, thus prevent vomiting andaspiration

7.3 Acute gastric dilatation – first sign of invasivesepsis7.4 Hemorrhagic gastritis – bleeding from congested

capillaries in the gastric mucosa

III. BURNS


INTEGUMENTARY



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


INTEGUMENTARY



9. Neuromusculoskeletal changes – are all due toinfection, immobilization and metabolic changes

9.1 Contractures9.2 Tendon dislocation9.3 Joint dislocation

9.4 Limb amputations9.5 Weakness due to neuropathy

III. BURNS


INTEGUMENTARY



C. Management1. First-aid treatment in the home: apply cold water 2. In the hospital

2.1 Replacement of fluids – most important goal ofinitial therapy2.1.1 Solution: Ringer’s Lactate is the choice

because it most closely resembles thecomposition of the extracellular fluidcompartment

2.1.2 Dosage: 3-4 ml/KBW/%TBSA2.1.3 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


INTEGUMENTARY



3. Remove foreign adherent material by gentlewashing with iodine-based solution orhexachlorophene and water, then thoroughly

rinsing with NSS

4. Shave hair from burned area and area immediatelysurrounding it

5. Excision of fragments of dead and devitalizedtissues

III. BURNS


INTEGUMENTARY



6. Application of topical agents

6.1 0.5% silver nitrate – unknown action; not verypopular because it stains the skin

6.2 Gentamicin cream6.3 Mafylon/Sulfamylon or silver sulfadiazine

(Silvadene) – the “burn butter”

6.3.1 Purpose: to prevent bacterial invasion

III. BURNS


INTEGUMENTARY



6.3.2 Method of application: applied evenly 1/8 inch inthickness

6.3.3 Side effects- Reduces buffering capacities of the bloodbecause it increases bicarbonate excretion(when bicarbonates are broken down, theyprovide a heavy acid load). Remember:Monitor pH level of blood

- Causes burning sensation for 20 minutesafter application

III. BURNS


INTEGUMENTARY



7. Dressings may (closed method) or may not (openmethod) be used. If closed method is used, dressingsare changed everyday.

8. Wound debridement is done with each dressing change

to prevent eschar (a tough coagulum of necrotictissues). Necrotic tissues are not only good media forbacteria, but also promote growth of granulationtissues.

9. Daily removal of dried cream by soaking in whirlpool

bathtub prior to debridement10. Morphine sulphate, gr. ¼ to relieve pain of second-

degree burns11. Use of Bradford frame for ease of turning and

maintenance of good body alignment.

III. BURNS


INTEGUMENTARY



12. Position flat on bed with legs extended specia;;yduring the first 24-48 hours in order to:

12.1 Avoid postural shock – because of fluid loss,circulation to the head may becomeinadequate

12.2 Support healing of burn wounds

12.3 Prevent hip contractures12.3.1 Proper splinting12.3.2 Active and passive range of motion

exercises

III. BURNS


INTEGUMENTARY



13. Grafting is done to minimize growth of granulationtissues which results in contractures and ugly

scars

13.1 Xenograft – from animals13.2 Homograft – from other individuals

13.3 Autograft – oneself

III. BURNS




NEUROLOGIC

DISORDERS

NEUROLOGIC DISORDERS



A. Classification1. Occulta – L5 and S1 are affected, with no protrusion of

spinal contents. Skin over the defect may reveal adimple, a small fatty mass or a tuft of hair.

2. Cystica2.1 Meningocoele – contains fluid - penetrated by

fluorescent bulb2.2 Myelomeningocoele – congenital failure of the

arches of one or more vertebrae to unite at thecenter of the back, so that the bony wall normallysurrounding the spinal canal at that place ismissing. There is external protrusion, through atransparent sac, containing spinal fluid, meninges,spinal cord and/or nerve roots. It is the most

severe of the spinal deformities.

I. SPINA BIFIDA – congenital problem in which

there is a defective closure of the spinal column.





B. Associated clinical problems – depend on thelocation; all body parts below the lesion are affected.

1. Motor function

1.1 Feet maybe deformed1.2 Joints of ankles, knees or hips may be immobile1.3 Variable degrees of weakness in the lower

extremities1.4 Spontaneous and induced movement are

decreased or absent

I. SPINA BIFIDA





2. Sensory function

2.1 Sensations usually absent below the level of thedefects

2.2 Ulcerations of the skin are common2.3 Impaired functioning of the autonomic nervous

system

2.3.1 Skin is dry and cool2.3.2 Sweating ability is impaired

I. SPINA BIFIDA





2.4 Urinary and bowel problems

2.4.1 Inefficient bladder causes constant urinary

dribbling2.4.2 Stasis of urine causes UTI2.4.3 Possible renal destruction2.4.4 Fecal incontinence or retention due to poor

innervation of the anal sphincter and bowelmusculature.2.5 Hydrocephalus – occurs in 65% of children;

usually develops within the first 6 weeks of life.

I. SPINA BIFIDA





C. Preoperative management/conservative treatment1. Careful handling to avoid rupture, pressure, irritation or

leakage from the protruding mass by putting the childon prone position, with the hips abducted

2. Meticulous skin hygiene to prevent irritation; steriledonut ring over the lesion

3. Watch for signs of increased intracranial pressure3.1 Anterior fontanel for tenseness, fullness, pressure3.2 Shrill, high-pitched cry

3.3 Increased head circumference3.4 Vomiting; irritability3.5 Increasing BP, decreasing PR and RR and widening

pulse pressure

I. SPINA BIFIDA





D. Surgical correction1. Early excision of the sac if it is small and then

primary closure is done2. 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 position2. Monitor urine output – bladder injury is a high

possibility in operations involving the spinal column3. Measure head circumference daily4. Monitor movement of lower extremities; passive

range of motion (ROM) exercise to impaired lower

extremities

I. SPINA BIFIDA





F. Complications1. Meningitis2. Severe neurologic deficits

3. Hydrocephalus3.1 Types3.1.1 Noncommunicating – blockage within

the ventricles which prevents CSF fromentering the subarachnoid space.

3.1.2 Communicating – obstruction in thesubarachnoid cistern at the base of thebrain and or within the subarachnoidspace.

I. SPINA BIFIDA





3.2 Management

3.2.1 1.5-2 grams Mannitol 20%/KBW for 10-15minutes – since Mannitol is a diuretic, an

indwelling castheter should be inserted foraccurate 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 theprocedure, the child should be positioned onthe side where the shunt is to prevent suddendecrease in intracranial pressure.

I. SPINA BIFIDA




Sample Question

The nurse is caring for an infant withhydrocephalus. She has a shuntinserted. Which of the followinf signs

indicates that the shunt is functioningproperly?A. The sunset sign

B. A bulging anterior fontanelC. Decreasing daily head circumferenceD. Widened suture lines

Answer: C Decreasing daily



Answer: C. Decreasing daily

head circumference

With improved drainage of theCSF, the head circumference shouldbecome smaller. All the other signs

indicate an increased ICP.




A. Definition: Disorders created by damage to themotor centers of the brain, specifically thepyramidal tracts of the CNS. There is difficulty incontrolling the voluntary muscles due to brain

injury (which is not progressive, through). Since itinvolves voluntary muscles, therefore, it can notbe diagnosed early in life, not until the child hasstarted to move about.

B. Incidence: Occurs most frequently amongpreemies and those who were in occipitoposteriorpositions while in utero.

II. CEREBRAL PALSY




C. Etiology1. Prenatal causes

1.1 Hereditary factors1.2 Irradiation of lower abdominal area especially

during the first trimester1.3 Infections. Eg., rubella, meascles, mumps,

chickenpox, etc.1.4 Anoxia – due to placenta previa, abruption

placenta, maternal blood loss, allergy to analgesics,

reaction to anesthesia1.5 Cord anomalies1.6 Fetal cerebral hemorrhage1.7 Prematurity1.8 Maternal history of abortion, diabetes or toxemia

II. CEREBRAL PALSY




2. Natal causes2.1 Abnormal delivery situations, e.g., prolonged labor,

forceps delivery, CS, precipitate delivery2.2 Use of analgesics and anesthetics

2.3 Placental abnormalities2.4 Poor natal care2.5 Fetal anoxia

2.5.1 Mechanical respiratory obstruction

2.5.2 Ateslectasis; RDS2.5.3 Neonatal infections2.5.4 Kernicterus; hemolytic disease2.5.5 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 monoxidepoisoning or internal hydrocephalus

II. CEREBRAL PALSY




D. Manifestations – vary according to the portion ofthe brain that has been damaged

1. Weakness

2. Paralysis and incoordination of voluntarymovements of the muscles

3. Seizures

4. Visual and hearing difficulties

II. CEREBRAL PALSY




5. Emotional disorders5.1 Irritability5.2 Overactivity

5.3 Impulsiveness5.4 Short attention span5.5 Mood swings

6. Speech problems

7. Mental retardation – not always present

II. CEREBRAL PALSY




E. Classification – based on brain areas involved and resultingpatterns of movement1. Spastic – muscles are hyperactive, hypertonic, hyperirritable,

hyperelastic, react readily to stimuli; exaggerated stretchreflex

2. Flaccid – (+) deep tendon reflexes and (+) plantar response3. 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 incoordination6. Tremor – uncontrollable, involuntary motions of a rhythmic,alternating, pendular patter

7. Atonic – lack of tone; no response of muscles to volitionalstimulation

8. Mixed

II. CEREBRAL PALSY




F. Management: the overall aim of treatment is musclere-education. Maximize assets and minimizeliabilities.

1. Physiotheraphy – provide a period of quietrelaxation before starting sessions

2. Drugs - muscle relaxants; anticonvulsants3. Maintain safe environment – seizure precautions

and use of safe toys

4. Prevent accidental falls – because of scissoring andtoe-pointing gait which results from tension on hipadductors, hip internal rotators and calf muscles(for this same reason, it is advisable to carry CPchildren astride the hips).

II. CEREBRAL PALSY




5. Encourage independence while providing adequate nutrition5.1 Cut food into small pieces5.2 Serve foods that stick to the spoon5.3 Position properly; do not feed when child is tired or excited5.4 Disregard messy eating

5.5 Allow child to hold spoon, guiding it to his mouth. Toestablish a hand-to-mouth pattern to serve as a basis forbeginning self-feeding5.5.1 Encourage finger foods5.5.2 Play games that call for pointing out mouth, nose,

eyes, etc.

5.5.3 Practice raising an empty glass to the mouth andsetting it down again

5.5.4 Place food at the back of the tongue because CPchildren have a tendency to push their tongue forward

6. Discipline is necessary for the child to feel loved and secure – donot overprotect

II. CEREBRAL PALSY

S l Q ti



Sample Question

Which of the following is the mostcommon permanently disability inchildhood?

A. Developmental dysplasia of thehip

B. Cerebral palsyC. Muscular dystrophyD. Scoliosis

Answer: B. Cerebral palsy



Answer: B. Cerebral palsy

CP is a group of disabilitiescaused by injury or insult to thebrain either before or during birth, or

in early infancy. Developmentaldysplasia of the hip and scoliosisshould not cause permanent

disability.

S l Q ti



Sample Question

Which of the following statements made by themother of a 4-month-old would indicate that thechild may have cerebral palsy?A. “ I am very worried because my baby has not

rolled all the way over yet.” B. “ “ my baby’s left hip tilts when I pull him to astanding position.”

C. My baby won’t lift her head up and look at me;

she is so floppy.” D. “ he holds his leg so stiff that I have a hardtime putting on his diapers.”

.

.head up and look at me; she is so



head up and look at me; she is so

floppy.”

Hypotonia or floppy infant is an earlymanifestation of CP. Typically, the infantlifts his head to a 90 degree angle by 4months with only a partial head lag by 2months. Rolling completely over usuallydoes not occur until the infant is 6 monthsold. Tilting of the hip and limitation in one

leg suggest developmental dysplasia ofthe hip.




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 Irritability1.2 Anorexia1.3 Fever chill

1.4 Headache

III. MENINGITIS




2. Specific signs

2.1 Nuchal rigidity – chief sign2.2 Stupor; convulsions 2.3 (+) Kernig’s - pain on extending leg after it has been

flexed on the abdomen 2.4 (+) Brudzinski’s 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 bychildren seriously ill with meningitis

3. Signs of increased intracranial pressure3.1 Vomiting every 8-10 minutes – an early sign of increased ICP

in children3.2 Increased BP; decreased PR and RR and widening pulse

pressure3.3 Increasing head circumference3.4 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 reveals2.1 Increased ICP, unless CSF has just been obtainedprior to the tap

2.2 Cloudy, if bacterial, and bacteria can be isolated inculture and nasopharyngeal secretions

2.3 High in protein, low in glucose – a reversal onvalues means improvement in condition

III. MENINGITIS




E. Management1. Provide rest and quiet – minimal handling in darkened,non-stimulating environment to prevent convulsions

2. Phenobarb and Valium to control restlessness and preventconvulsions

3. Keep close watch over the 4 major components of neurological

status 3.1 Level of consciousness (LOC) – indicates highestdegree of cerebral activity; take note of alertness andorientation 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 thedark.

3.3. Vital signs3.4 Motor activity – let child move all 4 extremities or grasp

examiner’s hand

III. MENINGITIS




4. Prevent transient increase in ICP4.1 When with IV, the danger of increasing the ICP

is very real, so monitor fluid volume veryclosely

4.2 Non-constipating diet to prevent valsalvamaneuver, crying, sneezing, coughing orvomiting should be avoided

4.3 Do not burp on upright sitting position becausepressure on the jugular veins will increase ICP;

just turn to side and rub the back4.4. Move as little as possible; sitting and head

movement cause increased ICP4.5 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 spreadby direct contact or indirect droplet or

inhalation. Cardinal rule in the use of isolationmasks: discard when wet

III. MENINGITIS




F. Complications1. Hydrocephalus – common2. Peripheral circulatory collapse/Waterhouse –

Friderichsen syndrome – most seriouscomplication due to bilateral adrenal hemorrhageleading to acute adrenocortical insufficiency

2.1 Profound shock2.2 Petechiae; ecchymotic lesions2.3 Vomiting

2.4 Prostration2.5 Hypotension

G. Prognosis: Good, if treated early, but withcomplications and long-term effects

III. MENINGITIS

Sample Question



Sample Question

To meet the sensory need of achild with viral meningitis, nursingstrategies should include

A. Minimizing bright lights and noiseB. Promoting active range of motionC. Increasing environmental stimuli

D. Avoiding physical contact withfamily members

nswer: . n m z ng r glights and noise



lights and noise

Photophobia and hypersensitivity toenvironmental stimuli are common clinicalmanifestations of meningeal irritation and

infection. Comfort measures includeproviding an environment that that isquiet and has minimal stressful stimuli.Promoting active ROM at this time would

not be beneficial. Viral meningitis is notcontagious, so contact with familymembers is not contraindicated.




A. Definition: Inflammation of brain tissue due tobacteria, viruses, protozoa or fungi

B. Signs and symptoms : same as meningitis

C. Management and prognosis: same as meningitis

IV. ENCEPHALITIS




A. General considerations1. Occur most commonly in the 5-7 years age group2. Vomiting in the morning is the initial symptom;

signs of increased intracranial pressure occur early

3. Uncommon for children to have metastatic tumorsB. Types – depends on the location in the brain

1. Astrocytoma – in the cerebellum1.1 Course: insidious onset with a slow course

1.2 Signs and symptoms1.2.1 Increased ICP1.2.2 Hypotonia; diminished reflexes1.2.3 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; ataxia2.2.2 Anorexia; vomiting

2.2.3 Early morning headache2.2.4 Papilledema; drowsiness; nystagmus

V. BRAIN TUMORS




3. Gliomas – in the brain stem; most common typein children

3.1 Course: slow3.2 Signs and symptoms

3.2.1 Palsies, ataxia, sensory loss

3.2.2 Signs of increased ICP3.2.3 Headache

V. BRAIN TUMORS




4. Ependymona – in the first, second and fourthventricles 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 growth5.1.2 Myxedema5.1.3 Delayed puberty5.1.4 Visual defects

5.1.5 Alterations in personality and memory5.1.6 Increased ICP

V. BRAIN TUMORS




C. Diagnostic procedures

1. EEG

2. Pneumoencephalogram3. Skull series; brain scans4. Ventriculograms; arteriograms5. Lumbar tap

V. BRAIN TUMORS




D. Nursing Care – successful treatment is uncertain inmany instances because the location of the tumorrenders surgical removal difficult and sometimesimpossible.1. Preoperative management

1.1 Enema not given because of possibility ofincreased ICP

1.2 Monitor neurologic and vital signs1.3 Observe seizure precautions

1.4 Diet and fluids as tolerated1.5 Consider body image in shaving the head-

explain its necessity and allow child toverbalize his feelings

V. BRAIN TUMORS




2. Postoperative care

2.1 Assess ICP; level of consciousness2.2 Observe for hemorrhage and edema. Mark

stain or spot on head dressings in order todetermine any increase in size

2.3 Position: head elevated, with body turned onthe unoperated side.

2.4 When changing position, support the head andthe neck and turn the child “in one piece” (logrolling)

V. BRAIN TUMORS

Sample Question



Sample Question

Jack is 10 years old and is receivingcranial irradiation for a brain tumor. Hehas developed alopecia. Which of thefollowing is an appropriate nursingintervention?A. Have Jack identify famous movie stars

and sports heroes who are bald.

B. Assure Jack that his hair will grow inbefore 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 headwill help Jack deal with the change inbody image. The other suggestions

are all inappropriate.




A. Definition: A disease diagnosed primarily from ahistory of seizure episodes because of increasedbasal level of excitability of the CNS.

B. Classification and their description1. Grand Mal

1.1 Abrupt onset preceded by an aura (anypeculiar feeling, sight, sound, taste, smellor twitching and spasm of small musclegroup)

1.2 Child falls to the ground, becomes pale,

pupils dilate, with upward rolling of theeyeballs. Head is thrown backward or toone side; chest and abdominal muscles arerigid; limbs are rigid and contracted – thetonic phase

VI. EPILEPSY




1.3 As air is forced out of a closed glottis by suddencontraction of the diaphragm, the child lets out ashort, 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 clonicactivity involving spasms of the entire body

1.6 The child sleeps after the episodes; on awakening, heappears drowsy, stuporous and accomplishes routinetasks in an automatic fashion

1.7 When seizures are so frequent that they appear to beconstant, it is termed status epilepticus, a medicalemergency which may result in brain damagebecause of decreased oxygen supply to the cerebrum

VI. EPILEPSY




2. Petit Mal – seen mainly in children2.1 Transients losses of consciousness2.2 Eye-rolling; drooping of fluttering of eyelids;

drooping of the head; quivering of limb or trunkmuscles

2.3 On completion of the seizure, the child immediatelyresumes activity without knowledge of whathappened

2.4 Can be precipitated by hyperventilation or induced

by blinking light3. Jacksonian – convulsion starts with one muscle orgroup of muscles and then spreads to other parts ofthe body

VI. EPILEPSY




C. Management1. During seizures in Grand Mal, ease child on to the

floor and loosen clothes around the neck and theabdomen, remove mall chairs, tables and otherobjects that can harm the child. Keep the head onthe side or put his abdomen with the head on oneside to prevent the tongue from falling against orobstructing the airway.

2. May participate actively in sports, but not in

hazardous activities unless accompanied by aresponsible adult.3. Ketogenic (high fat) diet – believed to decrease

incidence of seizures

VI. EPILEPSY




4. Mainstays of treatment – anticonvulsant drugs

4.1 Important information4.1.1 Purpose: to allow the child to function as

normally as possible4.1.2 Choice of drug depends on the type

of seizure and the severity of thesymptoms

4.1.3 Drug alterations are doneinfrequently since it takes 1-2 weeksbefore they exert their maximaleffects

VI. EPILEPSY




4.1.4 When patient has been seizure-free,medications must still be continued on aregular basis for at least 4-5 years afterthe last seizure

4.1.5 Drug should not be discontinued suddenly(just like steroids) especially duringpuberty when incidence of seizures isagain on the rise

4.1.6 Dosage and drug are re-evaluated duringearly adolescence because they may needsome 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 preventmegaloblastic anemia.

VI. EPILEPSY




4.3 For Petit Mal4.3.1 Zarontin – blood dyscrasias are less

common4.3.2 Trimethadione (Tridione) – decreasesthe excitability of the motor area of thecerebral cortex; less hypnotic effect thanZarontin but has toxic effects: blood

dyscrasias; insomnia; fatigue;photophobia; skin rashes

VI. EPILEPSY

Sample Question



Sample Question

Henry, a 13-year-old who has beendiagnosed as having epilepsy. A positivesign that Henry is taking his Dilantinproperly isA. Hair growth on his upper lipB. Absence of seizuresC. Lowered hemoglobin and hematocritD. Drowsiness

Answer:



Answer:

Dilantin is an antiepilepticdrug that controls seizures. All theother signs and symptoms are side

effects of the medications.

VII MENTAL RETARDATION (DOWN’S




A. Definition: Condition characterized by subnormalmental, physical and physiological capacity fromearly in life and during the growth period, which is

shown by lack of maturation and ability to learnand 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 trainable3. IQ below 30 – severely retarded or of thecustodial type

VII. MENTAL RETARDATION (DOWN SSYNDROME/TRISOMY 21)





C. Possible causes (other than Down’s syndrome)

1. Micro-/hydrocephaly2. Craniosynostosis – premature closure of the

fontanel3. Rubella; sexually-transmitted disease; bloodincompatibility

4. Kernicterus

5. Meningitis; encephalitis6. Poisoning7. Brain tumors8. Deprivation; malnutrition






D. Characteristics1. Lateral upward slant of the eyes2. Flattened occiput

3. Short nose with flat bridge4. Protruding fissured tongue5. Single transverse palmar crease – simian

crease 6. increased spaces between first and second

fingers and toes






7. Broad and square hands and feet8. Congenital heart defect is common

9. Abnormally aligned teeth10. Prone to respiratory tract infections11. Less sensitive to heat , cold and pain12. 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

cooperation1.2 Child’s 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 beconsidered


Sample Question



Sa p e Quest o

Jeffrey, age 17, has Down’s syndrome. He4 is 57 inches tall andweighs 155 lbs. In planning his care,

it is most important for the nurse totake into considerationA. His mental age

B. His chronological ageC. His bone ageD. Growth chart percentiles.

Answer: A. His mental age



All Down’s syndrome children areretarded and care must be geared totheir mental age.

Sample Question



p Q

Down’s syndrome is caused byA. An autosimal recessive defectB. An extra chromosome.

C. A sex-linked defectD. A dominant gene

nswer: . n ex rachromosome.



In Down’s syndrome there is anextra chromosome on the 21st pair ,which is why the disease is also

called trisomy 21.

Sample Question



p Q

Louise was born with ameningomyelocele with accompanyinghydrocephalus. She has had a shuntprocedure to alleviate the hydrocephalus.

Louse should be placed in which of thefollowing positions?A. Trendelenburg’s

B. On her backC. With her legs abductedD. On her abdomen

Answer: D. On her abdomen



Pressure must be kept off thespinal sac. As there is paralysis ofthe lower extremities, the legs

should be abducted. Trendelenburgposition is contraindicated inhydrocephalus.

Sample Question



p

Jennifer Pine, 3 years old, is admittedwith a diagnosis of viral meningitis. Duringan initial assessment of Jennifer, thenurse would expect to find

A. Headache, fever, and petechiaeB. Seizures, lethargy, and hypothermiaC. Pallor, anorexia, and bulging fontanels

D. Fever, irritability, and nuchal rigidity

Answer: D. Fever, irritability,

and nuchal rigidity



and nuchal rigidity

The clinical symptoms of viralmeningitis (aseptic meningitis)include fever, irritability, and nuchal

rigidity. Other symptoms includeheadache, seizures, and lethargy.Bulging fontanels are a sign ofhydrocephalus.



MUSCULOSKELETAL

DISORDERS

MUSCULOSKELETALDISORDERS



A. Definition: A kind of paralysis caused by traumaticinjury to the upper brachial plexus. It occurs mostcommonly in childbirth from forcible traction

during delivery, with injury to one or more cervicalnerve roots.B. Causes

1. Lateral traction exerted on head and neckduring delivery of the shoulder in vertexpresentation

2. Excessive traction on the shoulders duringbreech presentation, especially when arms areexerted over the head

I. ERB-DUCHENNE PARALYSIS/BRACHIAL PLEXUS

INJURY

DISORDERS




C. Signs and symptoms1. Loss of sensation in the arm2. 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 arm6. Some sensory impairment in outer aspect of affected

arm


INJURY

DISORDERS




D. Treatment1. Initially, the arm and shoulder should be

immobilized to allow swelling and inflammationof 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 musclesand to prevent flexion contracture of theelbow.


INJURY

SO S




A. Incidence1. 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 betreated by total hip arthroplasty.

II. CONGENITAL HIP DYSPLACIA (CDH)




B. Types1. Teratological – develops in utero and is commonly

associated with other orthopedic problems

2. Typical2.1 Occurs just before, during or shortly after birth.2.2 Probably caused by the softening effects of the

maternal hormone relax in on the infant’s ligaments and the stress of labor and birth.

2.3 Classification2.3.1 Dislocation or luxation – the femoral head

is completely displaced from socket oracetabulum.





2.3.2 Subluxation or partial displacement – more common,occurring in approximately 1 in 60 births. Asubluxated hip may become completely dislocatedduring an infant’s care unless certain types ofmaneuver 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 ablanket.

- Since this problems may be overlooked on the initialexamination, these precautions should apply to thecare of all infants.

- Barring complications, 88% of newborns withsubluxation becomes normal by 2 months of age.





C. Signs and symptoms

1. On supine, there is resistance when legs areflexed on abdomen and abducted2. Ortolani’s sign – on supine, put thumbs on

groin while abducting the legs; a “click” is felt

3. On prone, baby has unequal gluteral folds





D. Treatment1. Goal: Immediate return of the femoral head to

the acetabulum since the hip socket becomes

progressively more distorted if reduction isdelayed. Early treatment can reduce therapy toapproximately 3 months’ duration.

2. Specific measures2.1 When on supine, put a pillow between the

thighs to abduct the affected hip2.2 Carry the child astride the hip





2.3 Apply 2 diapers instead of one2.4 Traction2.5 Hip spica cast – when child is around 6 months

old, before he learns how to walk, the cast isapplied from the waist to below the knee of theaffected leg and above the knee of the unaffectedleg.

2.6 Pavlic harness – allows flexion and abduction but

prevents extention or adduction.E. Prognosis: If the child’s x-ray film indicates normallocation of the hip at years of age, the condition may beconsidered cured.





A. Definition: Lateral curvature of the spineB. Age group at risk: schoolageC. Types

1. Postural/functional – can be corrected bycorrect posture and exercises

2. Structural – can be corrected only by surgery

III. SCOLIOSIS




D. Screening test to differentiate one type from theolder – have the child bend forward over at thewaist and inspect equality of shoulders, hips and

scapula

E. Clues to diagnosis

1. Uneven hemline

2. One hip is more prominent than the older3. One shoulder blade is higher than the other

III. SCOLIOSIS




Screening Procedure for Scoliosis

III. SCOLIOSIS




F. Management1. Conservative

1.1 Exercises1.1.1 Pelvic tilt – to increase musclestrength of the body so as to counteracteffects of splinting

1.1.2 Swimming is known to be therapeutic1.3 No contact sports or violent gymnastics1.4 Avoid obesity

III. SCOLIOSIS




2. Corrective2.1 Surgical spinal fusion with or without Harrington

rods. Postoperatively:

2.1.1 Do logrolling – changing position ofthe child in “one piece” 2.1.2 Use firm mattress2.1.3 Monitor intake and output, emphasizing

urine output – damage of nerves thatcontrol the bladder is a possiblecomplication in surgeries involving thespinal column.

III. SCOLIOSIS




2.2 Immobilization in Milwaukee brace – to providelongitudinal 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 whentaking a bath

2.2.3 Avoid strong deodorants which can causerashes

III. SCOLIOSIS




2.2.4 Skin care to prevent sore areas at contactpoints

2.2.5 Wear T-shirt underneath the brace toprevent skin irritations

2.2.6 Wear loose clothing over the brace toprotect body image

G. Prognosis: better when curvature begins at an olderage when less growth remains and when curve ismild at the time of initial diagnosis and treatment.

III. SCOLIOSIS




Pelvic Tilt

III. SCOLIOSIS

Sample Question



A routine physical examination on 2-day old Melissa Baylon uncoveredevidence of congenital dislocation of theright hip. When assessing Melissa, a signof one-sided hip dislocation isA. An usually narrow perineumB. Pain where her leg is abducted

C. Symmetrical skin folds near herbuttocks and thighs

D. Asymmetrical skin folds over the

b tt k d thi h

folds over the buttocks and

thighs



thighs

Displacement of the hip on oneside causes asymmetry of skin folds.

Sample Question



An infant is being treated for congenitalhip dislocation with a Pavlik harness. Thebaby’s mother asks if she can remove theharness if it becomes soiled. The best

response for the nurse to make isA. 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

l i

nswer: . o, e arnessmay not be removed.



The harness is not to be removeduntil the hip is stable within 90degrees of flexion and x-ray

confirmation. This usually occursafter about 3 weeks of in a Pavlikharness.



TETRALOGY OF

FALLOT

TETRALOGY OF FALLOT



- is a congenital heart defect which is classicallyunderstood to involve four anatomicalabnormalities (although only three of them are

always present). It is the most commoncyanotic heart defect, representing 55-70%,and the most common cause of blue babysyndrome. It was described in 1672 by NielsStensen, in 1673 by Edward Sandifort, and in

1888 by the French physician Étienne-LouisArthur Fallot, for whom it is named.

TETRALOGY OF FALLOT



Anatomic morphology

TETRALOGY OF FALLOT



As classically described, tetralogy of Fallot involvesfour heart malformations which present together:

1. A ventricular septal defect (VSD): a hole

between the two bottom chambers (ventricles) ofthe heart. The defect is centered around the mostsuperior aspect of the ventricular septum (theoutlet septum), and in the majority of cases issingle and large. In some cases thickening of the

septum (septal hypertrophy) can narrow themargins 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 ismostly caused by overgrowth of the heart muscle wall(hypertrophy of the septoparietal trabeculae), however

the events leading to the formation of the overridingaorta are also believed to be a cause. The pulmonicstenosis is the major cause of the malformations, withthe other associated malformations acting ascompensatory mechanisms to the pulmonic stenosis. The

degree of stenosis varies between individuals with TOF,and is the primary determinant of symptoms andseverity. This malformation is infrequently described assub-pulmonary stenosis or subpulmonary obstruction.

TETRALOGY OF FALLOT



3. Overriding aorta: An aortic valve withbiventricular connection, that is, it is situatedabove the ventricular septal defect and connectedto both the right and the left ventricle. The degree

to which the aorta is attached to the right ventricleis referred to as its degree of "override." The aorticroot can be displaced toward the front (anteriorly)or directly above the septal defect, but it is alwaysabnormally located to the right of the root of the

pulmonary artery. The degree of override is quitevariable, with 5-95% of the valve being connectedto the right ventricle.

TETRALOGY OF FALLOT



4. Right ventricular hypertrophy: The rightventricle is more muscular than normal, causing acharacteristic boot-shaped appearance as seen bychest X-ray. Due to the misarrangement of the

external ventricular septum, the right ventricularwall increases in size to deal with the increasedobstruction to the right outflow tract. This featureis now generally agreed to be a secondaryanomaly, as the level of hypertrophy generallyincreases with age.

TETRALOGY OF FALLOT



Other variations

There is anatomic variation between the heartsof individuals with tetralogy of Fallot. Primarily,the degree of right ventricular outflow tractobstruction varies between patients andgenerally determines clinical symptoms anddisease progression. In addition, tetralogy of

Fallot may present with other anatomicalanomalies, including:

TETRALOGY OF FALLOT



1. stenosis of the left pulmonary artery, in 40% ofpatients

2. a bicuspid pulmonary valve, in 40% of patients3. right-sided aortic arch, in 25% of patients4. coronary artery anomalies, in 10% of patients5. an atrial septal defect, in which case the

syndrome is sometimes called a pentalogy ofFallot

6. an atrioventricular septal defect7. partially or totally anomalous pulmonary venous

return8. forked ribs and scoliosis

Other variations

TETRALOGY OF FALLOT



Tetralogy of Fallot with pulmonary atresia ( pseudotruncus arteriosus) is a severe variant inwhich there is complete obstruction (atresia) ofthe right ventricular outflow tract, causing an

absence of the pulmonary trunk during embryonicdevelopment. In these individuals, blood shuntscompletely from the right ventricle to the leftwhere it is pumped only through the aorta. The

lungs are perfused via extensive collaterals fromthe systemic arteries, and sometimes also via theductus arteriosus.

TETRALOGY OF FALLOT



Epidemiology and etiology

Tetralogy of Fallot occurs in approximately 3 to 6 per10,000 births and represents 5-7% of congenital heartdefects. Its cause is thought to be due to environmentalor genetic factors or a combination. It is associated with

chromosome 22 deletions and diGeorge syndrome. Itoccurs slightly more often in males than in females.

Embryology studies show that it is a result of anteriormalalignment of the conal septum, resulting in the clinicalcombination of a VSD, pulmonary stenosis, and anoverriding aorta. Right ventricular hypertrophy resultsfrom this combination, which causes resistance to bloodflow from the right ventricle.

TETRALOGY OF FALLOT



Pathophysiology and Symptoms

Tetralogy of Fallot results in low oxygenation of blooddue to the mixing of oxygenated and deoxygenatedblood in the left ventricle via the VSD and preferentialflow of the mixed blood from both ventricles throughthe aorta because of the obstruction to flow throughthe pulmonary valve. This is known as a right-to-leftshunt. The primary symptom is low blood oxygen

saturation with or without cyanosis from birth ordeveloping in the first year of life. If the baby is notcyanotic then it is sometimes referred to as a "pinktet".

TETRALOGY OF FALLOT



Other symptoms include a heart murmur which mayrange from almost imperceptible to very loud, difficultyin feeding, failure to gain weight, retarded growth andphysical development, dyspnea on exertion, clubbingof the fingers and toes, and polycythemia.


TETRALOGY OF FALLOT



Children with tetralogy of Fallot may develop "tetspells". The precise mechanism of these episodes is indoubt, but presumably results from a transientincrease in resistance to blood flow to the lungs withincreased preferential flow of desaturated blood to thebody. Tet spells are characterized by a sudden,marked increase in cyanosis followed by syncope, and

may result in hypoxic brain injury and death. Olderchildren will often squat during a tet spell, which cutsoff circulation to the legs and therefore improves bloodflow to the brain and vital organs.


TETRALOGY OF FALLOT



Diagnosis

The abnormal boot-like appearance of a heart withtetralogy of Fallot is easily visible via chest x-ray, and

before more sophisticated techniques becameavailable, this was the definitive method of diagnosis.Congenital heart defects are now diagnosed withechocardiography, which is quick, involves noradiation, 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 Fallotmay 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 acuteepisodes may require rapid intervention with morphine toreduce ventilatory drive and phenylephrine to increase bloodpressure. Oxygen is ineffective in treating hypoxic spellsbecause the underlying problem is lack of blood flow throughthe lungs and not oxygenation within the lungs. There are

also simple procedures such as squatting in the knee-chestposition which increases aortic wave reflection, increasingpressure on the left side of the heart, decreasing the right toleft shunt thus decreasing the amount of deoxygenated bloodentering the systemic circulation.

TETRALOGY OF FALLOT



Palliative surgeryThe condition was initially thought untreatable until surgeon AlfredBlalock, cardiologist Helen B. Taussig, and lab assistant Vivien Thomasat Johns Hopkins University developed a palliative surgical procedure,which involved forming an anastomosis between the subclavian arteryand the pulmonary artery (See movie "Something the Lord Made"). It

was actually Helen Taussig who convinced Alfred Blalock that the shuntwas going to work. This redirected a large portion of the partiallyoxygenated blood leaving the heart for the body into the lungs,increasing flow through the pulmonary circuit, and greatly relievingsymptoms in patients. The first Blalock-Thomas-Taussig shunt surgerywas performed on 15-month old Eileen Saxon on November 29, 1944with dramatic results.

The Pott shunt and the Waterson procedure are other shunt procedureswhich were developed for the same purpose.Currently, Blalock-Thomas-Taussig shunts are not normally performedon infants with TOF except for severe variants such as TOF withpulmonary atresia (pseudotruncus arteriosus).

Treatment

TETRALOGY OF FALLOT



Total surgical repairThe Blalock-Taussig procedure was the only surgical treatmentuntil the first total surgical repair was performed in 1954.Between 1944 and when total repair became available at majorsurgical centers in the early 1960s, many infants and childrenwere treated palliatively with Blalock-Taussig procedures.This first total repair was performed by C. Walton Lillehei at theUniversity of Minnesota in 1954 on a 10-month boy. Total repairinitially carried a high mortality risk which has consistentlyimproved over the years. Surgery is now often carried out ininfants 1 year of age or younger with a <5% perioperative

mortality. The surgery generally involves making incisions intothe heart muscle, relieving the right ventricular outflow tractstenosis by careful resection of muscle, and repairing the VSDusing a Gore-Tex patch or a homograft. Additional reparative orreconstructive work may be done on patients as required bytheir particular anatomy.

Treatment

TETRALOGY OF FALLOT



Prognosis

Untreated, tetralogy of Fallot rapidly results in progressive rightventricular hypertrophy due to the increased resistance on theright ventricle. This progresses to heart failure (dilatedcardiomyopathy) which begins in the right heart and often leadsto left heart failure. Actuarial survival for untreated tetralogy ofFallot is approximately 75% after the first year of life, 60% byfour years, 30% by ten years, and 5% by forty years.Patients who have undergone total surgical repair of tetralogy ofFallot have improved hemodynamics and often have good toexcellent cardiac function after the operation with some to noexercise intolerance (New York Heart Association Class I-II).Surgical success and long-term outcome greatly depends on theparticular anatomy of the patient and the surgeon's skill andexperience with this type of repair.

TETRALOGY OF FALLOT



Ninety percent of patients with total repair as infants develop aprogressively leaky pulmonary valve as the heart grows to itsadult size but the valve does not. Patients also often havedamage to the electrical system of the heart from surgicalincisions, causing abnormalities as detected by EKG and/or

arrhythmias.Long-term follow up studies show that patients with total repairof TOF are at risk for sudden cardiac death and for heart failure.Therefore, lifetime follow-up care by an adult congenitalcardiologist is recommended to monitor these risks and to

recommend treatment such as interventional procedures or re-

Prognosis

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