Test 2 Flashcards

1
Q

Respiratory Failure

A
  • inability of the respiratory apparatus to maintain adequate gas exchange
  • obstructive (increased resistance to airflow)
  • restrictive (impaired lung expansion)
  • primary insufficient gas transfer

Cardinal Signs=restlessness, tachy, tachypnea, diaphoresis

Early Signs=mood changes, HA, increased WOB, HTN, exertional dyspnea, anorexia, increased CO and urinary output, CNS symptoms, nasal flaring, retractions, expiratory grunting, wheezing or prolonged expiration.

Signs of Severe Hypoxia=hypo or HTN, depressed respirations, dimness of vision, brady, somnolence, cyanosis (central or peripheral), stupor, coma, dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Anatomy/Phys Respiratory Differences

A
  • Diphragmatic Breathers until age 7
  • see retractions more readily
  • infant’s airways are 1/4 size of adults
  • neonates have 20 million alveoli, age 8 have 300 million
  • paradoxical chest movements are normal
  • have 2x oxygen consumption of adults
  • obligate nose breathers for 2-3 months
  • ALWAYS auscultate anterior/posterior and axillary!!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Manifestations of Respiratory Alterations

A
  • restlessness (increased anxiety, fussiness)*
  • tachy*
  • tachypnea*
  • diaphoresis*
  • flaring nostrils
  • retractions
  • change in LOC
  • perfusion: color, cyanotic, cold, increased cap refill, increased RR, *HR, lower O2 sats, BP changes, decreased urine output
  • cough (NB=chlamydial pneumonia)
  • dyspnea
  • for dark pigmented children–oral cavity
  • grunting (premature closure of glottis in effort to increase PEEP)-late sign
  • retractions
  • stridor (uppper airway)-can be inspiratory or expiratory
  • wheezing (bronchioles-lower)-typically on expiration
  • intercostal bulging-increased expiratory pressure needed to push air out.
  • chest pain
  • head bobbing, use of sternocleidomastoids and scalene
  • clubbing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Respiratory Distress

A
  • inadequate CO2 elimination
  • decrease in O2
  • severe=RR>60…give nothing by mouth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Respiratory Assessment

A
  • LOC/response
  • RR (know baseline)
  • WOB
  • color of skin/MM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Oxygen Delivery

A
  • Room air is 21%
  • each L adds 4%
  • don’t go higher than 5 L with nasal cannula (above 4L is irritating to nasopharynx)
  • cannula 25-45%
  • mask 35-60% (6-10L)
  • Face tent/shield-tolerated better than mask 40% @ 10-15L
  • plastic hood
  • croup tent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Peak Expiratory Flow Meter

A
  • max flow of air forcefully exhaled in 1 second
  • Green-80-100%-no sx, continue maintenance
  • Yellow-50-79%-acute exacerbation may be occuring-increase maintenance tx, call practioner if child stays in this range
  • Red-<50%-medical alert-severe airway narrowing-short-acting bronchodilator; notify PCP if child doesn’t return to yellow or green
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Bronchopulmonary Dysplasia

(BPD)

A

-iatrogenic effect of high O2 given to preemies (also retinopathy of prematurity and intra-ventricular brain bleeds, cerebral palsy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cystic Fibrosis

A
  • dysfunction of exocrine glands-mucous blocks vital structures: lung, pancreas, loss of Na and Cl in sweat
  • frequent respiratory infection, pulmonary congestion
  • barrel chest (increased anterior-posterior diameter) from air trapping
  • kidneys affected-diabetic
  • pancreatic enzymes before they eat (ok to sprinkle over food, do not crush)
  • high caloric needs-often have G-button for continuous feedings over night)
  • need fat soluble vitamins
  • need low carb, high protein, high fat diet
  • clubbing-chronic hypoxia
  • malabsorption (steatorrhea)
  • biliary cirrhosis, portal HTN
  • CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Croup Syndromes

A

-Acute Epiglottitis (Life Threatening!)-bacterial(H.influenzae–vaccine)-abrupt onset preceded by sore throat, drooling, toxic looking, tripod position–do NOT inspect throat or take throat culture (gag/cry-narrows airway) Airway obstruction. *Do not examine the throat d/t risk of obstructing the airway completely.

  • Acute Laryngotracheobronchitis (LTB)-viral, less acute than epiglottitis, more common, suprasternal retractions, cough, hoarseness, low fever, mild wheeze. cool mist, nebulized epi/corticosteroids
  • S/S-hoarseness, barky cough, inspiratory stridor, inflammation or obstruction of larynx; (not a lot of mucous), mostly inflm and edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Stridor

A
  • narrowing of the upper airway
  • inspiratory or expiratory
  • causes=croup, epiglotitis, FB, or tracheitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pneumonia

A
  • inflm of the pulmonary parenchyma
  • viral-more frequent than bacterial, associated with URIs; RSV in infants, parainfluenzae and adenovirus in older children
  • bacterial-Strep. pneumoniae (pneumococcus), neonate-group A strp, stah, enteric bacilli, chlamydia (suspect in neonate with cough), 3-5 yo-strep pneumoniae, haemophilus influenzae and staph aureus, >5yo mycoplasma pneumoniae; prevented by pneumococcal conjugate vaccine (PCV, Prevnar)
  • S/S=cough (productive or not), tachypnea, breath sounds = fine crackles, chest pain, dullness on percussion, retractions, nasal flaring, pallor to cyanosis. irritable, restless, lethargic, anorexia, vomiting, diarrhea, abd pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

RSV

(Bronchiolitis)

A
  • begins as simple URI
  • infection of the bronchioles
  • airway obstruction caused by edema, accumulation of mucous, dyspnea (faster breathing…collapses airway)
  • wheezing, nasal flaring, nasal congestion, prolonged expiratory phase
  • antiviral = ribavirin
  • Synagis for high risk (<2yo, prematurity, CHD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pertussis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Foreign Body

(FB)

A

-cannot speak, becomes cyanotic, collapses = 4 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Asthma

A
  • chronic inflammatory disorder
  • mast cells, eosinophils, T lymphocytes
  • airflow limitation or obstruction
  • bronchospasm and obstruction (inflm response, airway edema, spasm of smooth muscle)
  • reactive airway dz
  • commonly chronic
  • airways become edematous
  • airways become congested with mucus
  • smooth muscles of bronchi and bronchioles constrict
  • air trapping in alveoli
  • bronchodilatros to reverse bronchospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Categories of Congenital Heart Defects

A
  1. increased pulmonary blood flow (acyanotic); atrial septal defect, ventricular septal defect, patent ductus arteriosis, atrioventricular canal (ASD, VSD, PDA, AVC)
  2. decreased pulmonary blood flow (cyanotic); tetrology of Fallot, tricuspid atresia (TOF, TA)
  3. obstruction of blood flow from the heart (acyanotic); coarctation of aorta, pulmonic stenosis, aortic stenosis (COA, PS, AS)
  4. mixed blood flow (cyanotic); transposition of great arteries, total anomalous pulmonary venous connection, hypoplastic left heart syndrome, truncus arteriosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Heart Failure

A

-inability of the heart to pump adequate amt of blood to the systemic circulation at normal filling pressures to meet body’s metabolic demands

Causes:

  1. volume overload (esp L to R shunts)
  2. pressure overload
  3. decreased contractility
  4. high cardiac output demands (sepsis, hyperthyroid, severe anemia)

Assess weight and urine output

Other causes=cardiomyopathies, arrhythmias, HTN, PE, chronic lung disease, severe hemorrhage

Goals: improve cardiac function, increase contractility, decrease afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cor Pulmonale

A

-HF resulting from obstructive lung dz such as CF or bronchopulmonary dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Coarctation of the Aorta

(COA)

A
  • obstruction of blood flow from the heart
  • unequal BP between upper and lower extremeties (high in upper, low in lower) Dif of 8-10 mmHg should be evaluated
  • different O2 sats-upper and lower
  • can be pre-ductal arteriosis or post-ductal
  • infants present with CHF–acidotic and hypotensive
  • older children-present with dizziness, HA, fainting, epistaxis-resulting from HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

2 Manifestations of CHD

A
  1. Cyanosis-apparent when there is venous arterial shunting or obstruction of blood flow to the lungs
  2. CHF-occurs when CO is unequal to body demands. Blood dams up in the heart and pulmonary vasculature becomes engorged.
    also: murmur, FTT, frequent respiratory infections, fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Abnormal Weight Gain

(CHD)

A

50g/day–infant

200g/day–preschool

500g/d–older child

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

PMI

(point of maximal impulse)

A

4th intercostal space

left mid-clavicular

24
Q

Murmurs

A
  • Organic = pathological, associated with CHD or acquired HD
  • Innocent = no physiologic abnormality-80% of children
  • Functional = no anatomic cardiac defect–physiologic reason (anemia)

*if murmur goes away when child sits up–no CHD

Graded 1-6

25
Q

Eisenmenger Syndrome :(

A
  • Left to Right shunt becomes Right to Left Shunt
  • (large VSD’s do this)
  • leads to increasing cyanosis
  • progressive increase in pulmonary vascular resistance (PVR)
  • occurs after prolonged period of increased pulmonary blood flow
  • can be deadly
  • increased pulmonary pressure=increased stress on lungs=increased WOB=diaphoresis while eating=sudden R to L shunting=turns blue.
  • especially with AVC
26
Q

VSD

A
  • most common CHD
  • increased pulmonary blood flow
  • increased ventricular and pulmonary artery pressures
  • FTT, dyspnea, frequent URIs, CHF, thrill and murmur
  • spontaneous closure withing first 2 years
  • tx medically with digoxin, diuretics
  • Sx closure to prevent irreversible pulmonary dz
  • Pulmonary artery banding (palliative): tightening of band=O2 sats drop, increased WOB
27
Q

Prostaglandins

A

maintain patency of ductus arteriosis

28
Q

Indomethacin

(Indocin)

A

to close ductus arteriosis

29
Q

Clinical Manifestations

of CHF

A
  • tachy, tachy (HR>160)
  • sweating
  • S3 and S3 (gallop rhythm)
  • decreased urine output*
  • fatigue
  • edema, weight gain
  • restlessness
  • anorexia
  • pale, cool extremities
  • weak peripheral pulses
  • decreased BP
  • cardiomegaly
  • hepatomegaly
30
Q

Digoxin

A

+inotropic (increased force of contraction)

  • chronotropic (decr HR)
  • dromotropic (slow conduction)
  • MUST take apical pulse for 1 minute to assess for bradycardia
  • therapeutic = 0.8-2.0 mcg/L

indirectly enhances diuresis by increasing renal perfusion.

rapid onset, short half-life

digitizing dose (ECG bf initial dose)-bolus given IV or PO to bring level to therapeutic

maintenance dose is usually 1/8 of digitizing dose, give 2qday

*infants rarely receive >1ml (50mcg) in single dose

always compare calculation with another RN

decreased K+ enhances effects of digoxin (risk of dig toxicity)

increased K+ lowers effects of digoxin

normal range 3.5-5.5

signs of dig toxicity = early:VOMIT, anorexia, diarrhea, abdominal pain, later:brady, also fatigue, muscle weakness drowsiness

must be given at scheduled time

31
Q

ACE Inhibitors

A
  • cause vasodilation
  • decrease PVR, SVR, BP
  • reduce afterload
  • decrease R and L atrial pressures (decr work of heart)
  • K+ supplements may cause hyperkalemia
  • high K+ foods=avacados, bananas, potatoes, kiwi, strawberries, watermelon
  • Captopril, Enalapril (Vasotec)
  • Assess BP before administration
32
Q

Diuretics for CHF

A
  • Lasix SE-N/V/D, ototoxic, hypokalemia, postrual hypo
  • Chlorothiazide SE-N/V, dizziness, paresthesia, cramping, hypokalemia, acidosis
  • Spironolactone (K-sparing) SE-skin rash, drowsiness, ataxia, hyperkalemia
33
Q

Therapeutic Mgt of CHF

A
  • remove fluid and Na (diuretics, fluid restriction, Na restrictions)
  • decrease cardiac demands (thermal neutral environ, tx infections, reduce WOB-elev HOB, sedation (Chloral Hydrate or Ativan), rest, quiet, cluster care)
  • improve tissue oxygenation-cool humidified O2

*O2 is vasodilator which will decrease PVR and will increase blood flow to the lungs–they sat in 70’s-80’s

  1. reduce workload
  2. increase CO
34
Q

TOF

(Tetrology of Fallot)

A

Four Associated Defects=VSD, Overriding Aorta, Pulmonary Stenosis, R ventricular hypertrophy

Clincial Manifestations: cyanosis, clubbing, dyspnea, cardial thrill, infants have intense cyanosis when PDA closes, DOE, syncope, convulsions; squatting in older children, respiratory distress and fatigue during feedings, polycythemia,

TET spells (paroxysmal hypercyanotic episodes), spasm of RVOT, tachy, possible loss of consciousness, common in AM after good night’s sleep, ppt’d by crying, defecation, feeding…can progress to sz, CVA, death

*Knee-Chest to decrease venous return, increases SVR which diverts more blood to the pulmonary artery

  • give O2
  • meds=propanolol, morphine

Therapeutic Mgt:

  • inderal (beta blocker) to relax hypertrophied RV, enhancing pulmonary blood flow
  • Sx to increase pulmonary blood flow (Blalock-Taussig Shunt-subclavian to pulmonary artery)

2-3 Sx’s to fix, first is palliative. complete repair=close VSD, resect infundibular stenosis, pericardial patch to enlarge the RVOT

35
Q

combined defects

A

-Transposition of the great vessels (TGV): cyanosis is ALWAYS present, hypoxic spells esp with crying, usually also have PDA, ASD, VSD and pulmonary stenosis: clubbing, FTT, polycythemia. O2 doesn’t help, enlarge or create ASD for more mixing, nitric oxide to decrease PVR, Prostaglandin E to dilate ductus arteriosis, arterial switch (7-30d after birth) and closure of ASD and VSD

-Hypoplastic Left Heart Syndrome (HLHS): hypoplasia of all left heart structures, may include mitral valve stenosis/atresia, only blood flow is thru PDA: cyanosis, tachypnea, dyspnea, decreased BP in all extremities, grunting, flaring, hypothermia. 3-step Norwood Procedure, bi-directional Glen Shunt

36
Q

Right to Left Shunting

A
  • TOF and Transposition
  • Risk for air from venous system going directly to brain
  • All IV lines should have filters in place to prevent air from entering the system, check tubing and syringes for air, tape connections securely
37
Q

Terrible T’s

A
  • truncus arteriosis=pulmonary artery and aorta are one and the same, large VSD
  • TOF
  • Transposition of the Great Vessels-incompatible with life unless coexisting VSD, ASD, and/or PDA is present (keep PDA open with prostaglandin E)
  • Total anomalous pulmonary venous connection
38
Q

Rheumatic Fever

A
  • systemic, inflm, grp A beta hemolytic strep (GABHS) occurs in 50% of cases
  • ages 6-15
  • onset 3 wks post untreated URI with GABHS
  • Major criteria for Dx=carditis, polyarthritis, chorea, erythema marginatum, subQ nodules; minor criteria=fever, arthralgia, elevated sed rate (ESR), CRP. Positive strep test, tachy, GI, decr plts, HA, tinnitus
  • Tx=ATB (penicillin), life-long prophylaxis (daily!!), ASA, digoxin (to decrease workload, decr HR, incr contractility
39
Q

Kawasaki Disease

(Mucotaneous Lymph Node Syndrome)

A
  • acute systemic vasculitis
  • unknown cause (usually toddlers)
  • acute dz is self-limiting, but wo tx 2-25% dev cardiac dz
  • usually Dilation of the Coronary Arteries–Aneurysms!
  • Acute phase (10 d)-fever (104), conjuctivitis, strawberry tongue, erythema, edema of hands and feet, polymorphous exanthema (rash-full body), cervical lymphadenopathy, incr sed rate, incr plts
  • Subacute phase (11-25 d after onset)-desquamation of hands/feet; rash, fever, lymphadenopathy disappear, cardiovasc changes
  • convalescent phase-sed rate and plts return to normal
  • Goal=reduce infl within coronary artery, prevent thrombosis
  • Tx=single dose gamma globulin (IV), ASA within 10 d of dz onset
  • lots of ASA at first, then decr
40
Q

Systemic HTN

A
  • typically associated with renal issues (secondary HTN)
  • significant (95-99% for sex, age, ht) or severe (99%+)
  • Must be noted on 3 separate occassions bf diagnosis
  • Tx-non-pharm, pharm: ACE inhibs, Beta Blockers, CCB’s, Vasodilators (Apresoline), ARB’s (Losartan), Diuretics
  • BB’s can cause lipid abnormalities or mood disturbancs (depression)
  • ACE inhibs and ARBs are teratogenic–not for teenage girls
41
Q

Hyperlipidemia

A
  • begins in childhood, early intervention
  • screen at age 2 with family Hx
  • indiv risk factors=DM, HTN, KD, nephrotic syndrome
  • dietary changes
  • drug therapy (Cholestyramine or Colestipol-both bile acid binding resins or sequestrants)
42
Q

Dysrhythmias

A

-Bradydysrhythmias

-Tachydysrhythmias-supraventricular tachy is most common (200-300 bpm)

-Conduction Disturbances-irreg HR

  • SVT–decreased CO-Tx=vagal maneuvers, adenosine, cardioversion; propanolol, amiodarone, radiofreq ablation, digoxin, transesophogeal atrial overdrive pacing or synchronized cardioversion
  • s/s of SVT=poor feeding, pallor, extreme fussiness, older-palps, dizzy, diaphoresis
43
Q

NG Drainage

A
  • replace over 4 hours: ml to ml
  • with isotonic soln (LR or NS)
  • in addition to maintenance fluids!
44
Q

Peritonitis

A
  • r/t release of GI contents into abd cavity thru rupture or perforation of bowel or suture line
  • d/t build-up of pressure within the bowel
  • s/s=spike Temp, tachy, abd circumference-distended
45
Q

Otitis Media

A
  • risk for conductive hearing loss if untreated
  • enlarged lymph nodes
  • discharge from ear if drum is ruptured
  • UR symptoms
  • position on affected side
  • no smoking, don’t feed supine
46
Q

Tonsillitis

A
  • May be viral or bacterial
  • may be strep
  • breathing may be obstructed

Post tonsilectomy:

-avoid red fluids which mimic blood

-do not use straws

-ice collars

47
Q

Problems Associated with GI Dysfunction

A
  • F/E and acid/base imbalance
  • FTT
  • increased metabolic needs, decreased absorption
  • vomiting/aspirations
  • infection
  • pain
48
Q

Cleft Palate

A
  • prevent aspiration
  • provide nutrition
  • prevent infection
  • prevent delay in speech (sugery for cleft palate done bt 9-15 months)
  • Sx for cleft lip when baby weighs 10 lbs, 10 wks old
  • NO forks, spoons or straws post-op!!!
49
Q

Esophogeal Atresia

Tracheoesophageal Fistula

A
  • maternal polyhydraminos
  • excessive mucous
  • RD (continuous/sporadic)
  • regurgitation of feedings
  • acute gaseous abd distention, abnormal amt of flatus

*3 C’s of TE fistulas: coughing, choking, cyanosis

  • Also: frothy saliva in mouth and nose, drooling
  • Associated with VATER or VACTERL (vertebral, anal, Tracheoesophogeal fisutal, radial and renal dysplasia, cardiac, limb)
  • may become cyanotic and apneic

-tracheal malacia-barking cough, stridor, wheezing, recurrent respiratory tract infections, cyanosis, sometimes apnea=is a condition characterized by flaccidity of the tracheal support cartilage which leads to tracheal collapse especially when increased airflow is demanded.

50
Q

Hirschsprung Dz

(Aganglionic Megacolon)

A

*rectal biopsy=definitive Dx

  • pre-op: NG tube, ATB, vit K
  • vomit is bile stained
51
Q

Pyloric Stenosis

A
  • projectile vomiting=hallmark symptom, approx 2 wks afer initial sx; may occur right after feeding or may be delayed up to an hour or more
  • hungry after vomit
  • NOT bile stained
  • SEVERE F/E imbalances very quickly
  • ALKALOSIS
  • weight loss and FTT
52
Q

Degree of Dehydration

A

pre-illness (g) - post-illness (g) / pre-illness (kg)

=mls/kg loss

  • MILD < 50 mls/kg
  • MODERATE 51-99 mls/kg
  • SEVERE >100mls/kg
53
Q

GER/GERD

A
  • becomes dz when complications such as FTT, bleeding, dysphagia develop
  • sx within 1st wk of life
  • chronic vomit/regurg (not projectile)
  • FTT
  • cardiorespiratory sx’s
  • hematemesis
  • Barium esophogram, esophageal pH monitoring (leave in for 24hr), scintigraphic studies (radioactive nucleotide added to formula-looks at gastric emptying time)
  • non-pharmalogic: 1 tablespoon of RC / 1 oz formula
  • reflux harness in crib
  • pharmacologic: antacids/histamine receptor antagonists (Zantac, Cimetadine, Pepcid), Proton pump inhibitor (Omeprazole), prokinetic meds (reglan and Bethenechol)
  • may outgrow, but if not (premature, neuro issues)-recurrent aspiration pneumonia, apnea, cardiac issues…
  • Sx=Nissen Fundoplication-no more vomiting/burping (may have to vent G-tube)=passage of the gastric fundus behind the esophagus to encircle the distal esphagus
54
Q

Acquired GI issues

A
  • Intussusception-invagination/telescoping of one portion of intestine (often at ileocecal valve) = extremely painful-causes ischemia, child will be screaming, vomiting (bile stained), currant jelly stool (mucus/blood), abd distention; ischemia…pressure can cause perforation…death. Hydreostatic reduction-or Sx if unsuccessful; can recur! =intestinal obstruction
  • Acute Appendicitis-obstruction of lumen (stool)-perforation can cause peritonitis-Dx abd ultrasound or CAT scan, elevated WBCs (no higher than 20,000), elevated bands. If ruptured-triple ATB’s
55
Q

Malabsorption Syndromes

A
  • Short Bowel Syndrome (SBS)–decreased mucosal surface usually due to extensive resection of the small intestine; also caused by congenital anomalies (jejunal and ileal atresia or gastroschisis), ischemia (necrotizing enterocolitis), trauma or vascular injury (seat belts)
  • gastroschisis=herniation of intestine lateral to umbilical ring
  • omphalocele=abd contents herniate through the umbilical ring, usually with an intact peritoneal sac
  • anastamoses (post-resection) can narrow–vomiting is a sign
56
Q

Necrotizing Enterocolitis

A
  • tachy, very agitated, very distended abd
  • can perf
  • necrotic, ischemia…death
  • leads to SBS (resection)
57
Q

Biliary Atresia

(Extrahepatic Biliary Atresia)

EHBA

A
  • progressive inflammatory process-intra and extrahepatic bile duct fibrosis resulting in eventual bile duct obstruction
  • obstruction leads to polysplenia, intestinal atresia, malroation of the intestine
  • infants appear healthy at birth
  • suspect if jaundice persists after 2 weeks and if direct (conjugated) bilirubin is elevated
  • urine may be dark, stools progressively more gray
  • hepatomegaly occurs early
  • if untreated…cirrhosis of the liver, liver failure, death
  • serum aminotransferase, alkaline phosphatase and gamma glutamyl transpeptidase leves are usually elevated
  • kids need nutrional support-formulas with medium chain triglycerides, ADEK, vit’s, minerals, iron, zinc and selenium
  • continous tube feedings or TPN

-Kasai procedure to re-route the bile ducts

-orthotopic liver transplantation