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Patient Marc LabradorWard Bed 10
Age/Sex 5 days/MaleDate of Admission Nov. , 001
Informant aunt/mother (reliability 80%)
CLINICAL HISTORY
By Intern Sonny Cyrus Bata
General Data
M.L., 5-day-old male, from Muntinlupa City, admitted on November , 001 for yellowish discoloration of the skin.
History of Present Illness
The Pt was born full term, via spontaneous vaginal delivery to a -year-old GP (00) at home c/o a midwife. Weight=8. lbs. No significant maternal illnesses/infection during present pregnancy, no maternal drug intake during the pregnancy, (+) regular prenatal check-ups, and no perinatal complications. Minimal blood loss during the delivery. (-) cephalhematoma, (?) Vitamin K, (+) good cry, good activity, no cyanosis, good suck at birth. (+) UO, BM
Pt was apparently well until 1 day PTA, there was note of icteric sclerae and jaundice of the whole body. (-) fever, (-) seizures, (-) feeding problems. Pt was noted to be awake with good suck and activity.
1 hours PTA, note of upward rolling of eyeballs associated with stiffening of the extremities which lasted for less than a minute, (+) poor suck, (-) loss of consciousness, (-) cyanosis, (-) drooling, (-) dyspnea, no fever at this time, (-) vomiting.
hours PTA, Pt was noted to be febrile (temp .40C), with persistence of jaundice. He was given Paracetamol drops with lysis of the fever. Pt was immediately brought to RITM where assessment was sepsis neonatorum, to consider kernicterus probably 0 to ABO incompatibility. Pt was then referred to PGH for further evaluation.
Review of Systems
(-) diarrhea(-) bleeding(-) oliguria
(-) umbilical stump discharge(-) dyspnea(-) acholic stools
(-) vomiting(+) dark green stools(-) pallor
(-) skin rashes(-) umbilical stump discharge
(-) pruritus(-) dark-colored urine(-) easy bruisability
(-) edema(-) drug intake-sulfonamides
Past Medical History as above
Family Medical History
(-) DM
(+) bronchial asthma - grandfather
(+) jaundice - maternal cousin, double exchange transfusion done.
(-) hepatitis, infectious diseases, blood dyscrasia
Immunizations none yet
Nutritional History breastfed since birth
Personal and Social History youngest of three siblings. -year-old mother (housewife), year old father (unemployed), financial support from relatives.
Physical Examination
¢At the ER, Pt was received asleep but arousable, jaundiced, in extended position
¢HR 140, RR 40, Temp 7.00C
¢HC cm, CC cm, AC 8cm
¢Length 48cm, weight .kg (P5)
¢Pink conjunctivae, icteric sclerae, soft and flat anterior and posterior fontanelles. (-) cervical lymphadenopathy, yellowish oral cavity
¢Symmetric chest expansion, clear breath sounds, no retractions, no alar flaring, no wheezes and crackles
¢No heaves and lifts, distinct heart sounds, normal rate and regular rhythm, no murmurs appreciated
¢Flat abdomen, normoactive bowel sounds, soft, liver edge 1cm below right subcostal margin, no masses and tenderness, (+) reddish, swollen umbilical stump with foul-smelling discharge
¢Full pulses, pink nailbeds, no edema and cyanosis, (+) jaundice all over, no petecchiae
¢Grossly male external genitalia, descended testes
¢Neuro exam asleep, arousable, mm EBRTL, no preferential movement, no spasticity, supple neck, DTRs +++, (-) extensor toe sign, spontaneous movement of all extremities
Assessment at the ER
Hyperbilirubinemia probably secondary to
1.ABO incompatibility
.sepsis neonatorum
Management at the ER
Therapeutics
Pt was started on Penicillin G 00,000 units/kg/day, Amikacin 15mkd, Phenobarbital 5mkd, Tetanus toxoid IM, Vitamin K mg IV OD
Phototherapy
Diazepam 0. mkdose, 0.8mg IV for frank seizures
Diagnostics done
CBCHgb 148, Hct 0.45, Plt 40, WBC .60 (Neut 58, Lymph 4, B/E/M not indicated), RBC 5.15 (no PBS requested)
Blood chemTB 855.0 (0-17.1), DB 17.06 (0-5), IB 88.8 (.4-1.70)
BUN .6, Crea (dec)
Ca .4, Na 147, K 4., Cl 10
Alb 18 (dec), glob , Alk phos 104, AST 74 (inc), ALT (dec)
Blood typeMother O+, Baby B+
ABG7., 8, 105, 18, -8, 7%
(acidosis increases risk of kernicterus)
ProtimeActivity 0.0, INR .6
Stool examBrown, soft, no RBCs, no parasites, 10-0 WBCs
U/ADark yellow, hazy, 1.010, 7.0, + sugar, +1 alb, 0- RBCs, 10-15 RBCs
Other labs done Coombs test, baby gram APL, blood CS
Additional labs Serology (mother)
Reticulocyte count, PBS
ESR
T4/TSH
G6PD screen, galactosemia screening
TORCH, Hepa profile
Criteria that rule out physiologic jaundice
1.Jaundice in the first 4-6 hours of life.
.TB increasing by more than 5mg/dL (85umol/L) per day.
.TB exceeding 1. mg/dL in a FT infant or 15 mg/dL in a PT infant.
4.DB exceeding 1.5- mg/dL or 15% of TB
5.Clinical jaundice persisting for more than a week in a FT infant or weeks in a PT infant
Etiologies of jaundice 0 to unconjugated hyperbilirubinemia
Overproduction of Bilirubin
1.Increased rate of hemolysis
a.(+) Coombs test
-Rh incompatibility
-ABO incompatibility
-other minor blood groups
b.(-) Coombs test
-abnormal RBC morphology
-RBC enzyme abnormalities
c.Sepsis
.Nonhemolytic causes of increased bilirubin load (elevated IB, normal retic count)
a.Extravascular hemorrhage
b.Polycythemia
c.Exaggerated enterohepatic circulation of bilirubin (delayed stooling, bowel obstruction)
d.Inadequate caloric intake
e.Neonatal asphyxia
Decreased rate of conjugation
1.Physiologic jaundice
.Crigler-Najjar syndrome
.Gilberts syndrome
Prolonged hyperbilirubinemia Hypothyroidism, Down syndrome, Cyanotic heart disease
Increased direct bilirubin
1.Sepsis
.Intrauterine infection (Toxoplasmosis, CMV, Rubella, Herpes, syphilis)
.Severe hemolytic disease
4.Biliary atresia
5.Giant cell hepatitis
6.Choledochal cyst
7.Cystic fibrosis
8.Galactosemia
.Alpha1 antitrypsin deficiency
10.Tyrosinemia
ABO incompatibility
Isoimmune hemolytic anemia may result when ABO incompatibility occurs between mother and the newborn infant.
Common with blood type A or B infants born to type O mothers
Hemolysis begins in utero and is the result of active placental transport of maternal isoantibody (7S-IgG in type O)
In type A or B mothers, the 1S-IgM antibody is present which cannot cross the placenta
Mild hemolytic anemia with reticulocytosis, microspherocytosis, early-onset unconjugated hyperbilirubinemia
Risk is present in 1-15% of pregnancies, evidences of fetal sensitization (+ Coombs test) present in -4% only. Symptomatic ABO hemolytic disease occurs in 1%
S/S jaundice, anemia
Kernicterus
¢yellowish discoloration of the basal ganglia due to unconjugated bilirubin
¢bilirubin encephalopathy (opisthotonus, seizure, lethargy, high pitched cry)
¢mortality of 50%, survivors develop choreoathetoid cerebral palsy, sensorineural hearing loss, paralysis of upward gaze
Management
Phototherapy
- UV radiation converts unconjugated bilirubin in the skin into a stereoisomer compound which is water-soluble and can be excreted in the bile.
- may also use bili blankets
- may increase dose by increasing the BSA exposed to light and by moving the lights closer to the infant
- complications includediarrhea, dehydration, skin rash, tanning, bronze baby syndrome, lactose intolerance, skin burns
Guidelines for use of phototherapy in term infants without hemolysisGuidelines for treatment of the term infant with ABO incompatibility
Bili 15mg/dL, age days eval, PT
Bili 18mg/dL, age - days eval, PT
Bili 0-mg/dL, age -4 eval, PT, stop feeding with formula milk
Bili 5mg/dL as above + exchange transfusionPhototherapy if
10mg/dL at 1 hrs
1-14mg/dL at 18 hrs
15mg/dL at 4 hrs
Exchange transfusion
- double-exchange transfusion is necessary in cases of Rh isoimmunization, ABO incompatibility, hereditary spherocytosis.
- serves to decrease bilirubin level acutely by 50%, remove 80% of the sensitized or abnormal RBC and any offending Ab.
- invasive procedure
- 160-00 mL/kg BW or 85cc/kg X
- complications include infection, thromboembolic phenomenon, umbilical and portal vein perforation, acute NEC, arrhythmia and cardiac arrest, hypocalcemia, hypomagnesemia, hypoglycemia, metabolic acidosis, graft vs host
- mortality in 0.1-0.5%
Induction of UDPGT activity
- Phenobarbital acts on the conjugating enzyme and affects the microsomal hepatocyte activity
Inhibition of heme oxygenase activity
- metalloporphyrins are capable of inhibiting heme oxygenase, thereby blocking the enzymatic process for the formation of bilirubin from heme. Examples are tin protoporphyrin and tin mesoporphyrin
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