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BILI BOYKody Crowell MD PGY2

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Setting: 4 day old male who presents

for a newborn visit in clinic.

HISTORY: Born to a 29 year old G1 NSVD at 37 4/7weeks. Uncomplicated delivery and 2 dayhospital stay. Maternal labs were normal

including GBS and Blood O+/-. Discharged at93 % birth wt. Bili done prior to discharge was12.8 with LL of 15.3.

Fam Hx: No congenital diseases. Maternal uncle

with jaundice as an infant. Social Hx: Lives with both parents who are from

South Korea and PhD students at the University.

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PHYSICAL EXAM

PHYSICAL EXAM:

Wt: 90% Birth wt.

GEN: Fussy but consolable. Not ill appearing.

HEENT: Sclera icteric.

CV: Clear S1 and S2 with no murmurs rubs or gallops.

PULM: Moving air well with clear breath sounds. Noretractions , wheezes or nasal flaring.

ABD: Soft, nontender, nondistended. No palpablemasses.

SKIN: Jaundice to thigh. No rashes.

NEURO: normal infant reflexes, facial symmetry.

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INTERVAL HX: DOL 4

Breast Feeding

Mom feels her breast milk had just come in.

Feeding 15 minutes every 2-3 hours.

Stooling 2-3 times a day of dark green stool.

Bili 21.8 with LL 20. Started on phototherapy.

Parents do not wish to supplement withformula as mothers breast milk is now in.

Bili next day is 19.8

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NEXT CLINIC VISIT: DOL 7

Gained 15g. Now at 91% of birth wt.

Stool x8/day and transitioning

Mom does not like leaving under bili lightsbecause he gets fussy.

PHYSICAL EXAM: facial Jaundice

Bili 21.6. Sent to RTU

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RTU

Started on phototherapy.

Temp of 38.5 and full ROS done.

Transferred to inpatient service.

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DIFFERENTIAL DIAGNOSIS?

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DIFFERENTIAL DIAGNOSIS

GI: Breast feeding jaundice, Breast milk jaundice, Crigler-Najjar syndrome type I and II, Gilberts.

Conjugated bili: Cholestasis (Biliary atresia), Dubin Johnson

ID: Sepsis (viral and bacterial), Viral infection (CMV, HSV,

Hepatitis, etc),parasitic infection (ascaris, lumbricoides,liver flukes)

HEME: Pyruvate kinase deficiency, G6PD, Spherocytosis,ABO incompatibility. (Too early for thalassemia or sicklecell)

ENDO: Hyperthyroidism CV: Heart failure

TOX: Drug induced (not applicable here, but rather in olderkids). Rifampin, probenecid, some herbal medicines.

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LABS

Blood Cx, Urine Cx, CSF Cx: NGTD

Enterovirus & HSV PCR Serum/CSF: Negative

CBC: Normal

CSF: Gram Stain negative, RBC 1, WBC 1

U/A: Normal

BMP: Normal Hepatic function panel: Normal

Reticulocytes: 1 (Normal)

Bilirubin:

Sun. (05:37) Neonatal = 12.2, Unconjugated = 12.2, Conjugated = 0.

Sat. (06:15) Neonatal = 13.7, Unconjugated = 13.7, Conjugated = 0Friday (16:20) Neonatal = 15.5, Unconjugated = 15.2, Conjugated = 0.3Friday (06:25) Neonatal = 17.2, Unconjugated = 16.8, Conjugated = 0.4Thurs. (20:05) Neonatal = 19.6, Unconjugated = 19.1, Conjugated = 0.4

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DOL 10: Clinic Visit for Hospitalization

follow-up.

Off Phototherapy x1 day. 96% Birth Wt.Parent s supplementing with formula 2 oz

x5/day in addition to Q2-3H breast feeding.

Jaundice to chest. Bili 19.8!!!

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CBC normal.

Retics normal.

Periphera l Smear: Target cells, Tear drop cells,reticulocytes, spherocytes, schistocytes.

(normal for newborn)

G6PD assay normal

NMS has returned normal

Sent home with phototherapy.

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DOL 13

Above birth wt. Bili 18.4

Sent home with no lights and daily bili.

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DOL 16

Bili 19

Pump and Dump x 2days.

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DOL 18

BILI

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12!!

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Hyperbilirubinemia

35 weeks gestation defined as a Total Bili >95th percentile for hours of

age.

Bilirubin production is 2-3 times higher in infants than adults.

UGT activity in term infants is 1% of the adult at 7 days and does not reach

adult levels until 14 weeks of age. Bilirubin-induced Neurologic Dysfunction (BIND): Increased risk with a

Total Bili >25 - 30 mg/dL.

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Gilberts/Crigler-Najjar (I/II)

Gilberts:-Most common inherited disorder of bilirubin glucoronidation.

-Mutation in the promotor region of UGT 1A1 gene resulting in a reduced productionof UGT.

-Breast milk jaunidice during second week of life may be a result of a concurrent

manifestation of Gilberts.

CN-I:-More sever than CN-II.

-UGT is present, but there is little to no activity.

-Severe hyperbilirubinemia during the first 2-3 days.

-Lifelong phototherapy or Liver transplant is needed for treatment.

CN-II:-UGT is present and has low activity.

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Breast Feeding Jaundice

Due to Inadequate oral intake by the infant

leading to hypovolemia.

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Breast Milk Jaundice

Persistence of physiologic jaundice beyond the

first week of age.

Usually begins after first 3-5 days of life.

Peaks within 1-2 weeks after birth and may

peak again at 3 weeks of life.

May take up to 3 months to completely

resolve.

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Breast Milk Jaundice continued

Likely caused by deconjugation of bilirubin by

Beta-Glucuronidase in breast milk.

Unconjucated bili is then absorbed by the

intestine causing an increase in enterohepatic

circulation.

Benign, but bili should be monitored regularly

until normalizing.