Author: ASEERVATHAM , CHRISTOPHER

Basic Information
Review Chart:
01/24/2019 10:17 Bilirubin, Total 13.5 mg/dL HI
Bilirubin, Direct 0.4 mg/dL HI
01/24/2019 04:34 Bilirubin, Total 16.6 mg/dL CRITICAL
Bilirubin, Direct 0.6 mg/dL HI

Chief Complaint
CE is a 7 day old (ex37+2wk) male infant, born via NSVD to a GBS + mother, who was admitted to
11N on 1/24 for management of hyperbilirubinemia.

History of Present Illness

Over the past couple of days, mother notes that he sleeps often and when woken up to feed only
feeds for a little. Normally, she breast feeds him every 3-4 hours for about 10 minutes and then
supplements his feeding w/ 1 oz of Enfamil formula. During instances where she doesn't breast feed
him, he will intake about 2 oz of Enfamil formula. He has 4-5 wet diapers per day. He had one
bowel movement yesterday; the prior bowel movement had been 6 days prior. When he was taken
to his PCP yesterday (1/23) for WCC, he was found to be jaundice w/ T. bili 17.7. He was sent to
the ED, where a repeat T. bili showed 18.5 and D. bili showed 0.5. H/H was 18/50.9. His cord blood
was O+ (Mother also is O+). Mother endorses that he has had no vomiting, diarrhea, rash, difficult
breathing or blood in urine/stool. He has lost 11% of his bodyweight in the past week [3.57 kg -->
3.15 kg].

Health Status
Allergies:
Allergic Reactions (All)
NKA

Histories
Birth History: Pregnancy was complicated by Maternal Thrombocytopenia (likely secondary to ITP)
[newborn's platelets was 269 on 1/18] and Cholestasis of Pregnancy tx with Actigal PO Tid.
Maternal Prenatal Labs:
Blood type: O, Rh positive
Rapid plasma reagin: nonreactive
Hepatitis B: negative
HIV: negative
Group B Strep: positive
Chlamydia: negative
Gonorrhea culture: negative
Rubella: immune

Review of Systems
Constitutional: Decreased activity, No fever, No chills.
Eye: Icterus.
Ear/Nose/Mouth/Throat: No nasal congestion.
Respiratory: No shortness of breath, No cough.
Gastrointestinal: Constipation, No vomiting, No diarrhea.
Genitourinary: No hematuria, No urethral discharge.
Integumentary: Jaundice, No rash.
Neurologic: Alert.
Physical Examination
Vital Signs and Measurements:
Vital Signs
Temp Axillary 36.7 DegC (Jan 23 22:40)
Resp Rate 56 br/min (Jan 23 22:40)
SBP 95 mmHG (Jan 23 22:40)
DBP 53 mmHG (Jan 23 22:40)
SpO2 96% (Jan 23 22:40)
Head Circumference 35.5 cm (Jan 23)
BSA 0.2098 m2 (Jan 23)
Abdominal Girth 34.5 cm (Jan 16)
Neck Circumference 33.5 cm (Jan 16), Weight Trend (ST)
Weight Measurements:
Weight: 3.17 kg 01/23/19
Weight: 3.37 kg 01/17/19
Weight: 3.57 kg 01/16/19

Height Measurements:
Height: 51.00 cm 01/23/19
Height: 51.00 cm 01/23/19
Height: 51.00 cm 01/23/19

General
No acute distress.
HENT: Normocephalic, Oral mucosa is moist, No pharyngeal erythema, Anterior fontanelle
open/soft/flat, Ears normally set and rotated.
Neck: Supple, Non-tender, No lymphadenopathy.
Respiratory: Lungs are clear to auscultation, Respirations are non-labored, Breath sounds are equal,
Symmetrical chest wall expansion.
Cardiovascular: Normal rate, Regular rhythm, No murmur, Good pulses equal in all extremities,
Normal peripheral perfusion.
Gastrointestinal: Soft, Non-tender, Non-distended, Normal bowel sounds, Anus patent, Brownish-
green soft stool in diaper.
Genitourinary: Normal genitalia for age and sex, No lesions.
Integumentary: Warm, Dry, Jaundiced under the diaper region.
Musculoskeletal: Normal range of motion, Normal strength, No deformity, No hip clicks, Normal
Barlow's, Normal Ortolani's.
Neurologic: Alert, Moves all extremities appropriately, No focal defects, Normal Moro reflex, Hand
grasp present, Toe grasp present.

Review / Management
Results review: Lab results
01/24/2019 10:17 Bilirubin, Total 13.5 mg/dL HI
Bilirubin, Direct 0.4 mg/dL HI
01/24/2019 04:34 Bilirubin, Total 16.6 mg/dL CRITICAL
Bilirubin, Direct 0.6 mg/dL HI
01/23/2019 20:40 Bilirubin, Total 18.5 mg/dL CRITICAL
Bilirubin, Direct 0.5 mg/dL HI
Hemoglobin 18.0 g/dL HI
Hematocrit 50.9 %
Reticulocyte Count, Automated 1.49 %
 01/23/2019 15:58 Bilirubin, Total 17.7 mg/dL CRITICAL
Bilirubin, Direct 0.4 mg/dL HI
.

Impression and Plan

CE is a 7 day old male w/ no significant medical history who presented to the ED w/ jaundice and was
admitted to 11N for management of hyperbilirubinemia secondary to poor PO and weight loss. Cord
blood type match with maternal blood type makes ABO incompatibility an unlikely diagnosis.
Differential diagnosis includes breastfeeding jaundice vs breast milk jaundice vs erythrocyte enzyme
defects (G6PD) in order of likelihood. He is currently clinically well-appearing and hemodynamically
WNL.

PLAN:
- Phototherapy: Though he has no discernable risk factors (no siblings requiring hyperbili
management, no family hx of G6PD, no known hemolytic disease, not east asian), his gestational
age places him at the medium risk curve and thus phototherapy should be started. Recheck T/D bili
every 4-6 hours after initiating phototherapy and if it continues to rise: consider exchange
transfusion.
- Strict I's and O's: Poor PO, drop in birth wt over the 1st week by >10%, and decrease in bowel
movements leans towards the dx of breastfeeding jaundice so encourage mom to increase
feeding frequency
- Breast milk jaundice more unlikely since infant is not exclusively breastfed and the mother complains
of infant's reduced overall PO intake
- If jaundice persists or T/D bili levels continue to rise, may consider screening (fluorescent spot test)
for G6PD or other hemolytic disorders but currently seems unlikely (no family hx of G6PD).
- Patient may be discharged after improved feeding and downtrend in T/D bili levels.

Professional Services
Attending Physician Attestation

Signature Line
CHRISTOPHER ASEERVATHAM, MED STUDENT on
 Neonatal Jaundice due to unconjugated hyperbilirubinemia can be attributed to either

physiologic or pathologic reasons and being able to distinguish the source of elevated plasma

bilirubin (TB) is essential to its management. Bilirubin is produced during the catabolism of

heme via mainly erythrocyte hemoglobin breakdown. Bilirubin is then prepared for clearance via

hepatic uptake and conjugation with glucuronic acid using the enzyme UGT1A1. Conjugated

bilirubin is then secreted via bile into the intestines where it’s reduced by bacterial enzymes into

urobilinogen and either reabsorbed via enterohepatic circulation or excreted via feces

(stercobilin) or urine (urobilin).

Physiologic neonatal jaundice is due to both an increase in heme catabolism and a deficit

in the aforementioned clearance pathway. Full term newborns have increased red blood cell mass

(Hct around 60%)1 in response to a relatively hypoxic intrauterine environment as well as a

shorter RBC life span leading to increased turnover of red blood cells. This increase in bilirubin

production is paired with a decrease in bilirubin clearance due to a deficient UGT1A1 enzyme

(takes 14 weeks to reach adult levels of activity) leading to an increase in unconjugated bilirubin

being reabsorbed into enterohepatic circulation.2 The resulting low-risk unconjugated

bilirubinemia is delineated by mean TB levels ranging from 7 mg/dL to 14 mg/dL that peak at 48

to 96 hours with Caucasian and African-American infants falling within the lower end of this

range and East-Asian infants falling within the upper end.3 The difference between ethnicities is

due to polymorphisms in the UGT1A1 gene that decrease enzyme activity4 as well as a

Gly71Arg mutation that is more common among Eastern Asians5. Therefore, East Asian

ethnicity is considered a risk factor for the infant when determining the necessity of phototherapy

treatment.
 On the other hand, hyperbilirubinemia which necessitates concern for pathology and puts

the infant at risk is delineated as TB levels greater than 25 mg/dL or greater than the 95th

percentile on the hour-specific Bhutani nomogram.6 Other concerning clinical features is an early

presentation of jaundice within the first 24 hours or persistent/late presentation of jaundice after

two weeks of age. One pathological source of increased bilirubin production is due to hemolytic

processes. For example, the infant’s cord blood was tested against his mother’s blood in my

specific case to check for ABO/Rh(D) incompatibility which can lead to a Coombs positive

hemolytic anemia.7 Other defects that can lead to erythrocyte injury include cell membrane

defects (hereditary spherocytosis), enzymatic defects (G6PD), and sepsis (increased oxidative

stress)3 as well as others. Another concern is decreased bilirubin conjugation leading to

insufficient clearance that can be caused by an inherited UGT1A1 enzyme disorder. Both

Crigler-Najjar syndrome and Gilbert syndrome involve mutations in the UGT1A1 gene causing a

varying reduction in conjugation activity.8

Breast milk jaundice is correlated with infants who are exclusively breastfed with TB

levels >5 mg/dL that persists beyond the first few weeks.9 The mechanism behind the diagnosis

involves either elevated levels of beta-glucuronidase in breast milk that deconjugates intestinal

bilirubin and promotes reabsorption or a concurrent UGT1A1 polymorphic mutation. Regardless.

it should resolve within 12 weeks of age without necessary intervention. On the other hand,

lactation failure jaundice is due to suboptimal breastfeeding which slows down bilirubin

elimination and leads to jaundice presenting within the first week of life concurrently with

weight/fluid loss.10 Treatment for neonatal jaundice depends on its severity and the infant’s risks

factors. It can range from monitoring and increased PO intake to phototherapy or exchange

transfusion depending on clinically proven hour-specific nomograms.11

 Bibliography

1) Gallagher PG. The neonatal erythrocyte and its disorders. In: Nathan and Oski's Hematology and

Oncology of Infancy and Childhood, 8th ed, Orkin SH, Fisher DE, Look T, Lux SE, Ginsburg D,

Nathan DG (Eds), WB Saunders, Philadelphia 2015. p.52.

2) Kawade N, Onishi S. The prenatal and postnatal development of UDP-glucuronyltransferase activity

towards bilirubin and the effect of premature birth on this activity in the human liver. Biochem J.

1981;196(1):257-60.

3) Kaplan M, Wong RJ, Sibley E, Stevenson DK. Neonatal jaundice and liver disease. In: Neonatal-

Perinatal Medicine: Diseases of the Fetus and Infant, 9th ed, Martin RJ, Fanaroff AA, Walsh MC

(Eds), Elsevier Mosby, St. Louis 2011. Vol 2, p.1443.

4) Dennery PA, Seidman DS, Stevenson DK. Neonatal hyperbilirubinemia. N Engl J Med.

2001;344(8):581-90.

5) Akaba K, Kimura T, Sasaki A, et al. Neonatal hyperbilirubinemia and mutation of the bilirubin uridine

diphosphate-glucuronosyltransferase gene: a common missense mutation among Japanese, Koreans

and Chinese. Biochem Mol Biol Int. 1998;46(1):21-6.

6) Bhutani VK, Johnson L, Sivieri EM. Predictive ability of a predischarge hour-specific serum bilirubin

for subsequent significant hyperbilirubinemia in healthy term and near-term newborns. Pediatrics.

1999;103(1):6-14.

7) Kaplan M, Hammerman C, Vreman HJ, Wong RJ, Stevenson DK. Direct antiglobulin titer strength

and hyperbilirubinemia. Pediatrics. 2014;134(5):e1340-4.

8) Skierka JM, Kotzer KE, Lagerstedt SA, O'kane DJ, Baudhuin LM. UGT1A1 genetic analysis as a

diagnostic aid for individuals with unconjugated hyperbilirubinemia. J Pediatr. 2013;162(6):1146-52,

1152.e1-2.

9) Maisels MJ, Clune S, Coleman K, et al. The natural history of jaundice in predominantly breastfed

infants. Pediatrics. 2014;134(2):e340-5.

10) Gourley GR, Kreamer B, Arend R. The effect of diet on feces and jaundice during the first 3 weeks of

life. Gastroenterology. 1992;103(2):660-7.

11)

Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics Jul
2004, 114 (1) 297-316; 10.1542/peds.114.1.297

Phototherapy Nomogram

Exchange Transfusion Nomogram