Neonatal Jaundice

Neonatal Jaundice

WHAT IS KERNICTERUS AND WHAT IS THE CLASSIC TETRAD OF KERNICTERUS?
Chronic bilirubin encephalopathy, irreversible
Tetrad:
Choreoathetoid cerebral palsy
High frequency central hearing loss
Palsy of vertical gaze
Dental enamel hypoplasia

WHAT ARE SIGNS OF ACUTE BILIRUBIN ENCEPHALOPATHY?
Early:
Alteration in tone of extensor muscles(hypo or hypertonia)
Retrocollis (arching of neck)
Opisthotonus (arching of back)
Poor suck
Shrill cry
Irritability
Lethargy
Fever

Advanced:
Cessation of feeding
Bicycling movements
Irritability
Seizures
Fever
Altered LOC

HOW IS BILIRUBIN PRODUCED AND EXCRETED BY THE NEONATE?
Produced by the breakdown of hemoglobin (hemoglobin is degraded by heme oxygenase releasing iron, CO and biliverdin; biliverdin converted o bilirubin by biliverdin reductase)
Unconjugated bilirubin bound by albumin in blood stream
Unconjugated bili taken up by liver and conjugated by UDPGT (uridine diphophate glucuronosyltransferase)
Conjugated bili excreted into biliary system and intestine
Intestinal bili excreted as stool or becomes unconjugated and reenters bloodstream as unconjugated bili through enterohepatic circulation

WHAT ARE THE MAIN CAUSES OF HYPERBILIRUBINEMIA IN THE NEONATE?
Increase hemolysis
Decreased hepatic uptake of unconjugated bili from circulation
Delayed maturation or inhibition of conjugating mechanism in liver
Increased enterohepatic circulation of unconjugated bili

WHAT TYPE OF BILI PUTS A NEONATE AT RISK FOR ACUTE ENCEPHALOPATHY AND WHY?
Unconjugated only as is lipid soluble and passes the blood brain barrier, conjugated is water soluble and cannot pass the BBB

WHAT ARE RISK FACTORS FOR SEVERE HYPERBILIRUBINEMIA?
Jaundice in the 1st 24 hr of life
Visible jaundice before hosp d/c
Fetal-maternal blood type incompatibility
Prematurity
Exclusive breastfeeding
Significant weight loss
Maternal age > 25
Male
Delayed meconium
Excessive birth trauma
LGA (in late preterms)
G6PD and breast feeding (in late peterms)

WHAT IS PHYSIOLOGIC JAUNDICE?
Transient elevation in bili that self resolves in 7-10 days
Peaks at day 3-5

WHAT ARE SIGNS OF PATHOLOGIC JAUNDICE?
Onset in 1st 24 hr
Rapidly rising bili level
anemia
Prolonged jaundice (> 3 weeks)
Conjugated bili > 20% of total bili
Temperature instability
Unwell appearing neonate

WHAT IS YOUR DDX FOR CONJUGATED (DIRECT) HYPERBILI OF THE NEONATE?
Infection:
TORCH
Hepatitis
Sepsis

Anatomic:
Biliary atresia
Choledochal cyst
Cholestasis
Mass lesion
Alagille syndrome (ateriohepatic dysplasia)

Metabolic:
Inborn errors of metabolism
CF
Alpha-1-antitrypsin deficiency

WHAT IS YOUR DDX OF UNCONJUGATED (INDIRECT) HYPERBILI OF THE NEONATE?
Benign:
Physiologic
Breast milk jaundice

Hemolysis:
ABO incompatibility
Physiologic breakdown of birth trauma hematomas
IVH
Spherocytosis
G6PD
Pyruvte kinase deficiency
Sickle cell

Infection:
TORCH
Sepsis (esp UTI)

Obstructive:
Meconium ileus
Hirschsrung’s
Duodenal atresia
Pyloric stenosis

Metabolic/genetic:
Galactosemia
Congenital hypothyroidism
Crigler-Najjar syndrome (absence or deficient UDPGT)
Gilbert’s

WHY CAN BREASTFEEDING LEAD TO JAUNDICE?
Caloric derivation and dehydration from delayed milk production (takes 2-5 days before maternal milk production up to normal) leading to increased enterohepatic circulation
Inhibition of  hepatic B-UGT

WHAT PRESENTATIONS OF NEONATAL JAUNDICE REQUIRE A WORKUP?
Onset in the 1st 24 hr of life
Unwell appearing neonate (lethargy, irritability, poor feeding, temperature instability, vomiting)
> 20% TSB is conjugated
Onset after 7-10 d of life
Associated anemia
Persists after 3 weeks (exclude exclusively breast fed neonates without any of above and who appear well)

WHAT ARE 3 TREATMENT MODALITIES USED TO TREAT POTENTIALLY HARMFUL LEVELS OF HYPERBILIRUBINEMIA IN THE NEONATE?
Phototherapy:
Decreases bili level 15-25%
Blue light converts unconjugated bili to a water soluble compound that is excreted in urine and stool

Ivig:
Used with fetal maternal ABO or Rh incompatibility

Exchange Transfusion:
Decreases bili level by ~ 50%
Indicated if: signs of intermediate to severe acute bilirubin encephalopathy, level as per AAP guidelines, rising level despite phototherapy

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Posted on เมษายน 8, 2013, in บทความ. Bookmark the permalink. ใส่ความเห็น.

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