12: Neonatal Jaundice Flashcards Preview

Simmons NURP 501 Exam 3 Weeks 12 and 13 > 12: Neonatal Jaundice > Flashcards

Flashcards in 12: Neonatal Jaundice Deck (36):

What is the description and cause of Jaundice?

The accumulation of bilirubin in the skin -yellow tones
Becomes apparent when bilirubin level is >5-7
Advances Head to toe

Rise in bilirubin from 1.5 in cord blood to 5-6 on the third day of life, declining to a normal level (<1.3-1.5) by 10-12 days in Caucasian and AA infants

Asian infants reach 8-12 on day 4-5 and decline more slowly

Breastmilk jaundice: inadequate feeding can lead to increased jaundice because of slow moving bowels and inability to clear bili


What is Non-physiologic (pathologic) Jaundice?

Appears at <24 hours and may last longer than 8 days

The rate of increase is >0.5 mg/dL/hr

Total bili >12.5 before 48 hours old or direct bili exceeds 1.5-2

Kernicterus (bilirubin encephalopathy) involves toxicity of the nervous system resulting from high levels of bili

Consider exchange transfusion when bili levels reach 25-30


What are the causes of jaundice?

Increased rate of hemolysis
Decreased rate of conjugation
Abnormalities of excretion or absorption


What increases the rate of hemolysis to cause jaundice?

ABO incompatibility
Rh incompatibility
Abnormal RBC shapes
RBC enzyme abnormalities


What decreases the rate of conjunction and causes jaundice?

Immaturity of bilirubin conjugation (physiologic jaundice)
Congenital familial nonhemolytic jaundice
Breast milk jaundice


What are the abnormalities of excretion and absorption that cause jaundice?

Metabolic abnormalities
Biliary atresia
Choledochal cyst
Obstruction of ampulla of Vater


What family factors increase the risk of jaundice?

Significant hemolytic disease/anemia
Inborn errors of metabolism
Early or severe jaundice
Ethnic or geographic origin associated with hemolytic anemia
Hepatobiliary disease
Sibling received phototherapy


What maternal history factors can increase the risk of jaundice?

ABO or Rh incompatibilities in previous pregnancy
Sepsis risk for the infant - Prolonged ROM
Macrosomic infant of a diabetic mother


What color of skin is an infant suffering from the deposition of indirect bili in the skin?

Bright yellow or orange


What color of skin is an infant suffering from the obstructive type (direct bili)

Greenish or muddy yellow


Physical exam of an infant with jaundice?

Signs of infection
Poor feeding
Loss of Moro reflex - signs of bili toxicity to the brain
Diminished DTR's
Respiratory distress
Failure to suck
Bulging fontanelle
Twitching of face or limbs
Shrill, high pitched cry
Signs of kernicterus


What are diagnostic studies for jaundice?

TcB Noninvasive Transcutaneous bilirubin
TSB (indirect and direct) for infants with TcB >15, for darker skinned infants or for infants under phototherapy
Fractionated bili: provides the concentration of both unconjugated and conjugated bili

Additional Labs:
Blood type
Isoimmmune antibodies of mother
Coombs test on infant
Reticulocyte count


Elevated indirect (unconjugated) serum bili with a normal reticulocyte count and negative Coombs test

physiologic jaundice
breast milk jaundice
congenital familial nonhemolytic jaundice


Elevated indirect and direct serum bili with a negative Coombs test and a normal reticulocyte count

metabolic abnormalities
biliary atresia
choledochal cyst in the bile duct
GI or pancreatic obstruction


How is jaundice managed?

Monitoring of TcB and TSB
Frequent breast feeding, supplementation feeding
Phototherapy with overhead light, bili blanket and bilibed
Exchange transfusion


How is jaundice prevented?

Frequent breast feeding
Systematic assessment of the new born for the risk of hyperbilirubinemia
Early and focused follow-up based on risk assessment
Supplement feeding if infant is inadequate intake, weight loss >10%, infant dehydration


How is bilirubin produced?

The breakdown of RBC --> Heme --> bilirubin
1g of Hgb produces 24 mg of bilirubin

Unconjugated bilirubin binds to albumin and is taken to the liver where it becomes conjugated, conjugated bilirubin is then excreted from the liver via the bile duct into the intestine. There it is further metabolized and excreted in the stool. Without appropriate gut flora or prolonged time in the intestine it is turned back into unconjugated bili and absorbed by the intestines back into circulation.


What is Unconjugated Bilirubin?

Or indirect bilirubin

Bilirubin not yet conjugated and reversibly bound to albumin.

Unconjugated bilirubin builds up when glucouronyl transferase is deficient and conjugation is slow


What is conjugated bilirubin?

Or direct bilirubin

Bilirubin conjugated with glucuronide

Water soluble so it's easily excretable. It builds up with obstruction of bile flow (cholestasis)


What is free bilirubin?

A small amount of unconjugated bilirubin not bound to albumin so it can cross the BBB and cause damage to neurons


What causes physiologic jaundice?

Increased RBC mass in the newborn
Decreased activity of UDP glucuronyl transferase that correlates with gestational age, leading to decreased conjugation and excretion
Increased enterohepatic circulation due to lack of intestinal flora, decrease gut motility and small enteral intake


What increases the chances of nonphysiological jaundice?

Early jaundice: infants with jaundice in first 24-36 hours of life likely have increased production of bili (hemolysis) or excessive blood cell breakdown from polycythemia or bruising

Significant jaundice in a previous infant

Exclusive breast feeding: due to small intake in first few days, delayed institution of intestinal flora and increased enterohepatic circulation of bilirubin

Gestational age <38 weeks

East Asian race

Cephalhematomas and bruising

Maternal age >25

Male sex


What is hyperbilirubinemia?

Hemolysis leading to increased bilirubin production?


What are the leading causes of hyperbilirubinemia?

Excessive production of bilirubin
Decreased bilirubin clearance
Breastfeeding-Associated Jaundice


What causes excessive production of bilirubin?

Hemolysis leading to increased bilirubin production
Nonantibody-mediated hemolysis
Nonhemolytic causes of increased Bilirubin production


What causes hemolysis leading to increased bilirubin production?

Antibody-mediated: Directed Coombs test or indirect Coombs test - Positive
ABO incompatibility: Mother Type O, Baby type A or B

Rh incompatibility: Mom Rh neg, baby Rh pos - Usually prevented with RhoGam


What is nonantibody-mediated hemolysis: Direct Coombs test or direct antibody test - Negative

Red cell membrane defects
Red cell enzyme defects


What is nonhemolytic causes of increased bilirubin production?

Bruising: related to birth trauma
Polycythemia: Can be due to delayed cord clamping, twin-twin or maternal-fetal transfusion, or secondary to chronic intrauterine hypoxia, IUGR, or maternal diabetes


What can cause decrease bilirubin clearance?

Bowel obstruction/delayed passing of meconium

Inborn errors of metabolism:
Glycuronyl transferase deficiency - Crigler-Najjar Syndrome, Gilbert Syndrome


How does phototherapy work?

Light energy is absorbed by the bilirubin molecule and changes its stereochemical shape making it more water soluble. This can be excreted in the bile without conjugation. This makes the bilirubin less toxic as the serum levels fall.


What are the possible complications of phototherapy?

Retinal Effects: Wear an eye patch
Bronze-baby syndrome: transient gray-bronze discoloration of infants with cholestatic jaundice treated with photo therapy. Usually, disappears after stopping phototherapy. No known long last effects.


What are guidelines for therapy?

Screening TSB >95%

TSB >8 mg % at 24 hours
TSB >13 mg % at 48 hours
TSB >16 mg % at 72 hours


What are some future medications to treat hyperbilirubinemia?

Heme oxygenase inhibitors (tin-protoporphyrin and tin-mesoporphyrin): suppress formation of bilirubin

Phenobarbital: When administered before birth, to mother of infant with known severe hemolytic disease, it will induce the infant's hepatic enzymes and increase hepatic uptake of bili and excretion of bili into the bile.


What is the pathology of Kernicterus?

yellow staining of brain nuclei (kerns), with current management of hyperbilirubinemia, this is a rare complication


What are the clinical manifestations of Kernicterus?

Poor suck to severe
Largely irreversible disease associated with coma and seizures


What is the root cause of re-emergence of kernicterus?

Early discharge (<48 hrs) without early follow-up

Failure to check the bili level in an infant noted to be jaundiced before 24 hours of age

Failure to recognize the presence of risk factors

Underestimating the severity of jaundice by clinical (visual) assessment

Lack of concern regarding the presence of jaundice

Delay in measuring serum bili despite marked jaundice

Failure to respond to parental concerns regarding jaundice, poor feeding or lethargy.