Section 4: Jaundice and the Breastfed Infant Flashcards
What is jaundice?
a yellow discoloration of the skin and sclera caused by hyperbilirubinemia
When does jaundice usually become visible on the sclera?
FIRST
34 to 51 μmol/L
(2-3 mg/dl)
When does jaundice become visible on the face?
68 to 86 μmol/L
( about 4 to 5 mg/dL)
Jaundice advances in a
head-to-foot direction
When does jaundice appear at the umbilicis and feet?
- umbilicus at about 258 μmol/L (15 mg/dL)
- at the feet at about 340 μmol/ (20 mg/dl)
How many neonates become visibly jaundiced in the first week of life?
Slightly more than half
Hyperbilirubinemia may be harmless or harmful depending on
its cause and the degree of elevation
The threshold for concern for jaundice varies by
- Age
- Degree of prematurity
- Health status
Jaundice threshold for healthy term infants
more than 308 μmol/L
( 18 mg/dL )
Infants who are premature, small for gestational age, or ill (sepsis, hypothermia, hypoxia) are at
much greater risk than healthy newborns
Treament for hyperbilirubinemia is given based on
- age
- clinical factors
what is the major consequence of neonatal hyperbilirubinemia
Neurotoxicity
How does neurotoxicity manifest
- acute encephalopathy
- can be followed by neuro problems eg
- cerebral palsy
- sensorimotor deficits
- cognition is usually spared
What is the most severe form of neurotoxicity
Kernicterus
Does kernicterus still occur?
Yes, although rare
What is kernicterus?
- brain damage
- Also known as Bilirubin encephalopathy
Bilirubin is normally bound to
- Serum albumin
- therfore stays in the vascular space
When can bilirubin cross the blood-brain barrier and cuase kernicterus?
WHEN ALBUMIN ISN’T KEEPING IT IN THE VASCULAR SPACE
- VERY HIGH serum bilirubin
- VERY LOW serum albumin (eg preteruM)
- BILIRUBIN displaced from Albumin (competitive binders)
What are competitive binders for bilirubin?
- drugs (eg, sulfisoxazole, ceftriaxone, aspirin)
- free fatty acids
- hydrogen ions (eg, in fasting, septic, or acidotic infants).
Risk of hyperbilirubinemia in neonates ≥ 35 weeks gestation
Patho of jaundice
- most bilirubin produced from breakdown of Hb into unconjugated bilirubin
- U. bilirubin binds to albumin in blood for transport to liver
- in liver, it is taken up by hepatocytes and conjugated (made water-soluble) by an enzyme
- Conjugated bilirubin is excreted in bile into duodenum
- In adults, Con. Bili is reduced by gut bacteria into urobilin and excreated
- Neontates have fewer gut bacteria, so excrete less bilirubin -
- they also have an enzyme that deconjugates bili
- Unconjugated bili is reabsorbed and recycled into circulation
- This is called enterohepatic circculation of bilirubin
Mechanisms of hyperbilirubinemia
- Increased production of bilirubin
- Decreased hepatic uptake
- Decreased conjugation
- Impaired excretion
- Impaired bile flow (cholestasis)
- Increased enterohepatic circulation
Most cases of jaundice involve
unconjugated hyperbilirubinemia.
What may cause a conjugated or mixed hyperbilirubinemia.
LIVER PROBLEMS
- Liver dysfunction
- neonatal sepsis
- neonatal hepatitis
Physiologic hyperbilirubinemia main points
- occurs in almost all neonates
- Generally resolves in first 1-3 weeks of life
- Bilirubin levels can rise up to 18 mg/dL by 3 to 4 days of life (7 days in Asian infants) and fall thereafter.
What is Breastfeeding Jaundice also known as?
- starvation jaundice
- breast-non-feeding jaundice
What is breast milk jaundice?
- different from breastfeeding jaundice
- Usually in healthy, thriving infants
Pathologic hyperbilirubinemia in term infants is diagnosed if
- Jaundice appears
- in the first 24 h
- after the first week of life,
- lasts more than 2 wks
- Total serum bilirubin (TSB) rises by more than 5 mg/dL/day
- TSB is more than 18 mg/dL
- Infant shows symptoms or signs of a serious illness
Some of the most common causes of pathologic hyperbilirubinemia are
- hemolytic anemia
- G6PD deficiency (inc RBC breaskdown)
- Hematoma resorption
- Sepsis
- Hypothyroidism
What findings may indicate pathological jaundice?
- Jaundice in the first day of life
- Jaundice after 2 wk of age
- Lethargy, irritability, respiratory distress
Jaundice that develops in the first 24 to 48 h, or that persists > 2 wk, is most likely
pathologic
aundice that does not become evident until after 2 to 3 days is more consistent with
physiologic, breastfeeding, or breast milk jaundice
Diagnosis of hyperbilirubinemia
Diagnosis is suspected by the infant’s color and is confirmed by measurement of serum bilirubin
What bilirubin concentration in infants warrants further testing?
- > 10 mg/dL (> 170 μmol/L) in preterm infants
- or > 18 mg/dL in term infants
Treatment of hyperbilirubinemia is directed at
the underlying disorder.
Treatment for physiologic jaundice
- usually is not clinically significant and resolves within 1 wk
- Frequent formula feedings can reduce the incidence and severity ( by increasing GI motility and frequency of stools)
- The type of formula does not seem important in increasing bilirubin excretion.
with breastfeeding jaundice, it is not advisable to supplement with
- water or dextrose
- it may disrupt the mother’s production of milk.
in breastfeeding jaundice, assure mother that
hyperbilirubinemia has not caused any harm and that she may safely resume breastfeeding.
in breastfeeding jaundice, stopping breastfeeding is necessary for
- only 1 or 2 days
- mother should continue to express
in breastfeeding jaundice, what may be appropriate at higher bilirubin levels?
phototherapy
If the bilirubin level continues to increase > 18 mg/dL in a term infant with early breastfeeding jaundice
a temporary change from breast milk to formula may be appropriate
breastfeeding jaundice may be prevented or reduced by
increasing the frequency of feedings
Treatment for breastfeeding jaundice
- may be prevented or reduced by increasing the frequency of feedings
- If the bilirubin level continues to increase > 18 mg/dL in a term infant with early breastfeeding jaundice, a temporary change from breast milk to formula may be appropriate
- phototherapy also may be indicated at higher levels.
- Stopping breastfeeding is necessary for only 1 or 2 days (mother should continue to exress)
- assure mother that hyperbilirubinemia has not caused any harm and that she may safely resume breastfeeding.
- It is not advisable to supplement with water or dextrose because that may disrupt the mother’s production of milk.
Definitive treatment of hyperbilirubinemia involves
- Phototherapy
- Exchange transfusion
What is phototherapy
- Standard of care for hyperbilirubinemia
- most commonly uses fluorescent white light
- Blue light, wavelength 425 to 475 nm, is most effective for intensive phototherapy
- The light is absorbed by bilirubin, making it water soluble and able to be excreted in the stool and urine
- It provides definitive treatment of neonatal hyperbilirubinemia and prevention of kernicterus.
What is an exchange teansfucion
- For severe hyperbilirubinemia,
- rapidly removes bilirubin
- Small amounts of blood drawn and replaced through umbilical vein catheter
Where does bilirubin come from?
- disintegration of red blood cells and the breakdown of hemoglobin into globin and heme
- Heme is further broken down to iron, biliverdin, and carbon monoxide
- Biliverdin is reduced to bilirubin
Amount of jaundice in a newborn depends on
the balance of bilirubin production and elimination.
the balance of bilirubin production and elimination may be upset because of
- (a) increased bilirubin production
- (b) decreased ability to metabolize the bilirubin for elimination
- (c) decreased elimination and increased absorption of bilirubin in the intestines.
What leads to additional produciton of bilirubin in the neonate?
- In utero, low O2 environment stimulates production of extra RBCs
- LIfespan of fetal RBCs shorter than adult
- Large volume of heme + shorter lifespan produces additional bilirubin
what causes Increased bilirubin production after birth?
- blood is transferred from the placenta to the newborn, further increasing blood volume and hemoglobin concentrations.
- Immature or inactive RBCs are destryed –> inc bilirubin
In the newborn, unconjugated bilirubin enters the liver cells
slower than in an older chil
Conjugation of bilirubin is necessary for
bilirubin to be transferred into bile and moved into the small intestine and stool.