Transcript Hyperbilirubinemia - Stanford University

Hyperbilirubinemia
Monica Stemmle
Objectives
• Understand pathway where bilirubin comes
from
• Physiologic vs Pathologic Hyperbilirubinemia
• Understand the risk for Kernicterus
• Understand why we care about
hyperbilirubinemia
Physiology
Physiologic hyperbilirubinemia
• 1. Increased production: Increased RBC
volume and decreased lifespan of RBC in
neonates
• 2. Decreased Excretion: UGT activity is
decreased in neonates for first few days. Also
increased enterohepatic circulation
Pathologic Hyperbilirubinemia
• Can you name some of the risk factors :
1. Increased bilirubin load?
2. Decreased bilirubin clearance?
Increased bilirubin load
Hemolysis
– Immune mediated (ABO, rH, minor antigens)
– Heritable defects (RBC membrane defect, RBC enzyme
defects, hemoglobinopathies)
Sepsis/DIC
Hematomas
Polycthemia
Macrosomia
Increased enterohepatic ciculation
Decreased bilirubin clearance
• G6PD deficiency
• Meconium plug
• Imperforate anus
Risk of Hyperbilirubinemia
KERNICTERUS
Kernicterus
• Physiology not well understood
• Believed that exposure to bilirubin at a
sensitive window of neuronal development
may lead to apoptosis
• Requires PROLONGED HIGH bilirubin
Kerniticus studies
• 1. Outcomes among Newborns with Total Serum Bilirubin Levels of
25 mg per Deciliter or More Thomas B. Newman N Engl J Med
354;18 may 4, 2006
– Kaiser data. Infants with bili >24. No cases of kernicterus and no
neurologic difference
• 2. Outcomes in a Population of Healthy Term and Near-Term Infants
With Serum Bilirubin Levels of >19 mg/dL Who Were Born in Nova
Scotia, Canada, Between 1994 and 2000. Pediatrics. Jangaard et al.
122 (1): 119. (2008).
– Babies in Nova Scotia bw 1994-2000. No dif in neuro problems or
deafness between severe hyperbili (>19) and no hyperbili (<13).
• 3. Synopsis report from the Pilot USA Kernicterus Registry VK
Bhutani and L Johnson Journal of Perinatology (2009) 29, S4–S7.
– No cases of kernicterus at bili <20, very usual at 20-25 and 25-35 could
be reversible if acted on quickly
So who do you screen
• AAP recommends universal screening either with
TcB or TSB
• USPSTF recommends against universal screening.
– Risks: treating unneccesarily, interrupting
breastfeeding, increased treatment and cost of
hospitalization.
• Summary: Screen with TcB or TSB with clinical
judgment and weighing baby risk factors!
Risk Factors to Consider
Can you name a few for hyperbilirubinemia
needing photo AND nuerotoxicity?
Risk Factors for Hyperbili
• Predischarge TSB or TcB in the HR or HIR zone
• Lower Gestational age
• Exclusive breasfeeding (esp if not going well or
weight loss excessive)
• Jaundice in first 24 hours
• Isoimmune or other hemolytic disease
• Cephalohematoma or significant bruising
• East Asian Race
Risk factors for neurotoxicity
•
•
•
•
•
•
Isoimmune hemolytic disease
G6PD
Asphyxia
Sepsis
Acidosis
Albumin <3
Charts To help
• Do you know what the 3 charts and what they
look at are that we use?
AAP Charts
• Risk Zones
• Phototherapy
• Exchange Transfusion
Risk Zones
Phototherapy
So what does all this mean?
• Approach each baby individually
• Importance is WHY the baby is jaundiced not
that the baby is jaundiced
• Use clinical judgment and think about risks
when deciding when to recheck and when to
treat.
Questions
• You are the junior on at Valley and have a
baby that is being admitted for hyperbili.
Meanwhile 3 other kids hit the floor at the
same time. In order to triage you send the
intern to see the hyperbili first while you see
the sicker patients. When you reunite with
the intern what are your 4 top questions you
want to ask the intern?
•
•
•
•
Gestational age and chronologic age
Bili level (and hours that it was taken)
Baby vital signs and general appearance
Baby blood type and mom blood type
Intern Response
• 6 day old ex 36 0/7 with a bili of 15.8. Vitals
not done yet. Mom is A +, Ab neg. Which
places the baby at risk for severe hyperbili?
– Late preterm
– Mom’s blood type
– Male
– 6 days old
Late preterm
And
Male
A little more history
• Baby is 3% down from BW currently drinking
breast and bottle. Baby looks “fine”. Why do
you think the baby has hyperbili?
•
•
•
•
Breastfeeding jaundice
Breastmilk Jaundice
Exaggerated physiologic jaundice
Other
• Exaggerated physiologic jaundice or other reason
What labs do you want?
CBCd
Retic
Direct bili
Type and cooms
• You get all because you don’t have a good
explanation for the high bili level. While you
are waiting for the results the nurse mentions
the baby has low tone. You go to examine the
baby and notice the baby does not suck much.
You look back at the vitals and note the temp
was low. You also notice his perfusion is poor.
What next?
Rule out Sepsis Evaluation!
• What would you order?
– LP
– CBCd
– Blood culture
– Urine culture
– CRP
• You correctly order the full workup. During
the tap the baby has respiratory arrest. You
then transfer to the NICU. In transport you
get a call that the CBC shows a white count of
3.7 but the smear says “many bacteria”. What
were your warning signs that this was not a
simple case of neonatal jaundice?
• Abnormal vital signs (low temp).
• No clear cause for jaundice (older baby, not
that far from BW, not a risk with mom blood
type)
• Poor perfusion.
Objectives reviewed
• Understand pathway where bilirubin comes
from
• Physiologic vs Pathologic Hyperbilirubinemia
• Understand the risk for Kernicterus
• Understand why we care about
hyperbilirubinemia
Questions?
References
Hyperbilirubinemia in the Newborn Infant >35 Weeks’ Gestation: An Update With Clarifications
M. Jeffrey Maisels Vinod K. Bhutani, Debra Bogen, Thomas B. Newman, MD, Ann R. Stark, and Jon F.
Watchko
PEDIATRICS Volume 124, Number 4, October 2009
Screening of Infants for Hyperbilirubinemia to Prevent Chronic Bilirubin
Encephalopathy: US Preventive Services Task Force Recommendation Statement
US Preventive Services Task Force Pediatrics 2009; 124;1172-1177
Neonatal Jaundice
M. Jeffrey Maisels
Pediatr. Rev. 2006;27;443-454
Trends in Hospitalizations for Neonatal Jaundice and Kernicterus in the United States, 1988_2005
Bryan L. Burke, James M. Robbins, T. Mac Bird, Charlotte A. Hobbs, Clare Nesmith and John Mick Tilford
Pediatrics 2009;123;524-532