Download 3.1 Jaundice Management guidelines

3.1
JAUNDICE
1. Physiological Jaundice
• Occurs between day 2 and day 10 usually peaking about day 5
• Due to delayed maturation of conjugation, with bilirubin production exceeding
excretion, hence conjugated fraction of bilirubin is never raised.
• Is exacerbated by:
• Polycythaemia , e.g. delayed cord clamping, materno-fetal transfusion,
recipient of twin-to twin transfusion.
• Extravasated blood eg cephalhaematoma .
• Delayed passage of meconium or delay in establishing enteral feeding
• Swallowed blood
• Prematurity
• Breastfeeding
• Physiological jaundice does NOT imply that the bilirubin level does not require
treatment, should it exceed phototherapy or exchange levels.
2. Pathological Jaundice (jaundice due to an underlying pathological cause)
The following are associated with pathological jaundice until proven otherwise:
• Jaundice within the rst 24 hours.
• Prolonged jaundice (>14 days term, > 21 days preterm infants)
• Jaundice in a sick baby
• Jaundice requiring an exchange transfusion.
• Rapidly rising bilirubin (> 0.3 mgdL/hour)
• Conjugated bilirubin > 10% of the total (or > 2mg dL)
1)Investigations: Early onset jaundice (1st 24 hours)
Early onset jaundice is usually due to haemolysis
1st line:
• ALWAYS consider infection and a full septic screen.
• Group and Coombs: for Rhesus, ABO, Kell and others.
• FBC and lm: help diagnose haemolysis, and red cell abnormalities such as
spherocytosis.
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2nd line:
• Red cell enzyme abnormalities: Glucose-6-phosphate-dehydrogenase
deciency (G-6-PD) Most common in babies of Mediterranean, African or Asian
origin, and in boys. Important to diagnose, as exposure to certain foods (e.g.
ava beans) and drugs (e.g. aspirin, Chloroquine, see table below for more
comprehensive list) will trigger haemolysis.
• Urine for reducing substances (galactosaemia). Galactosaemia is due to a
deciency of Galactose-1-phosphate uridyl transferase, which helps break
down galactose, a monosaccharide found in milk. The jaundice associated with
Galactosaemia is unconjugated in the rst week, and conjugated thereafter.
Infants with Galactosaemia usually become acutely unwell after starting milk
feeds.
• Urine for CMV, serology for Syphilis , Toxoplasmosis , Rubella , Herpes and
Hepatitis (congenital infection screen).
Common Medicines/foods associated with haemolysis in G6PD deciency
Antibiotics
Others
Antimalarials
Sulphonamides,
Methylene blue
Primaquine
e.g. Co-trimoxazole
Napthalene (mothballs)
Pamaquine
Quinolones
Aspirin
e.g. Ciprooxacin,
(doses up to 1gram a day Quinine
Nalidixic Acid
may be tolerated) Quinidine
Nitrofurantoin
Menadione
Chloroquine
Dapsone and other
(water soluble vitamin K)
(but these 3 may be
sulphones
acceptable in severe
malaria)
Note: Phytomenadione
(used in neonates) NOT
contra-indicated
2)Investigations: Late onset jaundice (>14 days term, >21 days preterm) or early
conjugated hyperbilirubinaemia
1st line:
• Split Bilirubin: only a few causes of late onset unconjugated
hyperbilirubinaemia e.g. hypothyroidism, hypopituitarism, Tyrosinosis. For
conjugated hyperbilirubinaemia think of surgical causes such as bile duct
obstruction, choledocal cyst (pale stools and dark urine). The commonest
neonatal cause remains long term TPN.
• Liver function tests: a rising trend in gGT indicates cholestasis.
• Thyroid function test
• FBC and lm
• Urine culture for UTI
• Urine for reducing substances (galactosaemia)
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2nd line:
• INR
• CF screen (DNA)
• a-1- antitrypsin assay/phenotype
• Urine for CMV, serology for syphilis, Toxoplasmosis, Rubella, Herpes and
Hepatitis
• Serum amino acids (Tyrosinosis, Hypermethioninaemia)
• Liver ultrasound: for surgical cause such as biliary atresia or choledocal cyst
• Plasma cortisol
• If necessary, further tests, particularly radiological tests. These should be
discussed with the paediatric hepatology team at Kings College Hospital.
For babies with cholestatic jaundice, additional supplements/medicines may need to
be considered:
• Ketovite liquid/tablets
• Vitamin K
• Ursodeoxycholic acid
• Medium chain triglyceride based infant formula for those not being breastfed.
3.Treatment of unconjugated hyperbilirubinaemia – phototherapy, exchange
transfusion
1)Phototherapy
• Phototherapy should be started when the serum bilirubin (SB) rises above the
phototherapy chart for age and gestation. For an otherwise well baby, this
should be provided at the mother’s bedside.
• Doctor should write instructions about timing (usually 4-6 hourly) of
SB measurements in the notes.
• Transfer to NNU may be appropriate if concerned about rapidly rising bilirubin
/state of hydration of the baby, or biliruin >20 mg/dL (especially if drowsy).
• Discontinue phototherapy when there have been 2 bilirubin levels
below the phototherapy line.
• Babies may be discharged if the bilirubin level has remained stable 12 hours
after phototherapy has been discontinued.
• For babies who suffered from haemolytic jaundice, (Rhesus, ABO, Kell),
consider Folic acid 2.5 mg/day at discharge. A repeat comple hameogram
should be done at 2-3 weeks for late anaemia, with review in the neonatal
clinic the next week.
2)Exchange transfusion :
Indications
• Rapidly rising bilirubin (> 0.3-0.6 mg dL/ hour)
• Rapidly falling haemoglobin in the context of immune haemolysis (cord blood <
10 g/dl or < 8 within 1st week)
• Bilirubin level above ‘exchange line’ on chart.