Neonatal Jaundice

Question 1

What are the types of neonatal jaundice?

Answer 1

Physiological - unconjugated

Pathological - unconjugated/conjugated

Question 2

What is physiological jaundice due to?

Answer 2

Increased bilirubin production in neonates due to shorter RBC lifespan - high concentration of Hb breaks down releasing
Decreased bilirubin conjugation due to hepatic immaturity
Absence of gut flora impedes elimination of bile pigment
Exclusive breastfeeding (esp. if there are feeding difficulties -> reduced intake -> dehydration -> reduced bilirubin elimination -> increased enterohepatic circulation of bilirubin

Question 3

Describe the course of physiological jaundice

Answer 3

Starts at day 2-3, peaks at day 5, usually resolved by day 10
Can progress to pathological jaundice if baby is premature or there is increased red cell breakdown

Question 4

What can pathological jaundice be due to?

Answer 4

Sepsis

Haemolytic disease:
Rhesus, ABO incompatibility, Red cell anomalies Congenital spherocytosis, G6PD-deficiency

Dehydration

Metabolic: hypothyroid, galactosaemia
Breast milk jaundice
GI: biliary atresia

Question 5

What is prolonged jaundice? What can cause this?

Answer 5

Jaundice for over 14 days or 21 days in poems

Causes:
Breastfeeding
Sepsis
Hypothyroidism
CF
Biliary atresia if conjugated and pale stools
Galactosaemia

Question 6

What are risk factors for pathological jaundice

Answer 6

Prematurity
Low birth weight
Small for dates
Previous sibling requiring phototherapy
Exclusively breast fed
Jaundice < 24 hours
Diabetic mother

Question 7

What are clinical features of hyperbilirubinaemia?

Answer 7

Yellow discolouration
Drowsy - difficult to rouse, not waking for feeds, very short feeds
Neurologically - altered muscle tone, seizures - require immediate attention
Other: signs of infection, poor urine output, abdominal mass

Question 8

What investigations in neonatal jaundice?

Answer 8

Serum bilirubin if:
<35/40, <24hours old, or transcutaneous bilirubin >250micromol/L

Maternal blood group, baby blood group

Direct Coomb’s test for Rh haemolytic disease

FBC for haemoglobin and haematocrit
with blood film

U&E if excessive weight loss/dehydrated

Infection screen if unwell or < 24 hours

G6PD

LFT if hepatobiliary disorder

TFTs

Question 9

What is management for neonatal jaundice?

Answer 9

Refer to treatment threshold graph for neonatal jaundice

Phototherapy if above or on phototherapy line for their gestation and age in days

Exchange transfusion via umbilical artery or vein if on or above threshold line.

IV immunoglobulin can be used as adjunct to intensified phototherapy in Rh disease/ABO incompatibility.

Question 10

Describe phototherapy.
What if neonate is below phototherapy threshold?
How often should bilirubin be monitored during treatment?
When should phototherapy be stopped?

Answer 10

If <50micromol/L below line, repeat level within 18 hours (if risk factors) to 24 hours (no risk factors)
Ultraviolet isomerisation of bilirubin to its soluble for for excretion

During photo therapy:
Repeat bilirubin 4-6 hours post initiation to ensure no still rising, 6-12 hourly once level is stable or reducing

Stop phototherapy once level is >50micromol/L below treatment threshold
Check for rebound hyperbilirubinaemia 12-18h after stopping

Question 11

What is exchange transfusion?

Answer 11

Simultaneous exchange of baby’s blood with donated blood or plasma to prevent further bilirubin increase and decrease serum bilirubin levels.
Warme blood
Given ideally via umbilical vein IVI and removed via umbilical artery

Usually done when there are signs of acute bilirubin encephalopathy

Question 12

What is kernicterus?

Answer 12

Acute bilirubin encephalopathy
Lethargy
Poor feeding
Hypertonicity
Opisthotonus
Shrill cry

Chronic bilirubin encephalopathy

Yellow staining in the brain

Accumulation of bilirubin in the CNS grey matter causing irreversible neurological damage

Long term sequelae - athetoid movements, deafness, and low IQ
Prevented by phototherapy ± exchange transfusion

Question 13

Describe Rhesus haemolytic disease

Answer 13

When RhD-ve mother delivers RhD+ve baby, leak of fetal red cells into her circulation may stimulate her to produce anti-D IgG antibodies.
In subsequent pregnancies these can cross the placenta causing worsening Rh haemolytic disease in Rh+ve pregnancies

First pregnancies may be affected due to leaks - threatened miscarriage, APH, Mild trauma, amniocentesis, chorionic villous sampling

Question 14

What are signs of Rh disease

Answer 14

Jaundice on day 1
Yellow vernix (greasy covering of baby)
CCF (oedema, ascites)
Hepatosplenomegaly
Progressive anaemia
Bleeding
CNS signs
Kernicterus

Question 15

How is Rh disease managed?

Answer 15

Test for D antibodies in all Rh-ve mothers

Phototherapy (isomerisation of bilirubin to its soluble form)
Give extra water
Avoid heat loss
Protect the eyes
Keep baby naked
Keep breastfeeds short to maximise time under lights

Exchange transfusion:
If HB<7g/dl
Keep baby warm

Question 16

What is hydrops fetalis?

Answer 16

Severely affected oedematous fetus with stiff oedematous lungs is called a hydrops fetalis.

Anaemia associated CCF causes oedema as does hypoalbuminaemia (liver is preoccupied by producing new RBCs)

Question 17

Mx of hydrops fetalis?

Answer 17

take cord blood for Hb, PCV, bilirubin (conjugated and unconjugated), blood group, Coombs, serum protein, LFT and infection screen to find cause
- isoimmunisation, thalassaemia, infection, toxoplasmosis, syphilis, parvoviruses, maternal diabetes, hypoproteinaemia

Expect need to ventilate with high inspiratory peak pressure and positive end pressure
Monitor plasma glucose 2-4 hourly, treating any hypoglycaemia
Drain ascites, pleural effusions
Correct anaemia
Vitamin K to reduce risk of haemorrhage
Furosemide if CCF is present
Limit IV fluids

Question 18

Describe biliary atresia. Management?

Answer 18

Biliary tree occlusion
Jaundice, dark urine and pale stools
Spleen becomes palpabils
Early surgery