Neonatal Core Conditions Flashcards
What is Jaundice?
Jaundice is the yellow colouring of skin and sclera caused by the accumulation of bilirubin in the skin and mucous membranes.
How common is neonatal jaundice?
60% of term infants and 80% of preterm infants.
10% of breast fed babies are jaundiced at 1 month.
What is physiological jaundice?
Normal phenomenon in neonates, with no underlying pathology. High levels of unconjugated bilirubin. Presents in the first 2-7 days of life and usually resolves by 10 days.
What causes physiological jaundice?
-Marked physiological release of Hb from the breakdown of RBCs due to the high Hb conc at birth
-RBC lifespan of newborn infants (70 days) is much shorter than adults (120 days)
-Hepatic bilirubin metabolism is less efficient in the first few days of life
When is jaundice always pathological?
In the first 24 hours and if conjugated.
What are the main causes of jaundice in the first 24 hours?
-Neonatal sepsis
-Rhesus haemolytic disease
-ABO haemolytic disease
-Hereditary spherocytosis
-Glucose-6-phosphate dehydrogenase (G6PH) deficiency
What are the key causes of neonatal jaundice?
Increased production of bilirubin:
-Haemolytic disease of the newborn
-ABO incompatibility
-Haemorrhage
-Intraventricular haemorrhage
-Cephalo-haemorrhage
-Polycythaemia
-Sepsis and DIC
G6PD deficiency
Decreased clearance of bilirubin:
- Prematurity (immature liver)
-Breast milk jaundice
-Neonatal cholestasis
-Extrahepatic biliary atresia
-Endocrine disorders (hypothyroid and hypopituitary)
-Gilbert syndrome
-Neonatal hepatitis
When is jaundice classed as prolonged?
More than 14 days in full term. More than 21 days in premature babies.
What are key causes of prolonged jaundice?
-Biliary atresia
-Hypothyroidism
-Galactosaemia
-Haemolytic anaemia
-Infection (particularly UTI)
-Breast milk jaundice
-Prematurity
-High GI obstruction e.g. pyloric stenosis
-Congenital infections e.g. CMV, toxoplasmosis
How should jaundice be investigated?
Bilirubin:
- Transcutaneous bilirubinometer (TCB) in >35/40 gestation and >24hrs old.
-Serum bilirubin if <35/40 gestation, <24 hours old or TCB >250 ymol/L
Further:
-FBC (for Hb and haematocrit) anad blood film
-Direct antiglobulin test (Coombs’ test)
-TFTs
-LFTs
-U&Es
-Infection screen: blood, urine, CSF. Consider TORCH screen.
-G6PD levels
What is Gilbert’s syndrome?
Autosomal recessive disorder with reduced UGT enzyme ability to conjugate bilirubin, results in mild episodes or jaundice throughout life in response to certain triggers
What is Glucose-6-phosphate dehydrogenase (G6PD) deficiency?
X-linked recessive condition where lack of G6PD makes RBCs susceptible to oxidative damage and haemolysis. Can cause severe neonatal jaundice.
What is hereditary spherocytosis?
Inherited disease where defects in RBC skeletal proteins cause RBCs to assume a spherical shape with a reduced lifespan.
What is biliary atresia?
Congenital inflammatory disease of unknown cause. Results in complete obliteration of the extra-hepatic bile ducts after birth. Presents with prolonged conjugated jaundice, pale stools and dark urine.
How is neonatal jaundice managed?
Plot total bilirubin levels on treatment threshold chart. 2 options:
- Phototherapy - converts unconjugated bilirubin into isomers which are excreted in bile and urine without requiring conjugation in liver. Remove all clothing and use blue-light. Rebound level should be measured in 12-18 hrs to ensure levels haven’t risen above threshold levels.
- Exchange transfusion - not very common as high rate of complications. Swap the baby’s blood with donor blood. Required for dangerously high levels of bilirubin or if signs of bilirubin encephalopahy.
What is bilirubin encephalopathy (Kernicterus)?
Occurs with high levels of unconjugated bilirubin as can cross the blood-brain barrier. Accumulates in brain and is neurotoxic. Presents with lethargy, hypotonia and poor suck reflex (Floppy, drowsy, poor feeding). Progresses to hypertonia, opisthotonos, fever, seizures and high-pitched cry. Can lead to permanent damage causing cerebral palsy, learning disability and deafness. Rare due to effective treatment of jaundice.
When does a baby become clinically jaundiced?
At about 80 ymol/l
What are the causes of hypoxic ischaemic encephalopathy?
- Failure of gas exchange across the placenta: excessive or prolonged uterine contractions, placental abruption, ruptured uterus, placenta previa
-Interruption of umbilical blood flow - cord compression including shoulder dystocia, cord prolapse
-Inadequate maternal placental perfusion: maternal hypotension or hypertension
-Compromised fetus - intrauterine growth restriction, anaemia
-Failure of cardiorespiratory adaptation at birth - failure to breath
-Intrapartum haemorrhage
What are the stages of HIE?
Sarnat staging:
-Mild (grade 1) - poor feeding, general irritability and hyper-alert. Resolves within 24 hrs. Normal prognosis.
-Moderate (grade 2) - poor feeding, lethargic, hypotonic and seizures. Can take weeks to resolve, 40% develop cerebral palsy.
-Severe (grade 3) - reduced consciousness, apnoeas, flaccid and reduced/absent reflexes, multiorgan failure. 50% mortality, 90% develop cerebral palsy
How can HIE be identified?
aEEG (amplitude-integrated electroencephalogram) - detects abnormal background brain activity to confirm early encephalopathy and identify seizures.
How is HIE treated?
- Respiratory support, treatment of seizures, nutrition, acid base balance, circulatory support.
-Mild hypothermia. Cool down to 33-34 degrees (using cooling blanket and cooling hat, measured rectally) for 72 hours. Start cooling within 6 hours of birth.
What is the key complication of HIE?
Cerebral palsy
What is classed as premature?
Birth before 37 weeks gestation
What are the WHO stages of preterm delivery?
-Extreme preterm: before 28 wks
-Very preterm: 28-32 wks
-Moderate to late preterm: 32-37 wks
