Neonatal Jaundice Flashcards
When is jaundice pathological and when not?
Pathological if 24hrs may be physiological or pathological
Blanch skin at chest in natural light, it would look yellow.
Jaundice visible when bilirubin >40 minimol/l
Why is jaundice common in infants?
- Neonates have more RBCs in few days of life and when get destroyed Hb falls
- Half life of RBCs in neonates (70days) instead of 120.
- Immaturity of hepatic bilirubin metabolism: less efficient bilirubin uptake, comjugation + excretion
- Breastfeeding excluselvy unknown why
Which babies are at risk of developing sign hyperalbuminaemia?
Gestational age
Some causes of conjugated bilirubun in neonates?
Bile duct obstruction, eg biliary atresia
Cong infx : TORCH: Toxoplasmosis, other( Rubella, syphillis, CMV, HIv)
Sepsis
Neonatal hepatitis
Inborn error of metabolsm- galactosaemia, tyrosinosis
Whats bilirubin?
Lipid soluble, glucuronic acid in liver metabolised it to water soluble from body.
Once conjugated, goes into bile, excteted into small intestine and stool. Conjugated hyperbilirubinaemia is due to illness that reduce secretion rate of bilirubin into bile, or slow the flow of bile into intestines.
Biliary atresia: conjugated hyperbilirubinaemia. Inflammation of large bile duct outside liver. Pale stools and dark urine. Early dx: vital 8w of age improves outcome. Main cause of chronic cholestatic disease in children+ common liver transplant reason.
When does unconjugated hyperbilitubinaemia occur in neonates?
Too much bilirubin production- haemolysis- Rhesus and ABO incompatibility, spherocytosis, G6PD deficiency
F of bilirubin uptake (Gilbert syndrome)
Impaired bilirubin conjugation (Crigler Najjar syndrome)
Others: physiological or breast milk jaundice
Whats thenDirect Coombs Test? DCT
Direct antiglobulin test- detects the presence of antibody-coated red cells
This indicated immune-mediated haemolysis - Rhesus or ABO incompatibility
When is ABO incompatibility indicated?
Reduced Hb, elevated unconjucated bilirubin, midly +ve Coombs test.
Confirmed by maternal blood group O and neonatal blood group A.
Mum: will have anti-A and anti-B IgG abxs which can cross the placenta and cause immune mediated haemolysis.
Rhesus? Not possible if blood film N, making spherocytosis unlikely.
Light- blue and white converts by photodegation- into harmless water sol sybstances–> urine and bile.
How does phototherapy work?
What happens if unconjugated bilirubin reaches too high levels?
Neurotoxic
Kernicterus
Give some CFs of kernicterus and why?
Opithotonus (arched back) Seizures Poor feeding Low muscle tone Poor Moro response Sleepiness High pitched crying Irritability
Unconjugated bilir- lipid soluble- when levels exceed the binding capacity of albumin, they cross they BBB. Deposition in bAsal ganglia and brainstem -> neuro consequenses-> kernicterus- can have permanent damage.
What are the RFs and early dx signs for kernicterus?
RFs: serum bilirubin >340mmol/l
Rapid rising bilirubin >8.5 mmol/hr
Early signs: 3-4Days after birth
What are some complications of kernicterus?
Learning difficulties
Enamel dysplesia
CP ‼️ eg dyskinesia CP due to bilir. Deposition in basal ganglia: ataxia and choreathetosis)
Sensorineural deafness: undergo hearing tests (brainstem evoked audiometry) before discharge.
Appear 18-24hrs .
If phototherapy worksA folic acid later.
Followed up in clinic in 2w for FBC to ensure haemolysis not hapoeninh.