Jaundice (paeds) Flashcards
What are some benign causes of newborn jaundice?
Physiological - due to haemolysis of foetal haemoglobin, unable to be processed by the liver fast enough
Breast feeding jaundice - seen in breastfed babies during the first week of life. It is more likely to occur when babies do not nurse well or the mother’s milk is slow to come in
Breast milk jaundice - may appear in some healthy, breastfed babies after day 7 of life; likely to peak during weeks 2 and 3, but may last at low levels for a month or more - may be due to how substances in the breast milk affect the breakdown of bilirubin in the liver
What are some more concerning forms of newborn jaundice?
Red cell diseases e.g. sickle cell anaemia
Blood type mismatch between the mother and baby - Rh incompatibility
Bleeding underneath the scalp (cephalohematoma) caused by a difficult delivery
Polycythemia - more common in babies small-for-gestational age and some twins
Infection
Genetic diseases
Also things like liver problems, newborn infections and hypoxia can make bilirubin clearance harder
What is ABO incompatibility?
ABO incompatibility happens when a mother’s blood type is O, and her baby’s blood type is A or B
The mother’s immune system may react and make antibodies against her baby’s red blood cells
The consequences and treatment are similar to Rhesus disease
What is rhesus haemolytic disease? How is it prevented?
Mother Rhesus negative, baby rhesus positive
Mum undergoes a sensitising event in pregnancy:
Invasive prenatal diagnosis - eg, amniocentesis, chronic villus biopsy
Antepartum haemorrhage
External cephalic version of the fetus (including attempted)
Ectopic pregnancy
Evacuation of molar pregnancy
Intrauterine death and stillbirth
Intrauterine procedures (eg, insertion of shunts, embryo reduction)
Miscarriage or threatened miscarriage after 12 weeks of gestation
Therapeutic termination of pregnancy
Delivery - normal, instrumental or caesarean section
Mum creates antibodies against foetus blood, leading to = haemolytic disease of the newborn
In order to stop this, following potentially sensitising events, it is recommended that anti-D Ig should be administered as soon as possible and always within 72 hours of the event
Anti D also given to Rh-ve mothers routinely in the 3rd trimester - given at 28wks - to prevent ‘silent’ sensitisation; it is not offered to women who have already been sensitised
Kleihauer test - assesses extent of foetal-maternal blood mixing; Direct Coombs test - detects antibodies that are stuck to the surface of the red blood cells
After a Kleihauer test, anti-D should be given to every non-sensitised RhD-negative woman, within 72 hours of delivering a rhesus-positive infant; if the pregnancy is stillborn (and no sample can be obtained from the baby), anti-D should be given
What are different causes of jaundice by age?
<24hrs - always pathological:
ABO incompatibility
Rhesus haemolytic disease (Coombs test +ve)
Glucose-6-phosphate dehydrogenase/G6PD deficiency (blood film - bite+blister cells)
Spherocytosis (blood film - spherocytes)
Congenital infection (CMV, toxoplasmosis)
24hrs-3wks Haemolytic disease Slow burning infection e.g. UTI Polycythaemia Physiological or breast milk jaundice Biliary atresia (will be conjugated jaundice)
>3wks Infection Physiological Hypothyroidism Liver diseases (will be conjugated?)
What is kernicterus?
Buildup and deposition of unconjugated bilirubin in the basal ganglia (as can cross BBB)
Serious as can impact feeding/growth right up to causing seizures and death if untreated
How should you assess jaundice?
In natural light - not incandescent
Jaundice spreads from head to toes so highest concentrations/most obvious should be head (also sclera); also recedes in reverse
Transcutaneous bilirubinometer - can give a skin reading of jaundice level - not particularly sensitive as has an error range of 50: if within 50 below the treatment line, will need a serum bilirubin to confirm; if greater than 50 below the treatment line then can accept the reading (e.g. unlikely jaundice)
Other assessment:
FBC - signs of sepsis? low haematocrit? (haemolytic anaemia)
Blood film - specific pathological cells or evidence of haemolysis
Blood group - of mother an baby
Direct Coombs’ test - Rh/ABO incompatability
LFTs - may be increased in congenital infection
G6PD levels - deficiency?
Cultures (blood/urine/CSF) if infection suspected; TORCH screen
How do you manage jaundice?
SBRs are plotted on a graph to track progress
Phototherapy = 1st line; can add as many lights as you need to try to get the bilirubin down by covering as much surface area a possible
Exchange transfusion line - involves replacing 1/3 infants blood with donor blood, through umbilical artery/vein; really want to avoid - takes 1-2hrs, needs constant supervision by doctor, central lines, sterile field, risks of blood (anaphylaxis etc)
Treat any underlying infections
Early surgical referral for biliary atresia
How does phototherapy work? What are some side effects?
Breaks down deposits of unconjugated bilirubin into products that are more easily excreted in urine and faeces
SE: dehydration, loose stools, separation from mother
What is prolonged jaundice?
Any jaundice >2wks in term infants; >21 days in prems
Could be physiological but other pathology:
Investigations:
Split bilirubin - raised conjugated could be biliary atresia = emergency surgical referral
LFT - raised in infections
FBC - anaemia?
Blood film - sickle? Bite/blister? Spherocytes?
TFT - hypothyroidism
Urine MC+S - low lying grumbling UTI, poss secondary to renal malformation
What is biliary atresia?
Failure of the development of part of the biliary tree - an extrahepatic obstruction
Presentation: pale stools + dark urine + failure to thrive ; risk of cirrhosis if untreated
Investigation: radioisotope scan and liver biopsy
Management: biliary shunt - Kasai procedure (though shunts often fail too); ursodeoxycholic acid - for symptoms + hepatoprotective; liver transplant
