Neonatal Jaundice, Hypoglycemia and Resus Flashcards
Outline Fetal Bilirubin metabolism, what is the way they removed it?
- Normal:
- haem - bilirubin, bound to albumin then gets to hepatoctye, gets conjugated, gets excreted into bile duct.
- Fetal:
- conjugation is rate limiting step - above 150 before you see something.
- unconjugated - enterohepatic circulation of bilirubin after birth (reabsorb) - bowel obstruction might get jaundiced.
- break down of haem - placenta to mother
- mother having high conjugated doesn’t cross placenta
What are the problems with neonatal jaundice?
- kerniterus - higher = worried about the sign.
- neurotoxic to grey matter (basal ganglia)
- signs of bilirubin encephalopathy:
- no feeding
- arching back/convulse (stop breathing/turn blue) - hypoxia
- type of cerebral palsy (athatoid - bulbar muscles so can’t talk, slow writhing movements, can’t hear - sensorineural deafness) - spastic the most common
- non verbal, deafness, intelligence not severely affected.
- erythroblastosis in the cord - cord is yellow.
What are causes of early onset rapidly rising bilirubin? What investigations and treatments would you use?
- hemolysis
- Antibodies:
- Anti-D
- ABO - most common because -most are IgM so don’t cross, some have IgD/E.
- Kell - more severe disease (16-18weeks gestation)
- Investigations:
- Kleihauer-Betke test = counts + fetal RBCs in materal blood - degree of haemorrhage.
- indirect coomb’s test = looks for maternal antibodies (titre)
- MCA PSV - will detect anaemia - if + use umbilical cord to measure Hb.
- treatment
- delivery
- blood transfusion (intravascular and peritoneum)
- Enzyme deficiency
- G6PD deficiency (anywhere equitorial)
- more common in males = XLR
- protective against malaria
- hemolysis triggered by (aspirin, naphthaline, moth balls, fava beans)
- membrane deficiency
- hereditary spherocytosis (autosomal dominant) - mum or dad can pass it on
- G6PD deficiency (anywhere equitorial)
- Antibodies:
- general investigations:
- bilirubin
- ABO
- direct antiglobulin test (direct coombs test)
- blood film (FBE) - funny shape
- Hb
- erythroblasts + reticulocyte count (left shift)
What are the causes of bilirubin rising late in neonatal babies?
- if bilirubin goes down then rises again its always disease state
- persisted - breastmilk jaundice
- conjugated
- galactosemia = cataracts, hypoglycemia, liver problems
- CF
- hepatitis virus
- parental nutrition
- unconjugated (G6PD)
- hypothyroidism = heel prick test, only measure TSH
- sepsis (septic ileus)
- bilieary atresia (present in 1month old)
- pale stools, dark urine, jaundice, FTT, sick
What do you do if the bilirubin is in the high but not too high? (3-4 day range (48-96hours)), what are the causes?
- dehydration/underfeeding = increased blood concentration - apparent jaundice
- weight drops too much
- stool fails to change colour (black to green to mustard)
- decreased wet nappies
- brusing (from traumatic delivery) - cephalohematoma
What is the treatment for bilirubinemia?
- most babies don’t require treatment
- monitor bilirubin (blue light threshold, exchange transfusion).
-
phototherapy (physical blue light, converts to isomered shape to get it into gut - get runny stools) - only unconjugated.
- complications (dehydration, hyperthermia)
- maxiamally exposed with covered eyes
-
exchange transfusion (340 or above) PIPER
- complications (acidosis pH=6.8 affects pulmonary ciruclation, calcium drops due to citrate (prevents clots), contamination
- 2 cycles of a kids whole blood - don’t tolerate well.
- citrate - binds calcium ions. Ionised calcium drop. Convulsions. Citrate part of Krebs cycle, converted to energy.
- stored for a few days pH drops - 6.8average. Pulmonary circulation (increased pul. vascular resistance, decreased oxygenation, increased pul HTN. desaturation).
- maths - wrong, not enough blood.
- inject viruses/bacteria.
- Air embolism, into a heart no circulation.
- catheter into umbilical vein.
- 2 cycles of a kids whole blood - don’t tolerate well.
- monitor SaO2 and give calcium
- complications (acidosis pH=6.8 affects pulmonary ciruclation, calcium drops due to citrate (prevents clots), contamination
After a normal vaginal delivery, a newborn has a normal check at 4 hours. He then has jaundice at 12 hours, but is otherwise normal. What is the most likely cause?
- normal physiological jaundice
- ABO incompatibility
- breast milk jaundice
- G6PD deficiency
- Infection
D - G6PD deficiency
Remeber when considering aetiology:
- too early = pathological if <24 hours
- too high = occuring within expected peak but too high (340)
- too late = >2-3weeks
This is too early <24 hours:
- hemolysis
- alloimmunization
- enzyme deficiency (G6PD - moth balls)
- membrane deficiency
Quickly summarise management of neonatal jaundice.
- jaundice in the first 24 hours is always pathological >35wks gestation:
- need to treat to avoid acute bilirubin encephalopathy (kernicterus - LT consequences - sensorineural, seizures, cognitive impairment, CP)
- rapid rise or >360micromol/L can cause it
- Screen with transcutaneous bilirubinometry (TcB)
- test the cord for DAT (direct antiglobulin - Coombs) - if + and jaundiced then do an immediate SBR.
- treatment - based on graph.
- phototherapy (1,2,3,4 lights, exchange transfusions)
- depends on 24hrs-14days.
- prolonged = 10% of babies ‘breast milk jaundice’, longer than 1 week assess
- conjungated = risk of biliary atresia, metabolic syndromes, hepatitis, liver failure.
- any age, rarely in first 24 hours.
What are some risk factors that predispose babies to hypoglycemia?
- GDM/DM (with uncontrolled hyperglycemia in labour or >7.5HbA1c)
- Preterm (<37weeks)
- SGA/IUGR (<2.5kg)
- macrosomia (>4kg)
What are some symptoms of hypoglycemia in neonates? What is the treatment?
- jittery or reduced GCS
- or measure BSL at 4 hours of age.
Management:
- TBG<1.5 - 40% glucose gel or IM glucagon
- 1.5-2.6mmol/L - then feed 2hourly, 90ml/kg/day
- >2.6mmol/L - feed 3 hourly
- bad - IV 10% glucose (can change volume/concentration)
- can’t do if less than 12.5% (blow line - central CVC instead) - transfer to a tertiary hospital.
don’t give glucagon to IUGR - less capacity.
if persistently low consider hyperinsulinism.
What are the principles of neonatal resuscitation?
- born:
- check gestation, breathing, tone - okay? give to mum
- no breathing/tone - check HR and give PEP
- check HR
- <100 - iPPV (intermittent positive pressure ventilation)
- <60 - compressions with 100% O2
- check 30seconds later - still bad
- increase pressure, increase oxygen
- check sats (always on right hand - branch to brain/right hand b4 ductus).
- check HR
- APGAR not super relevant. 1 minute (not for resus).