Neonatal Jaundice, Hypoglycemia and Resus Flashcards

1
Q

Outline Fetal Bilirubin metabolism, what is the way they removed it?

A
  • 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
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2
Q

What are the problems with neonatal jaundice?

A
  • 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.
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3
Q

What are causes of early onset rapidly rising bilirubin? What investigations and treatments would you use?

A
  • 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
  • general investigations:
    • bilirubin
    • ABO
    • direct antiglobulin test (direct coombs test)
    • blood film (FBE) - funny shape
    • Hb
    • erythroblasts + reticulocyte count (left shift)
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4
Q

What are the causes of bilirubin rising late in neonatal babies?

A
  • 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
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5
Q

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?

A
  • 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
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6
Q

What is the treatment for bilirubinemia?

A
  • 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.
    • monitor SaO2 and give calcium
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7
Q

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?

  1. normal physiological jaundice
  2. ABO incompatibility
  3. breast milk jaundice
  4. G6PD deficiency
  5. Infection
A

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
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8
Q

Quickly summarise management of neonatal jaundice.

A
  • 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.
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9
Q

What are some risk factors that predispose babies to hypoglycemia?

A
  • GDM/DM (with uncontrolled hyperglycemia in labour or >7.5HbA1c)
  • Preterm (<37weeks)
  • SGA/IUGR (<2.5kg)
  • macrosomia (>4kg)
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10
Q

What are some symptoms of hypoglycemia in neonates? What is the treatment?

A
  • 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.

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11
Q

What are the principles of neonatal resuscitation?

A
  • 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).
  • APGAR not super relevant. 1 minute (not for resus).
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