neonatal jaundice Flashcards

1
Q

what is jaundice

A

yellowing of the skin and sclera

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2
Q

what causes jaundice physiologically

A

due to high levels of bilirubin in blood

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3
Q

is the pathological or physiological in new borns

A

mainly physiological

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4
Q

-

A

-

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5
Q

what is gliberts disease

A

certain enzyme abnormalities which affects conjugation
mutation of UGT1A1 gene - reduces bilirubin uridine diphosphate glucuronosyltransferase by around30% (bilirubin-UGT) and can make jaundice worse

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6
Q

what can bilirubin crossing the BBB cause

A

encephalopthay which can lead to kernicterus

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7
Q

what is there a small risk of with high levels of bilirubin

A

cerebral palsy

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8
Q

what hours of birth is jaundice become pathological?

A

if still occuring late >14 weeks in term and 21 days in preterm
due to haemolysis, sepsis, metabolic disorders, liver disease

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9
Q

why does physiological jaundice develop?

A

increased productino; foetal RBC life span 2/3 of adults, high hct, brusing
decreased uptake and binding by liver cells
decreased conjugation
decreased excretion
increased enterohepatic circulation of bilirubin

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10
Q

to early jaundice is almost always pathological, what is this due to?

A

haemolysis, with excessive production of bilirubin, sepsis could be an underlying cause

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11
Q

when can babies be born with jaundice

A

severe haemolysis

hepatits

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12
Q

causes of haemolysis

A

ABO incompatibility
Rh immunisation
sepsis

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13
Q

how do you investigate early pathological jaundice?

A

total bilirubin conc (SBR)
maternal blood group and antibody titres (if Rh neg)
baby blood group, direct agglutination test, elution test to detect antiA or antiB antibodies on babys red cells
FBC - evidence of haemolysis
CRP - infection?

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14
Q

haemolysis investigations

A

blood group incompatibility (commonly with rhesus or ABO) identified with a positive direct agglutination test (DAT)or due to a glucose 6 phosphate dehydrogenase deficiency

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15
Q

haemolysis investigations

A

blood group incompatibility (commonly with rhesus or ABO) identified with a positive direct agglutination test (DAT)or due to a glucose 6 phosphate dehydrogenase deficiency

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16
Q

features of bilirubin encephalopathy

A
lethargy
poor feeding
temp instability
hypotonia
arching of the head, neck, and back
spasticity
seizure
17
Q

causes of SBR being too high

A
mild dehydration/insufficient milk supply
breakdown of extravasated blood
haemolysis
infection
increased enterohepatic circulation
17
Q

causes of SBR being too high

A
mild dehydration/insufficient milk supply
breakdown of extravasated blood
haemolysis
infection
increased enterohepatic circulation
18
Q

causes of persistent unconjugated hyperbilirubinaemia

A
breast milk jaundice
poor milk intake
haemolysis
infection
hypothyroidism
19
Q

causes of persistent conjugated hyperbilirubinaemia

A

hepatitis - infection or metabolic disorders

biliary atresia - pale stools dark urine, surgery with a kasai portoenterostomy before 3 months of age

20
Q

causes of persistent unconjugated hyperbilirubinaemia

A

hypothyroidism - persistent jaundice is the earliest sign
breast milk jaundice - normal conjugated portion, normal FBC and blood group to exclude haemolysis, no sign of infection UTI, thriving, reassurance

21
Q

treatment of jaundice

A

treat cause
adequate feeding
enteral feeding is best in order to reduce enterohepatic circulation of bilirubin
PHOTOTHERAPY - bluelight
exchange transfusion for haemolytic disease
IV IMMUNOGLOBULIN with imfants with isoimmune haemolytic disease and rising bilirubin despite intensive phototherapy

22
Q

onset day 1, peak variable, prolonged after day 14

symptoms and signs of aetiological cause eg lethargy for sepsis; pale stool for hepatitis

A

likely pathological

23
Q

onset day 2
peak day 5
resolve day 10-14
otherwise well

A

physiological