Neonatal/Infant Jaundice - Neonatal sepsis, Hereditary spherocytosis, G6PD deficiency, Biliary atresia, Congenital hypothyroidism, TORCH, Physiological, Breastfeeding, Breastmilk Flashcards

1
Q

Neonatal sepsis
-casusative organism
-risk factors
-why jaundice?

A

GBS - within 1st 72hrs of life
-transmitted from mother to neonate in delivery

Current maternal GBS colonisation
-prenatal screening
-current bateruria
-intrapartum temp 38C+
-membrane rupture 18hrs+
-current infection throughout pregnancy
Premature
Low birth weight (U2.5kg)
Maternal chorioamnionitis

Sepsis affects liver’s ability to break down conjugated bilirubin

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2
Q

Neonatal sepsis
-presentation
-investigations
-management

A

Resp distress
HighHR, apnoea
Change in MS, lethargy
Jaundice
Temp can vary - febrile <=> hypothermic
Symptoms relating to source of infection

FBC - can exclude healthy neonates
CRP
Blood gas - metabolic acidosis
Blood culture - establish diagnosis
Urine MCS if urinary source
LP if meningitis source

IV benpen + gent unless resistant
CRP remeasured in 18-24hrs to monitor progress and guide duration of therapy
-if U10 and -ve culture => stop ABx at 48hrs
-otherwise, guided by investigations and clinical picture

Supportive
-O2, fluids and electrolytes
-prevent and manage hypoglycemia, metabolic acidosis

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3
Q

Jaundice in the 1st 24hrs
-causes

A

ALWAYS PATHOLOGICAL
Hemolytic blood issues
-Rhesus hemolytic disease
-ABO hemolytic disease
-hereditary spherocytosis
-glucose 6 phosphodehydrogenase deficiency

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4
Q

Hereditary spherocytosis
-what is it
-presentation
-investigations
-management

A

AD defect of RBC cytoskeleton => sphere shaped RBC
-lifespan reduced as destroyed by spleen => non conjugated bilirubin rises
Northern EU

Failure to thrive
Jaundice, gallstones
Splenomegaly - as RBCs destroyed sooner
Aplastic crisis triggered by parvovirus infection

If FHx
-clinical picture
-lab results (spherocytes, high MCHC, high reticulocytes

If unclear => EMA binding and cryohemolysis test

Acute hemolytic crisis
-supportive
-transfuse if needed

Long term
-folate
-splenectomy

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5
Q

G6PD deficiency
-what is it
-presentation
-hemolysis triggering drugs
-investigations
-management

A

X linked defect
-low G6PD => increased red cell susceptibility to oxidative stress

Jaundince
Intravascular hemolysis
Gallstones
Splenomegaly
Heinz bodies - tiny red dots of hemoglobin
Bite and blister cells - spleen removes Heinz bodies

Antimalarials - primaquine
Ciprofloxacin
Sulph drugs
Infection
Fava beans

G6PD assay done after 3 months of acute hemolysis - prevent false negative results

Treat jaundice symptoms
-phototherapy
-exchange transfusion - remove affected blood, replace with healthy blood

Avoid triggering drugs and fava beans

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6
Q

Jaundice in 2-14days
-causes

A

Physiological
-babies are born with more Hb, gets broken down
-alongside developing liver function

Breastmilk jaundice
-breastmilk substance inhibits liver’s ability to conjugate bilirubin

Breastfeeding jaundice
-not enough breastmilk + greater absorption of conjugated bilirubin
-resolved with more breastfeeding

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7
Q

Prolonged jaundice in 14days+
-causes

A

Biliary atresia - high conjugated bilirubin

Hypothyroidism - high unconjugated bilirubin
-UTD activity low => harder to conjugate bilirubin

Prematurity - immature liver function
-prolonged jaundice defined at 3wks after birth

TORCH infections

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8
Q

Biliary atresia
-what is it
-presentation
-investigation
-management
-complications

A

Obliteration/discontinuation of extrahepatic biliary system => cholestasis

Jaundice beyond physiological 2wks
Dark urine, pale stool
Appetite, growth disturbance

Hepatosplenomegaly
Abnormal growth

LFT
-high conjugated bilirubin
-cholestatic picture
a1at deficiency
Sweat chloride test - CF often involves biliary tract
Biliary and liver US => distension, tract abnormalities

VITAL TO PICK UP WITHIN 2WEEKS => REQUIRES URGENT SURGERY
-if missed, must wait for transplant, there is no interim treatment

Definitive - surgical recontruction
Medical ABx and bile acid enhancers postop

Surgical failure, may need transplant
Progressive liver disease => cirrhosis, hepatocellular carcinoma

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9
Q

Congenital hypothyroidism
-why does this happen
-presentation
-screening
-management

A

Thyroid underdeveloped/,issing/not producing thyroxine

Prolonged neonatal jaundice
Delayed mental and physical milestones
Short
Puffy face, macroglossia
Hypotonia

Heel prick test 5-7days

Levothyroxine

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10
Q

TORCH infection
-what are they
-presentation

A

Toxoplasmosis
Other infections (HIV, parvovirus, varicella, Zika)
Rubella
CMV
Herpes

Can be passed onto baby via
-placental
-vaginal delivery
-breastfeeding

Common features
-fever, difficulty feeding
-jaundice
-low birth weight
-hearing impairment
-PDA
-purpura, blueberry rash
-hepatosplenomegaly
-cataracts
-microcephaly

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