Neonatal and Newborn Flashcards

1
Q

What % of babies are visibly jaundiced in the first week of life?

A

50%

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2
Q

What is jaundice?

A

Jaundice = state of hyperbilirubinaemia

Serum bilirubin exceeds 85μmol/L

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3
Q

Describe the stages of bilirubin metabolism

A

1) Haemoglobin (from RBCs) is broken down into haem and iron in the spleen
2) Bilirubin is the main breakdown product of haem
3) Unconjugated bilirubin = lipid soluble. It is transported round the blood bound to albumin
4) In the liver, it is actively transported into hepatocytes where it is conjugated with glucoronic acid by the enzyme UDPGT
5) Conjucated bilirubin = water soluble. It is stored in the gallbladder and excreted as a component of bile
6) Bile is broken down by gut bacteria into stercobilinogen and urobilinogen
7) A small amount of urobilinogen is reabsorbed and then excreted by the kidneys

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4
Q

What are the 3 types of jaundice?

A

1) Pre-hepatic
2) Hepatocellular / intrahepatic
3) Post-hepatic

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5
Q

Outline what pre-hapatic jaundice is

What levels would be raised?

A

Excessive RBC breakdown overwhelms the livers ability to conjugate bilirubin

= Unconjugated hyperbilirubinaemia

Any bilirubin that managed to become conjugated will be excreted normally, it is unconjugated bilirubin that remains in the blood stream to cause jaundice

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6
Q

Outline what hepatocellular / intrahepatic jaundice is

What levels would be raised?

A

Results from dysfunction of the liver itself. Damaged hepatocytes lose the ability to metabolise and excrete bilirubin

= Unconjugated hyperbilirubinaemia

The small bile ducts may also become damaged or obstructed, meaning conjugated bilirubin leaks into the blood

= Conjugated hyperbilirubinaemia

Thus hepatic jaundice = MIXED PICTURE

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7
Q

Outline what post-hepatic jaundice is

What levels would be raised?

A

Obstruction of biliary drainage

= Conjugated hyperbilirubinaemia

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8
Q

What is physiological jaundice in a neonate?

A

= Slow change to conjugation

In foetus, bilirubin stays unconjugated to allow placental excretion

After birth, conjugation and hepatic excretion takes over

If this happens slowly = physiological (hepatocellular) jaundice

THIS IS NOT PATHOLOGICAL

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9
Q

Is jaundice within the first 24 hours of life concerning?

A

YES

JAUNDICE WITHIN THE FIRST 24HRS OF LIFE IS ALWAYS PATHOLOGICAL

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10
Q

What are some causes of neonatal jaundice <24hrs? (Unconjugated and conjugated)

A

Unconjugated:

  • Haemolytic disease
  • Neonatal Sepsis

Conjugated:

  • Neonatal hepatitis
  • Congenital infections (rubella, CMV, syphilis)
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11
Q

What are some causes of neonatal jaundice 24hrs - 2 weeks? (Unconjugated and conjugated)

A

Unconjugated:

  • Physiological (exacerbated by bruising, polycythaemia, dehydration)
  • Hypothyroidism
  • Haemolysis / sepsis

Conjugated:

  • Neonatal hepatitis
  • Congenital infections (rubella, CMV, syphilis)
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12
Q

What are some causes of neonatal jaundice >2 weeks? (Unconjugated and conjugated)

A

Unconjugated:

  • Breast milk jaundice
  • Haemolysis / sepsis
  • Hypothyroidism
Conjugated:
- Biliary atresia
- Choledochal cyst
- Neonatal hepatitis
(alpha-1 antitrypsin, TORCH, galactosaemia, CF)
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13
Q

What is breast feeding jaundice and what is breast milk jaundice?

A

Breast feeding jaundice = failure to establish breast feeding and so child dehydrated (thus less bilirubin excreted in urine so builds up)

Breast milk jaundice = substance passes through breast milk into baby which increases activity of glucouronidase, leading to build up of bilirubin NB not a reason to stop breast feeding

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14
Q

Jaundice within first 24 hrs is usually due to haemolysis. List 3 causes of haemolysis leading to neonatal jaundice

A

1) ABO incompatibility
- mOther has antibodies against bAby

2) Rhesus
- Rh-ve mother exposed to Rh+ve red cells during first pregnancy. In following pregnancy, she produces anti-D which breaks down child’s red cells = alloimmunisation

3) G6PD deficiency
- Lack of G6PD leads to rapid haemolysis during oxidative stress eg infection, medication, lava beans (X- linked recessive)

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15
Q

List some risk factors for neonatal jaundice (5)

A

1) Premature / low birth weight
2) Breast-fed babies
3) Diabetic mother
4) Male
5) East Asian ethnicity

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16
Q

How may physiological jaundice present?

A

Not apparent in first 24 hours, usually presents at 2-3 days

  • Child remains well
  • Serum bilirubin remains below treatment level
  • Jaundice fades by 14 days
17
Q

What investigations are done for neonatal jaundice?

A

1) Bilirubin level - transcutaneous bilirubinometer or serum bilirubin
2) LFTS - hepatitis or cholestatic disease
3) Infection screen - TORCH congenital infection screen, surface swabs, urine culture, blood culture, LP, CXR
4) Haemolysis = blood type, RH (mother and infant), reticulocyte count, direct Coomb’s test, Hb and haemaotcrit count, peripheral blood film for erythrocyte, red cell enzyme assays eg G6PD activity
5) Reducing substance in urine = screening test for galactosaemia (if infant has received sufficient quantities of milk)
6) TFTs

18
Q

What is Coombs test?

A

Coombs test = tests for autoimmune haemolytic anaemia

Direct antiglobulin test (DAT): tests for antibodies directly bound to RBC. A blood sample is taken and RBC are washed (to remove patients own plasma and unbound antibodies). A anti-human globulin (antibody to antibodies) is then added, if the red cells then agglutinate = positive result (shows there are antibodies bound to the surface of RBC)

NB Indirect antiglobulin test (IAT): tests for antibodies circulating in the patients blood (this is a prenatal test)

19
Q

What treatment can be done for neonatal jaundice?

A

Depends on cause. Give fluids and refer urgently if <24hr or unwell

1) Phototherapy
2) Exchange transfusion

20
Q

How does phototherapy help neonatal jaundice? How effective is it?

A

Blue light converts unconjugated bilirubin to harmless water soluble products done via a combination of overhead lights and fibre-optic blanket

Very effective - after 4hrs, 20% of total bilirubin is in harmless form

21
Q

What are some risks associated with phototherapy for neonatal jaundice?

A

Risk of hyper/hypothermia, worse attachment, loose stools

22
Q

When is exchange transfusion required for neonatal jaundice? What are some risks?

A

Rarely required but indicated in severe hyperbilirubinaemia. Up to 2x blood volume replaced

Risk of thrombosis, embolism, infection, metabolic and coagulation abnormalities

23
Q

What is Kernicterus?

A

= Bilirubin toxicity encephalopathy

Yellow staining of basal ganglia

25
Q

How should Kernicterus be treated?

A

Phototherapy

26
Q

Birth asphyxia been renamed?

A

Hypoxic ischaemic encephalopathy (HIE)

27
Q

What is HIE?

A

Supply of oxygen to the brain is compromised by both failure of gas exchange (hypoxia) and failure of cerebral blood supply (ischaemia)

28
Q

What is the pathophysiology of HIE?

A

Foetal hypoxia and ischaemiea leads to hypoxia, hypercapnia, metabolic acidosis and cardiorespiratory depression

Acute severe asphyxia can cause brain damage within 10-12 mins (HIE) and death within 20-30 mins

29
Q

What are some antepartum causes of HIE? (3)

A

1) Inadequate maternal placental perfusion caused by hypotension or HTN
2) Foetal anaemia
3) IUGR

30
Q

What are some intrapartum causes of HIE? (2)

A

1) Prolonged uterine contractions

2) Cord compression

31
Q

How may HIE present?

A
Increased respiratory effort
Apnoea
Irregular gasping
Bradycardia
Hypotension
32
Q

How may Kernicterus present?

A

Hypotonia + lethargy

Followed by seizures, coma, and death