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Year 4 Paediatrics > Neonatal and Newborn > Flashcards

Neonatal and Newborn Flashcards

1
Q

What % of infants are visibly jaundiced during the first week of life?

A

50%

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2
Q

What is the most common mechanism of neonatal jaundice?

A

Physiological - slow conjugation of bilirubin

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3
Q

What are the ‘golden rules’ of physiological jaundice? (4)

A
  1. Jaundice is not apparent in first 24 hours of life
  2. The infant remains well
  3. The serum bilirubin does not reach treatment level
  4. The jaundice has faded by 14 days
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4
Q

If jaundice is apparent within the first 24 hours of life, what is it strongly suggestive of?

A

Either excessive haemolysis or sepsis, it is never physiological

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5
Q

What is kernicterus?

A

Unconjugated bilirubin (never conjugated) can enter the brain and cause neuronal damage.

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6
Q

What can increase the risk of developing kernicterus? (4)

A
  1. High serum bilirubin
  2. Pre-term birth
  3. Acidosis
  4. Hypoxia
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7
Q

What is the first-line treatment if serum bilirubin is high?

A

Phototherapy treatment - light of a wavelength that converts unconjugated bilirubin to non-toxic isomers allows bilirubin excretion without conjugation

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8
Q

What are the haemolytic causes of neonatal jaundice, often presenting within 24 hours of birth?

A
  1. ABO incompatibility
  2. Rhesus or other isoimmunization
  3. Red cell defects (e.g. G6PD deficiency)
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9
Q

What is hypoxic ischaemic encephalopathy?

A

It is a form of brain damage caused by a lack of oxygen to the brain.

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10
Q

What are the causes of hypoxic ischaemic encephalopathy (HIE)? (5)

A
  1. Reduced umbilical blood flow e.g. cord prolapse
  2. Reduced placental gas exchange e.g. placental abruption
  3. Reduced maternal placental perfusion
  4. Maternal hypoxia from whatever cause
  5. Inadequate postnatal cardiopulmonary circulation
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11
Q

What grading system is used to determine the severity of HIE?

A

Sarnat grade - mild, moderate or severe

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12
Q

How can HIE present? (9 features to assess)

A

Many different clinical features and depends on the severity, but the following are signs to assess:

  1. Level of consciousness
  2. Muscle tone
  3. Posture
  4. Tendon reflexes
  5. Suck
  6. Moro
  7. Autonomic dysfunction
  8. Heart rate
  9. Seizures
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13
Q

How is HIE managed?

A
  1. Resuscitate at birth; insert IV +/- arterial line
  2. Assess history and examine for features of dysmorphism and birth trauma e.g. fractures
  3. Exclude other causes of encephalopathy e.g. meningitis, metabolic disturbances, maternal drugs, CNS malformation
  4. Monitor and maintain homeostasis
  5. Cranial USS
  6. Mild fluid resuscitation
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14
Q

What are the disabilities likely caused by HIE/what is the prognosis? (6)

A
  1. Spastic quadriplegia
  2. Cerebral palsy
  3. Severely reduced IQ
  4. Cortical blindness
  5. Hearing loss
  6. Epilepsy
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15
Q

What % of babies born <32 weeks have a cerebral haemorrhage and ischaemia?

A

10-15%

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16
Q

Where is the origin of most cerebral haemorrhages in newborns, and where does the bleeding extend to?

A

The vascular germinal matrix (subependymal), with bleeding extending into the lateral ventricles

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17
Q

What are the causes of cerebral haemorrhage in newborns? (5)

A
  1. Severe RDS
  2. Pneumothorax
  3. Hypotension
  4. Hypoxia
  5. Fluctuations in pCO2
    (anything that rapidly alters the cerebral blood flow)
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18
Q

When do most cerebral haemorrhages occur in newborns?

A

Within 72 hours of birth

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19
Q

How do cerebral haemorrhages in newborns present? (5)

A

50% are asymptomatic, larger bleeds:

  1. Systemic collapse
  2. Bulging fontanelle
  3. Neurological dysfunction e.g. seizures or abnormal movements
  4. Anaemia
  5. Jaundice
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20
Q

How is a suspected cerebral haemorrhage investigated?

A

Cranial USS

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21
Q

How can a cerebral haemorrhage in newborn be prevented? (5)

A
  1. Antenatal steroids
  2. Maintenance of BP, blood gases, coagulation
  3. Gentle handling
  4. Ventilation and suction
  5. Postnatal surfactant
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22
Q

What is the most common neonatal surgical emergency?

A

Necrotising enterocolitis (NEC)

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23
Q

What is NEC?

A

It is a condition characterised by a triad of abdominal distension, GI bleeding and pneumatosis intestinalis (air in bowel wall on abdominal X-ray)

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24
Q

What causes NEC?

A

Impaired blood flow through the bowel (intestinal ischaemia), which predisposes the mucosa to invasion by enteric organisms

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25
Q

How do babies present with NEC, and when is the most common time after birth? (7)

A
  1. Apnoea
  2. Temperature instability
  3. Bradycardia
  4. Lethargy
  5. Abdominal distension
  6. Bloody diarrhoea
  7. Emesis
    - most common time is in the second week after birth
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26
Q

In what % of cases of NEC does bowel perforation occur?

A

20%

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27
Q

What are the predisposing features to developing NEC? (6)

A
  1. Prematurity
  2. IUGR
  3. Hypoxia
  4. Polycythaemia
  5. Exchange transfusion
  6. Rapid increase in milk feeding
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28
Q

In addition to perforation of the bowel, what are the other complications if NEC is missed early on? (5)

A
  1. Shock
  2. DIC; multiorgan failure
  3. Oedema
  4. Pneumatosis intestinalis (‘soap bubble’ or ‘halo’ signs)
  5. Signs of intestinal perforation
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29
Q

What is the prophylactic management of NEC?

A

Antenatal corticosteroids and breast milk feeds, if baby is high risk then antibiotics

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30
Q

What are the investigations that can be performed in suspected NEC?

A
  1. FBC, U&Es, creatinine, coagulation screen, albumin, blood culture
  2. Blood gas
  3. AXR
  4. Stool culture
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31
Q

What is the management of confirmed/suspected NEC? (5)

A
  1. Stop milk feeds for 7-10 days
  2. Insert NG tube
  3. IV antibiotics for 7-10 days
  4. Systemic support
  5. Surgery if perforation, deterioration despite above steps taken, GI obstruction due to stricture formation
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32
Q

What is the % mortality of NEC?

A

22%

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33
Q

What is the useful acronym to remember the causes of transplacental/congenital infections?

A 
TORCH
toxoplasma 
other
rubella
CMV
herpes 
(other = herpes zoster, parvovirus B19, syphilis, enterovirus, HIV, hep B, group B strep)
34
Q

What is respiratory distress syndrome sometimes also known as?

A

Hyaline membrane disease (HMD)

35
Q

What is the incidence of RDS?

A

1 in 100 live births

36
Q

What is the biggest risk factors for RDS?

A

Prematurity (50% at 32 weeks, >90% at <28 weeks)

37
Q

What causes RDS?

A

Surfactant deficiency causes alveolar collapse during expiration. The increased work of breathing leads to exhaustion and hypoxia.

38
Q

In addition to surfactant deficiency, what are the other reasons prematurity contributes to RDS?

A

Poor muscle bulk and elastic ribcage in the preterm compound the situation

39
Q

What are the other risk factors that make developing RDS more likely? (7)

A
  1. C-section
  2. Hypothermia
  3. Perinatal hypoxia
  4. Acidosis
  5. Meconium aspiration
  6. Congenital pneumonia
  7. Maternal diabetes
40
Q

How may RDS present?

A

Cyanosis and/or respiratory distress - recession.

41
Q

What is the management for RDS?

A

Surfactant ASAP after birth

42
Q

Why in some cases is RDS self-limiting?

A

The stress of premature birth and developing RDS causes the release of corticosteroids from the adrenal gland, and this will in turn cause surfactant to be produced

43
Q

What is the cause of physiological jaundice?

A

Immaturity of the hepatic bilirubin conjugation

44
Q

When is action required in physiological jaundice and how do you know?

A

When serum bilirubin levels are above the safe gestation-corrected level. This should be evident when jaundice is below the umbilicus

45
Q

In which pattern does jaundice tend to appear?

A

In a cephalic - caudal direction is spreads

46
Q

What are the causes of elevated serum bilirubin in physiological jaundice?

A
  1. Sepsis
  2. Bruising
  3. Haemolytic disorders
  4. Hepatic disease
47
Q

What is the treatment for physiological jaundice that is above the acceptable level?

A

Phototherapy - converts bilirubin to water-soluble form that can be excreted in urine

48
Q

What are the causes of jaundice in the first 24 hours of life? (5)

A
  1. Haemolysis (rhesus haemolytic disease)
  2. Red cell enzyme defects (G6PD deficiency)
  3. Rec cell membrane defects (congenital spherocytosis)
  4. Sepsis
  5. Severe bruising
49
Q

When is jaundice classed as prolonged?

A

In term infants >14 days

In premature infants >21 days

50
Q

What are some of the causes of prolonged jaundice? (8)

A
  1. Breastfeeding
  2. Enclosed bleeding (cephalhaematoma)
  3. Prematurity
  4. Haemolysis
  5. Sepsis
  6. Hypothyroidism
  7. Conjugated jaundice
  8. Crigler-Najjar syndrome
51
Q

What would be the expected colour of stools in obstructive jaundice?

A

Clay/white coloured

52
Q

What are the causes of conjugated/obstructive jaundice? (7)

A
  1. Sepsis
  2. TPN
  3. Biliary tract obstruction (biliary atresia)
  4. Viral hepatitis
  5. TORCH infections
  6. Alpha-1-antitrypsin deficiency
  7. Cystic fibrosis
    …urgh not gonna lie, loads others..
53
Q

What is the classic triad for Shaken Baby Syndrome?

A
  1. Subdural haematoma
  2. Encephalopathy
  3. Retinal haemorrhages
54
Q

When are babies most at risk of retinopathy of prematurity?

A

If they are born before 32 weeks or weight less than 1500g when they are born.

55
Q

Why does retinopathy of prematurity occur, and what is the pathophysiology behind it?

A

Blood vessels in the eyes develop between weeks 16 and 36, and so when babies are born prematurely, blood vessel development is incomplete and there will be areas of the retina that do not receive enough oxygen. This neovascularisation, and the new vessels are weak and leak blood, leading to scarring. The scarring leads to retinal detachment.

56
Q

Why is the amount of oxygen given to new borns important in preventing retinopathy of prematurity?

A

Too much oxygen will cause the retinopathy, so the target sats are 85-93%

57
Q

How and why does retinopathy of prematurity occur?

A

Normally the retinal blood vessels grow in a relatively hypoxic environment. However when baby is born prematurely, they often have oxygen requirements, and if too much oxygen is given, it halts vascular growth leading to:
1. Tortuosity of vessels
2. Angiogenesis
3. Iris vessel dilatation and rubeosis iridis
Although vascular growth has halted, the eye continues to grow, leading to hypoxic areas of the retina, leading to scarring and retinal detachment (in worse case scenarios)

58
Q

What is rhesus haemolytic disease?

A

Usually when the mother has RhD -ve and the baby is RhD +ve any exchange of blood from the baby to the maternal circulation leads to maternal anti-D IgG production. Transplacental passage of this antibody leads to fetal RBC haemolysis. The condition is usually asymptomatic or only mild in the first affected pregnancy, however severity increases with subsequent pregnancies.

59
Q

How is the risk of rhesus haemolytic disease measured?

A

The maternal anti-Rh titre is measured. The risk of disease is predicted depending on the measure:

  • disease unlikely when maternal anti-Rh titre <4u/mL
  • 10% when titre is 10-100u/mL
  • 70% when fetal Hb <7g/dL or titre >100u/mL
60
Q

What happens in ABO incompatibility?

A

If the maternal blood group is type O, the isoimmunization occurs because the naturally occurring antibodies at IgG not IgM. The IgG antibodies can cross the placenta and cause haemolysis in the foetus.

61
Q

How does ABO HDN differ to Rh HDN?

A

With ABO HDN, half of the cases occur in a first born compared to Rh HDN where it is less likely to occur in a first born. Also with ABO it does not become more severe after further pregnancies.

62
Q

How is a neonate defined?

A

Up to 28 days of life

63
Q

What is the pattern of spread of jaundice?

A

From cranial to caudal end

64
Q

Why is jaundice common in a newborn?

A

Because they have more red blood cells and a higher breakdown of them, leading to haemolysis which the liver cannot conjugate due to immaturity

65
Q

In addition to premature babies, when else is physiological jaundice more common?

A

In first born babies when mums are having difficulty establishing feeds (normally when exclusively breast fed)

66
Q

When is jaundice always pathological?

A

If it occurs within the first 24 hours of life

67
Q

What is the most common cause of pathological jaundice?

A

Sepsis

68
Q

In addition to sepsis, what are the other two common causes of pathological jaundice?

A
  1. Rh disease

2. ABO incompatibility

69
Q

When is jaundice classed as prolonged?

A

In a term baby 14 days

In a premature baby 21 days

70
Q

What is the most common cause of prolonged jaundice?

A

Breast milk jaundice

71
Q

What is the main concern with prolonged jaundice - what is the possible pathology? (2)

A
  1. Biliary atresia / neonatal liver disease

2. G6PD

72
Q

What is the cause of conjugated jaundice?

A

Neonatal liver disease - neonatal hepatitis, biliary atresia

73
Q

What investigations are performed with neonatal jaundice? (3)

A
  1. Bilirubin (conjugated/unconjugated/total)
  2. FBC, blood group and direct coomb’s test (shows if haemolytic anaemia)
  3. U&Es
74
Q

Why is jaundice treated?

A

Unconjugated jaundice can cross blood brain barrier leading to kernicterus.

75
Q

When is phototherapy stopped?

A

When the total serum bilirubin falls 50 below treatment line

76
Q

What is an exchange transfusion?

A

Taking small amounts of the babies blood out, and transfusing donor blood back in

77
Q

Which diseases are tested for using the Guthrie test?

A
  1. Maple syrup urine disease
  2. Phenylketonuria
  3. Sickle cell disease
  4. Galactosaemia
  5. Hypothyroidism
  6. CF
78
Q

Chewing gum should not be given to children with which disease and why?

A

Phenylketonuria due to it containing the sweetener aspartame

79
Q

What is an Epstein’s pearl?

A

A congenital cyst found in the mouth. They are common on the hard palate, but may also be seen on the gums where the parents mistake it for an erupting tooth. No treatment is generally required as the tend to spontaneously resolve over the course of a few weeks

80
Q

In a baby with prolonged jaundice and white stools, what is the most important diagnostic test to perform?

A

Abdominal USS - want to rule out biliary atresia. The baby should have conjugated bilirubin levels measured too, as they will be high, however this won’t confirm a diagnosis.

Year 4 Paediatrics (18 decks)

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