Neonatology Flashcards

1
Q

What is the significance of jaundice in the first 24 hours of life

A

it is always pathological

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2
Q

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

A
  • rhesus haemolytic disease
  • ABO haemolytic disease
  • hereditary spherocytosis
  • glucose-6-phosphodehydrogenase deficiency
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3
Q

When is jaundice considered physiological in the neonatal period

A

2 - 14 days

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4
Q

Explain the pathophysiology of physiological neonatal jaundice

A
  • high [RBC] in fetus that are more fragile
  • fetal RBCs break down more rapidly than normal RBCs
  • less developed liver function means at birth, bilirubin can’t be excreted fast enough
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5
Q

In which type of infants is physiological jaundice more commonly observed?

A

more commonly seen in breastfed babies

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6
Q

What is prolonged jaundice in the neonate

A

jaundice after 14 days in term infants and 21 days in preterm

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7
Q

Give 5 causes of prolonged jaundice

A
  • biliary atresia
  • hypothyroidism
  • breast milk jaundice
  • prematurity
  • UTI/ congenital infections
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8
Q

How is neonatal jaundice investigated

A
  • FBC and blood film
  • conjugated and unconjugated bilirubin
  • Direct Coombs test - direct antiglobulin test
  • thyroid function tests
  • U&Es and LFTs
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9
Q

How is neonatal jaundice managed

A
  • bilirubin monitored and plotted on treatment threshold charts for specific gestation
  • phototherapy if above threshold
  • closely monitor bilirubin during phototherapy
  • Recheck bilirubin 12-18 hours after stopping
  • exchange transfusion if bilirubin is extremely high
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10
Q

What is a complication of neonatal jaundice

A

Kernicterus

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11
Q

What is kernicterus

A

bilirubin induced encephalopathy and irreversible neurological damage

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12
Q

What is necrotising enterocolitis

A

acute inflammatory disease affecting premature neonates, where part of the bowel becomes necrotic

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13
Q

Give 3 RFs of necrotising enterocolitis

A
  • very low birth weight/ prematurity
  • antibiotic therapy >10 days
  • formula feeds
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14
Q

How does necrotising enterocolitis present

A
  • new feed intolerance
  • Vomiting, particularly with green bile
  • Generally unwell/ sepsis
  • Distended, tender abdomen
  • Absent bowel sounds
  • fresh blood in stools
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15
Q

What blood tests are conducted for necrotising enterocolitis ?

A
  • FBC - check for thrombocytopenia and neutropenia
  • CRP to assess inflammation
  • blood gas to check for metabolic acidosis
  • Blood culture for sepsis
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16
Q

What is the imaging investigation of choice for diagnosing necrotising enterocolitis?

A

abdominal X-ray, performed in the supine position (lying face up).

17
Q

What X-ray findings are indicative of necrotising enterocolitis?

A
  • Dilated bowel loops
  • Bowel wall oedema (thickened bowel walls)
  • Pneumatosis intestinalis - gas in the bowel wall
  • Pneumoperitoneum is free gas in the peritoneal cavity and indicates perforation
  • Gas in the portal veins
  • Rigler sign - air both inside and outside of the bowel wall
18
Q

How is necrotising enterocolitis managed

A
  • nil by mouth with parenteral nutrition
  • IV fluids
  • bowel decompression by NG tube
  • broad spec IV antibiotics
  • surgical emergency - remove necrotic bowel
19
Q

What are the serious complications associated with necrotising enterocolitis?

A
  • Death of bowel tissue, which can lead to bowel perforation
  • Bowel perforation leading to peritonitis and shock
  • sepsis
  • death
20
Q

What is the pathophysiology of respiratory distress syndrome

A
  • Inadequate surfactant leads to high surface tension within alveoli, resulting in lung collapse
  • This hinders lung expansion, causing inadequate gaseous exchange and leading to hypoxia, hypercapnia and respiratory distress
21
Q

Which maternal condition is linked to higher rates of neonatal respiratory distress syndrome?

A

more common in infants born to mothers with diabetes mellitus

22
Q

What causes increased risk of neonatal respiratory distress syndrome in infants of diabetic mothers?

A

increased insulin inhibits surfactant production and maturation of the fetal lungs.

23
Q

What is the role of antenatal steroids in managing respiratory distress syndrome

A

Antenatal steroids (e.g., dexamethasone) given to mothers with suspected or confirmed preterm labour increases surfactant production, reducing the incidence and severity of RDS in the baby

24
Q

What management options are available for premature neonates with respiratory distress syndrome

A
  • Intubation and ventilation for severe respiratory distress
  • artificial surfactant delivered via an endotracheal tube
  • Continuous positive airway pressure (CPAP) via a nasal mask
  • Supplementary oxygen to maintain saturations between 91-95%
  • Gradual reduction of support as the baby develops
25
Q

What are the short-term complications of respiratory distress syndrome

A
  • Pneumothorax
  • Infection
  • Apnea
  • Intraventricular haemorrhage
  • Pulmonary haemorrhage
  • Necrotising enterocolitis
26
Q

What are the long-term complications of respiratory distress syndrome

A
  • Chronic lung disease of prematurity
  • Retinopathy of prematurity
  • Neurological, hearing, and visual impairment
27
Q

When is neonatal blood spot screening performed?

A

5-9 days of life.

28
Q

Give 4 conditions that are screened for in neonatal blood spot screening?

A
  • Congenital hypothyroidism
  • Cystic fibrosis
  • sickle cell disease
  • Phenylketonuria