Neonatology Flashcards

1
Q

Whom does respiratory distress syndrome affect

A

Mainly premature neonates, commonly before 32 weeks

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2
Q

What causes respiratory distress syndrome

A

Lungs haven’t started producing adequate surfactant yet (type 2 pneumocytes) . Leading to high surface tension within alveoli. Leads to lung collapse, as more difficult for alveoli and lungs to expand.

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3
Q

Presentation of RDS

A
  • Tachypnoea (>60 breaths/min)
  • Labored breathing, chest wall recession, nasal flaring
  • cyanosis
  • hypoxia, hypercapnia
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4
Q

Mx of RDS

A
  • Antenatal corticosteroids - dexamethasone to mothers with suspected or confirmed pre term.
  • intubation + ventilation
  • endotracheal surfactant, artificial surfactant
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5
Q

Definition of bronchopulmonary dysplasia

A

CHRONIC LUNG DISEASE

- oxygen dependence at 36 weeks of corrected gestational age (gestational age + postnatal age)

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6
Q

Whos mostly affected by bronchopulmonary dysplasia

A

premature birth babies (usually 23-28 week) and low birth weight

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7
Q

Presentation of bronchopulmonary dysplasia

A

Baby that needs ventilation/CPAP/supplementary O2 at and passed 36 weeks of postmenstrual age

  • Most have initial RDS and then depend on O2
  • Many babies continue to have tachypnoea + signs of resp. distress (intercostal recession, nasal flaring), wheezing
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8
Q

Ix for bronchopulmonary dysplasia

A

CXR, ABG - acidosis, hypercapnia, hypoxia

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9
Q

Mx of bronchopulmonary dysplasia

A

Resp support - intubation/ventilation, CPAP, O2

Medicine - dexamethosone, diuretics

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10
Q

Complications of bronchopulmonary dysplasia

A

Developmental delay, hospital readmission, risk of infection

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11
Q

Why is physiological jaundice common in neonates

A
  • Marked release of haemoglobin due to high RBC no.s (hypoxic intrauterine environment)
  • red cell life span is shorter in newborn infants
  • hepatic bilirubin metabolism is less efficient in first few days of life
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12
Q

What 2 things need to be wary of with neonatal jaundice

A
  1. May be sign of another disorder e.g. haemolytic anaemia, infection, metabolic or liver disease
  2. Unconjugated bilirubin (=fat soluble + can stick to cells) can be deposited in brain, particularly basal ganglia causing kernicterus.
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13
Q

What is Kernicterus

A

Deposition of unconjugated bilirubin in basal ganglia and brainstem. Bilirubin is fat soluble so can cross bbb.
Px: can vary; lethargy, poor feeding, irritability, increased muscle tone, seizures, coma.

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14
Q

Causes of increased production of bilirubin

A
  • physiological
  • haemolytic disease of newborn
  • ABO incompatibility
  • G6PD deficiency
  • sepsis + DIC
  • heammorhage
  • polycythemia
  • normal urine (unconjugated bilirubinaemia insoluble in water)
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15
Q

Causes of Decreased clearance of bilirubin:

A
  • Prematurity (liver development)
  • Neonatal cholestasis
  • Extrahepatic biliary atresia
  • Endocrine disorders (hypothyroid and hypopituitary)
  • Gilbert syndrome
  • Pale stools (bilirubin not excreted in faeces) + dark urine (bilirubin principally excreted by kidneys)
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16
Q

What time frame is neonatal jaundice considered pathological or physiologocial

A
  • first 24 hours of life = pathological - neonatal sepsis common cause.
  • 2-14 days = physiological in full term
  • 2-21 days = physiological in premature
17
Q

Why is jaundice exaggerated in premature neonates

A

immature liver - increases risk of kernicterus.

18
Q

Ix for neonatal jaundice

A
  • FBC + blood film: polycythaemia (high RBC/haematocrit) or anaemia (low RBC, Hb)
  • Conjugated bilirubin: high indicate hepatobilliary cause
  • Unconjugated: high = increased production of bilirubin
  • G6PD levels for deficiency
  • Blood type testing: ABO incompatibility
  • Thyroid function: hypothyroid
19
Q

Mx of neonatal jaundice

A
  • Total bilirubin levels plotted on treatment threshold charts
  • phototherapy (breaks down unconjugated bilirubin so can be excreted into bile and urine)
20
Q

Common Causes of jaundice in baby less than 24 hours

A

ALWAYS ABNORMAL

  • rhesus hemolytic disease (mum is rhesus negative, baby is rhesus positive)
  • ABO incompatibility (mother is type O and baby is type A or B. Mum can develop anti B or anti A antibodies. Coombs test to diagnose)
  • G6PD def.
  • Hereditary spherocytosis
21
Q

Common causes of jaundice in baby 2-14 days

A
  • Physiological (HbF lifespan + liver immaturity)
  • Breastmilk jaundice (feeding difficulties, dehydration, impaired bilirubin elimination)
  • Infection
  • Can be exacerbated by bruising and polycythaemia
22
Q

Common causes of jaundice in baby older than 2 weeks

A
  • Breast milk jaundice
  • Congenital hypothyroidism (slows everything down including bilirubin excretion)
  • Cystic fibrosis
  • Biliary atresia (surgery improves outcomes, failure of biliary tree development).
23
Q

Why does meconium aspiration occur

A
  • meconium (dark green, sticky faecal material) is usually released from the bowels after birth (within 48hrs)
  • in some pregnancies baby can pass meconium in utero, and aspirate the meconium amniotic fluid
24
Q

What is presentation of meconium aspiration

A
  • Respiratory distress, can be life threatening: tachypnoea, tachycardia, cyanosis, nasal flaring, intercostal recession, gasping or unable to breath
25
Q

Mx of meconium aspiration

A
  • may need no extra support
  • ventilatory support: via nasal canula, CPAP, intubation
  • surfactant
26
Q

What is Hypoxic ischaemic encephalopathy

A
  • occurs in neonates as a result of hypoxia during birth.
  • prolonged or severe hypoxia leads to ischaemic brain damage. HIE can lead to permanent damage to the brain, causing cerebral palsy. Severe HIE can result in death.
27
Q

Causes of HIE

A
  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord, causing compression of the cord during birth
  • Nuchal cord, where the cord is wrapped around the neck of the baby
28
Q

HIE Px

A

Mild: Poor feeding, generally irritability and hyper-alert,
Resolves within 24 hours,
Normal prognosis

Moderate: Poor feeding, lethargic, hypotonic and seizures,
Can take weeks to resolve,
Up to 40% develop cerebral palsy

Severe: Reduced consciousness, apnoeas, flaccid and reduced or absent reflexes,
Up to 50% mortality,
Up to 90% develop cerebral palsy

29
Q

Mx of hypoxic ischeamic encephalopathy

A
  • supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance and treatment of seizures
30
Q

What is TORCH infection

A

Infection of the developing fetus or newborn that can occur in utero (via placenta), during delivery (birth canal) or post delivery (through breast milk)

31
Q

What are the TORCH infective organisms

A
  • Toxoplasma gondii
  • Other agents - VZV, parvovirus B19, HIV
  • Rubella
  • Cytomegalovirus
  • Herpes simplex virus
32
Q

Presentation of TORCH infections

A
  • Can vary depending on underlying infection but share non-specific signs + symptoms
  • fever, lethargy, decreased birth weight, rash, jaundice
  • cataracts, congenital heart disease, hearing loss
  • can cause a miscarriage, stillbirth or intrauterine growth restriction.
33
Q

Who does necrotising enterocolitis affect, what is it? What can lead to?

A
  • disorder affecting premature neonates
  • part of the bowel becomes necrotic
  • bowel perforation - peritonitis and shock. Life threatening emergency
34
Q

Px of necrotising enterocolitis

A
  • intolerance to feeds
  • vomiting, green bile (bilious vomiting)
  • distended abdomen
  • absent bowel sounds
  • blood in stools
35
Q

Dx of NEC

A
  • abdominal xray = gold standard - may show gas in bowel wall (NEC) or free gas in peritoneal cavity (perforation)
36
Q

Mx of NEC

A
  • nil by mouth, IV fluids
  • Abx
  • immediate surgery to remove dead bowel tissue
37
Q

How is group B strep passed to baby, what impact does it have on mother? How to prevent?

A
  • common bacteria found in vagina, passed on during labour
  • doesnt cause any problems for mother but can cause neonatal sepsis
  • prophylactic Abx during labour if mother is found to have GBS in vagina during pregnancy