Neonatology Flashcards

(37 cards)

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
Mx of meconium aspiration
- may need no extra support - ventilatory support: via nasal canula, CPAP, intubation - surfactant
26
What is Hypoxic ischaemic encephalopathy
- 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
Causes of HIE
- 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
HIE Px
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
Mx of hypoxic ischeamic encephalopathy
- supportive care with neonatal resuscitation and ongoing optimal ventilation, circulatory support, nutrition, acid base balance and treatment of seizures
30
What is TORCH infection
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
What are the TORCH infective organisms
- Toxoplasma gondii - Other agents - VZV, parvovirus B19, HIV - Rubella - Cytomegalovirus - Herpes simplex virus
32
Presentation of TORCH infections
- 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
Who does necrotising enterocolitis affect, what is it? What can lead to?
- disorder affecting premature neonates - part of the bowel becomes necrotic - bowel perforation - peritonitis and shock. Life threatening emergency
34
Px of necrotising enterocolitis
- intolerance to feeds - vomiting, green bile (bilious vomiting) - distended abdomen - absent bowel sounds - blood in stools
35
Dx of NEC
- abdominal xray = gold standard - may show gas in bowel wall (NEC) or free gas in peritoneal cavity (perforation)
36
Mx of NEC
- nil by mouth, IV fluids - Abx - immediate surgery to remove dead bowel tissue
37
How is group B strep passed to baby, what impact does it have on mother? How to prevent?
- 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