Paediatric Respiratory conditions Flashcards

1
Q

Pathophysiology of Neonatal Infant Respiratory DIstress Syndrome

A

*Deficiency in surfactant —> collapse of terminal air-spaces (the future site of alveolar development)

*deficiency may by due to inhibition from the insulin (produced in the newborn of diabetic mothers)

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2
Q

X ray changes seen in neonatal respiratory distress syndrome (3)

A
  • ‘Ground glass’ changes -> fine reticular granularity of the lung parenchyma
  • ‘white lung’
  • decreased lung volumes
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3
Q

Prevention of neonatal RDS

A
  • pregnancy should be prolonged for as long as possible
  • Glucocorticoids (antenatal)—> speed up production of surfactant

12mg Bethamethasone 12 hourly -> 2 doses; 2nd dose 12 - 24 hours before birth

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4
Q

What’s a disadvantage of CPAP use (e.g. neonate with RDS)

A

Positive pressure ventilation can damage the lungs -may lead to chronic bronchopulmonary dysplasia

(BPD) due to over-ventilation or underventilation

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5
Q

Management of neonatal RDS

A
  • oxygen
  • CPAP
  • IV fluids - to stabilise BM, BP etc
  • endotracheal tube (mechanical ventilation) - in severe cases
  • antibiotics - to prevent infection
  • exogenous surfactant
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6
Q

What’s the management (soon after delivery) of an extremly premature baby?

A

Usually: baby born at e.g. 28 weeks -> intubated ASAP (often at delivery room) -> surfactant

given through NG into the lungs (resistance will disappear as we administer surfactant) ->CPAP

for short time

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7
Q

What patients is bronchopulmonary dysplasia seen in?

A
  • chronic lung disease
  • usually in premature infants who were treated with supplemental oxygen / who required longterm oxygen support

*but improvements in care, prevention - incidence decreased

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8
Q

Cause of bronchopulmonary dysplasia

A

Prolonged high O2 delivery —> Necrotizing bronchiolitis (acute inflammatory lesion of lower

airway) and alveolar septal injury with inflammation and scarring—> hypoxemia

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9
Q

What’s bronchiolitis?

  • usual cause
A

Infection of the bronchioles (small airway)

Cause: usually Respiratory Syncytial Virus (RSV)

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10
Q

Most common patient (age) in bronchiolitis

A
  • can be diagnosed in children up to 2 years of age
  • most common in children under 6 months
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11
Q

What can be heard in bronchiolitis on baby’s chest? (3)

A
  • wheeze
  • crackles
  • harsh breath sounds
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12
Q

Signs and symptoms of bronchiolitis

A
  • Choryzal symptoms (common cold symptoms – runny / snotty nose, mucus in throat)
  • Dyspnoea
  • Poor feeding
  • Mild fever (<39C)
  • Apnoeas
  • Signs of respiratory distress (recessions, tracheal tube, nasal flaring, head bobbing)
  • Auscultation: wheeze and crackles
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13
Q

Where bronchiolitis is most commonly managed?

A

At home with safety netting

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14
Q

Reasons for admission with bronchiolitis

A
  • Any pre-existing condition (e.g. prematurity, Downs, cystic fibrosis) predisposes to more severe infection
  • Parent not confident in ability to manage at home or difficult access to medical help from home
  • <50% of normal intake or clinically dehydrated
  • Respiratory rate >70
  • Oxygen saturations <94%
  • Signs of respiratory distress
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15
Q

Typical management of bronchiolitis

A
  • Typically just supportive management
  • Ensure adequate feeding (NG tube if not managing orally)
  • Supplementary oxygen if saturations remain <92%
  • Rarely ventilatory support (CPAP) is required
  • Little evidence for other treatments such as nebulised saline / bronchodilators / steroids / antibiotics and are not routinely used
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16
Q

Management of CF

A
  • Most of the patients with CF need to have a constant IV access -> we try to avoid IV cannulas (long term e.g. Portacath -> providing long term IV access and preventing venous thrombosis)
  • Physiotherapy -> to improve sputum clearance and break cycle of continuous lung damage
  • Dornase Alpha (Pulmozyme) / recombinant human DNase = nubalised treatment -> treatment given before bed -> to help to clear the mucous in the morning

Lung transplant - but still high mortality rate (40%)

*treatments for class III mutation, where CFTR is non-functional -> to restore channel conductance (Ivacaftor)