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Neonatal Medicine > Respiratory Problems > Flashcards

Respiratory Problems Flashcards

1
Q

Risk factors for RDS

A
  • Male sex
  • Maternal diabetes
  • multiple birth (second twin esp)
  • Elective caesarean
  • Precipitous delivery
  • Family history
  • Sepsis
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2
Q

Protective factors for RDS

A
  • Female sex
  • PROM
  • Antenatal steroids
  • IUGR
  • Chronic or gestational hypertension
  • Maternal opiate or heroin use
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3
Q

What are the steps that occur in the normal transition to pulmonary respiration?

A
  • Before birth - increased levels of catecholamines, vasopressin, prolactin and glucocorticoid enhance lung fluid resorption
  • First breath triggered by decline in PaO2, acidosis and hypercapnia from interruption of placental circulation
  • Air entry into lungs displaces fluid to establish FRC
  • Increased pulmonary blood flow further enhances fluid resorption
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4
Q

Why do preterm infants have more difficulty in transition to pulmonary respiration?

A
  • Surfactant deficiency increases surface tension and impairs ability to establish FRC
  • Compliant chest wall means more energy required to generate sufficient negative pressure for first breath
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5
Q

3 types of apnoea and how do they differ?

A
  • Obstructive apnoea - absence of airflow but persistent chest wall motion
  • Central apnoea - no airflow or chest wall motion
  • Mixed apnoea - most common in apnoea of prematurity - usually obstructive apnoea precedes central apnoea
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6
Q

What is the mechanism behind apnoea of prematurity?

A

Immature brainstem respiratory centres - attenuated response to CO2 and paradoxical response to hypoxia (causes apnoea rather than hyperventilation)

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7
Q

What is the mechanism of action of methylxanthines for apnoea of prematurity?

A

Increase respiratory drive by lowering threshold of response to hypercapnia, enhance contractility of diaphragm, prevent diaphragmatic fatigue

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8
Q

What are 5 types of lung injury that can be seen in RDS? (largely ventilator-induced)

A
  1. Atelectrauma - injury resulting from repeated alveolar collapse and expansion (recruitment/derecruitment injury)
  2. Volutrauma - overdistension of alveoli resulting from mechanical ventilation
  3. Barotrauma - pressure injury from ventilation
  4. Oxygen toxicity - caused by oxygen free radicals
  5. Ischaemic injury
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9
Q

What is the primary pathological change seen in respiratory distress syndrome?

A

Hyaline membranes in alveolar spaces.- formed from effusion of proteinaceous material from damaged cells and cellular debris

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10
Q

What cell type produces surfactant?

A

Type 2 pneumocytes

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11
Q

What is the composition of surfactant (and what component contributes to reduction in surface tension)?

A
  • Phospholipids - lower surface tension
  • Other lipids e.g. surfactant proteins A-D - facilitate adsorption and spreading of surfactant and have immunoregulatory properties
  • Platelet activating factor
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12
Q

Typical radiological findings in RDS

A

Low lung volumes, ground glass appearance, air bronchograms

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13
Q

Below what gestation is routine antenatal corticosteroid administration recommended to reduce risk of RDS?

A

<37/40 (+consider before elective CS up to 38+6)

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14
Q

In relation to mechanical ventilation, what are the factors that affect oxygenation?

A
  • FiO2

- Mean airway pressure (which depends on PIP, i-time, PEEP, RR [and thus e-time])

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15
Q

In relation to mechanical ventilation, what are the factors that affect ventilation/CO2 elimination?

A

Determined by minute ventilation - tidal volume (determined by PIP and i-time) and RR

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16
Q

Why is volume-targeted ventilation particularly important in RDS?

A

Rapid changes in lung compliance occur with surfactant treatment - high risk of volutrauma and air leak with pressure-limited ventilation. With VTV, PIP varies depending on respiratory compliance to achieve a set tidal volume

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17
Q

What are indications for high-frequency ventilation?

A
  • Poor response to conventional ventilation
  • Severe RDS
  • Severe MAS
  • Pulmonary interstitial emphysema (PIE)
  • Recurrent pneumothorax
18
Q

Risks of surfactant administration

A
  • transient hypoxia, hypercapnia, bradycardia, hypotension
  • ETT blockage
  • Pulmonary haemorrhage
19
Q

Definition of bronchopulmonary dysplasia

A

Requirement for supplemental oxygen for ≥ first 28 postnatal days

20
Q

How is the severity of bronchopulmonary dysplasia classified?

A

Classified at 36/40 PMA

  • Mild BPD = breathing RA at 36/40
  • Moderate BPD = 22-29% O2 at 36/40
  • Severe BPD = positive pressure support or >30% O2
21
Q

What are proven strategies to reduce risk of BPD?

A
  • Early use of nCPAP
  • Early selective surfactant use
  • Use of volume targeted ventilation
  • Use of caffeine for apnoea of prematurity (load pre-extubation)
  • Systemic corticosteroids (reduce mortality and BPD but increase risk of CP and neurodevelopmental disability)
22
Q

Risk factors for TTN

A
  • Late prematurity
  • Twin gestation
  • Maternal asthma
  • Precipitous delivery
  • Gestational diabetes, macrosomia
  • Caesarian section without labour
23
Q

What is the pathophysiology of TTN?

A

ineffective expression or activity of ENaC or Na/K-ATPase -> slowed absorption of fetal lung fluid -> reduced pulmonary compliance and impaired gas exchange

24
Q

Risk factors for MAS

A
  • Term or post-term (esp >42/40)
  • SGA
  • Perinatal asphyxia
25
Q

What should be considered in the cause of in utero passage of meconium in a preterm infant (<34/40)

A

Congenital listeriosis

26
Q

What are 5 mechanisms by which meconium aspiration can effect lung function?

A
  1. Airway obstruction (complete causing atelectasis and V/Q mismatch, or partial creating ball-valve effect and air trapping)
  2. Chemical pneumonitis
  3. Surfactant deficiency/inactivation (lipid content of meconium displaces surfactant, and can reduce synthesis)
  4. Increased risk of infection - sterile but is good growth medium for E.coli; passage of meconium may result from intrauterine infection
  5. PPHN - from hypoxaemia, hypercapnia, acidosis; chronic fetal hypoxia causes remodelling of pulmonary vasculature
27
Q

Radiological features of MAS

A
  • Patchy infiltrates
  • Hyperinflation
  • Areas of air trapping
  • Homogenous opacification later from pneumonitis
28
Q

Treatments for MAS

A
  • Positive pressure ventilation - higher e-time to prevent air trapping
  • Surfactant replacement (reduces need for ECMO)
  • iNO for PPHN
  • HFOV or ECMO for MAS refractory to conventional ventilation
29
Q

Causes of pulmonary hypoplasia

A
  1. Reduced amniotic fluid production - Potter syndrome/sequence from renal agenesis, infantile ARPKD, posterior urethral valves etc
  2. Amniotic fluid loss - preterm rupture of membranes (only if ROM <26/40), amniocentesis w chronic leakage
  3. Lung compression - pulmonary space occupying lesions (CDH, CPAM, pleural effusion), thoracic abnormalities (thoracic dystrophies)
  4. Reduced fetal movements - neuromuscular disease, oligohydramnios
30
Q

What is the most common type/location of congenital diaphragmatic hernia?

A

Bochdalek hernia (posterior portion of diaphragm) - 90% (80-90% on the left)

31
Q

What other anomalies are associated with CDH?

A
  • Pulmonary hypoplasia
  • Intestinal malrotation (20%)
  • Chromosomal abnormalities - T21, T13, T18, Fryn’s, Cornelia-de-lange, Turners
  • Omphalocoele
  • Esophageal atresia
  • CNS lesions, cardiac lesions
32
Q

Predictors of outcome in CDH

A
  • Liver position in chest (poor prognosis)
  • expected:observed lung ratio
  • lung:head size ratio
33
Q

Clinical signs of congenital diaphragmatic hernia

A
  • Respiratory distress (may occur after ‘honeymoon period’ >48hrs as gut becomes more air filled)
  • Scaphoid abdomen, incr chest wall diameter
  • Reduced breath sounds (often bilateral)
  • Bowel sounds in chest
  • Mediastinal shift
34
Q

Key principles in management of CDH

A
  • Avoid mask PPV
  • Early intubation for respiratory distress
  • Widebore NG tube to decompress gut
  • Gentle ventilation with permissive hypercapnia to reduce lung injury (may need HFOV or ECMO)
  • Delayed surgical repair (at least 48hrs after stabilisation improves outcome)
35
Q

Predictors of poor outcome for CDH

A
  • Size of defect - strongest predictor
  • Early onset of symptoms
  • Associated major anomaly
  • Severe pulmonary hypoplasia
  • Herniation to contralateral lung
  • Need for ECMO
36
Q

Complications following CDH repair

A
  • GORD
  • Recurrence
  • intestinal obstruction
  • Poor growth
  • Pectus excavatum
  • Pulmonary problems/BPD
  • Neurocognitive deficits
37
Q

What is subcutaneous emphysema in a newborn nearly always indicate?

A

Pneumomediastinum

38
Q

What type of patient does pulmonary interstitial emphysema usually effect?

A

VLBW infants with RDS (occurs in up to 25%)

39
Q

Risk factors for pulmonary haemorrhage

A
  • Acute pulmonary infection
  • Severe asphyxia
  • RDS
  • Assisted ventilation
  • PDA
  • Bleeding diathesis (HDN, thrombocytopenia)
  • Surfactant treatment
40
Q

Treatments for acute pulmonary haemorrhage

A
  • Blood replacement
  • Intratracheal adrenaline
  • Tamponading by increasing mean airway pressure
  • Surfactant administration (intraalveolar blood can displace/inactivate surfactant)

Neonatal Medicine (2 decks)

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