Acute Lung Injury - ARDS (12/12/16) - Sunderram

Question 1

What is acute respiratory distress syndrome?

Answer 1

• Diffuse damage to alveolar-capillary interface (diffuse alveolar damage)
• Not only are you not able to exchange gas but you’re not able to keep air sacs open as well
• Leakage of protein-rich fluid → edema
  
  • Edema combines w necrotic epithelial cells → hyaline membranes in alveoli

Question 2

Clinical Features

Answer 2

Hypoxemia + cyanosis w respiratory distress

• Cause: due to thickened diffusion barrier and collapse of air sacs (increased surface tension)
  ​

‘White-out’ on CXR

Question 3

A major event usually precedes ARDS (9).

Timing of ARDS presents within 1 week of a known event.

Answer 3

• Sepsis
• Infection
• Shock
• Trauma
• Aspiration
• Pancreatitis
• DIC (disseminated intravascular coagulation)
• Hypersensitivity rxns
• Drugs

Activation of neutrophils induces protease- and free radical-mediated damage of type I and II pneumocytes.

Question 4

Answer 4

1. Insult (i.e. sepsis, trauma, severe pancreatitis) triggers:
2. Inflammatory cells + cytokines which cause:
3. Capillary endothelial + alveolar epithelial injury
4. Inc. permeability → protein-rich interstitial and alveolar edema
5. Dec. surfactant production + function → atelectasis

DIFFUSE ALVEOLAR DAMAGE:

• Acute inflammation
• Edema
• Hyaline membranes
• Hemorrhage

Question 5

ARDS Treatment

Answer 5

• Treat underlying cause
• Ventilation with positive end-expiratory pressure (PEEP)
  
  • However, this may lead to ventilator induced lung injury (VILI)
    
    • Barotrauma (popping of alveoli)
      
      • Pneumothorax
      • Pneumomediastinum
      • Subcutaneous emphysema

Note: recovery may be complicated by interstitial fibrosis; damage and loss of type II pneumocytes → scarring and fibrosis

Question 6

Neonatal Respiratory Distress Syndrome

Answer 6

Respiratory distress due to inadequate surfactant levels

• Surfactant made by Type II pneumocytes (lecithin = major component)
• Decreases surface tension in lung, preventing alveolar collapse post-expiration
• Lack of surfactant → alveolar collapse + hyaline membrane formation

Question 7

NRDS is associated with:

Answer 7

• PREMATURITY
  
  • Surfactant production begins at 28 weeks; adequate levels not reached until 34 weeks.
• Caesarian section delivery
  
  • Due to lack of stress-induced steroids
    
    • Steroids inc. surfactant synthesis
• Maternal diabetes
  
  • Insulin decreases surfactant production

Question 8

NRDS

Clinical features

Answer 8

• Increasing respiratory effort after birth
  
  • Tachypnea w use of accessory muscles, and grunting
• Hypoxemia w cyanosis
• Diffuse granularity of the lung (‘ground-glass’ appearance) on x-ray

Question 9

NRDS

Complications

Answer 9

• Hypoxemia inc. risk for persistence of PDA and necrotizing enterocolitis (due to dec. oxygen going to gut)
• Supplemental oxygen inc. risk for free radical injury
  
  • Retinal injury → blindness
  • Lung damage → bronchopulmonary dysplasia