Acute Respiratory Distress Syndrome (ARDS)

Acute respiratory distress syndrome (ARDS) occurs when the permeability of alveolar capillaries increases, leading to fluid (hyaline) accumulation in the alveoli. This type of fluid accumulation is known as non-cardiogenic pulmonary oedema.

It peaks between 60 and 70 years of age and has a mortality of ~ 50 – 75%.

Definition (diagnostic criteria) of ARDS

1. Onset: < 7 days from time of insult
2. Imaging: Bilateral alveolar infiltrates on chest radiography or CT scan
3. Origin: No evidence of cardiac disease (PCWP ≤ 18 mmHg); If there is cardiac disease the infiltrates are beyond the degree of heart failure
4. Hypoxia: Severe hypoxaemia – PaO2/FiO2 ≤ 200

+/- Total thoracic compliance < 30 mL/cmH20

Causes of ARDS

• Risk factors
  • Advanced age
  • Cigarette smoking
  • Genetic polymorphisms related to inflammation, coagulation, and endothelial dysfunction
  • Obesity
  • Diabetes
  • Chronic liver disease
  • Mechanical ventilation strategies which can exacerbate lung injury
    • High tidal volumes
    • High airway pressures
  • Fluid management
    • Excessive fluid administration
  • Oxygen toxicity
    • Prolonged exposure to high FiO2
• Pathophysiology (stages)
  1. Inflammation
     • The insult causes release of inflammatory mediators → increased alveolar capillary permeability and endothelial dysfunction
  2. Exudation
     • Endothelial/epithelial injury → alveolar oedema → hyaline deposition → severe hypoxaemia
  3. Proliferation
     • Type II pneumocytes proliferate → repair begins
  4. Recovery vs fibrosis
     • The lungs may recover or undergo fibrosis
• Signs and symptoms
  • Acute onset
  • Severe shortness of breath
  • Cyanosis
  • Tachypnoea
  • Tachycardia
  • Peripheral vasodilation
  • Bilateral fine inspiratory crackles
• Differentials
  • Cardiogenic pulmonary oedema
  • Bilateral pneumonia
  • Acute interstitial pneumonia
  • Interstitial lung disease exacerbation
  • Diffuse alveolar haemorrhage
  • Pulmonary vasculitis
  • Acute eosinophilic pneumonia
  • Organising pneumonia
  • Disseminated malignancy
• Investigations
  • Complete blood count
  • UEC
  • LFTs
  • Amylase
  • Coagulation profile
  • CRP
  • Blood cultures, sputum cultures, and respiratory tract samples
  • Bronchoalveolar lavage if standard cultures are negative
  • Arterial blood gas to assess hypoxaemia and calculate PaO2/FiO2 ratio
  • B-lines (interstitial oedema) on lung POCUS
  • Chest X-ray
    • Bilateral lung infiltrates (alveolar opacities)
    • The history, normal heart size and lack of pleural effusion suggests ARDS
  • CT chest if the diagnosis is uncertain
  • Echocardiography to exclude cardiogenic pulmonary oedema
  • Pulmonary artery catheter to measure pulmonary capillary wedge pressure (PCWP)
• Treatment
  • ICU admission
  • Treat the underlying cause
  • Respiratory support
    • Continuous positive airway pressure (CPAP) or mechanical ventilation. Most patients require mechanical ventilation.
    • Increased PEEP of 8 – 12 cmH20. Note that a higher PEEP may cause overdistension, barotrauma, hypotension, and increased dead space.
    • Tidal volume of 4 – 6 ml/kg to keep Pplat < 30 cmH20. A tidal volume lower than this can cause atelectotrauma while a tidal volume higher than this can cause volutrauma.
    • Adjust RR up to 35/min to maintain acceptable pH
    • Avoid hyperoxygenation. Titrate FiO2 to < 60% as soon as possible while maintaining an SpO2 of 90 – 94%
    • Increase inspiratory time using an inverse I:E ratio of 1:1 or 2:1. More time is needed to inspire since the lungs have reduced compliance
    • Proning improves V/Q mismatch by perfusing the posterior lung – it has a larger volume – and reducing regional overdistension. Proning is done 8 – 16 hours a day but carries the risk of aspiration, tube dislodgement, difficult nursing, and difficult turning during CPR
    • Intermittent high pressures, i.e., raising the PIP and PEEP intermittently. PIP of 30 cmH20 for 30 seconds.
    • Neuromuscular blockade or sedation to prevent patient ventilator asynchrony.
  • Circulatory support
    • Keep assessing fluid status and avoid a positive fluid balance. A positive fluid balance exacerbates pulmonary oedema.
    • Invasive hemodynamic monitoring (arterial line or Swan-Ganz catheter) to monitor PCWP and cardiac output
    • Conservative fluid management
    • Inotropes, vasodilators, and blood transfusion to maintain cardiac output and oxygen delivery
    • Nitric oxide may be considered for pulmonary hypertension
    • Haemofiltration may be needed in renal failure to achieve negative fluid balance
  • Supportive treatment
    • Nutritional support: enteral feeding is preferred
    • DVT prophylaxis
    • Stress ulcer prophylaxis when indicated
    • Glycaemic control
    • Pressure-area care
    • Steroids for patients with fat embolization and pneumocystosis