Acute respiratory distress syndrome (ARDS)

‘Most of us are heaving through corrupted lungs’ – Daughter – ‘Youth’

Acute respiratory distress syndrome (ARDS) is an acute, diffuse, inflammatory lung insult, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue.

It is characterised by hypoxaemia and bilateral radiographic opacities, associated with increased physiological dead space and decreased lung compliance.

The “Berlin definition” (The ARDS Definition Task Force) clarified the criteria and classification of ARDS.

The four criteria are as follows:

  1. Onset: Syndrome occurring within 1 week of known clinical insult
  2. Imaging: Bilateral opacities consistent with pulmonary oedema (on either chest X-ray or CT scan)
  3. Oedema: Pulmonary oedema not fully explained by cardiac failure or fluid overload. Objective assessment of cardiac function (i.e. echo) may be required
  4. P:F ratio<39.9 (300 in old money)

And the classification:

  • Mild: P:F<39.9 but >26.6kPa (200-300 in old money)
  • Moderate: P:F<26.6 but >13.3kPa (100-200 in old money)
  • Severe: P:F<13.3kPa (<100 in old money)

The above are based on 5cmH20 PEEP. Oxygenation can be assessed on NIV for the mild classification. For moderate and severe the patient must be intubated and receiving ventilatory assistance.

Mortality for mild, moderate and severe ARDS is around 27%, 32% and 47%, respectively

Risk factors for ARDS can be classified as direct (pulmonary) and indirect (non-pulmonary)

Direct Indirect
Pneumonia Sepsis (non-pulmonary)
Aspiration of gastric contents Polytrauma
Lung contusion Massive transfusion
Fat embolism Pancreatitis
Near-drowning Cardiopulmonary bypass
Inhalational injury Pregnancy-related (amniotic embolism, eclampsia)
Reperfusion injury  Tumour lysis syndrome

”What is the pathophysiology of ARDS regarding cell types and cell mediators?”

…”ummmmm” – click here: ARDS – pathophysiology

”What are the management principles in ARDS?”

Management principles include close attention to mechanical ventilation, sedation, neuromuscular blockade, fluid balance and good housekeeping.

  • Lung protective ventilation (see below)
  • Sedation improves compliance with mechanical ventilation and reduces oxygen consumption. Must be balanced against the risks of excessive or prolonged sedation.
  • Neuromuscular blockade similarly improves compliance and decreases oxygen consumption. There is evidence to suggest that their use in the first 48 hours of severe ARDS decreases mortality.
  • Use of a ‘conservative’ fluid strategy leads to improved lung function and reduced number of ventilator days but no reduction in mortality, when compared to a ‘liberal’ fluid strategy. Avoid ‘drying out’ patients – often the lungs will be the last place to give up their water, and in the mean time the kidneys will suffer with no benefit to oxygenation
  • Keeping a good house – DVT prophylaxis, ulcer prophylaxis, nutrition, infection control

Low tidal volume ventilation is the mainstay of management

The ARDS network study demonstrated a significant mortality benefit associated with targeting a tidal volume of 6ml/kg predicted body weight and a plateau pressure of <30cmH2O. This was compared to a vT of 12ml/kg which was apparently decided over the phone as an arbitrary large number to increase the chances of positive study findings

ECMO

Referral of patients with potentially reversible severe ARDS to a regional ECMO centre improves mortality and is cost effective