ARDS is a clinical syndrome of acute, diffuse, inflammatory lung injury leading to increased pulmonary vascular permeability, bilateral pulmonary infiltrates, and severe hypoxaemia. It is defined by the 2012 Berlin definition, which requires four criteria to be met simultaneously:

• Timing: acute onset within one week of a known clinical insult or new/worsening respiratory symptoms
• Chest imaging: bilateral opacities on CXR or CT not fully explained by effusions, lobar/lung collapse, or nodules
• Origin of oedema: respiratory failure not fully explained by cardiac failure or fluid overload
• Oxygenation: PaO2/FiO2 ratio <300 mmHg with PEEP or CPAP ≥5 cmH2O

ARDS Severity	PaO2/FiO2 Ratio	Approximate Mortality
Mild	200–300 mmHg	~27%
Moderate	100–200 mmHg	~32%
Severe	<100 mmHg	~45%

Pathophysiology of ARDS

ARDS results from a dysregulated inflammatory response — triggered by either a direct pulmonary insult (pneumonia, aspiration, inhalation injury) or an indirect systemic insult (sepsis, pancreatitis, major trauma, transfusion-related injury). Inflammatory mediators damage the alveolar-capillary membrane, causing protein-rich fluid to leak into the alveolar spaces. This produces the characteristic diffuse bilateral infiltrates on imaging, reduces lung compliance dramatically, and causes the profound shunt physiology responsible for the refractory hypoxaemia.

A crucial concept in ARDS is the ‘baby lung’ — the available aerated lung volume in ARDS is dramatically reduced (sometimes to only 20–30% of normal), even though total lung weight is increased by the oedema. This means conventional tidal volumes (400–600 mL) are being delivered into a much smaller volume than expected, causing regional overdistension of the remaining aerated lung and perpetuating injury. This is the physiological basis for low tidal volume ventilation.

Lung-Protective Ventilation in ARDS

The cornerstone of ARDS management is lung-protective ventilation. The ARDSNet protocol, which demonstrated a 22% relative reduction in 28-day mortality with 6 mL/kg PBW versus 12 mL/kg PBW, established this as the definitive standard of care. Key principles are: VT 4–6 mL/kg PBW, plateau pressure <30 cmH2O, driving pressure <15 cmH2O, and titrated PEEP to maintain oxygenation with acceptable driving pressures. Permissive hypercapnia — accepting PaCO2 up to 8–10 kPa to avoid unsafe pressures and volumes — is an accepted part of the strategy.

Prone Positioning

Prone positioning — turning the patient face-down for 16 or more hours per day — redistributes ventilation and perfusion more evenly across the lung, reducing dorsal atelectasis, improving V/Q matching, and reducing driving pressure. The PROSEVA trial demonstrated a 16% absolute mortality reduction in severe ARDS (PaO2/FiO2 <150 mmHg) when proning was applied early and for prolonged sessions. Current guidelines recommend prone positioning for at least 16 hours per day in patients with moderate-to-severe ARDS (PaO2/FiO2 <150 mmHg) despite optimised conventional ventilation. It requires a coordinated team of at least 5 people and careful attention to pressure area care, line security, and airway management during the turn.

CLINICAL PEARL Prone positioning is one of the most evidence-based and impactful interventions in ARDS. The mortality benefit is large. If a patient has severe ARDS and is not being proned, there should be a clear documented reason why not.