Synopsis
Recognise ARDS as acute inflammatory hypoxaemic respiratory failure, treat its precipitant, and deliver lung-protective critical care with timely proning and ECMO referral when conventional support is failing.
- ARDS is acute hypoxaemic respiratory failure from diffuse inflammatory lung injury with bilateral opacities not primarily explained by heart failure, collapse or pleural fluid.
- Common precipitants are pneumonia, non-pulmonary sepsis, aspiration, pancreatitis, major trauma, transfusion and inhalational injury; more than one trigger may coexist.
- Establish timing, oxygenation severity and the level of PEEP or CPAP, but never delay supportive care to complete a formal label.
- Actively assess cardiac function and fluid status because cardiogenic oedema can mimic or coexist with ARDS.
- High-flow nasal oxygen may support selected patients, but tachypnoea, large respiratory effort, shock, hypercapnia, worsening acidosis or deteriorating mentation predicts failure.
- In invasive ventilation use low tidal volume based on predicted, not actual, body weight and limit plateau pressure; accept carefully monitored permissive hypercapnia when appropriate.
- Prone ventilation improves outcomes in moderate to severe ARDS when used early and for prolonged sessions by a trained team alongside lung-protective ventilation.
- After shock is controlled, a conservative fluid strategy usually reduces ventilator duration; ongoing positive balance worsens lung oedema.
- Do not use high-frequency oscillation routinely. Inhaled pulmonary vasodilators are rescue bridges, not proven mortality treatment.
- Discuss ECMO early with a commissioned centre for potentially reversible severe respiratory failure despite optimised protective ventilation and proning; transfer becomes riskier after collapse.
Key red flags
A recent insult followed by increasing oxygen need, tachypnoea and bilateral opacities with no dominant hydrostatic explanation should prompt early ICU review even before invasive ventilation.
Low PaO2 relative to FiO2 despite PEEP or CPAP, diffuse shunt physiology and reduced compliance indicate more severe disease and strengthen the case for early proning and advanced support.
Persistently high respiratory rate, vigorous inspiratory effort, worsening hypoxaemia, hypercapnia, acidosis, shock or altered mentation indicates that high-flow or NIV is not safely containing the illness.
Excess tidal volume for predicted body weight, high plateau or driving pressure, repeated derecruitment and patient–ventilator dyssynchrony can worsen otherwise reversible lung injury.
Falling haemoglobin with haematuria suggests alveolar haemorrhage; marked eosinophilia, immunosuppression, drug exposure or a focal bronchial distribution should redirect investigation.
Investigation priorities
Quantify oxygenation, ventilation and acid-base trajectory and support severity assessment.
Management branches
Acute hypoxaemia with new bilateral pulmonary opacities.
- Start monitored oxygen support and involve ICU early while documenting timing, FiO2, blood gases and work of breathing.
- Search immediately for pneumonia, sepsis, aspiration, trauma, pancreatitis, transfusion, inhalation, drug injury and immune haemorrhage.
- Use cardiac assessment to determine whether left-heart congestion is dominant, absent or coexisting.
- Treat the cause promptly, including antimicrobials and source control for high-risk sepsis, without waiting for every test.