Acute respiratory distress syndrome: recognition and protective ventilation

Manage now— do this, in order

• Identify and treat the precipitating condition first: more than 80% of deaths are from sepsis and non-pulmonary organ failure, not hypoxaemia — give broad-spectrum antibiotics early where infection is suspected and pursue source control. The ventilator buys time; only source control and antimicrobial therapy cure.Doctor / Nurse
• Sit the patient up and give a non-rebreathing reservoir mask at 15 L/min while unstable — severe hypoxaemia is more dangerous than hypercapnia. Once stable, titrate down to SpO2 88-95% with PaO2 above 55 mmHg (7.3 kPa), reducing FiO2 towards 0.6 or less as fast as is safe — hyperoxia injures the lung.
• CPAP or high-flow nasal oxygen only as a strictly time-limited trial with pre-specified criteria — e.g. CPAP 8 cmH2O at FiO2 0.6, reassessed at 60 minutes: intubate if the respiratory rate remains above 30, SpO2 is below 90%, or the P/F has not improved. Delay in a tiring patient is the commonest avoidable harm in this syndrome.Doctor / Nurse
• Intubate for severe distress despite maximal therapy, confusion or falling conscious level, rising PaCO2 above 8 kPa, PaO2 below 8 kPa despite oxygen, inability to protect the airway, or shock. Ketamine 1-2 mg/kg IV is first choice if shocked; propofol 1-2 mg/kg IV only if haemodynamically stable; suxamethonium 1-1.5 mg/kg or rocuronium 1-1.2 mg/kg IV. Anticipate hypotension — crystalloid running and a vasopressor immediately available.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
• Ventilate protectively — the only intervention with a large, reproducible survival benefit: tidal volume 6 mL/kg predicted body weight (range 4-8), plateau pressure ≤ 30 cmH2O, PEEP at least 5 (usually 5-15) cmH2O, rate 16-20/min up to 30-35 for CO2, FiO2 1.0 initially then ≤ 0.6, targeting SpO2 88-95%, pH ≥ 7.30, MAP ≥ 65 mmHg. Calculate PBW from height, never measured weight.Doctor / NurseNot available at your setup — Mechanical ventilator.
• Measure the plateau pressure with a 0.5-1 second inspiratory hold after every change; if it exceeds 30 cmH2O reduce tidal volume in 1 mL/kg steps to a minimum of 4 mL/kg PBW. Accept permissive hypercapnia — manage CO2 with a higher rate, never by abandoning the protective volume, aiming pH ≥ 7.30 and tolerating down to 7.20.Doctor / Nurse
• Keep the lung dry once out of shock: aim for a consistently negative fluid balance with furosemide 20-40 mg IV slowly (child 0.5-1 mg/kg, max 2 mg/kg/dose), or an infusion of 5-10 mg/h. In hypotensive patients give small aliquots only — 250-500 mL (child 10 mL/kg), reassessed after each — reaching for a vasopressor rather than repeating boluses into a leaking lung.Doctor / Nurse
• Prone the severe patient early: prone positioning is the one rescue manoeuvre with a demonstrated survival benefit — 28-day mortality fell from 32.8% to 16.0% in severe ARDS (P/F below 150 mmHg) when applied early and for longer periods prone than supine.Doctor / Nurse
• Suspect tension pneumothorax in any ventilated patient who deteriorates — new hypoxia, unexplained rise in airway pressure, hypotension, unequal expansion, tracheal deviation, hyper-resonant hemithorax: needle decompress the 2nd intercostal space mid-clavicular line, then a chest drain. On sudden deterioration, disconnect and hand-ventilate with 100% oxygen while causes are excluded.Doctor / NurseNot available at your setup — Chest drain / tube thoracostomy.