ICU · Respiratory
Acute severe community-acquired pneumonia: pulmonary complications and ARDS
Also known as CAP complicated by ARDS · Pneumonia-induced ARDS · Pulmonary ARDS vs non-pulmonary ARDS
Severe CAP can progress to ARDS (acute respiratory distress syndrome) — direct lung injury from pulmonary infection. Pulmonary ARDS (from pneumonia, aspiration) vs non-pulmonary ARDS (from sepsis, trauma, pancreatitis): pulmonary ARDS has more consolidation (less recruitable lung) and a worse response to PEEP. Diagnosis: Berlin definition (acute timing, bilateral infiltrates, not fully explained by cardiac failure, PaO2/FiO2 <300). Management: lung-protective ventilation (VT 6 mL/kg, plateau <30, minimise driving pressure), prone positioning (PaO2/FiO2 <150), conservative fluid strategy, treat underlying pneumonia.
Checked against its sources on 14 Oct 2026
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- Pulmonary ARDS (from pneumonia) has more consolidation, less recruitable lung, may respond poorly to high PEEP
- Distinguish ARDS from severe pneumonia without ARDS: ARDS has bilateral infiltrates + PaO2/FiO2 <300 + non-cardiogenic
- Prone positioning is beneficial in severe ARDS regardless of cause (PROSEVA)
- Conservative fluid strategy improves lung outcomes (FACTT) but may be challenging in septic shock
- Pulmonary ARDS tolerates LOWER PEEP — consolidation is not recruitable; high PEEP overdistends healthy lung
- Aggressive recruitment manoeuvres HARM (ART trial) — do not use routinely
- Pleural fluid pH <7.2 = complicated parapneumonic effusion — needs a chest tube, not antibiotics alone
- Loculated effusion failing drainage: use COMBINATION intrapleural tPA + DNase (MIST2), not either agent alone
- Lung abscess (in lung) is NOT empyema (in pleura) — CT with contrast distinguishes them; persistent abscess warrants bronchoscopy to exclude obstruction
- Bacteraemic CAP seeds distant sites — echo all S. aureus bacteraemia; rule out meningitis in invasive pneumococcal disease
- Rising lactate + falling platelets + prolonged PT in CAP = septic DIC (ISTH scoring) — escalate source control
- Refer EARLY for VV-ECMO in refractory ARDS (PaO2/FiO2 <80 despite optimisation + proning) — patients ventilated over 7 days were excluded from CESAR
Severe community-acquired pneumonia (CAP) is the single commonest cause of ARDS worldwide. The same pneumonia that fills alveoli with inflammatory exudate can, in a subset of patients, trigger the runaway diffuse alveolar damage (DAD) cascade that defines ARDS. Beyond the lung, bacteraemic CAP seeds the pleura (effusion, empyema), destroys parenchyma (abscess), disseminates (endocarditis, meningitis, septic arthritis), and drives systemic organ failure (AKI, DIC). This topic follows that chain: how severe pneumonia becomes ARDS, how to ventilate it, and how to recognise and manage the complications that determine who survives. [1][25]
Meet the patient
It is the small hours in the ICU. A middle-aged man with a five-day history of productive cough, fever, and rigors is intubated for type 1 respiratory failure. The CXR shows bilateral opacities with dense right-sided consolidation and a moderate left pleural effusion. On high PEEP and high FiO2 his saturation barely holds despite maximal support. Plateau pressure is above the lung-protective ceiling, driving pressure high. He is hypotensive on noradrenaline, lactate raised, platelets low with a prolonged INR and low fibrinogen, creatinine tripled from baseline. Urine pneumococcal antigen positive. The trainee asks: is this ARDS, and how do we ventilate it; what about the effusion, the DIC, the kidneys? Three questions wearing one disease. [1][2]
You answer in three moves. First, confirm ARDS by Berlin criteria and start lung-protective ventilation immediately. Second, look for the complications — pleural, parenchymal, systemic — because each one lifts the mortality curve. Third, treat the pneumonia, not just the syndrome. [1][3]
References27ShowHide
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