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Pulmonary and Critical Care Medicine›Condition·Updated Jul 11, 2026·v1

Acute Respiratory Distress Syndrome

ARDS is a common, life-threatening form of hypoxemic respiratory failure with a mortality of 30-40%; management centers on lung-protective ventilation, prone positioning for severe hypoxemia, and early dexamethasone, with ECMO and lung transplantation as rescue options for selected patients.

High Evidence461 references·3,030 words·13 min read·v1
ARDSacute respiratory distress syndromecritical caremechanical ventilationprone positioningcorticosteroidsECMOdriving pressurelung-protective ventilation

Quick Reference

RxDrug of choiceDexamethasone 20 mg IV daily for 5 days, then 10 mg daily for 5 days (for moderate-to-severe ARDS).
AltAlternativesMethylprednisolone may be considered if dexamethasone unavailable, but evidence is strongest for early dexamethasone; avoid late initiation (>14 days).
⊘AvoidHigh-frequency oscillation, statins (simvastatin, rosuvastatin), exogenous surfactant, beta-agonists, late corticosteroids (>14 days), prolonged recruitment maneuvers.
DxTest of choiceArterial blood gas to calculate PaO2/FiO2 ratio on PEEP ≥5 cm H2O.
ScKey scoreBerlin severity classification (PaO2/FiO2: mild 200-300, moderate 100-200, severe <100); driving pressure (ΔP <15 cm H2O) is the strongest modifiable predictor of mortality.
→When to referFor ECMO if PaO2/FiO2 <80 for >6 hours or pH <7.25 with PaCO2 ≥60 despite optimal ventilation. For lung transplant if irreversible ARDS after prolonged support (>47 ECMO days may predict oxygen need).
Lung-protective ventilation (6 mL/kg, Pplat ≤30, driving pressure <15) and early prone positioning for PaO2/FiO2 <150 are the most impactful interventions; dexamethasone reduces mortality in moderate-to-severe ARDS. ECMO and lung transplantation are rescue options for selected patients.
Acute respiratory distress syndrome (ARDS) is an acute, diffuse inflammatory lung injury characterized by increased pulmonary vascular permeability and hypoxemia. It occurs in ~10% of ICU admissions, with mortality 30-40%. Management centers on lung-protective ventilation, prone positioning, and addressing the underlying cause.

Overview and Recommendations

Background

  • •ARDS is an acute, diffuse inflammatory lung injury defined by the Berlin 2012 criteria: acute onset ≤1 week, bilateral opacities on imaging, and PaO₂/FiO₂ ≤300 mm Hg on at least 5 cm H₂O PEEP, not fully explained by cardiac failure or fluid overload. The 2024 New Global Definition extended eligibility to include high-flow nasal oxygen ≥30 L/min and SpO₂/FiO₂ ≤315 (if SpO₂ ≤97%) as a surrogate when ABG is unavailable.
  • •It affects approximately 10% of all ICU admissions and 23% of mechanically ventilated patients worldwide; in the U.S., over 190,000 cases occur annually. Despite declining mortality from ~50% in the 1990s to 30-40% in contemporary trials, ARDS remains a major cause of death, with hospital mortality rising from 27% (mild) to 35% (moderate) to 45% (severe) in the LUNG SAFE cohort.
  • •Two reproducible molecular subphenotypes, hyperinflammatory (≈35% of patients, elevated IL-6/IL-8, lower bicarbonate, more shock, higher mortality) and hypoinflammatory (≈65%), have been identified by latent class analysis across multiple RCT cohorts. These subphenotypes show differential treatment responses to PEEP, fluid management, and statins, driving a precision-medicine approach.
  • •The histologic hallmark is diffuse alveolar damage (DAD), characterized by hyaline membranes, edema, and type II cell hyperplasia. However, DAD is present in only 45% of patients meeting clinical ARDS criteria; its presence nearly doubles the odds of death (pooled OR 1.81, 95%). Alternative histologies include organizing pneumonia and pulmonary edema without DAD.
  • •Key risk factors include sepsis (most common), pneumonia (bacterial, viral), aspiration of gastric contents, major trauma, and transfusion. Elevated driving pressure (>12 cm H₂O) at intubation independently predicts ARDS development (OR 1.20 per cm H₂O). Modifiable factors include crystalloid volume in the first 6 hours after injury (aOR 1.19 per liter) and ambient air pollution (long-term PM₁₀ per 10 μg/m³ OR 2.24).

Evaluation

  • •Suspect ARDS in any patient with acute onset of hypoxemic respiratory failure, bilateral opacities on chest imaging, and no evidence of cardiogenic edema. The classic presentation is severe dyspnea, tachypnea >30 breaths/min, and refractory hypoxemia developing within 72 hours of an inciting event (sepsis, pneumonia, aspiration, trauma, transfusion).
  • •Ask about the timing and progression of dyspnea, presence of cough (initially dry, later productive of frothy sputum), fever, and risk factors. Orthopnea and paroxysmal nocturnal dyspnea are absent, helping differentiate from cardiogenic pulmonary edema. Inquire about smoking history, recent travel, drug exposures, and immunocompromised status.
  • •Examine for tachypnea, use of accessory muscles, intercostal retractions, and diffuse bilateral crackles on auscultation (present in >90%). Note dullness to percussion over consolidated areas. Cyanosis is a late sign correlating with severe hypoxemia (SpO₂ <85%). Wheezing is uncommon and should raise suspicion for alternative diagnoses.
  • •Order an arterial blood gas to calculate PaO₂/FiO₂ ratio. The Berlin definition requires PaO₂/FiO₂ ≤300 on at least 5 cm H₂O PEEP for mild ARDS. If ABG is unavailable, use SpO₂/FiO₂ ≤315 when SpO₂ ≤97% (New Global Definition). Note that in high-altitude regions, the corrected SpO₂/FiO₂ cutoff may be higher (e.g., 360.4 in Xining cohort).
  • •Obtain chest imaging (X-ray or CT) to confirm bilateral opacities not fully explained by effusions or atelectasis. CT is more sensitive for detecting underlying diffuse parenchymal lung disease. Lung ultrasound is an accepted alternative; the LUS-ARDS score (bilateral aeration scores and anterolateral pleural line abnormalities) has an AUC of 0.80.
  • •Perform echocardiography to exclude cardiogenic pulmonary edema, assess left ventricular function, valve pathology, and estimated filling pressures. Natriuretic peptides can be adjunctive but are not diagnostic. Right ventricular dysfunction is common and associated with worse outcomes.
  • •Apply the Berlin severity classification: mild (200-300 mm Hg), moderate (100-200 mm Hg), severe (<100 mm Hg) at minimum PEEP of 5 cm H₂O. Consider the PFP ratio (PaO₂/[FiO₂ × PEEP]) if PEEP varies, as it improves mortality discrimination (pooled AUC 0.84).
  • •In atypical presentations (e.g., no clear ARDS risk factor, eosinophilia, hemoptysis, rapid progression), perform bronchoscopy with bronchoalveolar lavage (BAL) for cultures, cytology, and fungal markers to rule out acute eosinophilic pneumonia, diffuse alveolar hemorrhage, DPLD exacerbation, or infection. Transbronchial lung cryobiopsy can provide histologic confirmation of DAD if needed.
  • •Assess for the hyperinflammatory subphenotype using plasma biomarkers (IL-8, bicarbonate, protein C), a parsimonious 3-variable model identifies phenotypes with AUC 0.94-0.95. While not yet standard of care, this informs clinical trial enrollment and may guide differential treatment (e.g., conservative fluids may harm hyperinflammatory patients).
  • •Do not delay initiation of lung-protective ventilation while awaiting diagnostic test results. Once the diagnosis is suspected, commence 6 mL/kg tidal volume and PEEP per the ARDSNet table immediately. A diagnostic pitfall is misclassifying cardiogenic edema, DPLD exacerbation, or bilateral pneumonia as ARDS, careful assessment for an ARDS risk factor and absence of left atrial hypertension is essential.

Management

  • •Initiate lung-protective ventilation with a target tidal volume of 6 mL/kg predicted body weight (PBW) and maintain plateau pressure ≤30 cm H₂O. Prioritize driving pressure <15 cm H₂O (ΔP = Pplat - PEEP), as it is the strongest modifiable predictor of mortality. The ARMA trial (n=861) showed a mortality reduction from 39.8% to 31.0% (NNT=12) with this strategy.
  • •Set PEEP using the ARDSNet lower PEEP/FiO₂ table. Consider -guided PEEP if available; in patients with high lung recruitability, EIT-guided PEEP assigned higher PEEP and reduced mortality (35.6% vs 60.0%; HR 0.49). Avoid prolonged recruitment maneuvers, they are harmful (RR 1.37 vs higher PEEP alone).
  • •Target oxygenation: SpO₂ 92-96% or PaO₂ 60-80 mm Hg. Avoid both hypoxemia and hyperoxia. The LOCO2 trial (n=205) found increased 90-day mortality with conservative PaO₂ targets of 55-70 mm Hg (44.4% vs 30.4%) and more mesenteric ischemic events. Five mesenteric ischemic events occurred in the conservative group.
  • •For PaO₂/FiO₂ <150 mm Hg, start prone positioning within 12 hours of ARDS onset, aiming for ≥16 continuous hours per session. The PROSEVA trial showed a dramatic 28-day mortality reduction (16.0% prone vs 32.8% supine; HR 0.39; NNT=6). Benefit is independent of baseline respiratory system elastance. In non-intubated COVID-19 patients, awake prone positioning reduced intubation (OR 0.35) and mortality (OR 0.38).
  • •Administer early dexamethasone 20 mg IV daily for 5 days, then 10 mg daily for 5 days. The DEXA-ARDS trial (n=277, moderate-to-severe ARDS) showed increased ventilator-free days (mean 4.8 days) and reduced 60-day mortality (21% vs 36%; NNT=7). Do not initiate corticosteroids after 14 days of ARDS (late methylprednisolone increases mortality).
  • •Use a conservative fluid strategy after initial resuscitation: target central venous pressure <4 mm Hg or pulmonary artery occlusion pressure <8 mm Hg, using diuretics or fluid restriction as needed. The FACTT trial showed increased ventilator-free days but no overall mortality benefit. Note: conservative fluids may increase mortality in the hyperinflammatory phenotype (interaction P=0.0039).
  • •Reserve neuromuscular blockade (cisatracurium infusion) for patients with severe ventilator dyssynchrony or driving pressure >15 cm H₂O despite deep sedation. The ROSE trial (n=1006) found no 90-day mortality benefit (42.5% vs 42.8%). A secondary analysis suggests benefit in patients with high respiratory system elastance (Ers ≥2 cm H₂O/[mL/kg]; median ARR 9%, posterior probability 96%).
  • •For very severe ARDS (PaO₂/FiO₂ <50 mm Hg for >3 h, or <80 mm Hg for >6 h, or pH <7.25 with PaCO₂ ≥60 mm Hg), refer for venovenous ECMO evaluation at a high-volume center. The EOLIA trial showed 60-day mortality 35% with ECMO vs 46% with conventional care (RR 0.76; 95% CI 0.55-1.04). A meta-analysis of VV-ECMO trials demonstrated a mortality benefit (RR 0.64).
  • •Provide pharmacologic VTE prophylaxis with low molecular weight heparin per institutional protocol. In patients on ECMO, a restrictive transfusion threshold of hemoglobin <8 g/dL was associated with lower hazard of death (aHR 0.48) in a retrospective cohort. Anticoagulation targets vary; monitor for bleeding (46% of ECMO patients) and thrombocytopenia (27%).
  • •Implement a daily sedation interruption and spontaneous breathing trial protocol to reduce duration of mechanical ventilation, prevent ventilator-associated pneumonia, and minimize ICU-acquired weakness. Early rehabilitation and physical therapy should be initiated as soon as hemodynamically stable; mobilization during ECMO is feasible and safe (2% adverse event rate).
  • •Avoid high-frequency oscillatory ventilation (increased mortality in OSCILLATE: 47% vs 35%; RR 1.33), statins (rosuvastatin in SAILS and simvastatin in HARP-2: no benefit), exogenous surfactant (no improvement in outcomes), and beta-agonists (increased 90-day mortality: RR 1.39; increased arrhythmias).
  • •Monitor for complications: barotrauma (pneumothorax, persistent air leak), VTE (53% incidence on ECMO), circuit thrombosis on ECMO, ventilator-associated pneumonia, pulmonary hemorrhage on ECMO (63% on autopsy), right ventricular dysfunction (prognostic determinant), and neuromuscular weakness (especially with prolonged NMB or corticosteroids).
  • •For patients with irreversible lung failure despite prolonged support (e.g., >47 ECMO days predicts oxygen need at 6 months), consider lung transplant evaluation at a specialized center. In a European cohort, 70% of ARDS lung transplant survivors returned to work. Selection criteria include absence of multiorgan failure, potential for rehabilitation, and psychosocial stability.

Board Review — High Yield

  • •Berlin definition, Acute onset (≤1 week), bilateral opacities, PaO2/FiO2 ≤300 on PEEP ≥5 cm H2O, not fully explained by cardiac failure or fluid overload.
  • •PROSEVA trial, Prone positioning for ≥16 h/day in severe ARDS (PaO2/FiO2 <150) reduces 28-day mortality from 32.8% to 16.0% (HR 0.39; NNT=6).
  • •DEXA-ARDS trial, Early dexamethasone 20 mg IV daily ×5, then 10 mg ×5, reduces 60-day mortality from 36% to 21% (NNT=7) and increases ventilator-free days by 4.8.
  • •Driving pressure, ΔP = Pplat - PEEP. Target <15 cm H2O; it is the strongest modifiable predictor of mortality, and the benefit of low tidal volume varies by elastance.
  • •Hyperinflammatory phenotype, Identified by IL-8, bicarbonate, protein C; ~35% of ARDS patients; higher mortality (39% vs 17% at 28 days); responds differently to PEEP, fluids, and statins.
  • •EOLIA trial, VV-ECMO for very severe ARDS (PaO2/FiO2 <50 for >3h, <80 for >6h, or pH<7.25 with PaCO2 ≥60) showed 60-day mortality 35% vs 46% (RR 0.76; 95% CI 0.55-1.04; p=0.09).
  • •ROSE trial, Routine neuromuscular blockade (cisatracurium) for moderate-severe ARDS does not improve 90-day mortality (42.5% vs 42.8%); benefit may be limited to high-elastance patients.
  • •ARMA trial, Low tidal volume (6 mL/kg PBW) reduces mortality from 39.8% to 31.0% compared with 12 mL/kg (NNT=12); remains the strongest mortality benefit signal in ARDS history.
  • •Avoid, High-frequency oscillation (increased mortality), statins (no benefit), exogenous surfactant (no benefit), beta-agonists (increased mortality), late corticosteroids (>14 days) (harm).
  • •DAD, Diffuse alveolar damage is the histologic hallmark but present in only 45% of clinical ARDS; doubles odds of death (OR 1.81).

Deep Dive — Evidence Details

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