Life-threatening acute lung injury characterized by diffuse alveolar damage, leading to increased capillary permeability (noncardiogenic pulmonary edema) and severe hypoxemic respiratory failure.
Common final pathway in critical illness (∼10–15% of ICU ventilated patients) with high mortality (∼40% overall, up to 45% in severe ARDS). Recognition and prompt lung-protective management improve outcomes, and distinguishing ARDS from cardiogenic edema is a frequently tested clinical skill.
Acute onset (within <1 week of precipitating insult) of dyspnea, tachypnea, and refractory hypoxemia often requiring intubation. Exam: diffuse crackles, respiratory distress (accessory muscle use), and possibly cyanosis despite supplemental O₂.
Common triggers: sepsis (most common), aspiration (gastric contents), pneumonia, severe trauma (e.g., pulmonary contusion), acute pancreatitis, massive transfusion (TRALI), burns, etc. Symptoms typically worsen 12–48 hours after the inciting event, progressing to respiratory failure.
Imaging: Chest X-ray – bilateral diffuse infiltrates (pulmonary edema) sparing costophrenic angles, often with normal heart size (no cardiomegaly), consistent with noncardiogenic edema. Chest CT – patchy areas of consolidation with normal lung regions (dependent lobes often denser). Lung ultrasound – B-lines (wet lung) in both ARDS and cardiogenic edema, but ARDS shows a patchy pattern (B-lines interspersed with normal aerated "spared" areas) plus subpleural consolidations and thick, irregular pleural line; cardiogenic edema shows diffuse uniform B-lines, a thin pleura, and often pleural effusions.
Laboratory studies: Arterial blood gas (ABG) reveals acute hypoxemicrespiratory failure (low PaO₂) with PaO₂/FiO₂ ≤ 300 mmHg (defining ARDS; severity: mild 200–300, moderate 100–200, severe ≤100). Early ARDS often causes respiratory alkalosis (low PaCO₂, high pH) from hyperventilation, though CO₂ may rise (acidosis) as fatigue and ventilatory failure ensue.
Suspect ARDS in any patient with acute respiratory failure and a known risk factor (e.g., sepsis, trauma). Exclude cardiogenic pulmonary edema: assess volume status and cardiac function (e.g., bedside echocardiogram, BNP). Historically, a pulmonary capillary wedge pressure (PCWP) < 18 mmHg supports ARDS over cardiac edema.
Confirm ARDS: obtain chest imaging to identify bilateral infiltrates and perform an ABG to calculate the PaO₂/FiO₂ ratio (ensure PEEP ≥5 cm H₂O or CPAP when assessing P/F ratio). Classify severity (mild/moderate/severe) based on P/F ratio. Rule out alternate diagnoses (e.g., diffuse alveolar hemorrhage, acute exacerbation of chronic lung disease) with appropriate tests (e.g., bronchoscopy if hemoptysis, CT scan if a focal process is suspected).
If ARDS is present, address any underlying cause (e.g., broad-spectrum antibiotics for pneumonia/sepsis, surgical management of trauma or pancreatitis, etc.) while providing supportive care. In mild cases (P/F 200–300) with minimal symptoms, high-flow nasal oxygen or noninvasive support can be tried; moderate to severe ARDS usually requires intubation and mechanical ventilation.
Monitor oxygenation and ventilation closely (continuous pulse ox and repeat ABGs). Prevent complications: use sedation to facilitate ventilation, elevate head of bed to reduce aspiration risk, provide stress ulcer and DVT prophylaxis, and watch for barotrauma or ventilator-associated pneumonia.
Condition
Distinguishing Feature
Cardiogenic pulmonary edema
Acute heart failure (e.g., MI) can mimic ARDS but with elevated JVP, S3 gallop, cardiomegaly, and often rapid improvement with diuretics.
Diffuse alveolar hemorrhage
Pulmonary capillaritis (e.g., vasculitis, Goodpasture) causes similar infiltrates and hypoxemia; look for hemoptysis and blood in alveoli (hemosiderin-laden macrophages) on bronchoalveolar lavage.
Acute eosinophilic pneumonia
Presents like ARDS in young patients (often smokers) but bronchoalveolar lavage shows eosinophils; responds dramatically to corticosteroids.
Mechanical ventilation (lung-protective strategy): Most ARDS patients require intubation. Use low tidal volumes (~6 mL/kg ideal body weight) and moderate-to-high PEEP to improve oxygenation, while limiting plateau pressure ≤30 cm H₂O. Accept permissive hypercapnia if needed (target pH >7.2) to avoid excessive pressures. Monitor driving pressure and adjust ventilator settings to minimize barotrauma.
Adjunctive therapies for severe ARDS: If PaO₂/FiO₂ remains <150 despite optimal ventilation (FiO₂ ≥0.6, PEEP high), employ prone positioning (turn patient prone ~16 hours/day) to improve V/Q matching. Consider short-term neuromuscular blockade (paralysis) in early severe ARDS to improve ventilator synchrony. Refractory cases may benefit from ECMO (extracorporeal membrane oxygenation) in specialized centers.
Conservative fluid management: Avoid fluid overload – use diuretics if necessary to achieve euvolemia, as a dry lung strategy is associated with better outcomes. Ensure adequate organ perfusion but prevent unnecessary IV fluids that can worsen pulmonary edema.
Medications: No specific drug reverses ARDS, but corticosteroids are often considered in moderate-severe ARDS (especially early in the course) to reduce inflammation. Manage symptoms with sedation/analgesia for comfort and to reduce oxygen demand. If severe hypoxemic pulmonary hypertension is present, inhaled pulmonary vasodilators (e.g., nitric oxide) may transiently improve oxygenation (no proven mortality benefit).
Underlying cause: Treat it aggressively (e.g., antibiotics for infection, surgery for trauma, etc.) alongside supportive care. Recovery from ARDS can take weeks; many survivors require rehabilitation due to lingering lung injury or fibrosis.
Think ARDS when a critically ill patient has refractory hypoxemia with bilateral infiltrates not due to heart failure. The key is noncardiogenic edema – normal heart size on X-ray and normal PCWP, distinguishing it from cardiogenic pulmonary edema.
Management cornerstone is low tidal volume ventilation (≈6 mL/kg ideal body weight) with adequate PEEP; this approach prevents ventilator-induced lung injury and is the only intervention proven to improve survival. Permissive hypercapnia (allowing higher CO₂) is often accepted to avoid high ventilatory pressures.
Always search for and treat the underlying cause of ARDS – ARDS is a syndrome, not a specific disease. For example, prompt treatment of sepsis or pancreatitis can halt ongoing lung injury.
Tension pneumothorax: Sudden unilateral absence of breath sounds or subcutaneous emphysema in an ARDS patient on a ventilator suggests barotrauma (alveolar rupture). Immediately decompress the chest (needle/chest tube) and adjust ventilator settings to prevent further injury.
Refractory hypoxemia: If oxygen saturation remains critically low (SaO₂ < 88–90% on maximal support) or PaO₂/FiO₂ continues to fall despite optimal settings, this is an emergency – initiate rescue therapies (proning, paralysis, ECMO) or risk cardiac arrest from hypoxemia.
Multi-organ failure: Signs of other organ failures (acute kidney injury, shock, elevated LFTs) alongside ARDS indicate a severe systemic process. Escalate care (e.g., vasopressors for shock, dialysis if needed) and consider prognosis (high mortality when ARDS is part of MODS).
Obtain chest X-ray (look for bilateral infiltrates) and ABG (calculate PaO₂/FiO₂ ratio). Evaluate for alternative causes (cardiac vs pulmonary). If bilateral opacities and P/F ≤300 (with PEEP ≥5) and no evidence of volume overload/heart failure → diagnose ARDS.
Admit to ICU. If moderate or severe oxygenation impairment, intubate and start lung-protective ventilation (low tidal volume, adequate PEEP). Place central access if needed for hemodynamic monitoring and medications.
Treat the underlying cause (e.g., antibiotics for pneumonia/sepsis, operative intervention for trauma) in parallel with respiratory support.
If oxygenation remains poor on ventilator (high FiO₂ requirement), escalate support – add prone positioning, consider neuromuscular blockade, and optimize PEEP. For extreme hypoxemia not improving, consult an ECMO center early.
Continually reassess gas exchange and lung compliance. Wean FiO₂ as tolerated to avoid oxygen toxicity. As the lung injury resolves (often in 1–2 weeks), lighten sedation and assess readiness for extubation.
A septic pancreatitis patient in ICU develops worsening respiratory distress 24 hours later. Chest X-ray shows bilateral patchy infiltrates, PaO₂ 60 mmHg on FiO₂ 0.6 (P/F = 100) → ARDS from pancreatitis (systemic inflammation causing noncardiogenic pulmonary edema).
An ICU patient with multiple trauma and massive transfusions becomes difficult to oxygenate on 100% O₂. Chest imaging reveals "white-out" diffuse infiltrates but a normal cardiac silhouette → ARDS (e.g., transfusion-related acute lung injury).
