ARDS (Acute Respiratory Distress Syndrome)
Diffuse alveolar damage from direct or indirect lung injury — Berlin criteria: bilateral infiltrates + PaO2/FiO2 <300 + not fully explained by cardiac failure + acute onset within 1 week; usually ICU
Symptoms / Associated Sx
Severe progressive dyspnea and tachypnea
Refractory hypoxia — SpO2 <88% despite high FiO2
Bilateral crackles (diffuse alveolar damage)
Tachycardia, agitation, altered mentation
Signs of the underlying trigger: fever (sepsis/pneumonia), abdominal tenderness (aspiration/pancreatitis), trauma injuries
Denies
Elevated BNP + cardiomegaly + bilateral effusions (rules out cardiogenic pulmonary edema as primary — though can coexist; PCWP <18 in ARDS)
Onset >1 week from insult (Berlin criteria require <1 week from triggering event)
Unilateral infiltrates (rules out ARDS — must be bilateral; consider pneumonia, atelectasis)
Social History (SHx)
Sepsis source (pneumonia, abdominal — most common triggers), aspiration event, recent trauma or surgery, alcohol use, transfusion history (TRALI — transfusion-related ARDS), immunosuppression, prior lung disease, baseline ABG values.
Main Etiology
Pulmonary (direct): Pneumonia (most common), aspiration, pulmonary contusion, near-drowning, toxic inhalation
Extrapulmonary (indirect): Sepsis (most common indirect cause), severe pancreatitis, massive transfusion, trauma, burns, DIC
TRALI: Transfusion-related acute lung injury — within 6h of transfusion; donor anti-HLA antibodies activate recipient neutrophils
Most Common DDx
Cardiogenic pulmonary edema (elevated BNP; JVD; bilateral effusions; cardiomegaly; responds to diuretics + vasodilators; PCWP >18; echo shows LV dysfunction)
Bilateral pneumonia (can be indistinguishable from ARDS; fever + leukocytosis + consolidation; cultures positive; responds to antibiotics — though severe bilateral pneumonia IS ARDS)
Diffuse alveolar hemorrhage (bilateral infiltrates + hemoptysis + falling Hgb; ANCA/anti-GBM; BAL progressively bloodier — see DAH section)
Acute eosinophilic pneumonia (fever + bilateral infiltrates; eosinophilia on BAL; new exposure; responds to steroids)
AIP (acute interstitial pneumonia / Hamman-Rich syndrome) — idiopathic ARDS without a trigger; bilateral GGO; diffuse alveolar damage on biopsy; poor prognosis)
TRALI (within 6h of blood product transfusion; bilateral infiltrates; non-cardiogenic; resolves within 48–96h with supportive care)
DATA
ABG (PaO2/FiO2 ratio = P/F ratio; Berlin severity: mild P/F 201–300; moderate 101–200; severe ≤100)
CBC, CMP, LFTs, coagulation panel (multiorgan failure assessment)
Procalcitonin, blood cultures × 2, respiratory cultures (infection trigger)
BNP/NT-proBNP + Echo (distinguish ARDS from cardiogenic pulmonary edema)
Lactate (sepsis severity; tissue perfusion)
CXR (bilateral airspace opacities; no cardiomegaly; no large effusions)
CT chest (better characterization if CXR equivocal; gravity-dependent distribution in ARDS — posterior lower lobes; heterogeneous)
Bronchoscopy + BAL (infection workup; DAH exclusion; BAL fluid if ARDS of unknown etiology)
ANCA panel, anti-GBM (if vasculitis/DAH suspected — bilateral infiltrates + hemoptysis + renal failure)
Home Meds
All medications (drug-induced ARDS — amiodarone, nitrofurantoin, bleomycin, checkpoint inhibitors)
Immunosuppressants (assess for opportunistic infections)
Plan
Treat the underlying cause first (most important intervention in ARDS)
Lung-protective mechanical ventilation (ARDSNet protocol — cornerstone of ARDS management):
Tidal volume: 6 mL/kg predicted body weight (PBW) — NOT actual body weight; reduces volutrauma
Plateau pressure: ≤30 cmH2O (prevents barotrauma)
PEEP: titrated (higher PEEP in moderate-severe ARDS improves oxygenation; ARDS Network PEEP tables)
FiO2: titrated to SpO2 88–95%; avoid hyperoxia (>96%)
Respiratory rate: 14–35/min; I:E ratio 1:2; allow permissive hypercapnia (pH >7.20 acceptable)
Driving pressure (plateau − PEEP) ≤15 cmH2O — mortality predictor; minimize
Prone positioning (PROSEVA trial — most important evidence-based intervention):
Indication: P/F <150 (moderate-severe ARDS) after 12–24h of mechanical ventilation
Duration: ≥16h per session; continue until P/F >150 consistently
Reduces 28-day mortality by ~50% in severe ARDS (PROSEVA); requires trained nursing team
Conservative fluid strategy (after initial resuscitation):
Target even to negative fluid balance once hemodynamically stable
FACTT trial: conservative fluid strategy reduces ventilator days without increasing organ failure
Avoid aggressive IV fluids in euvolemic ARDS patients
Neuromuscular blockade (NMB):
Cisatracurium 37.5 mg/h IV infusion × 48h for severe ARDS (P/F <150) — reduces patient-ventilator dyssynchrony, reduces volutrauma; deep sedation required (RASS −5)
ACURASYS trial showed benefit; ROSE trial did not — clinical judgment; severe dyssynchrony is main indication
Corticosteroids:
Dexamethasone 20 mg IV daily × 5 days → 10 mg IV daily × 5 days (DEXA-ARDS trial — reduces ventilator days in moderate-severe ARDS)
Methylprednisolone 1 mg/kg IV (alternative — unresolving ARDS after 7–14 days)
Avoid high-dose steroids for >14 days — increased mortality in late ARDS
Sedation protocol (Richmond Agitation-Sedation Scale — RASS −2 to 0 target unless NMB); analgesia-first approach
Spontaneous awakening trial (SAT) + spontaneous breathing trial (SBT) daily when improving
Stress ulcer prophylaxis (pantoprazole 40 mg IV daily)
DVT prophylaxis (enoxaparin 40 mg SQ daily)
Enteral nutrition within 24–48h (gastric or post-pyloric feeds; 25–30 kcal/kg/day)
Vasopressors if septic shock (norepinephrine first-line)
Critical care/pulmonology in ICU
Serial ABG q4–6h; daily CBC, BMP, lactate; CXR; RASS/sedation level assessment
PT/OT post-extubation — ICU-acquired weakness rehabilitation
Discharge: Pulmonary rehabilitation; PCP and pulmonology follow-up 2–4 weeks; repeat PFTs at 3 months (ARDS survivors have restrictive defects); PTSD screening (ICU survivors); cognitive rehabilitation; oxygen if needed on discharge
Red Flags
P/F <100 (severe ARDS) + not prone → prone immediately; mortality >45% without prone positioning
Plateau pressure >30 cmH2O → reduce tidal volume to 4 mL/kg PBW and/or increase PEEP; barotrauma imminent
Refractory hypoxia (SpO2 <85% despite P/F protocol + prone + optimal PEEP) → ECMO consideration (veno-venous ECMO as rescue therapy)
Barotrauma (pneumothorax in ARDS on MV) → emergent chest tube; reduce TV + PEEP until lung re-expands
Multiorgan failure (renal + hepatic + hematologic + respiratory) → ICU; supportive care; poor prognosis
Senior IM Resident Pearls
ARDSNet protocol (6 mL/kg PBW tidal volume) is the most important intervention in ARDS — reduces mortality by 22% compared to 12 mL/kg; calculated from HEIGHT not weight; use PBW calculator (men: 50 + 2.3 × [height in inches − 60]; women: 45.5 + 2.3 × [height in inches − 60])
Prone positioning reduces mortality by ~50% in severe ARDS (P/F <150) — PROSEVA trial; improves V/Q matching (dependent dorsal regions become non-dependent); requires skilled nursing team; prone 16h/day
Driving pressure (plateau − PEEP) is the strongest predictor of ARDS mortality — target ≤15 cmH2O; can be used to titrate PEEP and tidal volume simultaneously
ECMO (veno-venous) for refractory ARDS — P/F <80 despite optimal MV + prone; considered in young patients without multiorgan failure; transfer to ECMO center early
Common mistake: Using actual body weight instead of predicted body weight for tidal volume calculation — in obese patients, 6 mL/kg of actual weight causes massive over-distension and volutrauma; always use PBW
Common mistake: Not prone positioning a severe ARDS patient — prone is one of the most evidence-based interventions in critical care; it is underutilized due to nursing complexity; advocate strongly for it