- Clinical science
Acute respiratory distress syndrome (ARDS) is a severe inflammatory reaction of the lungs to pulmonary damage. Sepsis is the most common cause, but various other systemic or pulmonary factors – such as pneumonia or aspiration – can lead to ARDS. Patients initially present with acute onset cyanosis, dyspnea, and tachypnea. Over the course of the next weeks, most patients will improve significantly, although some progress to pulmonary fibrosis, which prolongs their hospital stay and delays resolution of symptoms. The chief finding in ARDS is hypoxemic respiratory failure with decreased arterial oxygen pressure, which usually progresses to hypercapnic respiratory failure. Chest x-ray typically shows diffuse bilateral infiltrates (“butterfly pattern”). Management of ARDS focuses on maintaining adequate oxygenation, which often requires intubation and (lung protective) mechanical ventilation, as nasal prongs and/or mask ventilation are insufficient. Moreover, any treatable causes of ARDS should be addressed. However, even if adequate treatment is initiated, ARDS remains an acutely life-threatening disease with a high mortality rate.
(most common cause)
- E.g., secondary to trauma, infection or peritonitis
- Massive TRALI” for details) (See “
- Hematopoietic stem cell transplantation
- Medication (e.g., salicylic acid, tricyclic antidepressants, bleomycin)
- Recreational drug overdose (e.g., cocaine)
Primary damage to the lungs
- Inhaled toxins
- Pulmonary contusion
- Inhalation injury (e.g., inhalation of hyperbaric oxygen)
- Near drowning
- Fat embolism (e.g., through blunt trauma)
- Amniotic fluid embolism (e.g., during labor)
- Lung transplantation
Sepsis is the most common cause of ARDS!
Tissue damage (pulmonary or extrapulmonary) → release of inflammatory mediators (e.g., interleukin-1) → inflammatory reaction → injury to alveolar capillaries and endothelial cells leading to:
- Excess fluid in interstitium and on alveolar surface → pulmonary edema
- Exudation of neutrophils and protein-rich fluid (hyaline membrane) into the alveolar space → diffuse alveolar damage (DAD) to type I and type II pneumocytes → decrease in surfactant → intrapulmonary shunting → late stage: proliferation of type II pneumocytes and infiltration of fibroblasts → progressive interstitial fibrosis
- Impaired gas exchange, reduced compliance, hypertension and a right-to-left pulmonary shunt (increased shunt fraction) → hypoxemia → compensation through hyperventilation → respiratory alkalosis
- Acute onset
- Disease course
- Most patients begin to improve after the first 1–3 weeks and symptoms usually resolve fully.
- Some develop pulmonary fibrosis with prolonged resolution of symptoms and extended ventilator dependence.
- Arterial blood gas
- Additional findings depend on the underlying cause (e.g., abnormal white blood count in sepsis) or associated complications (e.g., increased creatinine levels in acute tubular necrosis).
- Imaging: chest x-ray
ARDS is a likely diagnosis in the presence of both typical causes and therapy-resistant hypoxemia. The diagnosis is further supported by characteristic findings on chest x-ray that are not explained by underlying cardiac disease.
- Cardiogenic pulmonary edema: presents with signs of cardiac dysfunction (e.g., murmurs, jugular venous congestion)
- Acute exacerbations of interstitial lung diseases: examine patient history and past chest x-rays
- Transfusion-related acute lung injury (TRALI)
- Transfusion-associated circulatory overload (TACO): a rapid, high-volume infusion, which causes symptoms similar to ARDS
- See differential diagnoses for dyspnea
The differential diagnoses listed here are not exhaustive.
- The primary objective is achieving sufficient oxygen saturation (while avoiding oxygen toxicity).
- Treat the underlying cause (e.g., sepsis).
- Sedation (benzodiazepines, opioids)
- If oxygenation is insufficient:
- Description: Pressure-controlled ventilation with a low tidal volume and low peak inspiratory pressure to avoid further pulmonary damage. However, increasing the positive end-expiratory pressure (PEEP) is often necessary during treatment. With this type of ventilation, higher levels of CO2 can be tolerated (permissive hypercapnia).
- Goal: SaO2 > 90% (or PaO2 > 55 mm Hg)
- Definition: ECMO is a method of artificially supporting the circulatory system. In patients with severely reduced or no pulmonary function, the O2/CO2 exchange is achieved through the use of artificial lung membranes. Depending on the exact technique/machinery used, several other terms are employed as well (e.g., extracorporeal membrane oxygenation).
All patients with ARDS
- Quantify hypoxemia: Use the P/F ratio to evaluate ARDS severity. 
- Mild: P/F 200–300 mm Hg
- Moderate: P/F 100–200 mm Hg
- Severe: P/F < 100 mm Hg
- Start lung protective ventilation strategy 
- Identify and treat the underlying cause.
- Ensure euvolemia.
- Hemodynamic monitoring
- Pain management and sedation
- Consider further diagnostics.
- CT scan of the chest
- Consider bronchoscopy if the etiology remains unclear.
- ICU admission
- Consider transfer to ARDS/ECMO center of care.
Moderate or severe ARDS
- Prone positioning for > 12 hours/day 
- Higher PEEP (use incremental FiO2-PEEP combinations according to local protocols)
- Airway recruitment maneuvers
- Neuromuscular blockade in the first 48 h