Acute respiratory distress syndrome

Acute Respiratory Distress Syndrome (ARDS) is a severe, life-threatening condition characterized by acute lung dysfunction and respiratory failure. It occurs when the lungs suffer widespread inflammation and increased permeability, leading to fluid accumulation in the alveoli and impaired oxygen exchange. ARDS is not a primary lung disease but rather a complication of various systemic illnesses or injuries, such as sepsis, major trauma, pneumonia, aspiration, and severe viral infections.

ARDS, Severe

Micrograph of diffuse alveolar damage, the histologic correlate of ARDS. H&E stain.

A chest x-ray of transfusion-related acute lung injury (left) which led to ARDS. Right is the same patient with resolved injury 72 hours after ventilator support. Note the clearance of bilateral diffuse infiltrates.

Epidemiology

ARDS affects individuals of all ages but is more common in critically ill patients. Risk factors include:

• Sepsis – The most common cause of ARDS.
• Pneumonia – Bacterial, viral, or fungal lung infections.
• Aspiration of gastric contents – Entry of stomach acid or food particles into the lungs.
• Severe trauma – Blunt force injuries, burns, or near-drowning incidents.
• COVID-19 and other viral infections – Severe respiratory viral infections can precipitate ARDS.
• Pancreatitis – Systemic inflammation affecting the lungs.
• Multiple blood transfusions – Transfusion-related acute lung injury (TRALI).

Clinical Features

Patients with ARDS typically present with:

• Severe shortness of breath (dyspnea) that develops rapidly.
• Hypoxemia (low blood oxygen levels) despite oxygen therapy.
• Tachypnea (rapid breathing) and respiratory distress.
• Bilateral pulmonary infiltrates on chest imaging.
• Cyanosis (bluish skin coloration) due to oxygen deprivation.

Without immediate intervention, ARDS can progress to multi-organ failure and death. Early recognition and aggressive treatment in an intensive care unit (ICU) setting are critical for survival.

Pathophysiology and Stages of ARDS

ARDS results from direct or indirect lung injury, leading to a cascade of inflammatory processes that disrupt normal lung function.

Pathophysiology

• 1. Damage to the alveolar-capillary membrane – Inflammatory mediators cause increased permeability, leading to fluid leakage into the alveoli.
• 2. Pulmonary edema – The accumulation of fluid in the alveoli reduces lung compliance and impairs gas exchange.
• 3. Severe hypoxemia – Due to ventilation-perfusion mismatch and lung collapse.
• 4. Inflammatory response – The release of cytokines and immune cells further worsens lung injury.
• 5. Fibrosis and lung remodeling – In chronic ARDS, prolonged inflammation leads to fibrotic scarring, reducing lung function.

Phases of ARDS

ARDS progresses through three overlapping stages:

Exudative Phase (Acute Phase, 0-7 days)

• Pulmonary edema and alveolar collapse occur due to increased permeability.
• Lung compliance decreases, requiring mechanical ventilation.
• Severe hypoxemia develops.

Proliferative Phase (7-21 days)

• Inflammation persists, but alveolar re-epithelialization begins.
• Some patients improve, while others progress to lung fibrosis.

Fibrotic Phase (Chronic Phase, >21 days)

• Excessive collagen deposition leads to lung scarring and fibrosis.
• Reduced lung capacity may cause long-term respiratory impairment.

Diagnosis and Classification of ARDS

ARDS is diagnosed based on clinical, radiologic, and oxygenation criteria, following the Berlin Definition of ARDS.

Diagnostic Criteria

1. Acute onset – Symptoms develop within 1 week of a known clinical insult. 2. Bilateral lung opacities on chest X-ray or CT scan, not fully explained by other causes (e.g., heart failure). 3. Severe oxygenation impairment defined by the PaO₂/FiO₂ ratio (arterial oxygen to inspired oxygen fraction):

• Mild ARDS: PaO₂/FiO₂ 200–300 mmHg
• Moderate ARDS: PaO₂/FiO₂ 100–200 mmHg
• Severe ARDS: PaO₂/FiO₂ <100 mmHg

4. No evidence of heart failure as the primary cause of lung injury.

Imaging and Laboratory Tests

• Chest X-ray or CT scan – Shows bilateral infiltrates (white-out lungs).
• Arterial blood gas (ABG) analysis – Confirms severe hypoxemia.
• Lung ultrasound – Detects fluid accumulation and lung consolidation.
• Bronchoscopy and bronchoalveolar lavage (BAL) – Helps identify infectious causes.

Treatment and Prognosis of ARDS

Currently, there is no specific cure for ARDS; treatment is supportive and aims to improve oxygenation, reduce lung injury, and treat the underlying cause.

Ventilatory Support and Mechanical Ventilation

• Low tidal volume ventilation (lung-protective strategy) – Prevents ventilator-induced lung injury.
• Positive end-expiratory pressure (PEEP) – Keeps alveoli open and improves gas exchange.
• Prone positioning – Placing patients face down enhances oxygenation in severe ARDS.
• High-flow nasal cannula (HFNC) or non-invasive ventilation (NIV) – Used for mild ARDS before intubation.

Fluid Management and Pharmacologic Therapy

• Conservative fluid management – Avoids pulmonary edema and improves oxygenation.
• Corticosteroids – May be beneficial in some cases to reduce inflammation.
• Neuromuscular blockers – Improve oxygenation and reduce ventilator-induced lung injury in early severe ARDS.
• Antibiotics – Given if ARDS is secondary to bacterial pneumonia or sepsis.

Extracorporeal Membrane Oxygenation (ECMO)

For severe, refractory ARDS, ECMO may be used as a last resort:

• Veno-venous ECMO (VV-ECMO) – Oxygenates the blood outside the body when conventional ventilation fails.
• Veno-arterial ECMO (VA-ECMO) – Provides both respiratory and cardiac support in circulatory collapse.

Prognosis and Long-Term Complications

The mortality rate of ARDS ranges from 35% to 50%, with higher rates in severe cases. Survivors often face long-term complications such as:

• Pulmonary fibrosis – Persistent lung scarring causing chronic respiratory impairment.
• Post-intensive care syndrome (PICS) – Includes muscle weakness, cognitive dysfunction, and psychological distress.
• Increased risk of infections and ICU-acquired complications.

Prevention Strategies

While ARDS cannot always be prevented, the following strategies reduce the risk:

• Early sepsis treatment – Prompt use of antibiotics and fluid resuscitation.
• Avoidance of ventilator-associated lung injury – Using lung-protective strategies.
• Reducing aspiration risk – Careful intubation and aspiration precautions in high-risk patients.
• Preventing hospital-acquired infections – Hand hygiene and early mobilization protocols.

See Also

• Sepsis
• Mechanical ventilation
• Pulmonary fibrosis
• Extracorporeal membrane oxygenation
• Critical care medicine
• Lung-protective ventilation

This article is a medical stub. You can help WikiMD by expanding it!
Most recent articles Ongoing trials	Wikipedia