Acute Respiratory Distress Syndrome (ARDS)
Related Subjects: Asthma
|Acute Severe Asthma
|Exacerbation of COPD
|Pulmonary Embolism
|Cardiogenic Pulmonary Oedema
|Pneumothorax
|Tension Pneumothorax
|Fat embolism
|Hyperventilation Syndrome
|Acute Respiratory Distress Syndrome (ARDS)
|Respiratory Failure
|Non invasive ventilation (NIV)
|Intubation and Mechanical Ventilation
ARDS is due to an acute, diffuse pulmonary inflammatory response to either direct (via airway or chest trauma) or indirect blood-borne insults from extrapulmonary pathology. It must occur within 1 week of a clinical insult or worsening respiratory symptoms. Chest Imaging: Bilateral opacities visible on chest X-ray, CT scan, or ultrasound. Oedema: ARDS should not be fully explained by cardiac failure or fluid overload. There is progressive hypoxia. It is characterised by neutrophil sequestration in pulmonary capillaries, increased capillary permeability, and protein-rich pulmonary oedema.
📖 About
- ARDS is a systemic disease with acute hypoxia and multi-organ dysfunction.
- Seen as a manifestation of trauma, sepsis, tissue damage, or other severe illnesses.
- Mild ARDS was once called “acute lung injury.”
- May progress to a fibroproliferative phase with lung fibrosis.
🧬 Aetiology & Pathophysiology
- Type 1 respiratory failure without cardiac dysfunction.
- Loss of type II pneumocytes → ↓ surfactant.
- Protein-rich alveolar oedema due to ↑ capillary permeability.
- Neutrophil sequestration → inflammatory damage.
- Capillary leak → alveolar flooding and collapse.
- Lungs become stiff, poorly compliant → impaired gas exchange.
📝 Global Definition Criteria (2024, building on Berlin 2012)
- Timing: Within 1 week of known insult or worsening symptoms.
- Chest imaging: Bilateral opacities not fully explained by effusions, collapse, or nodules (X-ray, CT, or ultrasound).
- Origin of oedema: Not explained by cardiac failure or fluid overload (echo if uncertain).
- Oxygenation severity: (on respiratory support: ventilator, CPAP, BiPAP, or HFNO ≥30 L/min)
- Mild: PaO₂/FiO₂ 200–300 mmHg (26.7–40 kPa) or SpO₂/FiO₂ 235–315 (if SpO₂ ≤97%) with PEEP/CPAP ≥5 cmH₂O.
- Moderate: PaO₂/FiO₂ 100–200 mmHg (13.3–26.7 kPa) or SpO₂/FiO₂ 148–235 (if SpO₂ ≤97%) with PEEP/CPAP ≥5 cmH₂O.
- Severe: PaO₂/FiO₂ <100 mmHg (<13.3 kPa) or SpO₂/FiO₂ <148 (if SpO₂ ≤97%) with PEEP/CPAP ≥5 cmH₂O.
Note: In resource-limited settings, no PEEP requirement; use SpO₂/FiO₂ on ≥5 L/min oxygen.
👩⚕️ Clinical Features
- Occurs in context of severe illness (e.g. sepsis, trauma, pneumonia).
- Increasing breathlessness, cyanosis, inspiratory basal crackles.
- Tachycardia, refractory hypoxaemia. Bronchial breath sounds may be heard.
- Hypotension, worsening cyanosis, and potentially death.
🧾 Causes
- Direct lung injury: burns, smoke inhalation, pneumonia, aspiration, high altitude, near drowning, O₂ toxicity, fat/air embolism.
- Indirect/systemic: sepsis, trauma, eclampsia, pancreatitis, heroin/barbiturates, transfusion-associated lung injury, cardiopulmonary bypass, malignancy.
🔍 Differentials
- Congestive cardiac failure.
- Bilateral pneumonia (VAP, community-acquired).
- Alveolar haemorrhage (e.g. Wegener’s, Goodpasture’s).
- Acute interstitial pneumonia.
- Acute eosinophilic pneumonia or hypersensitivity pneumonitis.
📊 Severity Levels
- Mild: PaO₂/FiO₂ 200–300 mmHg, mortality ~27%, managed with low tidal volume ventilation + conservative fluids.
- Moderate: PaO₂/FiO₂ 100–200 mmHg, mortality ~32%, requires higher PEEP, prone positioning.
- Severe: PaO₂/FiO₂ <100 mmHg, mortality ~45%, may need ECMO, advanced ventilation strategies.
🧪 Investigations
- ABG: Mild to severe hypoxia. Type 1 RF. PaO₂/FiO₂ ratio confirms severity (on PEEP ≥5). In late stages, severe hypoxaemia (low PaO₂) and severe hypercapnia (high PaCO₂) may occur.
- FBC: anaemia, ↑ neutrophils.
- U&E: AKI, ↑ lactate, ↑ LFTs.
- CXR/CT: Initially normal but then develops bilateral opacities, ground glass changes. Features usually develop 12-24 hours after initial lung insult. Alveolar pulmonary oedema (hyaline membrane) occurs due to type 1 pneumocyte damage and proteinaceous interstitial oedema.
- Echo: exclude LV dysfunction.
- Blood cultures: look for sepsis.
- Coagulopathy: DIC may develop (↑ APTT/PT, ↓ platelets).
- BAL: useful in unclear infection.
💊 Management
- Initial: ABCs, treat underlying cause (e.g. sepsis, trauma).
- Supplemental Oxygen & Targets: Titrate O₂ to conservative targets — SpO₂ 88–95% (commonly 90–94% or 92–96%), PaO₂ 55–80 mmHg to avoid hyperoxia while preventing severe hypoxaemia; start supplemental O₂ if SpO₂ <90–92% and minimize FiO₂ as tolerated.
- Ventilation: Low tidal volume (4–6 mL/kg ideal body weight), avoid barotrauma (plateau pressure <30 cmH₂O).
- PEEP: Prevent alveolar collapse, titrate as needed; higher PEEP without recruitment maneuvers in moderate-severe ARDS.
- Prone positioning: Improves V/Q matching in moderate–severe ARDS (at least 12-16 hours).
- Neuromuscular blockade: Early in severe ARDS to improve synchrony (conditional for P/F <150 mmHg).
- Fluid management: Conservative strategy to reduce oedema.
- Rescue therapies: ECMO if refractory; inhaled NO as temporary bridge.
- Steroids: Suggested for adults with ARDS (conditional recommendation, moderate certainty; e.g., if persists or early moderate-severe).
⚠️ Complications
- Pneumothorax.
- Ventilator-associated pneumonia.
- Multi-organ failure.
- Pulmonary fibrosis.
- Mortality ~30–50%.
📖 References
- Matthay MA et al. (2024) A new global definition of acute respiratory distress syndrome. Am J Respir Crit Care Med, 209:37-47.
- Qadir N et al. (2024) An Update on Management of Adult Patients with ARDS: ATS Guideline. Am J Respir Crit Care Med, 209:24-36.
- Grasselli G et al. (2023) ESICM guidelines on acute respiratory distress syndrome. Intensive Care Med, 49:727-759.
- Barrot L et al. (2020) Liberal or Conservative Oxygen Therapy for Acute Respiratory Distress Syndrome. N Engl J Med, 382:999-1008 (LOCO2 trial).
- Chaudhuri D et al. (2024) 2024 Focused Update: Guidelines on Use of Corticosteroids in Sepsis, ARDS, and CAP. Crit Care Med.
- De Haro et al. (2013) ARDS: prevention and early recognition. Annals Int Care, 3:11.
- Ferguson et al. (2005) Development of a clinical definition for ARDS. J Crit Care, 20:147.
