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 must occur within 1 week of a clinical insult or worsening respiratory symptoms.
Chest Imaging: Bilateral opacities should be visible on chest X-ray or CT scan.
Oedema: ARDS should not be fully explained by cardiac failure or fluid overload.
There is progressive hypoxia.
đź“– 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.”
- PaOâ‚‚ < 10 kPa on FiOâ‚‚ = 0.5 corresponds to ~20 kPa.
- 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.
📝 Berlin Criteria
- Timing: Within 1 week of known insult or worsening symptoms.
- Chest imaging: Bilateral opacities not fully explained by effusions, collapse, or nodules.
- Origin of oedema: Not explained by cardiac failure or fluid overload (echo if uncertain).
- Oxygenation severity:
- Mild: PaO₂/FiO₂ 200–300 mmHg (26.7–40 kPa) with PEEP ≥ 5 cmH₂O.
- Moderate: PaO₂/FiO₂ 100–200 mmHg (13.3–26.7 kPa) with PEEP ≥ 5 cmH₂O.
- Severe: PaO₂/FiO₂ < 100 mmHg (<13.3 kPa) with PEEP ≥ 5 cmH₂O.
👩‍⚕️ Clinical Features
- Occurs in context of severe illness (e.g. sepsis, trauma, pneumonia).
- Progressive breathlessness, cyanosis, basal crackles.
- Tachycardia, refractory hypoxaemia.
đź§ľ Causes
- Direct lung injury: burns, smoke inhalation, pneumonia, aspiration, high altitude, near drowning, Oâ‚‚ 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: PaOâ‚‚/FiOâ‚‚ <100 mmHg, mortality ~45%, may need ECMO, advanced ventilation strategies.
đź§Ş Investigations
- ABG: PaO₂/FiO₂ ratio confirms severity (on PEEP ≥5).
- FBC: anaemia, ↑ neutrophils.
- U&E: AKI, ↑ lactate, ↑ LFTs.
- CXR/CT: bilateral opacities, ground glass changes.
- Echo: exclude LV dysfunction.
- Blood cultures: look for sepsis.
- Coagulopathy: DIC may develop (↑ APTT/PT, ↓ platelets).
- BAL: useful in unclear infection.
đź’Š Management
- Initial: ABCs, treat underlying cause (e.g. sepsis, trauma).
- Ventilation: Low tidal volume (4–6 mL/kg), avoid barotrauma.
- PEEP: Prevent alveolar collapse, titrate as needed.
- Prone positioning: Improves V/Q matching in moderate–severe ARDS.
- Neuromuscular blockade: Early severe ARDS to improve synchrony.
- Fluid management: Conservative strategy to reduce oedema.
- Rescue therapies: ECMO if refractory; inhaled NO as temporary bridge.
- Steroids: Sometimes used if ARDS persists beyond acute phase.
⚠️ Complications
- Pneumothorax.
- Ventilator-associated pneumonia.
- Multi-organ failure.
- Pulmonary fibrosis.
- Mortality ~30–50%.
đź“– References
- 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.