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 = acute hypoxaemic respiratory failure caused by diffuse inflammatory lung injury.
🔑 Core mechanism: alveolar–capillary leak → protein-rich oedema → surfactant loss → alveolar collapse → shunt physiology → refractory hypoxaemia.
🇬🇧 UK note: no single dedicated NICE ARDS guideline; management is based mainly on ICU/FICM/ICS practice plus treatment of the underlying cause (for example, sepsis).
📖 Definition
- Acute onset: within 1 week of a known insult or worsening respiratory symptoms.
- Imaging: bilateral opacities on CXR/CT not fully explained by effusions, collapse, or nodules.
- Oedema origin: not fully explained by cardiac failure or fluid overload.
- Hypoxaemia: severity based on PaO₂/FiO₂ ratio with PEEP ≥5 cmH₂O.
📊 Severity (Berlin)
- Mild: PaO₂/FiO₂ 200–300 mmHg
- Moderate: PaO₂/FiO₂ 100–200 mmHg
- Severe: PaO₂/FiO₂ <100 mmHg
🆕 2024 update
- May include patients on HFNO ≥30 L/min.
- SpO₂/FiO₂ ratios can be used if ABG unavailable.
- Good exam extra, but Berlin criteria remain the main framework to know.
🧾 Common causes
- Direct: pneumonia, aspiration, smoke inhalation, pulmonary contusion.
- Indirect: sepsis, trauma, pancreatitis, TRALI, major systemic inflammation, some drugs.
🧬 Pathophysiology
- Diffuse alveolar damage injures endothelium + epithelium.
- Neutrophil-driven inflammation increases permeability.
- Protein-rich oedema floods alveoli.
- Type II pneumocyte dysfunction → ↓ surfactant.
- Alveolar collapse + reduced compliance = “stiff lungs”.
- Shunt physiology means oxygen alone may not fully correct hypoxia.
- Can progress to a fibroproliferative phase with fibrosis.
👩⚕️ Clinical features
- Usually occurs during a severe illness such as sepsis.
- Rapidly worsening breathlessness and tachypnoea.
- Refractory hypoxaemia despite oxygen.
- Fine inspiratory crackles.
- May have hypotension, lactataemia, renal injury, or other multi-organ dysfunction.
🔍 Differentials
- Cardiogenic pulmonary oedema / LV failure
- Bilateral pneumonia
- Diffuse alveolar haemorrhage
- Acute eosinophilic pneumonia
- Acute interstitial lung disease flare
🧪 Investigations
- ABG: type 1 respiratory failure; late hypercapnia may occur.
- CXR: bilateral diffuse opacities.
- CT chest: ground-glass / dependent consolidation.
- Echo: helps exclude cardiogenic oedema.
- Bloods: FBC, U&E, LFT, CRP, clotting, lactate.
- Microbiology: blood cultures, sputum, relevant infection work-up.
💊 Management
- Treat the cause first: sepsis, aspiration, trauma, pancreatitis, etc.
- Escalate oxygen/respiratory support as needed.
- Low tidal volume ventilation: 4–6 mL/kg ideal body weight.
- Limit plateau pressure to <30 cmH₂O.
- PEEP to prevent derecruitment and alveolar collapse.
- Proning for moderate–severe ARDS: usually 12–16 h/day.
- Conservative fluid strategy once haemodynamically appropriate.
- Neuromuscular blockade may be considered in severe cases.
- ECMO referral if refractory hypoxaemia despite optimal care.
🚫 Not routine
- Inhaled nitric oxide: may transiently improve oxygenation but no routine mortality benefit.
- Steroids: controversial; not a universally standard UK ARDS treatment line for every patient.
⚠️ Complications
- Ventilator-associated pneumonia
- Pneumothorax / barotrauma
- Multi-organ failure
- Pulmonary fibrosis
- Death
🧠 Exam pearls
- ARDS = non-cardiogenic pulmonary oedema.
- Sepsis is the classic trigger.
- Low tidal volume + prone positioning are the key tested interventions.
- Hypoxia that is hard to correct = think intrapulmonary shunt.
- Do not diagnose ARDS purely from “white lungs” — exclude cardiac failure/fluid overload.
