ARDS: Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) is an acute non-cardiogenic pulmonary oedema due to abnormalities in alveolar permeability, occurring in certain clinical conditions.
ARDS represents the severe end of the spectrum of acute lung injury, caused by increased microvascular permeability. The threshold between acute lung injury and ARDS is arbitrary and generally based on the severity of hypoxia.
Obsolete terms include “shock lung” and “adult respiratory distress syndrome”.
Pathophysiology
Mechanism of Pulmonary Oedema
Pulmonary oedema results from disruption of Starling’s forces:
Net fluid out = K × [(Pc – Pi) – σ × (πc – πi)]
Where:
- Pc = capillary hydrostatic pressure
- Pi = interstitial hydrostatic pressure
- πc = plasma oncotic pressure
- πi = interstitial oncotic pressure
- K = filtration coefficient (water permeability)
- σ = protein permeability factor
Three mechanisms of pulmonary oedema:
- Cardiogenic: ↑ capillary hydrostatic pressure (Pc)
- Low oncotic pressure: ↓ plasma oncotic pressure (πc) — rare
- Increased permeability: ↑ K — the primary mechanism in ARDS
Causes of Increased Alveolar Permeability in ARDS
- Direct lung injury (e.g., surfactant loss)
- Secondary to systemic illness
Pathology
ARDS progresses through three overlapping phases over 2–3 weeks:
- Exudative
- Inflammatory
- Fibroproliferative (reparative)
Consequences:
- Refractory hypoxaemia from:
- V/Q mismatch
- Physiological shunting
- Atelectasis
- Reduced compliance
Rare complications:
- Progressive pulmonary fibrosis
- Pulmonary hypertension
→ Both are markers of poor prognosis
Causes of ARDS
Direct Lung Injury | Indirect (Secondary) Lung Injury |
---|---|
Aspiration | Severe/prolonged shock |
Near drowning | Renal or hepatic failure |
Inhalation of noxious gases | Severe pancreatitis |
Severe pulmonary trauma | Generalised sepsis |
Severe pneumonia | Fat embolism |
Radiation | Anaphylaxis (rare) |
HAPE (high-altitude pulmonary oedema) | |
Raised ICP (“neurogenic” pulmonary oedema) | |
TRALI (transfusion-related acute lung injury) | |
Severe burns | |
Multitrauma |
Clinical Assessment
ARDS typically develops 12–72 hours post-insult.
Diagnostic Criteria:
- Known precipitating condition
- Acute respiratory failure:
- Acute lung injury: PaO₂/FiO₂ < 40 kPa
- ARDS: PaO₂/FiO₂ < 26 kPa
- Bilateral pulmonary infiltrates on CXR
- Exclusion of hydrostatic causes (PCWP < 18 mmHg)
Note: Hydrostatic or oncotic pulmonary oedema may coexist or precede ARDS.
Investigations
Bloods
- FBC
- CRP
- U&Es, glucose
- Lipase
- Troponin
- ABGs, lactate
- Blood cultures
- Others as indicated
Imaging
- CXR: bilateral infiltrates
- CT Chest: more sensitive for pulmonary causes
Other
- ECG: arrhythmias, ischaemia
- Echocardiography: exclude cardiogenic causes
Management
Key Principles
- Oxygenation and ventilation support
- Treat underlying cause
- General supportive care
1. Respiratory Support
Non-invasive ventilation may be appropriate in mild cases.
Mechanical ventilation is usually required for ARDS.
Aim: Maintain oxygenation to allow time for lung recovery.
ARDS mortality is often due to sepsis and multi-organ failure, not hypoxia.
Ventilation Strategy
Parameter | Approach |
---|---|
Mode | Volume or pressure-limited modes (SIMV, PCV, etc.) |
FiO₂ | Start at 1.0, then titrate to maintain SpO₂ > 90% |
Tidal Volume | Max 6 mL/kg IBW (↓ to 3–4 mL/kg in severe cases) |
Respiratory Rate | 18–25/min to maintain minute ventilation |
PEEP | Start low, ↑ in 5 cm H₂O steps; aim FiO₂ < 0.6, SpO₂ ≥ 88% |
I:E Ratio | ↑ to >1:1; consider 2:1 to 3:1 if hypoxia persists |
Avoid:
- Prolonged high FiO₂ (>0.6 >24 hrs)
- High peak/plateau pressures
- Overdistension (permissive hypercapnia may be needed)
ECMO
- No proven benefit for ARDS to date
2. Treat Underlying Cause
- Prompt treatment of infection or other triggers
3. Supportive Measures
- Early enteral nutrition
- Judicious fluid therapy — avoid fluid overload
4. Therapies of Uncertain Benefit
- Inhaled nitric oxide: reduces pulmonary vascular resistance, unclear impact
- Nebulised prostacyclin: potential vasodilation
5. Corticosteroids
- No proven benefit
Prognosis
- Mortality up to 60% (varies with definitions and comorbidities)
- Common causes of death: sepsis, multi-organ failure
- Survivors often recover with good function, but mild long-term pulmonary impairment is possible.
References
FOAMed
- Nickson C. Acute Respiratory Distress Syndrome – ARDS. CCC
- Nickson C. Acute Respiratory Distress Syndrome Definitions. CCC
- Nickson C. ARDSnet Ventilation Strategy. CCC
- Nickson C. ARDS Literature Summaries. CCC
- Nickson C. Improving Oxygenation in ARDS. CCC
Publications
- Leaver SK, Evans TW. Acute respiratory distress syndrome. BMJ. 2007 Aug 25;335(7616):389-94.
Fellowship Notes
Educator, magister, munus exemplar, dicata in agro subitis medicina et discrimine cura | FFS |