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:

  1. Cardiogenic: ↑ capillary hydrostatic pressure (Pc​)
  2. Low oncotic pressure: ↓ plasma oncotic pressure (πc​) — rare
  3. 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:

  1. Exudative
  2. Inflammatory
  3. 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 InjuryIndirect (Secondary) Lung Injury
AspirationSevere/prolonged shock
Near drowningRenal or hepatic failure
Inhalation of noxious gasesSevere pancreatitis
Severe pulmonary traumaGeneralised sepsis
Severe pneumoniaFat embolism
RadiationAnaphylaxis (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:
  1. Known precipitating condition
  2. Acute respiratory failure:
    • Acute lung injury: PaO₂/FiO₂ < 40 kPa
    • ARDS: PaO₂/FiO₂ < 26 kPa
  3. Bilateral pulmonary infiltrates on CXR
  4. 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
ParameterApproach
ModeVolume or pressure-limited modes (SIMV, PCV, etc.)
FiO₂Start at 1.0, then titrate to maintain SpO₂ > 90%
Tidal VolumeMax 6 mL/kg IBW (↓ to 3–4 mL/kg in severe cases)
Respiratory Rate18–25/min to maintain minute ventilation
PEEPStart 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

Publications

Fellowship Notes

Dr James Hayes LITFL Author Medical Educator

Educator, magister, munus exemplar, dicata in agro subitis medicina et discrimine cura | FFS |

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