- ARDS defined as
- Respiratory distress
- Stiff lungs – ↓compliance, resulting in ↑inflation pressures
- CXR – infiltrates
- Cardiac – no apparent cause of pulmonary oedema
- Gas exchange abnormalities
- Mild – PaO2 / FiO2 = 300-200mmHg
- Moderate – PaO2/FiO2 = 200-100mmHg
- Severe – PaO2/FiO2 <100mmHg
Etiology
Direct lung injury
- Pneumonia
- Aspiration of gastric contents
Indirect lung injury
- Sepsis (MCC)
- Trauma
- Drug overdose – aspirin/heroin
Pathophysiology
- ARDS is an early manifestation of a generalised inflammatory response with endothelial dysfunction
- Frequently associated with MODS
Non-cardiogenic pulmonary oedema – cardinal feature of ARDS
- First clinical sign of generalised ↑vascular permeability – neutrophils play a key role
- Damage of pulmonary epithelium → ↓surfactant production → predisposes for alveolar collapse
Pulmonary hypertension
- Interstitial oedema → vascular compression → mechanical obstruction of pulmonary circulation
- Activation of coagulation cascade → thrombosis + obstruction of pulmonary microvasculature
- ↑ANS activity → ↑catecholamines + thromboxanes → pulmonary vasoconstriction
Haemorrhagic intra-alveolar exudates
- Exudates is rich in platelets, fibrin, fibrinogen, clotting factors – inactivates surfactant + stimulates inflam
- Promotes hyaline membrane formation
- Promotes fibroblast migration into alveoli
Resolution, fibrosis, repair
- Within a few days formation of a new epithelial lining begins
- Activated fibroblasts accumulate in the interstitial spaces – can lead to progressive interstitial fibrosis
Physiological changes
- ↑dead space and shunts
- ↓lung compliance – airflow limitation
Clinical features
- Unexplained tachypnoea
- Central cyanosis (lips and membranes) + dyspnoea – as hypoxaemia increases
- Chest pain
- Fine crackles
Diagnosis
- ABGs – low oxygen
- CXR – bilateral, diffuse infiltrates
- Swan-Ganz catheter – measures PCWP (indirectly measures LAP)
- Has to be <19mmHg to consider a diagnosis of ARDS
Treatment
- Treatment underlying cause
- Mechanical ventilation – CPAP (if PaO2 remains <8kPa then intubate and give mechanical ventilation)
- Limit pulmonary oedema – fluid restriction, diuretics (furosemide)
- Prone position – improves gas exchange by redistribution of lung densities and perfusion
- Inhaled NO – increases perfusion of ventilated lung areas, reduces pulmonary hypertension
- Prostacyclin – similar effect to NO, but better at monitoring
- Aerosolised surfactant