Acute respiratory distress syndrome (ARDS)

Definition:

Defined as:

• Diffuse pulmonary infiltrates
• Non-cardiogenic pulmonary oedema
• Refractory hypoxaemia
• Stiff lungs
• Respiratory distress

Commonest predisposing factor, by far, is sepsis (20-40% of patients with severe sepsis will develop ARDS)

Disorders associated with ARDS:

Shock

Infection (e.g. sepsis, pneumonia)

Trauma

Pulmonary aspiration

Inhalation injury (e.g. smoke, corrosive gases)

Haematological (e.g. DIC, massive transfusion)

Obstetric (e.g. amniotic fluid embolism)

Drug overdose (e.g. heroin, barbiturates)

Miscellaneous (e.g. pancreatitis, CP bypass)

Pathophysiology:

ARDS can be considered as the earliest manifestation of a generalized inflammatory response and is, therefore, frequently associated with the development of MODS (multiple organ dysfunction syndrome)

Non-cardiogenic pulmonary oedema:

• Cardinal feature of ARDS
• Is the first and clinically most evident sign of a generalized increase in vascular permeability (caused by the microcirculatory changes and release of inflammatory mediators)
• The pulmonary epithelium is also damaged in the early stages of ARDS, reducing surfactant production and lowering the threshold for alveolar flooding

Pulmonary hypertension:

Common feature of ARDS

Initially, mechanical obstruction of the pulmonary circulation may occur as a result of vascular compression by interstitial oedema and, subsequently, oedema of the vessel wall itself

Later, constriction of the vasculature may develop in response to increased ANS activity and circulating substances (e.g. catecholamines)

Fibrosis:

• Starts to occur within 7 days of the onset of ARDS
• Is progressive, and causes a loss of elastic tissue and obliteration of the lung vasculature, together with lung destruction and emphysema

Physiological changes:

• Increased dead-space
• Decreased compliance
• Evidence of airflow limitation

Clinical presentation of ARDS:

• Unexplained tachycardia
• Increasing hypoxaemia
• Dyspnoea
• Laboured breathing
• Fine crackles bilaterally

Management of ARDS:

This is based on treatment of the underlying cause and supportive measures

Limit pulmonary oedema:

• Fluid restriction
• Diuretics
• Haemofiltration (if severe)

Body position changes:

• When the patient is changed from the supine to the prone position, lung densities in the dependent regions are redistributed and gas exchange may improve
• Repeated position changes between prone and supine may, therefore, allow reduction in airway pressures and the inspired oxygen concentration

High dose steroids:

• Only shown to be beneficial when administered during the late fibroproliferative phase of ARDS

Inhaled nitric oxide:

• Can improve V/Q matching and oxygenation by increasing perfusion in ventilated lung units
• Also reduces pulmonary hypertension

Aerosolized prostacyclin:

• Has similar effects to inhaled NO

Aerosolized surfactant:

• Yet to be established
• Beneficial in animal models of ARDS

Prognosis:

• Mortality is >50%
• Prognosis is very dependent on aetiology
• When ARDS occurs in association with septic shock, mortality can be as high as 90%
• ~40% of uncomplicated cases die
• The major cause of mortality is not so much impaired gas exchange but MODS and haemodynamic instability