17th January 2024

Background

Acute respiratory distress syndrome (ARDS) is defined by the acute onset of lung inflammation, causing a diffuse, non-cardiogenic pulmonary oedema and respiratory failure. Due to the nature of the diagnostic criteria, it is almost exclusively a diagnosis made and managed in a critical care setting.

Epidemiology

There are various estimates for the prevalence of ARDS, ranging from 1 case per 100,000 to 79 per 100,000. One large, multi-centre study projected incidence as 86 per 100,000 person-years. Prevalence in the intensive care patient population is thought to be around 10%, rising to 23% in the mechanically ventilated patient group. Mortality from ARDS is estimated to be around 40%, increasing depending on severity group. It can affect many different patient groups, but incidence increases with age (1).

Pathophysiology

ARDS is an umbrella term encompassing multiple different disease processes leading to a distinct clinical syndrome. The most common causes are sepsis, pneumonia (including COVID-19 pneumonitis), aspiration, trauma, pancreatitis and transfusion of blood products. All causes of ARDS result in an increased vascular endothelial permeability, allowing for accumulation of protein-rich fluid in the alveolar spaces. This initiates the release of pro-inflammatory cytokines, such as Tumour Necrosis Factor (TNF), IL-1 and IL-6, creating a further cycle of damage, whereby neutrophils are recruited to accumulate in the alveolar spaces, and toxic free radical production causes extensive oxidative cell damage. This diffuse alveolar damage results in impaired gas exchange, reduced lung compliance and pulmonary hypertension (2).

The pathophysiology of ARDS can be divided into three distinct stages (3):

• Early exudative stage – the acute reaction to lung injury from various sources, involving inflammation and alveolar oedema. This lasts for around 7-10 days.
• Fibroproliferative stage – remodelling of the alveolar cell walls with fibroblastic invasion and collagen deposition, reducing compliance.
• Fibrotic stage – not all patients progress to this final stage. It involves the complete destruction of the alveolar architecture, with cyst formation and further fibrosis.