Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS) is a form of acute, diffuse inflammatory lung injury in which damage to the alveolar-capillary barrier floods the alveoli with protein-rich fluid, causing severe hypoxaemia and reduced lung compliance. It is a syndrome rather than a single disease, triggered by varied insults such as pneumonia, sepsis, or trauma, and is defined by clinical and physiologic criteria.

Definition

ARDS is an acute, diffuse inflammatory injury of the lung, defined by the Berlin criteria as acute onset within a week of a known insult, bilateral opacities not fully explained by cardiac failure or fluid overload, and hypoxaemia graded by the ratio of arterial oxygen tension to inspired oxygen fraction (ARDS Definition Task Force, 2012).

Scope

This topic covers ARDS as a manifestation of acute injury to the pulmonary microvasculature and alveolar epithelium: the underlying alveolar-capillary barrier disruption, the resulting hypoxaemia and stiff lungs, and the consensus criteria that define and grade severity. It is a reference account of how the syndrome is conceived and defined, not a guide to ventilatory or pharmacologic management.

Core questions

• What injury to the alveolar-capillary barrier underlies ARDS?
• How do the Berlin criteria define and grade the syndrome?
• Why is the hypoxaemia of ARDS often severe and refractory?
• What range of insults can precipitate diffuse alveolar injury?

Key concepts

• Diffuse alveolar damage
• Alveolar-capillary barrier disruption
• Increased-permeability (non-cardiogenic) pulmonary oedema
• Severe hypoxaemia and reduced lung compliance
• Berlin definition and severity grading by PaO2/FiO2
• Heterogeneous precipitating insults (pneumonia, sepsis, trauma)

Mechanisms

In ARDS, an inciting insult provokes an inflammatory response that injures the alveolar epithelium and the pulmonary capillary endothelium, breaking down the barrier that normally keeps the alveoli dry. Protein-rich fluid and inflammatory cells flood the air spaces, surfactant function is impaired, and the lungs become stiff and prone to collapse. The result is increased-permeability pulmonary oedema with severe ventilation-perfusion mismatch and shunt, producing hypoxaemia that is often refractory; because injury is patchy, aerated lung volume is markedly reduced (Ware, 2000; Thompson, 2017).

Clinical relevance

ARDS is recognised when acute, severe hypoxaemia and bilateral lung opacities develop after a precipitating insult and cannot be attributed primarily to heart failure, with severity graded by the degree of hypoxaemia. This entry describes how the syndrome is defined and understood and is not a basis for individual diagnosis or for ventilatory or drug management decisions.

Epidemiology

ARDS is an important cause of acute respiratory failure and intensive-care admission, with population-based work documenting a substantial incidence and high mortality among those affected; estimates vary with the definition used and the population studied (Rubenfeld, 2005).

Evidence & guidelines

The standard case definition is the Berlin definition (ARDS Definition Task Force, 2012), with mechanism and clinical features summarised in widely cited reviews (Ware, 2000; Thompson, 2017) and incidence characterised in population-based cohort work (Rubenfeld, 2005); these are cited for definition and orientation rather than as care directives.

History

ARDS was first described as a distinct clinical entity in the late 1960s under the label adult respiratory distress syndrome, and its definition was progressively standardised, culminating in the consensus Berlin definition that replaced earlier criteria and graded severity by the degree of hypoxaemia (ARDS Definition Task Force, 2012). Population-based studies then clarified its incidence and outcomes (Rubenfeld, 2005).

Debates

How should ARDS be defined and its severity graded?

The Berlin definition refined earlier criteria by grading severity through the PaO2/FiO2 ratio and tightening the requirements, but the boundaries of the syndrome and how to capture milder or evolving injury remain matters of ongoing refinement.

Key figures

• Arthur Slutsky
• Lorraine Ware
• Michael Matthay
• Gordon Rubenfeld

Seminal works

• ardstaskforce-2012
• ware-2000
• rubenfeld-2005

Frequently asked questions

Is ARDS a type of heart failure?

No. The pulmonary oedema of ARDS results from increased permeability of the injured alveolar-capillary barrier rather than from elevated cardiac filling pressures, and the Berlin definition requires that the findings are not fully explained by cardiac failure or fluid overload.

What kinds of conditions can lead to ARDS?

A range of direct and indirect insults can precipitate it, including pneumonia, aspiration, sepsis, severe trauma, and other systemic inflammatory states.