Part of the TeachMe Series

Acute Respiratory Distress Syndrome

star star star star star
based on 6 ratings

Original Author(s): Omar Ahmed
Last updated: January 12, 2019
Revisions: 20

Original Author(s): Omar Ahmed
Last updated: January 12, 2019
Revisions: 20

format_list_bulletedContents add remove


Acute respiratory distress syndrome (ARDS) is a form of acute lung injury, which is characterised by severe hypoxemia in the absence of a cardiogenic cause.

It occurs when there is inflammatory damage to the alveoli, which leads to pulmonary oedema, respiratory compromise, and ultimately acute respiratory failure.


The most up-to-date definition of acute respiratory distress syndrome is the Berlin Definition, which broadly consists of 4 key points:

  • Acute onset within 7 days
  • PaO2:FiO2 ratio <300
  • Bilateral infiltrates on CXR
  • Alveolar oedema not explained by fluid overload or cardiogenic causes

The degree of ARDS severity can be further defined, based on degree of hypoxemia via the PaO2:FiO2 ratio: Mild = 200-300mmHg, Moderate = 100-200mmHg, Severe ≤100mmHg.


The causes of acute respiratory distress syndrome can be divided into direct and indirect:

Direct Indirect

Smoke inhalation


Fat embolus


Acute pancreatitis


The pathophysiology is complex, and poorly understood. It is thought that direct injury or activation of the systemic inflammatory cascade results in breakdown of the alveolar-capillary barrier. Consequently, its permeability increases, and this leads to fluid infiltration and pulmonary oedema.

The fluid infiltration impairs ventilation and gas exchange, leading to hypoxaemia. In addition, damage to the type II alveolar cells impairs surfactant production, reducing the lung compliance and further worsening ventilation.

ARDS is self-perpetuating. The affected alveoli begin to expand more and more, with the shear forces from this expansion resulting in barotrauma and more cell damage.

Figure 1 – The microscopic diffuse alveolar damage seen in acute respiratory distress syndrome

Clinical Features

Acute respiratory distress syndrome presents with (worsening) dyspnoea, usually in the presence of a related risk factor or underlying cause.

This then rapidly leads to hypoxia, tachycardia, and tachypneoa, with inspiratory crackles on auscultation.


All patients with suspected acute respiratory distress syndrome should have the following basic investigations:

  • Routine bloods (including full blood count, urea and electrolyte, amylase, and C-reactive protein)
  • Blood cultures
  • Arterial blood gas
  • Chest radiograph (CXR)
    • Classically shows diffuse bilateral infiltrates, similar to that of pulmonary oedema.

The suspected underlying cause of the acute respiratory distress syndrome will determine which further investigations are required.

Figure 2 – Two separate chest radiographs demonstrating extensive bilateral infiltrates from acute respiratory distress syndrome


The management of acute respiratory distress syndrome is twofold; (i) supportive treatment with ventilation, and; (ii) focused treatment of the underlying cause. It is highly likely that patients will require emergency intubation and ITU admission for respiratory and circulatory support.

The specific goals of ITU management of ARDS are complex, focusing on limiting the inflammatory cascade and alveolar oedema. However, the main aspects of management involve:

  • Maintaining the minimum intravascular volume required to ensure adequate tissue perfusion, thus limiting excess oedema
  • Lower tidal volumes used in ventilation, reducing shear forces from over-distension and ventilator-associated lung injury
  • Positive end-expiratory pressure, splinting airways and avoids the damage caused by the cyclical opening of alveoli

Pharmacological Treatment of ARDS

Pharmacological treatments of ARDS have in the past involved the use of artificial surfactant and corticosteroids, however are used less and less in modern practice.

Use of artificial surfactant can be effective in neonatal cases, however has yielded no advantage in adults, whilst the use of corticosteroids are not effective in the acute phase of ARDS (but may reduce ventilation days when used 7-14 days after onset).


Acute respiratory distress syndrome remains associated with a high mortality (~40% in Western centres), although it varies dependent on the underlying cause, age and degree of multi organ failure.

Survivors can develop pulmonary fibrosis, although in many patients, lung capacity returns to normal within 12 months. Only 50% of patients will return to work after one year.

Key Points

  • Acute respiratory distress syndrome remains associated with a high mortality
  • Its causes can be divided into either direct or indirect
  • Management of ARDS comprises both of supportive treatment with ventilation and focused management of the underlying cause