Acute Respiratory Distress Syndrome

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.

In this article, we shall look at the aetiology, clinical features and management of acute respiratory distress syndrome.

Definition

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.

Aetiology and Pathophysiology

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

Direct Indirect
Pneumonia

Smoke inhalation

Aspiration

Fat embolus

Sepsis

Acute pancreatitis

Polytrauma

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.

Fig. 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 cyanosis, hypoxia, tachycardia, and tachypneoa, with inspiratory crackles on auscultation.


Investigations

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 x-ray (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.

Fig 2 – Chest x-rays demonstrating the extensive bilateral infiltrates seen in acute respiratory distress syndrome.

Management

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 is used to splint 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. Artificial surfactant is effective in neonates but has yielded no advantage in adults.

Corticosteroids are not effective in the acute phase of ARDS, but may reduce ventilation days when used 7-14 days after onset.


Prognosis

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). 50% of patients 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.

Quiz

Question 1 / 3
Which of the following is a 'direct' cause of acute respiratory distress syndrome?

Quiz

Question 2 / 3
What is a feature of acute respiratory distress syndrome on examination?

Quiz

Question 3 / 3
Which of the following pathologies has similar x-ray features to acute respiratory distress syndrome?

Results

Further Reading

Acute respiratory distress syndrome: new definition, current and future therapeutic options
Fanelli V et al., Journal of Thoracic Disease

Rate This Article

Average Rating:

Not yet rated