Acute respiratory distress syndrome (ARDS)
An acute form of respiratory failure caused by diffuse pulmonary infiltrates and alveolar damage occurring hours to days after a pulmonary or systemic insult. Previously called adult respiratory distress syndrome it has been renamed as it also occurs in children.
Occurs in 20–40% of patients with severe sepsis.
Many conditions are recognised as precipitants, most commonly systemic sepsis.
· Lung-related causes include aspiration and smoke inhalation, pneumonia, near drowning and lung contusion.
· Other systemic causes include shock from any cause, major trauma/burns, disseminated intravascular coagulation (DIC), air, fat or amniotic fluid embolism and heroin overdose. It is also well reported following cardiopulmonary bypass and pancreatitis.
1. Acute exudative phase:
Increased vascular permeability and epithelial damage due to neutrophilderived toxins, mechanical damage, cytokines and possibly abnormal clotting mechanisms lead to pulmonary oedema (non-cardiogenic) and exudation of a protein-rich fluid into alveolar spaces.
Type I pneumocytes, which make up 90% of the alveolar epithelium mostly die, and Type II pneumocytes, which produce surfactant are disrupted in function.
During this phase, there is alveolar collapse, lung compliance falls (i.e. the lungs become stiff) and gas exchange is impaired, and there may also be evidence of airflow obstruction. Increased shunting and deadspace occurs (ventilation–perfusion mismatch) and hypoxaemia results.
2. In some cases the acute phase resolves with complete recovery within a week. In other cases, where damage to lung tissue has been severe the disease progresses to a fibrosing alveolitis phase:
The mechanism is unclear, but interstitial fibrosis develops with loss of the normal architecture of the lung, obliterating the vasculature and leading to pulmonary hypertension, worsening lung compliance and in the long-term emphysema and honeycomb lung.
The first sign is tachypnoea, followed by hypoxia, worsening dyspnoea and fine bibasal crackles that become widespread. ARDS is often the first manifestation of multiple organ failure, so the features of other organ failure may develop such as renal and liver failure.
Often complicated by secondary infection (nosocomial pneumonia).
Chest X-ray and CT scan show bilateral diffuse shadowing with an alveolar pattern. Later the picture may progress to a complete whiteout. With the fibrotic phase, linear opacities become visible.
Blood gases are used to detect and monitor respiratory failure, other investigations such as U&E and liver function tests may be required, as multiorgan failure is common.
The pulmonary wedge pressure should be measured by insertion of a Swan–Ganz catheter. In ARDS the pulmonary wedge pressure is normal (although pulmonary arterial pressure is raised) unlike in cardiogenic pulmonary oedema.
Other investigations to look for an underlying cause (e.g. blood cultures coagulation screen and d-dimers for DIC, amylase for pancreatitis).
1. Identification and eradication of any underlying cause such as sepsis.
2. Supportive treatment with following:
· Ventilatory support – low volume, pressure-limited cycles reduce further damage.
· Fluid restriction and removal if necessary to minimise pulmonary oedema.
· To attempt to improve ventilation/perfusion mis-match the patient can be alternately nursed prone and supine, or treated with nebulised prostacyclin or nitric oxide.
· High dose steroids are no longer recommended in ARDS for treatment or prophylaxis.
Dependant on the underlying cause, mortality can be very high in patients with septic shock who develop multi-organ failure. Increasing age and pre-existing disease worsen the outcome.