Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Symptoms include shortness of breath, rapid breathing, and bluish skin coloration. Among those who survive, a decreased quality of life is relatively common.
Causes may include sepsis, pancreatitis, trauma, pneumonia, and aspiration. The underlying mechanism involves diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction of the body’s regulation of blood clotting. In effect, ARDS impairs the lungs’ ability to exchange oxygen and carbon dioxide. Diagnosis is based on a PaO2/FiO2 ratio of less than 300 mmHg despite a PEEP of more than 5 cm H2O. Heart related pulmonary edema, as the cause, must be excluded.
The primary treatment involves mechanical ventilation together with treatments directed at the underlying cause. Ventilation strategies include using low volumes and low pressures. If oxygenation remains insufficient lung recruitment maneuvers and paralysis may be tried. If this is insufficient ECMO may be an option. The syndrome is associated with a death rate between 35 and 50%.
Acute Respiratory Distress Syndrome Symptoms
ARDS affects about 3 million people a year. The condition was first described in 1967.
Although the terminology of “adult respiratory distress syndrome” has at times been used to differentiate ARDS from “infant respiratory distress syndrome” in newborns, the international consensus is that “acute respiratory distress syndrome” is the best term because ARDS can affect people of all ages. There are modified diagnostic criteria for children and areas of the world with less resources.
The signs and symptoms of ARDS often begin within two hours of an inciting event, but can occur after 1–3 days. Signs and symptoms may include shortness of breath, fast breathing, and a low oxygen level in the blood due to abnormal ventilation
Diagnostic criteria for ARDS have changed over time as understanding of the pathophysiology has evolved. The international consensus criteria for ARDS were most recently updated in 2012 and are known as the “Berlin definition“. In addition to generally broadening the diagnostic thresholds, other notable changes from the prior 1994 consensus criteria include discouraging the term “acute lung injury,” and defining grades of ARDS severity according to degree of decrease in the oxygen content of the blood.
According to the 2012 Berlin definition, ARDS is characterized by the following:
- lung injury of acute onset, within 1 week of an apparent clinical insult and with progression of respiratory symptoms
- bilateral opacities on chest imaging (chest radiograph or CT) not explained by other lung pathology (e.g. effusion, lobar/lung collapse, or nodules)
- respiratory failure not explained by heart failure or volume overload
- decreased PaO2/FiO2 ratio (a decreased PaO 2/FiO 2 ratio indicates reduced arterial oxygenation from the available inhaled gas)
Note that the Berlin definition requires a minimum positive end expiratory pressure (PEEP) of 5 cm H2O for consideration of the PaO2/FiO 2 ratio. This degree of PEEP may be delivered noninvasively with CPAP to diagnose mild ARDS.
Treatment Of Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome is usually treated with mechanical ventilation in the intensive care unit (ICU). Mechanical ventilation is usually delivered through a rigid tube which enters the oral cavity and is secured in the airway (endotracheal intubation), or by tracheostomy when prolonged ventilation (≥2 weeks) is necessary. The role of non-invasive ventilation is limited to the very early period of the disease or to prevent worsening respiratory distress in individuals with atypical pneumonias, lung bruising, or major surgery patients, who are at risk of developing ARDS.
Treatment of the underlying cause is crucial. Appropriate antibiotic therapy is started as soon as culture results are available, or if infection is suspected (whichever is earlier).
Empirical therapy may be appropriate if local microbiological surveillance is efficient. Where possible the origin of the infection is removed. When sepsis is diagnosed, appropriate local protocols are followed.
The overall goal of mechanical ventilation is to maintain acceptable gas exchange to meet the body’s metabolic demands and to minimize adverse effects in its application. The parameters PEEP (positive end-expiratory pressure, to keep alveoli open), mean airway pressure (to promote recruitment (opening) of easily collapsible alveoli and predictor of hemodynamic effects) and plateau pressure (best predictor of alveolar overdistention) are used.
Previously, mechanical ventilation aimed to achieve tidal volumes (Vt) of 12–15 ml/kg (where the weight is ideal body weight rather than actual weight). Recent studies have shown that high tidal volumes can overstretch alveoli resulting in volutrauma (secondary lung injury). The ARDS Clinical Network, or ARDSNet, completed a clinical trial that showed improved mortality when people with ARDS were ventilated with a tidal volume of 6 ml/kg compared to the traditional 12 ml/kg.
Low tidal volumes (Vt) may cause a permitted rise in blood carbon dioxide levels and collapse of alveoli because of their inherent tendency to increase shunting within the lung. Physiologic dead space cannot change as it is ventilation without perfusion. A shunt is perfusion without ventilation.
Low tidal volume ventilation was the primary independent variable associated with reduced mortality in the NIH-sponsored ARDSnet trial of tidal volume in ARDS. Plateau pressure less than 30 cm H2O was a secondary goal, and subsequent analyses of the data from the ARDSnet trial and other experimental data demonstrate that there appears to be no safe upper limit to plateau pressure; regardless of plateau pressure, individuals with ARDS fare better with low tidal volumes.
Irwin RS, Rippe JM (2003)
Irwin and Rippe’s Intensive Care Medicine
Lippincott Williams & Wilkins. ISBN 978-0-7817-3548-3
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