Acute respiratory distress syndrome


Acute respiratory distress syndrome 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. For those who survive, a decreased quality of life is 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. Adult diagnosis is based on a PaO2/FiO2 ratio of less than 300 mm Hg despite a positive end-expiratory pressure of more than 5 cm H2O. Cardiogenic 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 neuromuscular blockers may be used. If these are insufficient, extracorporeal membrane oxygenation may be an option. The syndrome is associated with a death rate between 35 and 46%.
Globally, ARDS affects more than 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 separate diagnostic criteria for children and those in areas of the world with fewer resources.

Signs and symptoms

The signs and symptoms of ARDS often begin within two hours of an inciting event, but have been known to take as long as 1–3 days; diagnostic criteria require a known insult to have happened within 7 days of the syndrome. Signs and symptoms may include shortness of breath, fast breathing, and a low oxygen level in the blood due to abnormal ventilation. Other common symptoms include muscle fatigue and general weakness, low blood pressure, a dry, hacking cough, and fever.

Complications

Complications may include the following:
Other complications that are typically associated with ARDS include:
  • Atelectasis: small air pockets within the lung collapse
  • Complications that arise from treatment in a hospital: blood clots formed by lying down for long periods of time, weakness in muscles that are used for breathing, stress ulcers, and issues with mental health and depression.
  • Failure of multiple organs
  • Pulmonary hypertension or increase in blood pressure in the main artery from the heart to the lungs. This complication typically occurs due to the restriction of the blood vessel due to inflammation of the mechanical ventilation

    Causes

There are direct and indirect causes of ARDS depending whether the lungs are initially affected. Direct causes include pneumonia, aspiration, inhalational lung injury, lung contusion, chest trauma, and near-drowning. Indirect causes include sepsis, shock, pancreatitis, trauma, cardiopulmonary bypass, TRALI, burns, increased intracranial pressure. Fewer cases of ARDS are linked to large volumes of fluid used during post-trauma resuscitation.

Pathophysiology

ARDS is a form of fluid accumulation in the lungs not explained by heart failure. It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. Additional common findings in ARDS include partial collapse of the alveoli and low levels of oxygen in the blood. The clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage. Of these, the pathology most commonly associated with ARDS is DAD, which is characterized by a diffuse inflammation of lung tissue. The triggering insult to the tissue usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells.
Neutrophils and some T-lymphocytes quickly migrate into the inflamed lung tissue and contribute in the amplification of the phenomenon. The typical histological presentation involves diffuse alveolar damage and hyaline membrane formation in alveolar walls. Although the triggering mechanisms are not completely understood, recent research has examined the role of inflammation and mechanical stress.
One research group has reported that broncho-alveolar lavage fluid in later-stage ARDS often contains trichomonads, in an amoeboid form which makes them difficult to identify under the microscope.

Diagnosis

Diagnostic criteria

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, adult ARDS is characterized by the following:
  • lung injury of acute onset, within 1 week of an apparent clinical insult and with the progression of respiratory symptoms
  • bilateral opacities on chest imaging not explained by other lung pathology
  • respiratory failure not explained by heart failure or volume overload
  • decreased Pa/Fi ratio :
  • * mild ARDS: 201 – 300 mmHg
  • * moderate ARDS: 101 – 200 mmHg
  • * severe ARDS: ≤ 100 mmHg
  • * The Berlin definition requires a minimum positive end expiratory pressure of 5 cm for consideration of the Pa/Fi ratio. This degree of PEEP may be delivered noninvasively with CPAP to diagnose mild ARDS.
The 2012 "Berlin criteria" are a modification of the prior 1994 consensus conference definitions.

Medical imaging

Radiologic imaging has long been a criterion for diagnosis of ARDS. Original definitions of ARDS specified that correlative chest X-ray findings were required for diagnosis, the diagnostic criteria have been expanded over time to accept CT and ultrasound findings as equally contributory. Generally, radiographic findings of fluid accumulation affecting both lungs and unrelated to increased cardiopulmonary vascular pressure may be suggestive of ARDS.
Ultrasound findings suggestive of ARDS include the following:
  • Anterior subpleural consolidations
  • Absence or reduction of lung sliding
  • "Spared areas" of normal parenchyma
  • Pleural line abnormalities
  • Nonhomogeneous distribution of B-lines

    Treatment

Acute respiratory distress syndrome is usually treated with mechanical ventilation in the intensive care unit. Mechanical ventilation is usually delivered through a rigid tube which enters the oral cavity and is secured in the airway, or by tracheostomy when prolonged ventilation 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. 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.

Mechanical ventilation

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, mean airway pressure, and plateau pressure are used.
Previously, mechanical ventilation aimed to achieve tidal volumes of 12–15 ml/kg. Recent studies have shown that high tidal volumes can overstretch alveoli resulting in volutrauma. 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 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 a perfusion without ventilation within a lung region.
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 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.