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Definition
Adult Respiratory Distress Syndrome (also known as Acute Respiratory Distress Syndrome or ARDS) is a form of rapid onset lung injury often seen in previously healthy patients. ARDS is characterized by rapid breathing and a profound sensation of shortness of breath. The clinical definition consists of severely low bloodstream oxygen levels unresponsive to supplemental oxygen and widespread lung infiltrates (fluid and protein) not caused by heart failure or fluid overload.
Incidence
100,000 cases occur in the USA each year. 40,000 deaths occur as a result of ARDS annually in the USA
Prognosis
ARDS is fatal in 40% of all cases. Chances for survival are highest when ARDS occurs as a single entity in otherwise healthy individuals, and lowest when ARDS occurs in conjunction with multi-organ failure. The simultaneous presence of pneumonia is also associated with a much greater risk of fatality.
Cause
ARDS can occur from a wide variety of lung based and systemic injury, but 80% of cases result from systemic bodily infections (sepsis), localized lung infection (pneumonia), severe trauma or inhalation into the lungs of stomach contents (aspiration). The likelihood of development of ARDS is highest in individuals with systemic bodily infection (sepsis) or those in shock as a result of sepsis, and is increased in the presence of multiple risk factors (see table below) and/or multiple organ failure. The generic term ARDS belies the non-uniformity of possible causes and diversity of precipitating events. (see table 1)
TABLE 1 - Disorders Associated with ARDS
Aspiration (into the trachea) Gastric contents Fresh and salt water Hydrocarbons
Hematologic alterations Disseminated intravascular coagulation Massive blood transfusion Leukoagglutination reactions
Metabolic disorders Pancreatitis Uremia and diabetes mellitus seem to contribute to other risk factors
Central nervous system Trauma Anoxia (no oxygen) Seizures Increased intracranial pressure
Infection Sepsis (gram-positive or -negative) Pneumonia: bacterial, viral, fungal Tuberculosis Shock (rare in cardiogenic or embolic; uncommon in pure hemorrhagic)
Drug overdose or reactions Acetylsalicyclic acid Heroin Hydroxychloroquine (Plaquenil) Propoxyphene Paraquat
Inhalation of toxins Oxygen Smoke Corrosive chemicals (NO2 , Cl2 , NH3 , phosgene)
Trauma Fat emboli (long bones usually) Lung contusion Non-thoracic (severe) Cardiopulmonary bypass
Mechanism of onset
Despite the variety of specific conditions that can give rise to ARDS, the common intiating event is release of enzymes and other chemicals from injured tissues that cause excessive leakage of fluid from tiny blood vessels (capillaries) in the lung, as well as damage to the microscopic air sacs (alveoli) that directly interface with the capillaries. The excessive fluid leakage may lead to abnormal amounts of fluid in the lungs (pulmonary edema), while the alveolar damage may lead to irreversible scarring of lung tissue (fibrosis). The full extent of injury depends on the severity and persistence of the initial process (ie- systemic infection). Experimental and clinical evidence shows that some cases of ARDS resolve rapidly while others progress relentlessly through several stages to severe scarring (fibrosis) and ultimately death from respiratory failure.
Treatment
Treatment of the underlying causes of ARDS (ie- sepsis, pneumonia) is the only approach shown to be effective in leading to good outcomes for individuals so afflicted. Effective treatments for capillary leakage and alveolar tissue damage have thus far been elusive. Use of corticosteroids (ie-prednisone), non-steroidal anti inflammatories, prostoglandins and nitric oxide have all proven unsuccessful, as have trials with agents designed to antagonize or block receptors for the injurious infection and trauma related chemicals and enzymes which lead to ARDS. Preliminary trials with "free-radical scavengers" in infection-related ARDS have been encouraging, but practical treatments with these compounds are not yet a reality.
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