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.
Click here to view an animation of capillary leakage and
pulmonary edema in ARDS
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"