A brief overview of acute respiratory distress syndrome

The low pO: (2) in traumatic and septic shock was first documented at Walter Reed Army Medical Center starting in 1960. It was postulated that this respiratory failure was due to the occlusion of the pulmonary microcirculation by the microclots of disseminated intravascular coagulation (DIC).

Animal studies showed that pulmonary failure and death could be caused by intravenous injection of a killed culture of either Escherichia coli or pneumococcal organisms or by severe muscle contusion. Severe clinical septic and traumatic shock cases were studied.

Injection of either killed E. coli or killed pneumococci resulted in acute respiratory distress syndrome (ARDS) and death in pigs. Muscle contusion also resulted in ARDS and death in pigs. Both ARDS and death were prevented by administration of a plasminogen activator, and ARDS in human septic or traumatic shock were safely and effectively treated by administration of a plasminogen activator.

Acute respiratory distress syndrome can be caused by DIC, which blocks the microcirculation of any and all organs. These microclots can be safely lysed by a plasminogen activator, thus treating ARDS and saving lives.