Mannose-binding lectin deficiency provides a genetic basis for the use of SIRS/sepsis definitions in critically ill patients

Excerpt

Over a decade ago, Roger Bone and colleagues [1, 2] developed clinical criteria to identify critically ill patients with systemic inflammation. They reasoned that abnormal body temperature, tachycardia, tachypnea, and abnormal white blood cell counts were the accepted clinical signs of systemic inflammation. In an effort to capture all critically ill patients with systemic inflammatory response syndromes, “systemic inflammatory response syndrome” (SIRS) was defined by the presence of two or more of the four signs in the absence of any other clinical conditions known to cause these abnormalities. For example, a hemorrhaging trauma patient in pain with tachypnea and tachycardia would not be considered to have SIRS. However, if tachycardia and tachypnea persisted in this patient after hemorrhage and pain was controlled and blood volume restored, the patient would be considered to have SIRS. Because systemic inflammation can occur as a result of infection as well as a result of tissue injury without infection, Bone and colleagues also defined SIRS in the presence of suspected or proven infection as “sepsis.” Investigators then applied these clinical definitions to their respective critically ill populations and found that the incidence of SIRS/sepsis ranged from 50%–80%! This caused concern in some intensivists who thought that criteria which defined the majority of critically ill patients were of little utility, but satisfaction in other intensivists who thought that most “sick” patients with critical illness were in fact suffering from the side effects of systemic inflammation. …