Searching for the etiology of systemic inflammatory response syndrome: is SIRS occult endotoxemia?

Excerpt

It has been estimated that as many as 60% of critically ill patients develop systemic inflammatory response syndrome (SIRS), manifested by tachycardia, tachypnea, fever, and/or leukocytosis [1]. When this response occurs in the presence of living infection, it is called sepsis. When it occurs in the absence of living infection, it is called SIRS. In Intensive Care Medicine Stephens and colleagues now continue their investigation into the immunological etiology of SIRS in critical illness [2]. They previously reported in this journal that mannose binding lectin (MBL) deficiency is a predisposing factor to the development of SIRS in children after trauma or noncardiac surgery. [3] This lectin is the immediate (first 12 h) soluble immune response to infection. It is responsible for antibody independent complement mediated localization and killing of microbes. When MBL is deficient, infection cannot be localized, and if unchecked for the first 12 h it spreads until the antibody mediated complement system is recruited. If this infection is alive then this spread of infection can be identified as culture positive sepsis. However, if the infection is dead, it can be identified as culture negative sepsis, or if the physician does not think the patient has infection, it can be identified as SIRS. When one thinks of the component of dead infection in humans most likely to cause SIRS, it is endotoxin. The human gastrointestinal tract contains 25 × 10⁹ ng endotoxin as microflora [4]. Any perturbation of intestinal, portal system, or liver permeability can result in spilling of endotoxin into the circulation. If not localized by MBL, this endotoxin has an additional 12 h to spread and cause SIRS (Fig. 1).

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