Rewarming from hypothermia leads to elevated plasma lipopolysaccharide concentrations

Rewarming victims of hypothermia such as divers or immersion victims, parti cipants in winter sports and military operations, and surgical patients on cardiopulmonary bypass (CPB) may lead to vascular instability, multiorgan f ailure, shock, and even death. While the causes of these rewarming symptoms are unknown, they may be related to bacterial lipopolysaccharide (LPS) tra nslocated from the intestines into the circulation due to splanchnic ischem ia. We have determined LPS during the cooling (to 31.5 degrees-34.0 degrees C) and rewarming phases of hypothermic surgery in 11 patients at the Stanf ord University Medical Center. During rewarming, there was an LPS spike in 6/11, in one more patient there was an LPS spike during surgery but not dur ing rewarming, and in 4/11 there was no rise in LPS, i.e., a temporary endo toxemia occurred in 7/11 (63.6%) patients, usually at the commencement of r ewarming. All four patients with no LPS spike received dexamethasone for at least 7 days before surgery. We propose that hypothermia reduced splanchni c blood flow (BF), causing ischemic damage to the gut wall and translocatio n of LPS from the gut into the vascular space. Upon rewarming, splanchnic B F is restored, the translocated LPS transits from the splanchnic to the sys temic circulations as a bolus, and the gut wall is healed. No sequelae occu rred in these patients because of their adequately functioning immune syste ms. However, had they been immunocompromised, symptoms might have occurred. Rewarming of accident victims probably also incurs a similar risk of endot oxemia, and dexamethasone may have protected the gut wall. Further studies are indicated.