06 Feb

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Impact of the liver

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Impact of the liverSeveral anatomic factors account for the impact of the liver on control of systemic endotoxemia and bacteremia: (1) its strategic location immediately downstream from the large gastrointestinal (GI) reservoir of these substances; (2) the characteristics of the splanchnic circulation—receiving 25 percent of the cardiac output and comprising 20 to 25 percent of the systemic blood volume—which constitutes portal blood flow (approximately 75 percent of total hepatic blood flow); and (3) the extensively anastomosing sinusoidal microvasculature through which this volume must pass. Consequently ample opportunity exists for blood-cell contact and hepatic clearance prior to reentry of blood into the systemic circulation. An intact GI mucosal barrier prevents significant entry of intestinal endotoxin into the portal vein, but small amounts of endotoxin and, occasionally, bacteria gain access to portal blood; however, the in-series intestinal barrier and efficient Kupffer cell uptake of these substances in portal blood normally constitutes an effective first line of defense in host control of systemic endotoxemia and bacteremia. there

Even with normal preexisting hepatic function, failure of this defense to contain endotoxin and bacteria can trigger irreversible shock and multiple organ dysfunction owing to their “spillover” from endogenous intestinal sources past the liver into the systemic circulation. Several mechanisms may alter the gut-liver axis, permitting endogenous endotoxemia and bacteremia by overwhelming hepatic clearance capacity. Gut factors include augmented endotoxin production or absorption from the intestinal lumen. Stasis with Gram-negative coliform and Pseudomonas overgrowth changes the homeostatic balance among gut microbial populations, altering total body endotoxin load and susceptibility to endotoxin itself.’ Acute mesenteric ischemia increases the permeability of the gut wall to intestinal endotoxin. This can lead to cardiovascular collapse, an effect exacerbated by vasoactive drugs which further reduce mesenteric inflow but ameliorated by decreasing the gut flora with nonabsorbable antibiotics. As an example of a positive amplification mechanism, systemic endotoxemia can become a self-sustaining process in which the associated hemodynamic effects mobilize additional GI endotoxin and lead to bacterial translocation across the intestinal wall.

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