Intraoperative splanchnic hypoperfusion, increased intestinal permeability, down-regulation of monocyte class II major histocompatibility complex expression, exaggerated acute phase response, and sepsis.

BACKGROUND: A compromised gut barrier function may be associated with systemic inflammatory response syndrome, sepsis, and multiple organ dysfunction syndrome in patients after major trauma or critical illness, and inadequate oxygenation of the gut mucosa has been incriminated as an underlying mechanism. The focus of this study was the relationship of splanchnic hypoperfusion to regional and systemic immune responses after major surgery.

METHODS: Patients (n=20) undergoing curative oncologic resection of the esophagus or esophagogastric junction were studied. Gastric mucosal pH level was monitored by gastric tonometry. The expression of class II major histocompatibility complex antigen (human leukocyte antigen-DR) and L-selectin on systemic monocytes was assessed before surgery, during surgery (as well as portal monocytes), and for 1 week after surgery, along with C-reactive protein levels. Intestinal permeability was measured before surgery and on the first and seventh postoperative days by using dual sugar probes.

RESULTS: Significant mucosal acidosis (pH<7.1) intraoperatively was evident in 5 patients (25%), and a further 7 patients (35%) had a nadir gastrointestinal mucosal pH level between 7.1 and 7.2. Severe (<7.1) mucosal acidosis was associated significantly (P< .05) with postoperative septic complications, an increase in postoperative intestinal permeability, C-reactive protein and L-selectin expression, and a decrease (P< .05) in monocyte human leukocyte antigen-DR expression.

CONCLUSIONS: Intraoperative splanchnic hypoperfusion is associated significantly with down-regulation of monocyte function, increased intestinal permeability, and an exaggerated acute phase response. This suggests that splanchnic hypoperfusion alters local and systemic immune function, supporting the thesis that the gut has a central role in the immunoinflammatory response to major surgery.