Severe mesenteric traction syndrome is associated with increased systemic inflammatory response, endothelial dysfunction, and major postoperative morbidity.

UNLABELLED: This study aimed to determine if mesenteric traction syndrome (MTS) triggers increased systemic inflammation and endothelial cell dysfunction. Patients developing severe MTS had pronounced early IL6 elevations followed by endothelial cell damage. Furthermore, these processes were associated with increased postoperative morbidity.

OBJECTIVE

To determine whether mesenteric traction syndrome (MTS) leads to increased systemic inflammation and dysfunction of the glycocalyx and endothelial cell and whether this correlates with the degree of postoperative morbidity.

INTRODUCTION

Severe MTS is associated with increased postoperative morbidity following major gastrointestinal surgery, but the pathophysiological mechanism has not been previously explored. Systemic inflammatory response and impaired glycocalyx and endothelial cells may be responsible for the development of symptoms.

METHODS

The study analyzed prospectively collected data from two cohorts (n = 67). The severity of the MTS response was graded intraoperatively and blood samples for PGI2, catecholamines, IL6, and endothelial biomarkers obtained at predefined time points.

RESULTS

Patients undergoing either esophagectomy (n = 45) or gastrectomy (n = 22) were included. Surgery led to significantly increased plasma concentrations of all biomarkers. Yet, patients who developed severe MTS had higher baseline epinephrine levels (p < 0.05) and higher levels of PGI2 (p < 0.05), Syndecan-1 (p < 0.001), and sVEGFR1 (p < 0.001). Peak values of IL6, Syndecan-1, sVEGFR1, and sTM all correlated to peak PGI2. Lastly, patients with high postoperative morbidity had higher baseline epinephrine (p = 0.009) and developed higher plasma IL6 (p = 0.007) and sTM (p = 0.022).

CONCLUSION

The development of severe MTS during upper gastrointestinal surgery is associated with preoperative elevated plasma epinephrine and further a more pronounced proinflammatory response and damage to the vascular endothelium. The increased postoperative morbidity seen in patients with severe MTS may thus, in part, be explained by an inherent susceptibility towards an inappropriate secretion of PGI2, which leads to an increased surgical stress response and endothelial damage. These findings must be confirmed in a new prospective cohort.