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1999 Abstract: 2150 PREDICTION OF SEVERE AND SEPTIC COURSES OF ACUTE PANCREATITIS BY NONINVASIVE INTRAMUCOSAL PH-MEASUREMENTS OF THE SIGMA

Abstracts
1999 Digestive Disease Week

# 2150 PREDICTION OF SEVERE AND SEPTIC COURSES OF ACUTE PANCREATITIS BY NONINVASIVE INTRAMUCOSAL PH-MEASUREMENTS OF THE SIGMA
Jens Werner, T Keck, J Schmidt, C Kuntz, M M Gebhard, M Aulmann, Univ of Heidelberg, Heidelberg Germany; Christian Herfarth, Ernst Klar, Univ of Heidelberg, Dept. of Surg, Heidelberg Germany

Prognosis of acute pancreatitis is mainly dependent on septic complications. Sepsis is characterized by intestinal ischemia, subsequent mucosal barrier failure and bacterial translocation. Unfortunately, a predictor of severe fatal disease does not exist. The present study investigated whether measurement of intramucosal pH of the sigma (pHi) correlates with the intestinal microcirculatory disturbances, whether it can differentiate between severe necrotizing and mild pancreatitis, and whether it can predict septic courses of pancreatitis. Methods: Noninvasive measurement of the pHi was performed with a sigmoid catheter in Wistar rats at baseline, and 1, 3, 6, 12, and 24 hours, and 3 and 7 days after induction of mild (caerulein i.v.) or severe necrotizing pancreatitis (intraductal glycodeoxycolic acid and caerulein i.v.) and compared with control animals (Ringer i.v.; n=20 per group). Pancreatic and intestinal injury were evaluated by histology and myeloperoxidase activity, and bacterial translocation was analyzed by bacteriological assessment of mesenteric lymphnodes. In additional animals (n=6 per group) intestinal mucosal perfusion and leukocyte adhesion in postcapillary venules were investigated by intravital microscopy at all timepoints and correlated with intramucosal pHi-measurements of the sigma. Results: Intramucosal pH of the sigma showed a constant pHi in control animals and animals with mild pancreatitis at all timepoints compared to baseline (pHi 7.36 ± 0.27), but was significantly decreased in severe necrotizing disease at 3 hours (pHi 7.13 ± 0.47; p<0.01). PHi was still reduced at 24 hours after induction of severe pancreatitis, but increased again after 3 days (p<0.05). Animals which did not survive showed massive reduced pH-measurements of the sigma (pHi <7.1). In severe pancreatitis mucosal perfusion as assessed by intravital microscopy was significantly reduced already at 1 hour (p<0.01), and leukocyte adhesion was increased (p<0.05). In contrast, mild pancreatitis did not change intestinal microcirculation. Leukocyte infiltratioin and inflammation of the mucosa was observed in severe disease at 12 hours, but not in mild pancreatitis. Bacterial translocation was apparent after 1 day only in necrotizing disease. Conclusion: Decreased intramucosal pH of the sigma positively predicts severe courses of acute pancreatitis. The reduction of pHi is the consequence of decreased mucosal perfusion and can be observed long before failure of the mucosal barrier, bacterial translocation and sepsis. As pHi-measurements are simple and noninvasive, clinical evaluation should be performed in humans with acute pancreatitis.

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