ABSTRACT
Perforated duodenal ulcers are rare complications seen after roux-en-Y gastric bypass (RYGP). They often present as a diagnostic dilemma as they rarely present with pneumoperitoneum on radiologic evaluation. There is no consensus as to the pathophysiology of these ulcers; however expeditious treatment is necessary. We present two patients with perforated duodenal ulcers and a distant history of RYGP who were successfully treated. Their individual surgical management is discussed as well as a literature review. We conclude that, in patients who present with acute abdominal pain and a history of RYGB, perforated ulcer needs to be very high in the differential diagnosis even in the absence of pneumoperitoneum. In these patients an early surgical exploration is paramount to help diagnose and treat these patients.
ABSTRACT
We have previously shown that serotonin type-3 (5-HT3) receptors mediate cholecystokinin (CCK)-induced satiation and that this effect is dependent on postoropharyngeal feedback. However, the independent contributions of gastric and intestinal feedback in 5-HT3 receptor mediation of suppression of food intake by CCK have not been determined. Using a sham-feeding preparation combined with intraduodenal sucrose infusion, we show that blockade of 5-HT3 receptors by ondansetron (1 mg/kg ip) had no effect on suppression of sham feeding by intraduodenal 15% sucrose infusion (4 ml/10 min), CCK (2 microg/kg ip) administration, or the combination of the two treatments. In separate experiments consisting of either sham-feeding rats that received gastric distension with the use of a balloon or real-feeding rats whose stomachs were distended using gastric loads of saline after the occlusion of the pylorus, we tested the hypothesis that gastric feedback signals are necessary for activation of 5-HT3 receptors. Ondansetron significantly attenuated suppression of sham sucrose intake after a 10-ml gastric balloon distension (30.5 +/- 2.2 vs. 20.2 +/- 2.2 ml, respectively) and gastric distension combined with CCK (21.9 +/- 1.4 vs. 12.0 +/- 1.7 ml, respectively). When intestinal feedback was eliminated in a real-feeding paradigm by closing the pylorus using a cuff preparation, ondansetron attenuated suppression of sucrose intake produced by a 10-ml saline gastric load (6.8 +/- 0.7 vs. 4.2 +/- 0.4 ml, respectively). Finally, when CCK (1 microg/kg) was administered in combination with a 5-ml saline gastric load in a real-feeding preparation, ondansetron significantly attenuated suppression of sucrose intake by CCK (9.0 +/- 0.9 vs. 6.3 +/- 0.5 ml, respectively), as well as the enhanced suppression of intake by CCK plus gastric load (6.9 +/- 0.6 vs. 4.6 +/- 0.5 ml, respectively). These findings demonstrate that CCK-induced activation of 5-HT3 receptors requires gastric, but not intestinal feedback.
