12 research outputs found

    Ulcer Disease in the Excluded Segments after Roux-en-Y Gastric Bypass: a Current Review of the Literature.

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    Ulcer disease in excluded segments after Roux-Y gastric bypass (RYGB) is rare but can evolve into a life-threatening situation. The excluded segments exhibit a different behavior from that of non-altered anatomy; perforated ulcers do not result in pneumoperitoneum or free fluid, and therefore must be met with a low threshold for surgical exploration. The anatomical changes after RYGB impede routine access to the remnant stomach and duodenum. There are various options to address bleeding or perforated ulcers. While oversewing and drainage preserves the anatomy and forgoes resection, remnant gastrectomy offers a definitive solution. The importance of traditional risk factors such as smoking or use of non-steroidal anti-inflammatory drugs is unclear. Eradication of Helicobacter pylori and secondary prophylaxis with proton-pump inhibitors is advisable, albeit in double-dose

    Perforated duodenal ulcers after Roux-Y Gastric Bypass.

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    Even though the incidence of complicated peptic ulcer disease (PUD) has decreased in the last decades, it remains a condition with a significant mortality. Whilst diagnosis and treatment of PUD in morbidly obese patients can be challenging, patients with excluded segments - such as after Roux-Y Gastric Bypass (RYGB) - present an even greater problem, as the subsequent altered anatomy impedes the common modalities used for diagnostic and therapeutic measures. We report the cases of two patients after RYGB with perforated duodenal ulcers in the intention to highlight problems regarding diagnosis and treatment. Patients with perforation after RYGB usually present without signs of hollow organ perforation in clinical examination but also in computed tomography scans. Diagnostic laparoscopy was performed to address the discrepancy between pain and non-diagnostic examinations. An aggressive approach in case of unexplained symptoms in these patients is not only justified but mandatory

    De novo gastroesophageal reflux disease after sleeve gastrectomy: role of preoperative silent reflux.

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    BACKGROUND Laparoscopic sleeve gastrectomy (LSG) has become the most frequently performed bariatric procedure to date. However, LSG is known to worsen pre-operative and result in de novo gastroesophageal reflux disease (GERD). Pre-operative evaluation reveals a high percentage of silent GERD of so far unknown influence on post-operative GERD. METHODS Prospective data of patients undergoing primary LSG between 01/2012 and 12/2015 were evaluated. Pre-operative GERD-specific evaluation consisted of validated questionnaires, upper endoscopy, 24 h-pH-manometry, and esophagograms. Patients were followed-up with questionnaires every 6 months, upper endoscopies after 1 year and 24 h-pH-metry after 2 years. Silent GERD was defined as esophagitis grade > B and/or abnormal esophageal acid exposure in absence of symptoms. LSG was performed over a 32F bougie, hiatal hernias > 1 cm were addressed with posterior hiatoplasty. Excluded were patients with hiatal hernias > 4 cm, patients with incorrect anatomy (stenosis, fundus too large) and conversion to RYGB for early leaks. RESULTS 222 patients were included. Mean follow-up was 32 ± 16 months, mean preoperative body mass index 49.6 ± 7.2 kg/m. 116 patients (52%) presented with post-operative GERD-symptoms, of which 85 (73%) had de novo symptoms. Of those, 48 (of 85, 56%) had no preoperative GERD and 37 (of 85, 44%) silent GERD. 57 patients (26%) had neither pre- nor post-operative GERD, 7 (3%) had silent pre-operative and no postop GERD, and in 19 patients (9%) GERD was cured with LSG. 31 patients (14%) stayed symptomatic. Of 56 patients (25%) with pre-operative silent GERD, 37 (of 54, 66%) became symptomatic. CONCLUSION LSG leads to a considerable rate of post-operative GERD. De novo-GERD consist of around half of pre-operative silent GERD and completely de novo-GERD. Most patients with pre-operative silent GERD became symptomatic

    Pretreatment with helium does not attenuate liver injury after warm ischemia-reperfusion

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    Preconditioning with noble gases serves as an effective strategy to diminish tissue injury in different organs. The aim of this study was to investigate the influence of pretreatment with the nonanesthetic noble gas helium on hepatic injury after warm ischemia and reperfusion (IR) in comparison to ischemic preconditioning (IPC). Anesthetized and ventilated rats were randomized into six groups (n = 8/group): sham: after laparotomy, the portal triad was exposed without clamping; IPC was performed with 10 min of partial liver ischemia and 10 min of reperfusion; HePC: three cycles of 5 min with inhalation of helium 70 vol% and intermittent washout; IR: 45 min of ischemia followed by 240 min of reperfusion; IPC-IR: IPC followed by hepatic IR; HePC-IR: pretreatment with helium 70 vol% followed by hepatic IR. Hepatic injury was evaluated by measurement of serum enzymes aspartate aminotransferase and alanine aminotransferase. Hepatic mRNA expression and serum levels of tumor necrosis factor α (TNF-α) and interleukin 10 (IL-10) were measured with real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Myeloperoxidase in liver tissue was assessed spectrophotometrically as a marker of neutrophil accumulation. mRNA levels of heme oxygenase 1 in liver tissue were assessed to investigate a protein of the most abundant protective system in the liver. Aspartate aminotransferase and alanine aminotransferase serum activities increased after hepatic IR (sham vs. IR; P < 0.05). The serum levels of liver enzymes after IR were significantly diminished with IPC (P < 0.05), whereas helium pretreatment had no effect. mRNA expression of TNF-α increased in all groups except IPC-IR compared with sham, whereas mRNA expression of IL-10 increased only after helium pretreatment. Serum levels of IL-10 were not affected by any intervention, whereas serum levels of TNF-α and liver myeloperoxidase were increased after IR, but not after HePC-IR. In conclusion, pretreatment with inhaled helium does not attenuate hepatic injury after warm IR of the liver, although there is evidence for a modulation of the inflammatory respons

    DE NOVO GASTROESOPHAGEAL REFLUX DISEASE AFTER SLEEVE GASTRECTOMY: ROLE OF PREOPERATIVE SILENT REFLUX

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    INTRODUCTION Laparoscopic sleeve Gastrectomy (LSG) has become the most frequently performed bariatric procedure to date. However, LSG is known to worsen preoperative and result in de novo GERD. Preoperative evaluation reveals a high percentage of silent GERD of so far unknown influence on postoperative GERD. METHODS AND PROCEDURES Prospective data of patients undergoing primary LSG between 01/2012 and 12/2015 were evaluated. Preoperative GERD-specific evaluation consisted of validated questionnaires (GERD-HRQL), upper endoscopy, 24h-pH-manometry, and esophagograms. Patients were followed-up with questionnaires every 6 months and gastroscopies after 1 year. Silent GERD was defined as esophagitis grade >B and/or abnormal esophageal acid exposure in absence of symptoms. LSG was performed over a 32F bougie, hiatal hernias >1cm were addressed with posterior hiatoplasty. Excluded were patients with hiatal hernias >4cm, patients with incorrect anatomy (stenosis, fundus too large) and conversion to RYGB for early leaks. RESULTS 222 patients were included. Overall mean follow-up was 3216 months, 3 patients (1%) were lost to follow-up. 124 patients (56%) presented with postoperative GERD symptoms, of which 85 (69%) had de novo symptoms. Of those, 48 (of 85, 56%) had no preoperative GERD and 37 (of 85, 44%) silent GERD (p=0.2). 61 patients (27%) had neither pre- nor postoperative GERD, 17 (8%) had silent preoperative and no postop GERD, and in 18 patients (8%) GERD was cured with LSG. 31 patients (14%) stayed symptomatic. Of 54 patients (24%) with preoperative silent GERD, 37 (of 54, 69%) became symptomatic. Postoperative GERD-symptoms were typical in 116 (of 124, 94%), respiratory in 12 (10%), obstructive in 19 (15%), and pain in 21 patients (17%). CONCLUSION LSG leads to a considerable rate of postoperative GERD. De novo GERD consist of around half of preoperative silent GERD and completely de novo GERD. Most patients with preoperative silent GERD became symptomatic. These data justify a comprehensive preoperative evaluation
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