Successful treatment with a combination of endoscopic injection and irrigation with coca cola for gastric bezoar-induced gastric outlet obstruction.

We report a case of gastric bezoar-induced gastric outlet obstruction that was successfully treated with a combination of endoscopic injection and irrigation with Coca Cola. A 73-year-old diabetic woman had a history of perforated peptic ulcer and had received pyloroplasty more than 20 years previously. She had been ingesting Pho Pu Zi (Cordia dichotoma Forst. f.) as an appetizer for 1 month. She presented with epigastric pain, nausea, and vomiting. Upper gastrointestinal endoscopy, performed at a local hospital, showed 2 gastric bezoars in the stomach, and 1 of them impacted at the pylorus. She was referred to our emergency department for removal of the gastric bezoars that were suspected to be causing gastric outlet obstruction. All attempts at endoscopic removal using a polypectomy snare, biopsy forceps and Dormia basket failed. We then injected Coca Cola directly into the bezoar mass, followed by irrigation with Coca Cola. Follow-up endoscopy was performed the next day, which revealed that the gastric bezoars had dissolved spontaneously.

Clinical significance and prediction factors of gastric varices in patients with hepatocellular carcinoma.

BACKGROUND/AIMS: Hepatocellular carcinoma is part of the natural history of liver cirrhosis. Gastrointestinal bleeding and hepatic failure are the leading causes of death in hepatocellular carcinoma patients. With gastrointestinal bleeding, variceal bleeding is the most prominent, and most variceal bleeding is of esophageal origin. Gastric varices bleeding is often a massive and severe bleeding episode. The role of gastric varices among patients with hepatocellular carcinoma remains to be clarified. In this study, we aimed to evaluate the prevalence, clinical significance and prediction of gastric varices in patients with hepatocellular carcinoma. METHODOLOGY: From 1998 to 2000, we reviewed 304 patients with hepatocellular carcinoma receiving upper gastrointestinal endoscopic examinations. Patients' clinical characteristics, physical findings, laboratory data, image studies, endoscopic examinations and treatment were reviewed. RESULTS: Among 304 patients with HCC, twenty-one (6.9%) had gastric varices among 304 patients with hepatocellular carcinoma. The location of gastric varices were the posterior wall in 12 (57%), the lesser curvature in 1 (5%), the greater curvature in 4 (19%) and the fundus in 4 (19%). Three (14%) of these 21 patients with hepatocellular carcinoma and gastric varices had clinical evidence of bleeding. One of them died due to uncontrollable bleeding. Child-Pugh classification, hepatic encephalopathy, portal vein or splenic vein dilatation, ascites, splenomegaly, albumin level, prothrombin time and platelet count were significantly different between hepatocellular carcinoma patients with gastric varices and without gastric varices under the univariate analysis. Ascites (Odds ratio: 5.45; 95% confidence interval: 2.12-14.01) and portal vein or splenic vein dilatation (Odds ratio: 4.38; 95% confidence interval: 1.77-10.86) were the two most important predictors under the stepwise logistic regression analysis. CONCLUSIONS: The prevalence of gastric varices in patients with hepatocellular carcinoma is 6.9% and the risk of bleeding is low in this study. The Predictors of gastric varices among hepatocellular carcinoma are related to liver cirrhosis, Child-Pugh classification, hepatic encephalopathy, portal vein or splenic vein dilatation, ascites, splenomegaly, albumin level, prothrombin time and platelet count.