Cases of gallstone ileus account for 1% to 4% of all instances of mechanical bowel obstruction. The majority of obstructing gallstones are located in the terminal ileum. Less than 10% of impacted gallstones are located in the duodenum. A gastric outlet obstruction secondary to a gallstone ileus is known as Bouveret syndrome. Gallstones usually enter the bowel through a biliary enteral fistula. Little is known about the formation of such fistulae in the course of gallstone disease.
We report the case of a 72-year-old Caucasian woman born in Germany with a gastric outlet obstruction due to a gallstone ileus (Bouveret syndrome), with a large gallstone impacted in the third part of the duodenum. Diagnostic investigations of our patient included plain abdominal films, gastroscopy and abdominal computed tomography, which showed a biliary enteric fistula between the gallbladder and the duodenal bulb. Our patient was successfully treated by laparotomy, duodenotomy, extraction of the stone, cholecystectomy, and resection of the fistula in a one-stage surgical approach. Histopathological examination showed chronic and acute cholecystitis, with perforated ulceration of the duodenal wall and acute purulent inflammation of the surrounding fatty tissue. Four months prior to developing a gallstone ileus our patient had been hospitalized for cholecystitis, a large gallstone in the gallbladder, cholangitis and a small obstructing gallstone in the common biliary duct. She had been treated with endoscopic retrograde cholangiopancreatography, endoscopic biliary sphincterotomy, balloon extraction of the common biliary duct gallstone, and intravenous antibiotics. At the time of her first presentation, abdominal ultrasound and endoscopic examination (including esophagogastroduodenoscopy and endoscopic retrograde cholangiopancreatography) had not shown any evidence of a biliary enteral fistula. In the four months preceding the gallstone ileus our patient had been asymptomatic.
In patients known to have gallstone disease presenting with symptoms of ileus, the differential diagnosis of a gallstone ileus should be considered even in the absence of preceding symptoms related to the gallbladder disease. Gallstones large enough to cause intestinal obstruction usually enter the bowel by a biliary enteral fistula. During the formation of such a fistula, patients can be asymptomatic.
Gallstone ileus accounts for approximately 1% to 4% of all cases of mechanical bowel obstruction. However, in the population over the age of 65 it is the cause of 25% of non-strangulated small bowel obstructions. Diagnosis is often delayed and mortality is high, ranging at 15% to 18%, which may also reflect the age and comorbidity of affected patients . Gallstones usually enter the bowel through a biliary enteric fistula, which complicates 2% to 3% of cases of cholecystolithiasis with associated episodes of cholecystitis . Due to the sedimentation of intestinal content, gallstones increase in diameter as they pass the bowel. The majority of obstructing gallstones are located in the terminal ileum (50% to 75%), followed by the proximal ileum and jejunum (20% to 40%). Gallstones impacted in the duodenum account for less than 10% . A gastric outlet obstruction secondary to an impacted gallstone in the duodenum or pylorus is called Bouveret syndrome. It was first described in 1896 by the French internist Leon Bouveret, and up to 1999 only 175 cases had been described in the medical literature . Our case is a rare description of Bouveret syndrome developing four months after successful treatment of symptomatic gallstone disease and after a four-month period with no symptoms.
A 72-year-old Caucasian woman born in Germany was admitted to our hospital with acute onset of nausea, vomiting and diffuse abdominal pain. Her only medications were metoprolol tartate and ramipril for arterial hypertension and chronic compensated heart failure. Physical examination was normal apart from diffuse pain on abdominal palpation. There were no signs of peritonitis. Laboratory findings (Table 1) included a white blood count of 14.3 cells/nL, an elevated C-reactive protein (CRP) level of 25.9 mg/dL, mildly elevated plasma aspartate aminotransferase and alanine aminotransferase (AST and ALT) levels of 51 U/L and 83 U/L, a moderate elevation of the γ glutamyl transpeptidase (GGT) level of 487 U/L and an alkaline phosphatase (AP) level of 368 U/L. Her total bilirubin level was elevated to 1.17 mg/dL and her serum creatinine level was 1.84 mg/dL. An abdominal ultrasonography scan showed thickening and edema of the gallbladder (GB) wall (12 mm), double wall sign, the presence of a large gallstone and a local hypoechogenic mass in the GB adhering to the GB wall with no signs of vascularization on color flow imaging. The common biliary duct (CBD) was dilated to 10 mm. Endoscopic retrograde cholangiopancreatography (ERCP) performed on the day of admission revealed a normal pancreatic duct and a small pigmented gallstone of the CBD that was extracted with an extraction balloon after endoscopic biliary sphincterotomy. Esophagogastroduodenoscopy (EGD) findings were normal without any signs of perforation or fistula. Under antibiotic treatment (ceftriaxon 2 g intravenously a day and metronidazole 400 mg intravenously four times a day for 10 days), our patient recovered completely. Her white blood count normalized and CRP and GGT levels fell (CRP 1.6 mg/dL, GGT 284 U/L two days before discharge). She was discharged after 11 days. After discharge our patient continued her antibiotic treatment (cefuroxim 500 mg orally twice a day and metronidazole 500 mg orally three times a day) for another four days.