Cases reported "Dilatation, Pathologic"

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1/19. Undiagnosed Mirizzi's syndrome: a word of caution for laparoscopic surgeons--a report of three cases and review of the literature.

    The mirizzi syndrome is often undiagnosed before surgery and can carry a high risk of iatrogenic damage to the common bile duct when encountered during open or, especially, laparoscopic surgery. Endoscopic management has recently been reported, but this treatment can be performed only when there is a high index of suspicion based on clinical criteria that the condition is present and therefore suggests the indication for endoscopic retrograde cholangiopancreatography (ERCP). This is not always the case. Consequently, in a considerable percentage of patients, the syndrome is discovered only after the bile ducts have been damaged during surgery. Three cases of Mirizzi's syndrome were observed in our experience of 896 laparoscopic cholecystectomies (0.3%). All patients were without typical symptoms, and the syndrome was unsuspected in spite of preoperative intravenous cholangiography. All patients required conversion to an open procedure, with two injuries of the common bile duct (a complete transection and a tear) being promptly repaired. We conclude that when this syndrome is suspected or found during surgery, the surgeon should follow these guidelines: (1) perform intraoperative cholangiography when possible, even through the gallbladder wall; and (2) dissect the gallbladder from above and, if necessary, open it to extract the stone. dissection of Calot's triangle should never be attempted. Great expertise is required to complete the operation laparoscopically. The reported cases in the literature refer to a high percentage of conversion, underlining the technical difficulties and making this syndrome, when undiagnosed and unsuspected, a real challenge for laparoscopic surgeons.
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2/19. Ultrasound of gallbladder wall thickening and its relation to cholecystitis.

    A prospective ultrasound study of gallbladder wall thickness in patients with suspected gallbladder disease was performed over a 9 month period. gallbladder walls thicker than 3 mm in fasting patients whose gallbladders were wider than 2 cm were considered abnormal. gallstones were documented by ultrasound in 62 patients, a thickened gallbladder wall was demonstrated in 12 of these. Five patients without cholelithiasis had thick-walled gallbladders and were diagnosed as acalculous cholecystitis.
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ranking = 4.5
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3/19. Synchronous carcinoma of the gallbladder in a patient with intrahepatic bile duct carcinoma.

    An 83-year-old woman, diagnosed as having cholelithiasis, was admitted to the Department of Surgery, Nippon Medical School, with right hypochondrial pain. ultrasonography and computed tomography revealed a mass in the gallbladder fundus and a hypovascular tumor in the anterior segment of the liver. magnetic resonance imaging showed stenosis of the intrahepatic bile duct and dilatation of its proximal portion. She was diagnosed as having intrahepatic bile duct carcinoma combined with gallbladder carcinoma. At laparotomy, there was evidence of multiple peritoneal metastases and intraoperative histological examination of the gallbladder tumor revealed adenocarcinoma. Accordingly, only cholecystectomy and needle biopsy of the liver tumor was performed. Histological examination of the gallbladder revealed papillary adenocarcinoma invading the muscularis propria with medullary growth or intermediate stroma. There was no microvessel invasion, no perineural invasion and no lymph node involvement. On the other hand, the liver tumor was a cholangiocarcinoma with a well-differentiated tubular pattern. Therefore, this was a rare case of synchronous carcinoma of the gallbladder associated with intrahepatic bile duct carcinoma.
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4/19. Spontaneous necrosis of gallbladder carcinoma in patient with pancreaticobiliary maljunction.

    While gallbladder carcinoma is occasionally associated with pancreaticobiliary maljunction, spontaneous necrosis of carcinoma is extremely rare. We herein present a case of spontaneous necrosis of gallbladder carcinoma associated with direct invasion of viable cancer cell nests to the muscularis propria and subserosal layer located beneath the primary nodules. A 65-year-old Japanese man was admitted to a local hospital, complaining of repeated discomfort in the right hypochondrium. ultrasonography and computed tomography scanning revealed cholecystitis associated with gallstones. cholecystectomy was performed, and operative cholangiography demonstrated pancreaticobiliary maljunction. The resected gallbladder showed multiple mixed stones filled with necrotic debris and bile sludge. Scrutiny of the mucosal surface revealed multiple small necrotic nodules in the fundus, which were histologically confirmed to be necrotic remnants of a cancerous glandular structure. Small nests of papillary adenocarcinoma were found beneath the nodules in the muscularis propria and in the venous structure located in the connective tissues next to the divided margin of the gallbladder bed. Resection of S4a and S5 of the liver and resection of the extrahepatic bile duct was then performed to remove the remaining cancerous tissues and/or micrometastasis in the liver and bile duct. The biliary tree was reconstructed with a hepaticoduodenostomy. No cancer nests or any precancerous lesions were found in the additionally resected specimens. This case indicates a unique morphological feature of gallbladder carcinoma associated with pancreaticobiliary maljunction, which provides some insight into the pathogenesis of spontaneous necrosis of gallbladder carcinoma.
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5/19. Intestinal type cholangiocarcinoma of intrahepatic large bile duct associated with hepatolithiasis--a new histologic subtype for further investigation.

    Intestinal metaplasia is regarded as a possible predisposing factor of cancer, particularly of the intestinal type adenocarcinoma. The clinicopathologic features of intestinal type adenocarcinoma have been well documented in the stomach, and intestinal metaplasia and intestinal type adenocarcinoma has also been reported in the gallbladder. However, regarding the intrahepatic bile ducts, the clinicopathologic features are not yet clear and there have been no reports in English literature on intestinal type intrahepatic cholangiocarcinoma. We report a case of intestinal type cholangiocarcinoma associated with hepatolithiasis in the large intrahepatic bile duct. The tumor showed mainly intraductal papillary growth primarily composed of absorptive columnar cells. Particularly, Paneth cell metaplasia of carcinoma cells was widespread, and goblet cells and neuroendocrine cells were also observed in the carcinoma tissue, to a varied degree. It showed an intraluminal spread along the dilated intrahepatic ducts with minimal ductal stromal invasion. In the vicinity of the tumor, intestinal metaplasia was also identified in the adjacent hyperplastic and dysplastic bile duct epithelium. Some bile ducts contained stones and the mural glands of the bile ducts showed hyperplastic change secondary to stones. This case is considered to provide the evidence supporting the concept of the metaplasia-dysplasia-carcinoma sequence via intestinal metaplasia in the stone-containing intrahepatic bile ducts.
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6/19. Rapid progression of intrapulmonary arteriovenous shunting in polysplenia syndrome associated with biliary atresia.

    This report describes a patient with biliary atresia (BA) associated with polysplenia syndrome who showed a rapid progression of intrapulmonary arteriovenous shunting (IPS), resulting in a fatal outcome. Intrauterine ultrasonography at 36 weeks of gestation revealed fetal abnormalities, including situs inversus, absent retrohepatic inferior vena cava, and azygous connection. She was diagnosed postnatally as BA because of persistent acholic stool and neonatal jaundice. She underwent hepatic portoenterostomy at age 158 days. The gallbladder and the hepatic ducts were hypoplastic, and the common bile duct was absent. Magnetic resonance image and operative findings also identified polysplenia and an absent portal trunk. Liver histology showed cirrhotic changes and bile duct proliferation. Postoperatively, she achieved good bile secretion, with gradual decrease of total bilirubin. However, she had repeated febrile episodes, and computerized tomography at age 7 months showed multiple liver cysts. Thereafter, she presented with exertional dyspnea. Contrast-enhanced echocardiography showed IPS with a degree of 2/III at age 8 months and 3/III at 10 months. (99m)technetium-labeled macroaggregated albumin ((99m)Tc-MAA) scintigraphy revealed a shunt ratio of 25.5% at 9 months and 39.7% at 10 months. Percutaneous transhepatic drainage of the bile cysts was performed without success. Sludged bile was obtained. However, respiratory distress rapidly progressed, and she died at age 11 months. In the present patient, the association of polysplenia syndrome and absent portal vein with BA, as well as liver cirrhosis, seemed to be contributing factors to rapid progression of IPS in early life.
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keywords = gallbladder
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7/19. Transient gallbladder distention in sick premature infants: the value of ultrasonography and radionuclide scintigraphy.

    Transient gallbladder distention in sick premature infants has been reported with increasing frequency over the last few years. It is important to be aware of this entity of gallbladder disease which resolves spontaneously and to be able to differentiate it from other problems that require surgical correction. We believe that ultrasonography is most helpful in confirming the diagnosis, excluding stone formation, and documenting any changes in size or appearance. However, there are no reliable ultrasonic criteria for distinguishing inflamed or pathologically distended gallbladders from noninflamed or temporarily enlarged gallbladders. Radioisotope imaging, though useful in demonstrating malfunction of the hepatobiliary system, should be interpreted with caution. In the final analysis, the dilemma as to whether gallbladder distention is a transient or persistent malfunction can be settled best by thoughtful clinical judgement.
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ranking = 4.5
keywords = gallbladder
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8/19. Visceral ischemia secondary to gastric dilatation: a rare complication of Nissen fundoplication.

    Antireflux operations are now commonly performed for severe gastroesophageal reflux with life-threatening presentations like recurrent aspiration pneumonia and apnea. We report a child who presented 2 years after Nissen fundoplication with jejunal volvulus resulting in massive gastric dilatation, gastric rupture, pneumoretroperitoneum, pneumomediastinum, and severely compromised circulation to the lower extremities. Because of the intense intraabdominal pressure from the gastric dilatation, there was severe ischemia of the pancreas, duodenum, small bowel, colon, and gallbladder. We suggest that gastrointestinal symptoms in a child who has had Nissen fundoplication should be promptly evaluated to avoid delay in recognition of acute gastric dilatation and to prevent a fatal outcome.
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keywords = gallbladder
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9/19. Acute gallbladder dilatation in a neonate: emphasis on ultrasonography.

    A neonate with giant-cell hepatitis developed gallbladder dilatation that was identified on ultrasonography and treated by tube cholecystostomy. Previous reports of hydrops and cholecystitis in neonates are reviewed. Ultrasound identifies gallstones and dilated bile ducts, establishes a large gallbladder as the cause of a palpable mass, and is the ideal way to follow the course of gallbladder dilatation.
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ranking = 3.5
keywords = gallbladder
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10/19. The dilated common duct sign. A potential indicator of a sphincter of oddi dyskinesia.

    The cholescintigraphic findings of a sphincter of oddi dyskinesia (SOD) in a 45-year-old woman with persistent right upper quadrant pain and biliary colic are reported. After an overnight fast, the patient was injected with 5 mCi of Tc-99 disofenin and .02 micrograms/kg of cholecystokinin (CCK) post maximal gallbladder filling. Pre and postcholescintiscans were obtained and gallbladder ejection fractions determined. The hepatobiliary scan was normal, except for a delay in biliary-bowel transit. The gallbladder responded normally to CCK, however, the sphincter of oddi responded abnormally, as there was a paradoxical response to CCK manifested by a marked dilatation of the common bile duct. We postulate that this dilatation (the dilated common duct sign) was due to an inappropriate response of the smooth muscle of the sphincter of oddi (contraction vs relaxation) to CCK and was the cause of this patient's biliary colic. The dilated common duct sign should alert the physician to the possibility of a Sphincter of Oddi dyskinesia.
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