[Morphine induced biliary pain. Case report]. / Cólico biliar inducido por morfina.

Morphine produces contraction of Oddi’s sphincter, which can be severe and of longer duration in some pathological conditions. This exaggerated response can manifest as a colicky biliary pain, frequently accompanied by a dramatic increase in hepatic enzymes. We report a 32 years old female who consulted in the emergency room for severe low abdominal pain of gynecologic origin, which was completely controlled by morphine. However, she presented a sudden epigastric colicky pain irradiating in the back, which persisted for several hours in spite of the repeated administration of analgesics. Transaminases elevated from previously normal value to over 1,000 U/L, and returned to the normal level without further treatment after several days. Magnetic resonance cholangiography showed normal fine bile duct, without stones. This transient increase in hepatic enzymes was considered as a consequence of high biliary pressure secondary to morphine-induced spastic contraction of Oddi’s sphincter and a consecutive hepatocellular necrosis.

Cólico biliar inducido por morfina / Morphine induced biliary pain: case report

Morphine produces contraction of Oddi’s sphincter, which can be severe and of longer duration in some pathological conditions. This exaggerated response can manifest as a colicky biliary pain, frequently accompanied by a dramatic increase in hepatic enzymes. We report a 32 years old female who consulted in the emergency room for severe low abdominal pain of gynecologic origin, which was completely controlled by morphine. However, she presented a sudden epigastric colicky pain irradiating in the back, which persisted for several hours in spite of the repeated administration of analgesics. Transaminases elevated from previously normal value to over 1,000 U/L, and returned to the normal level without further treatment after several days. Magnetic resonance cholangiography showed normal fine bile duct, without stones. This transient increase in hepatic enzymes was considered as a consequence of high biliary pressure secondary to morphine-induced spastic contraction of Oddi’s sphincter and a consecutive hepatocellular necrosis.

Vanishing bile duct syndrome in the context of concurrent temozolomide for glioblastoma.

Temozolomide, an oral alkylating agent, is used in the treatment of glioblastoma. We describe a case of a 62-year-old woman developing jaundice with significant derangement of liver function tests on day 17 of focal radiotherapy with concomitant temozolomide. There was no structural abnormality on imaging and liver biopsy was performed. Pathology revealed absence of small terminal bile ducts affecting up to 60% of sampled portal tracts and senescence of many of the remaining small bile ducts, in keeping with a diagnosis of acute vanishing bile duct syndrome. This is a rare syndrome. It has been documented in association with Hodgkin's lymphoma and viral causes. Drugs implicated as precipitating this condition include antiseizure medications, some antibiotics, ibuprofen and antifungals. Temozolomide was stopped. The patient received supportive care, ursodeoxycholic acid 750 mg daily and cholestyramine 4 g twice daily. She was otherwise asymptomatic and her blood results returned to normal by day 129.

Oddi sphincter fibrosis due to chemotherapy agents in small cell lung cancer: case report.

A 62-year-old, man patient was diagnosed as small cell lung cancer. Cisplatin (80 mg/m(2), first day) and etoposide (100 mg/m(2), three days) chemotherapy was started for once 21 days. As the patient received third course of chemotherapy, jaundice and hyperbilirubinemia were detected. Hepatic ultrasonography showed dilated choledochus and intrahepatic biliary tract. Hepatic markers and serologic tests for viral hepatitis were found as normal. Finally endoscopic retrograde cholangiopancreatography (ERCP) was performed. Endoscopic sphincterotomy was performed in the first ERCP and two days later, second ERCP was performed and oddi sphincter was seen as fibrotic and stenotic and stent was placed. One day after the stent placement, direct bilirubin was found as 6.2 mg/dL and 10 days later laboratory parameters were detected as normal. Oddi sphincter fibrosis occurred due to lung cancer chemotherapy treatment is an interesting case for fibrosis not having been reported due to cisplatin or etoposide before.

Sphincter of Oddi dysfunction in patients addicted to opium: an unrecognized entity.

BACKGROUND: Opiate-induced sphincter of Oddi dysfunction (SOD) as a clinical entity has not been described. METHODS: Eight chronic opium addicts (all men, mean age 61.3 years, mean duration of addiction 24.75 years) presenting with pancreatobiliary pain and a dilated bile duct with or without dilated pancreatic duct on abdominal US were studied. All patients underwent ERCP and biliary sphincterotomy. In addition, pancreatic sphincterotomy was performed in 4 patients with a dilated pancreatic duct. OBSERVATIONS: At ERCP, the bile duct was dilated in 8 and pancreatic duct in 4 patients. There was delayed drainage of contrast (>45 minutes) from the bile duct in all 7 patients studied, whereas delayed drainage from the pancreatic duct (>9 minutes) was incidentally observed in 3 patients. In 6 patients followed after sphincterotomy for at least 2 years, there was marked relief of symptoms. Transabdominal US at 2 years follow-up revealed a normal bile duct in 5 and persistent albeit minimal dilatation in 1 patient. Acute pancreatitis developed in 4 patients after ERCP and sphincterotomy, which was fatal in one. No patient had any abnormality in the gallbladder on initial or follow-up transabdominal US. CONCLUSION: SOD in opium addicts is a distinct clinical entity, mainly seen in men in this population, that is characterized by a long history of opium addiction and the absence of prior cholecystectomy or associated gallstone disease. Most patients are seen with the classic clinical picture of SOD with marked long-term improvement in symptoms after endoscopic sphincterotomy.

Dilated bile duct in patients receiving narcotic substitution: an early report.

Narcotic substitution is now widely used. Morphine can induce a spasm of the sphincter of Oddi but dilation of bile duct has been reported only in an anecdotal case. In June 1995, we observed a first case of dilation of the common bile duct without organic obstacle in a hepatitis C virus (HCV)-infected patient who was under narcotic substitution, suggesting a causal relationship. We conducted a prospective study to evaluate the precise prevalence of bile duct abnormalities related to narcotic substitution in active intravenous drug or ex-intravenous drug users referred to our liver unit for histologic evaluation of HCV infection. We conducted a prospective study in a 30-month period of 334 HCV-infected patients, including 36 receiving narcotic substitution with methadone or buprenorphine. Biliary tract was analyzed by ultrasonography and by endoscopy ultrasound in cases of bile duct abnormalities. Of the 36 patients under narcotic substitution, 3 (8.3%) had asymptomatic dilated bile duct without organic obstacle--defined as a common bile duct > or =9 mm--compared to 1 of 298 (0.03%; p < 0.001) of those who did not receive substitution. Narcotic substitution may lead to bile duct dilation that does not require invasive diagnosis procedures.

Acute pancreatitis complicating a bone marrow harvest.

A patient developing acute pancreatitis with pseudocyst formation after an uncomplicated bone marrow harvest is reported. The diagnosis was confirmed by elevated serum amylase and lipase, and by CT scan. We suggest that the pancreatitis may have been precipitated by spasm of the sphincter of Oddi secondary to opiates administered as premedication and for pain relief.

Lack of tolerance of morphine-induced spasm of guinea pig sphincter of Oddi.

To determine whether guinea pigs chronically exposed to morphine would develop tolerance to the morphine-induced contraction of the sphincter of Oddi (SO), adult male guinea pigs were implanted with morphine pellets (100 mg morphine). The effect of increasing IV doses of morphine on the SO was assessed by determining the duration of which saline perfusate stopped flowing into the duodenum of morphine-treated guinea pigs (MTGP) vs nonimplanted animals (non-MTGP). Isolated bovine and guinea pigs SO were also challenged with morphine. In the in vivo experiments the spasmogenic response of the SO from MTGP to morphine was greater than that of SO from non-MTGP. However, morphine had no effect on isolated SO. These results indicate that chronic morphine exposure does not result in tolerance of the SO to the spasmogenic effects of morphine. On the contrary, chronic morphine even sensitized the SO to morphine, in addition, the in vitro data indicated that morphine does not act directly on the smooth muscle of SO to cause its spasmogenic effect.

Lack tolerance of morphine induced spasm of Guinea pig sphincter of Oddi

To determine whether guinea pigs chronically exposed to morphine would develop tolerance to the morphine-induced contraction of the sphincterof Oddi (SO), adult male guinea pigs were implanted with morphine pellets (100 mg morphine). The effect of increasing IV doses of morphine on the SO was assessed by determining the duration of which saline perfusate stopped flowing into the duodenum of morphine-treated guinea pigs (MTGP) vs monimplanted animals (non-MTGP). Isolated bovine and guinea pigs SO were also challenged with morphine. Int the in vivo experiments the spasmogenic response of the SO from MTGP to morphine was greater than of SO from non-MTGP. However, morphine had no effect on isolated SO. These results indicate that chronic morphine exposure does not results in tolerance of the SO to the spasmogenic effects of morphine. On the contrary, chronic morphine even sensitized the SO to morphine, in addition, the in vitro data indicated that morphine does not act directly on the smooth muscle of SO to cause spasmogenic effect

[Sclerosing cholangitis after chemotherapy by continuous hepatic intra-arterial infusion of fluorodeoxyuridine]. / Cholangite sclérosante après chimiothérapie par perfusion intra-artérielle hépatique continue de fluorodésoxyuridine (FUDR).

A case of sclerosing cholangitis after a two-month treatment by hepatic artery infusion of FUDR is reported. The patient presented with jaundice and a marked increase in serum alkaline phosphatase activity which persisted after withdrawal of FUDR infusion. Endoscopic retrograde cholangiogram revealed a stricture of the middle part of the common bile duct, which was treated by endoprosthesis insertion. From this report, as well as those previously published, it is concluded that sclerosing cholangitis may complicate continuous hepatic artery infusion with FUDR. This lesion could be secondary to an FUDR-induced arteritis in the branches of hepatic artery which supply bile ducts.

Common duct stricture associated with hepatic artery infusion of FUDR.

A case report is presented giving the first detailed description of a benign common duct stricture occurring in a patient receiving hepatic artery infusion of FUDR for metastatic colon cancer. It is postulated that the stricture results from a combination of drug toxicity, and hypoxemia of the duct, with the lesion occurring more often than is recognized. A guide is given for the evaluation of the FUDR-infused patient with suspected nonmalignant duct stricture, and for the methods of alleviating extrahepatic blockage in these individuals.

Unusual causes for abnormal hepatobiliary scans.

Cholescintigraphy with Tc-99m iminodiacetic acid (IDA) agents has proved to be a convenient, non-invasive method for evaluating patients with suspected cholecystitis. (1,2) We recently examined two patients who were being evaluated for abdominal pain. The etiology of the two abnormal cholescintigrams was later proven to be due to nonhepatobiliary pathology.

Narcotics and spasm of the sphincter of Oddi. A retrospective study of operative cholangiograms.

The operative cholangiograms of 112 patients undergoing elective cholecystectomy were reviewed independently and retrospectively by two radiologists who were not aware of the anaesthetic technique used. Fifty four patients who received opioid drugs either pre- and/or intra-operatively comprised one study group whilst 58 patients who received no opioids comprised the other. Spasm of the sphincter of Oddi was observed in two patients in the opioid group and in one patient in the non-opioid group. The use of opioid drugs as part of the anaesthetic management for cholecystectomy did not appear to interfere with the radiological interpretation of operative cholangiography nor to increase the low incidence of spasm of the sphincter of Oddi.

Necrotizing choledochomalacia after use of monooctanoin to dissolve bile-duct stones.

A 72-year-old man with choledocholithiasis, demonstrated radiologically, was treated by constant perfusion through the gallbladder of monooctanoin (glyceryl-1-monooctanoate) following cholecystostomy for a perforated gallbladder. The monooctanoin was given at a rate of 7.5 ml/h and monitored to ensure that delivery pressure did not rise above 20 cm H2O. Perfusion was carried out for 60 hours, but could not be continued because of abdominal pain, nausea and vomiting. This was followed by progressive jaundice, anorexia and fever. The patient was treated with penicillin G and cefoxitin intravenously and metronidazole orally, but he died 5 weeks after the perfusion. Autopsy showed acute pancreatitis and cholangitis, and a biliary tree filled with pus and a black biliary cast. No calculi were present. The authors consider the possible causes for this patient's death.

Incidence of choledochoduodenal sphincter spasm during fentanyl-supplemented anesthesia.

One hundred patients were studied prospectively to assess the incidence of spasm of the choledochoduodenal sphincter during biliary tract surgery performed under a fentanyl-supplemented anesthetic technique. The incidence of failure of passage of contrast medium into the duodenum was 3%. In each of the three patients with cholangiographic evidence of sphincter spasm, contrast medium flowed freely into the duodenum after the intravenous administration of 2 mg of glucagon. It is concluded that spasm of the choledochoduodenal sphincter is an uncommon occurrence during fentanyl-supplemented anesthesia and that this method of anesthesia is suitable for biliary tract surgery.