[Bile duct anomalies. Cholecystohepatic ducts].
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Biomedical subjects
Publications and source records attributed to F Burcharth.
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Oesophageal stricture and dysphagia after endoscopic sclerotherapy of oesophageal varices were assessed with regard to occurrence and severity and the relation to the treatment. We followed 34 patients for three to 47 months who had two to 25 treatments with submucosal, paravenous injections of polidocanol (3%). Twenty patients (59%) developed stricture or dysphagia; 14 both dysphagia and endoscopically verified stricture, two dysphagia without stricture, and four stricture without dysphagia. Both phenomena occurred intermittently and often independent of each other, but occupied median 38% of the observation time in these 20 patients. The patients developing strictures had received significantly more treatments and greater amount of sclerosant, and they had significantly more preceding mucosal necroses. The varices were eradicated to about the same degree and the incidence of recurrent haemorrhage was the same as in the patients who had not developed stricture.
To evaluate the effect of tube decompression of the stomach after elective colorectal operations, 97 patients were randomly allocated to postoperative treatment with or without nasogastric tubes. Flatus passed earlier in the patient group without tubes. However, no significant differences were found between the two groups with respect to duration and severity of postoperative paralysis, as measured by occurrence and duration of nausea and vomiting, postoperative peroral fluid intake and time for defecation. The frequencies of postoperative complications were small in both groups and without any difference between groups. Tube decompression of the stomach does not relieve intestinal paralysis after elective colorectal operations. Tube decompression should be used only in patients with paralytic ileus.
In 26 patients simple cysts of the liver were diagnosed by ultrasonography. Half of the patients had no symptoms, and half presented with abdominal pain and a palpable mass; 14 patients with small cysts required no treatment. Nine patients were operated upon, while 3 patients with large cysts were treated exclusively by ultrasonically guided drainage. Further, ultrasonically guided drainage was successful in two patients with recurrences after surgical treatment. Patients with small asymptomatic cysts of the liver, incidentally diagnosed should be left without treatment. Ultrasonically guided puncture is advocated as the first treatment in patients with large symptomatic cysts.
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The free portal pressure was measured by percutaneous transhepatic catheterization of the portal vein in 106 patients with cirrhosis of the liver and in 19 patients without liver disease and with normal portography. Patients with cirrhosis had a median portal pressure of 38 cmH2O and patients without liver disease had a median portal pressure of 16 cmH2O. Among the cirrhotic patients the free portal pressure showed no relationship to etiology of cirrhosis, ascites, variceal bleedings or extrahepatic shunting. The median portal pressure was significantly higher in patients with (40 cmH2O) than without (30 cmH2O) gastroesophageal varices (p less than 0.01). The pressure was not related to the size of the varices.
We compared the diagnosis of oesophageal varices obtained by oesophagoscopy and percutaneous transhepatic portography in 78 patients with hepatic cirrhosis who were suspected of having oesophageal varices because of ascites and/or preceding upper gastrointestinal haemorrhage. Portograms were evaluated independently of the clinical and endoscopical findings. Endoscopy showed varices in 59 patients and portography in 54 patients. The two methods agreed on the presence of varices only in 46 patients (59%), on the absence of varices in 11 patients (14%), and disagreed in 21 patients (27%). Among the patients showing varices by endoscopy, portography agreed on the diagnosis in 78%, and among patients without endoscopical varices, portography agreed in 58%. The corresponding rates of agreement expected by chance alone are 69% and 31%, respectively. The free portal pressure was lowest in patients with no varices according to both techniques, highest in patients with varices by both techniques and intermediate in patients in whom there was disagreement on the diagnosis. Modification of the criteria for endoscopical and portographical diagnosis of varices and distinction between patients with and without ascites and preceding haemorrhage had no appreciable effect on the agreement. We conclude that endoscopy and portography show only moderate agreement in the diagnosis of oesophageal varices.
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Sixtyfour jaundiced patients were randomly allocated to have fine needle PTC performed with or without prior ultrasonographical localization of the porta hepatis. The general success rate was 97% and complications occurred in two patients (3%). Ultrasonography prior to PTC did not significantly reduce the number of needle passes in the liver parenchyma, the failure rate or the number of complications. Ultrasonic scanning, however, should precede PTC to disclose patients with obstructive jaundice and reveal hepatic and perihepatic abnormalities.
Percutaneous transhepatic portography was performed in 57 patients with cirrhosis and portal hypertension. The portographic findings, the free portal pressure and the coagulation tests were analyzed. Moderate or severe abnormality of the coagulation system was significantly associated with extrahepatic shunting, large gastric varices and collaterals from the splenic vein and splenic hilum. Reduced levels of prothrombin, factor X and thrombocyte counts were the factors mainly accounting for this association. As severe variceal bleeding is associated with these changes in the portal circulation, identification of patients at high risk may be based on portography combined with examination of the coagulation system.
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Experience with splenoportography suggests that patency of the umbilical vein occurs in about 9% of the patients with portal hypertension. A widely patent umbilical vein might serve as a decompressive portosystemic shunt. Percutaneous transhepatic portography was performed in 107 patients with cirrhosis of the liver and portal hypertension. A patent umbilical vein was found in 28 patients (26%). This finding significantly paralleled the number and size of other collateral veins, apart from gastroesophageal varices. No significant relation was found between umbilical vein patency and portal pressure, extrahepatic shunting, variceal bleeding, or ascites. It is concluded that a large patent umbilical vein does not effectively relieve portal hypertension, prevent gastroesophageal varices, or protect against variceal bleeding or ascites.