Although, total paracentesis associated with human albumin substitution has shown to be a rapid, effective and safe treatment of diuretic refractory ascites in advanced liver cirrhosis, it implies high costs and has a limited availability. Therefore an alternative procedure the reinfusion of concentrated ascites has gained popularity in recent years (Smart et al. 1990; Grazioto et al. 1997). It was the aim of the study to compare human albumin substitution vs. reinfusion of ascitic-ultrafiltrate after total paracentesis. 35 patients with cirrhosis and tense ascites received total paracentesis associated with either human albumin (5-8 g/l ascites) (= group A) or reinfusion of an ascitic-ultrafiltrate fluid by means of hemofiltration technique (= group B). The mean volume of ascites removed was 9.41 (2.1-20.0) in group A and 11.41 (6.5-21.0) in group B. No significant differences in serum electrolytes, liver and renal function, coagulation profiles and hormones of the renin-angiotensin-aldosterone system were observed during hospitalization. In both groups sodium excretion increased significantly. 43% of the patients in group B developed pyrexia and chill after reinfusion of the ascitic-ultrafiltrate fluid. In one patient an anaphylactic bronchospasm occurred requiring IUC-treatment. The treatment cost in case of human albumin were 326.-DM vs. 290.-DM for each patient treated with ascitic-ultrafiltrate fluid reinfusion. The probabilities of hospital readmission and survival were similar in both groups during follow-up. The results indicate that i.v. infusion of ascitic-ultrafiltrate fluid is as effective as total paracentesis and albumin infusion in case of diuretic refractory ascites. However, according to the costs of instruments and staff and due to the significant allergic reactions caused by ascitic fluid it cannot be considered as a real alternative to albumin substitution.

No abstract

No abstract

The files of patients who underwent emergency endoscopy in a 2-yr period (January 1985 to January 1987) in the Heinz-Kalk Hospital were analyzed to establish the frequency, significance and therapy of the Mallory-Weiss syndrome associated with portal hypertension, an association observed in 55 of 339 patients (16.2%). Portal hypertension was caused by cirrhosis in 53 patients and by a prehepatic block in two patients. For 21 of these patients (37%) with portal hypertension, Mallory-Weiss syndrome was the first bleeding manifestation. They numbered 6.2% of the whole population. In the remaining 34 patients (63%) sclerotherapy treatment had been previously performed. No lesions that suggested peptic esophagitis were seen in these 55 patients, although in 25 of them (45.4%) a gastroesophageal reflux was observed. The frequency of bleeding from a Mallory-Weiss tear was significantly higher in patients with advanced liver disease, particularly with Child-Pugh classifications C and B. In patients with prehepatic block, a hemorrhage from a Mallory-Weiss tear may occur, but the frequency is significantly lower than it is in patients with cirrhosis. The bleeding tear was treated by transendoscopic esophageal and cardial wall sclerosis (paravariceal technique) and was, in all cases, successfully controlled. Mallory-Weiss syndrome is observed more frequently in patients with portal hypertension and cirrhosis. Gastroesophageal reflux apparently does not play a major role in the pathogenesis of this syndrome. It may simply be the manifestation of an abnormal gastroesophageal function. Mallory-Weiss syndrome can also be observed as a cause of rebleeding in patients treated with chronic sclerotherapy. Paravariceal endoscopic sclerotherapy is apparently the treatment of first choice to stop hemorrhage.

From January 1, 1978, to January 1, 1980, a prospective controlled randomized trial comparing conservative treatment to prophylactic endoscopic paravariceal injection sclerotherapy of esophageal varices prior to hemorrhage was carried out. In all 71 patients liver cirrhosis was confirmed histologically. The two randomly assigned groups were comparable with respect to age, sex and degree of liver diseases and its histological type was also similar. Indications for endoscopic treatment were the existence of degree III to IV varices bearing telangiectasias on their top, and degree II to IV varices without telangiectasias but coagulation factors below 30%, or both. Six patients had to be excluded. In group IA--treatment by conservative means, clinical and endoscopic monitoring--a high rate of variceal bleeding (66%) and death (42%) was observed. Comparing these results with those of group IB treated by sclerotherapy, bleeding and death rates (6 and 6%) were found to be highly significantly lower. From January 1, 1980, to January 1, 1984 another 70 non-randomized patients were treated by prophylactic endoscopic paravariceal injection sclerotherapy. In this group II the frequency of hemorrhage was 4.5% and in-hospital mortality 13%. The main causes of death were hepatic coma, followed by hemorrhage from esophageal varices. After four years another 14 patients had died despite regular monitoring and re-injection (20%); the main causes of death were hepatic coma and hepatocellular cancer. Five patients (7%) were lost to follow up, while 42 (60%) are still living.(ABSTRACT TRUNCATED AT 250 WORDS)