Prospective study comparing human albumin vs. reinfusion of ultrafiltrate-ascitic fluid after total paracentesis in cirrhotic patients with tense ascites.

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.

[Small unilocular hepatocellular carcinoma (0 < 5 cm) in patients with liver cirrhosis. Early diagnosis, surgical indications, resection and prognosis]. / Singuläres, hepatozelluläres Karzinom (0 < 5 cm) beim Leberzirrhotiker. Frühdiagnose, chirurgische Indikation, Resektion und Prognose.

In 151 (17.5%) of 861 patients with liver cirrhosis regularly screened by sonography and determination of alpha-fetoprotein a hepatocellular carcinoma (HCC) was detected. Diagnosis was verified by sonographically guided fine needle puncture and exceptionally by laparoscopy and direct puncture. In 34 patients (22.5%) selection criteria for operation were a tumour diameter under 5 cm, no central localisation in the liver and at least 5 mm distant from the main structures; furthermore multilocular HCC and intra- and extrahepatic metastases were contraindications. Additionally Child-Pugh-classification should be A + B and urea synthesis rate 6 g per day. 27 patients (80%) had esophagogastric varices seen at endoscopy and 20 (59%) had bleeding episodes from varices managed endoscopically or surgically. Types of surgical resections were segmentectomy [17], bisegmentectomy [10] and oncologically defined wedge resections [7] using controlled hypotension and interrupted occlusion of the hepatoduodenal ligament. 4 patients (11.8%) died within 30 days of liver failure [3] and sepsis [1]. All patients could be followed up for eleven years: 18 patients died after 1.5-10 years of liver failure, tumour recurrence or second tumour and a cause not associated with HCC, 12 patients are living. Kaplan-Meier survival curves show that survival at 5 years is 50% and at 10 years 34%. The main indicators for a good prognosis were clinically the HBsAG-activity, the Child-Pugh-classification and the application of autologous blood, pathologic-anatomically the classification and grading and histologically the absence of vascular invasion, absence of satellites and a number of mitoses under 7 in the visual field. For tumour recurrence dysplasia is of positive influence.--Liver resection remains the most widely used therapeutic option for treatment of HCC in cirrhosis. The early and long-term results can be improved by early diagnosis, strict selection of patients for operation and the use of well defined clinical, pathological and histological criteria.

Causes and pathomechanisms of oesophageal varices development.

Portal hypertension is a common clinical syndrome with chronic liver diseases and is characterised by a pathological increase in portal pressure. Moreover, portal hypertension is associated with increased portal blood flow. Increased vascular resistance in portal hypertension is because of an increase in both intrahepatic and portosystemic collateral resistance. Chronic elevations in systemic and splanchnic blood flow have been documented as key elements of hyperdynamic circulatory state of hypertensive animals and humans. Peripheral vasodilatation initiates the development of the classic profile of decreased systemic elevated splanchnic blood flow and elevated cardia index that characterises this state. Portosystemic collaterals develop as a result of portal hypertension. This is the central pathophysiological event that leads to bleeding from oesophagogastric varices and portosystemic encephalopathy. Collateral vessels respond to various vasoconstrictors and vasodilators.--Varices in the distal 5 cm of the distal oesophagus are easily identified by endoscopy because of their superficial location in the lamina propria and therefore are must apt to bleed and why the current practise of endoscopic therapy is likely to be successful in obliterating the varices. In patients with oesophageal varices the dilated deep intrinsic veins displace the superficial venous plexus, assume a supepitheal position and are endoscopically visible as teleangiectasia, cherry red spots, red colour signs, hemocystic spots, red wale markings or varices on varices. As alternative endoscopic way of treatment the paravariceal injection has been propagated by our group thus preserving the pathophysiologic collaterals and preventing early new formation of collaterals and rebleeding. Pathophysiologically the concept of erosion has been abandoned and replaced by the explosion theory: bleeding probably occurs when the expanding force by pressure and flow can no longer be counter-balanced by the variceal wall tension; at this point the varices rupture and bleed. When the varix distension has increased, the radius has increased and the wall thickness decreased. Thus early diagnosis of patients with a high tendency to bleed can easily be made by endoscopy, measuring portal and/or oesophageal-variceal pressure and characteristising the chronic liver disease according to the Child-Pugh-classification.

Appraisal of surgical resection of gallbladder carcinoma with special reference to hepatic resection.

Carcinoma of the gallbladder a gastrointestinal malignancy with an extraordinarily poor prognosis. However, aggressive surgery, with special reference to hepatic resection, may improve survival. To prove this, we performed a retrospective analysis over an 18-year period to investigate the experience of a center that began employing liver resection in patients with gallbladder cancer in 1978. The analysis was based on patients' documentation and regular follow-up to January 1996. The standard procedures were extended cholecystectomy (cholecystectomy with lymphadenectomy and wedge hepatic resection), anatomic segmentectomy of segments IVa and V, and extended hepatectomy. Significance was assessed by the log-rank test. Thirty-nine patients were resected, curatively in 41% (n = 22; group I) and palliatively in 31% (n = 17; group 2). In 28% (n = 15; group 3) a palliative or no operation was performed. Only curatively resected patients were analyzed and followed up to January 1996. No patients in group 1 died postoperatively. The actuarial 5-year survival rate of the patients with curative resection was 55%. Four patients had stage I, two had stage II, four had stage III, and two had stage IV disease according to TNM-classification. Six of the 16 patients without lymph node metastasis survived more than 5 years. A significant difference in long-term survival was recognised between stage II and stage IV patients and between stage (pT1a)- and (look table 1b) (pT1b)-patients (P < 0.01). Diagnostic efforts should focus on detecting early stages I and II gallbladder cancer. In advanced cases, aggressive surgery, particularly with hepatic resection, is the method of choice and is successful even in patients 70 years and older.

Analysis of factors affecting outcome after hepatectomy of patients with liver cirrhosis and small hepatocellular carcinoma.

OBJECTIVE: To review our policy of screening patients at risk of developing hepatocellular carcinoma (HCC), and to present 10 years' experience of hepatic resection for small HCC (< 5 cm). DESIGN: Retrospective study. SETTING: Teaching hospital, Germany. SUBJECTS: 861 patients with hepatic cirrhosis and oesophageal varices of whom 151 (18%) had HCC confirmed histologically; 30 of these tumours (20%) were less than 5 cm in diameter and suitable for resection. INTERVENTIONS: Segmentectomy (n = 14) bisegmentectomy (n = 10), and oncologically defined wedge resection (n = 6). MAIN OUTCOME MEASURES: Mortality, morbidity, and survival. RESULTS: 4 patients died within 30 days of liver failure and sepsis (n = 20, liver failure (n = 1), and bronchopneumonia (n = 1). The main beneficial prognostic factors were Child classification, donation of autologous blood, and an encapsulated tumour. The main indicators of a poor prognosis were invasion of the liver, venous invasion, invasion of the resection margin, and the presence of microsatellite tumours and nodules. 12 of the 26 survivors developed recurrences during the first five years postoperatively (46%). Kaplan-Meier survival curves showed that survival at 1 year was 80%, at 3 years 65%, and 5 years 50%, and at 10 years 30%. CONCLUSION: Hepatic resection is a useful treatment for small HCC, but its success depends on early detection and careful selection of patients.

Prophylactic endoscopic sclerotherapy in patients with liver cirrhosis, portal hypertension, and esophageal varices.

A major cause of death among patients with cirrhosis and portal hypertension is bleeding from esophago varices. The reasons for variceal haemorrhage and which varices have a high risk of bleeding are discussed. In addition, the question as to whether prophylactic endoscopic sclerotherapy is a viable solution to prevent variceal haemorrhage.

[Ruptured pseudoaneurysm of the splenic artery. A complication of chronic pancreatitis]. / Rupturiertes Pseudoaneurysma der Arteria lienalis. Komplikation der chronischen Pankreatitis.

HISTORY AND FINDINGS: A pale looking 33-year-old man with a history of perforated gastric ulcer and pancreatitis with surgically drained pseudocyst was admitted because of painless anal bleeding. Heart rate was 100/min, blood pressure 90/60 mm Hg. INVESTIGATIONS: Haemoglobin concentration (6.3 g/dl) and RBC count (2.4 mill./microliters) indicated anaemia due to bleeding. Sonography and computed tomography demonstrated chronic calcifying pancreatitis and thrombosis of splenic and mesenteric veins. There were grade 1 oesophageal varices on endoscopy. The source of bleeding was found by coloscopy to be a submucous pulsating tumour in the region of the left flexure, which on angiography was an aneurysm of the splenic artery. TREATMENT AND COURSE: The pseudoaneurysm of the splenic artery, which had perforated into the colon, was resected together with a partial pancreas excision and splenectomy. There were no complications and the patient was discharged symptom-free after 15 days, and there had been no further bleeding 6 months later. CONCLUSION: Pseudoaneurysm of a visceral artery is a rare, but life-threatening, complication of pancreatitis. Treatment options are operation and/or interventional catheter embolisation.

[The value collateralization and venous obstruction operations in acute bleeding esophageal varices in patients with cirrhosis of the liver]. / Zum Stellenwert von Kollateralisations- und Venensperroperationen bei der akuten Oesophagusvaricenblutung des Lebercirrhotikers.

Despite the development of new techniques and the great successes in recent years in Japan, the value of surgical venous obstruction in the treatment of oesophageal and gastric variceal bleeding remains controversial. For this reason we chose to evaluate our own results over a period of 10 years. Splenectomy is the only curative operation that eliminates the local portal hypertension in peripheral thrombosis of the splenic vein. Transposition of the spleen to the thoracic cavity with establishment of splenopulmonary anastomoses is indicated in the case of prehepatic block in childhood. The most widespread and successful of the operations to achieve venous obstruction are extended oesophagogastric disconnection (devascularisation with selective proximal vagotomy and fundoplication) as introduced by our group; para-oesophagogastric devascularisation and oesophageal transection according to Johnston using the clip suture device; and devascularisation of the upper two-thirds of the stomach and half of the abdominal oesophagus with transection, splenectomy and pyloroplasty after Sugiura and Futagawa. In the 10-year period analysed, we operated on 90 patients with acute bleeding oesophageal varices, many of them as emergencies. 66% were classified as Child-Pugh type C. Early mortality amounted to 26% (n = 24), and the morbidity rate was 42%. The 5- and 10-year survival rates were 50% and 38% respectively with regular endoscopic follow-up and repeat sclerotherapy. In an emergency, the choice between a shunt operation and a venous obstruction procedure depends on the individual case and the surgeon's experience.(ABSTRACT TRUNCATED AT 250 WORDS)

[Narrow-lumen mesocaval interposition shunt in liver cirrhosis and recurrent esophageal varices hemorrhage. Standard surgery of the future in failure of sclerotherapy?]. / Englumiger mesokavaler Interpositions-Shunt bei Leberzirrhose und rezidivierender Osophagusvarizenblutung. Standardoperation der Zukunft bei "Sklerosierungsversagen"?

In a prospective study, conducted between 1.1.1987 and 31.12.1992, 72 consecutive patients (50 men, 22 women; mean age 59.8 [16-72] years) with cirrhosis of the liver and recurrent bleeding from oesophageal or fundal varices, were treated with a mesocaval interposition shunt, made of reinforced Goretex 10 or 12 mm in diameter. Further selection criteria were Child-Pugh class A (n = 39) or B (n = 33), liver volume (by ultrasound) between 1000 and 2500 ml, portal vein perfusion index of at least 10% and histological exclusion of activity or progression of the cirrhosis. Four patients (5.6%) died during the first 30 days after the intervention, and four had recurrent bleeding from the varices, three of them during the postoperative period, one during the second postoperative year. The cumulative shunt patency rate was 94.4% (up to 84 months). An acute encephalopathy occurred in six patients (8.3%), which was successfully treated with protein restriction and neomycin administration. Intra- and post-operative hemodynamic investigation confirmed maintenance of portal-vein perfusion in all patients, but there was a significant tendency towards reduction after 3 years in all patients. The overall survival rate after 7 years was 75%, with 85% for patients in Child-Pugh class A and 65% for those in class B. The results indicate that the described method can achieve satisfactory portal decompression with maintenance of portal-vein flow. It is especially suitable as a standard method if sclerotherapy has failed.

Mesocaval interposition shunt with small-diameter polytetrafluoroethylene grafts in sclerotherapy failure.

Fifty-seven patients with failed sclerotherapy received a mesocaval interposition shunt with an externally supported, ringed polytetrafluoroethylene prosthesis of either 10 or 12 mm diameter. Thirty-one patients had Child-Pugh grade A disease and 26 grade B; all had a liver volume of 1000-2500 ml. Follow-up ranged from 16 months to 6 years 3 months. Three patients (5 per cent) died in the postoperative period. There were two postoperative recurrences of variceal haemorrhage and one recurrent bleed in the second year after surgery. The cumulative shunt patency rate was 95 per cent and the incidence of encephalopathy 9 per cent; the latter was successfully managed by protein restriction and/or lactulose therapy. The actuarial survival rate for the whole group at 6 years was 78 per cent, for those with Child-Pugh grade A 88 per cent and for grade B 67 per cent. Small-lumen mesocaval interposition shunting achieves portal decompression, preserves hepatopetal flow, has a low incidence of shunt thrombosis, prevents recurrent variceal bleeding and is not associated with significant postoperative encephalopathy.

Prophylactic sclerotherapy for esophageal varices in high-risk cirrhotic patients selected by endoscopic and hemodynamic criteria: a randomized, single-center controlled trial.

Controlled trials of sclerotherapy for the prevention of the first variceal hemorrhage in cirrhotics have given conflicting results, in spite of an initial positive controlled trial. We designed therefore a new study in which only 89 of 396 investigated patients were randomized to sclerotherapy (44 patients) or a control group (45 patients). The admission criteria were: no history of variceal bleeding, the presence of high risk varies, i.e., varices of degrees III and IV with minivarices on the surface of them, and portal pressure over 16 mmHg. Sclerotherapy sessions were performed at 0, 7, 14, 21, and 28 days, until the varices were reduced in size and completely covered by fibrous tissue. Follow-up endoscopy was performed at four-month and thereafter at six-month intervals. The control patients underwent repeated clinical investigation and endoscopy at six-month intervals. Bleeding episodes were treated by emergency endoscopic sclerotherapy in both groups, whenever possible. The mean follow-up was 33 months. The results were analyzed using Student's t-test and the log-rank test. Variceal bleeding occured in 11 sclerotherapy patients (25%) and 34 controls (75.6%) (p < 0.05). The overall mortality was 25% (11 patients) among the sclerotherapy patients and 69% (31 patients) in the controls (p < 0.01). Prophylactic endoscopic sclerotherapy was able to prolong survival in Child-Pugh classes A and B, but not in C. It is concluded that prophylactic endoscopic sclerotherapy does reduce the incidence of first variceal bleeding in cirrhotic patients, and is able to prolong survival if only high-risk patients are selected and the treatment is performed by endoscopic experts.

Current therapeutic strategy in bleeding esophageal varices in babies and children and long-term results of endoscopic paravariceal sclerotherapy over twenty years.

71 consecutive babies and children with bleeding esophageal varices managed primarily by emergency or elective paravariceal endoscopic sclerotherapy (PES) have been reviewed and followed up for twenty years. In 36 of them 53 different operations to prevent further variceal hemorrhage had been performed without permanent success. In 50 children (70 per cent--Group Ia), portal vein obstruction, in 2 (3 per cent--Group Ib), congenital hepatic fibrosis and in 19 (27 per cent--Group II) babies and children different types of cirrhoses were the cause of portal hypertension. Emergency PES was necessary for 29 and successful for 28 children (96.5 per cent). Recurrent bleeding in one child stopped after introduction and inflation of the Sengstaken-Blakemore tube. In one case an urgent transthoracic esophageal resection and fundoplication was performed because of recurrent hemorrhage in spite of repeated PES. 6 children--3 foreigners--were lost to follow-up after 3, 5, 6, 7, 11 and 12 years. Under regular PES there were 3 rebleedings (4 per cent) during the first month managed successfully by PES or conservatively; another 3 rebleedings (4 per cent) occurred during the first year. In "sclerotherapy failures" (recurrent hemorrhage in spite of chronic PES in 6 children aged more than 10 years 6 elective and selective shunts were carried out 3, 5, 6, 8, 10 and eleven years after the first PES. The number of complications was high, but the vast majority was asymptomatic and no complications was responsible for death. There was no death in children with portal vein obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)

Massive and recurrent gastrointestinal hemorrhage due to jejunal varices in an afferent loop--diagnosis and management.

Bleeding from "ectopic" varices outside the gastroesophageal region is an uncommon complication of portal hypertension. Although the high mortality rate of bleeding duodenal varices has been emphasized (1-4), an awareness of the condition and its characteristic presentation may enable diagnostic and therapeutic procedures to be performed rapidly with an increased likelihood of a successful outcome. This report describes a patient with recurrent, frequent and massive hemorrhage from jejunal varices in the afferent loop after a Billroth II resection, chronic pancreatitis and portal hypertension; the diagnosis and management of this unusual case of recurrent gastrointestinal bleeding are discussed.

[Correlation between pulmonary hypertension and portal hypertension--2 case reports of different forms of pre-sinusoidal portal hypertension]. / Zum Zusammenhang zwischen pulmonaler Hypertonie und portaler Hypertension--zwei Kasuistiken von unterschiedlichen Formen von präsinusoidaler portaler Hypertension.

Since its first description in 1951 by Mantz and Craig pulmonary hypertension in combination with portal hypertension has been observed more and more frequently. In a recent prospective study Hadengue et al. reported an incidence of 2%. Thus this simultaneous occurrence can no longer be considered to be coincidental. The etiology remains still unclear. It is most probable that the development is due to vasoactive substances which bypass the liver or which are produced in the lung itself, and which, due to a long-term vasoconstriction, causes irreparable damage to the arterioles and arteries in the lung. Such pulmonary hypertension can develop in the presence of a pre- as well as an intrahepatic block, even when the portal hypertension is partially or completely alleviated by a portosystemic anastomosis. This last circumstance can be illustrated by two cases which were observed by our group. Case A is of particular interest because it is the first documentation of a case of an intrahepatic block due to a (so-called) macronodular transformation of the liver in the absence of portal thrombosis (a so-called NRH: nodular regenerative hyperplasia) in combination with pulmonary hypertension. This type of non-cirrhotic portal hypertension can be associated with micronodular transformation of the liver as well. Post-hepatic blocks or the so-called BUDD-CHIARI Syndrome type appear to carry no risk of development of pulmonary hypertension. It remains unclear which particular etiologies increase susceptibility to later development of pulmonary hypertension.