Intraabdominal pressure and resorption of ascites in decompensated liver cirrhosis.

We determined the levels of total intraabdominal pressure and the tension resulting from the distention of the abdominal wall in 12 patients with ascites resulting from alcoholic cirrhosis of the liver. The measurements were performed first when ascites was tense, and were repeated later when ascites became non-tense with treatment. Using intraperitoneal injections of 131I-labeled human serum albumin, we measured the ascites volume and the resorption of albumin from the ascitic compartment at the same time as the pressure studies. Reduction in intra-abdominal pressure from 29.5 +/- 4.1 to 21.7 +/- 6.0 cm H2O (p less than 0.001) and in tension from 8.3 +/- 2.7 to 2.9 +/- 1.6 cm H2O (p less than 0.001) did not result in significant changes in resorption of albumin from the peritoneal cavity. Lowering of intra-abdominal pressure was not associated with any change in the volume of the resorbed ascitic fluid or the amount of albumin resorbed. We conclude that the ascites resorption rate in cirrhosis is not linearly related to intra-abdominal pressure and that in tense ascites, the decreased permeability of the parietal peritoneum counteracts the effects of the increased intra-abdominal pressure on albumin resorption. Cirrhotic ascites is associated with a changing permeability of the peritoneal membrane.

Intraabdominal pressure and ascitic fluid volume in decompensated liver cirrhosis.

Tense ascites is a widely used clinical concept lacking a quantitative correlate. In 13 patients with tense cirrhotic ascites we measured total intraabdominal pressure (IAP), hydrostatic pressure (HP), and tension. HP was defined as the level of ascitic fluid determined by percussion of the abdominal wall, and tension was the fluid level in the manometer above the HP. The total IAP is the sum of HP and tension. At a later, second measurement 11 patients significantly decreased their IAP. As expected in early stages of ascites resolution, major changes were found to be due to the reduction of the tension component, which accounted for 68% of the decrease in IAP. The HP seemed to show a definite decline only at a late stage of resolving ascites. Five patients, two with an essentially unchanged IAP and three with declining IAP, increased their ascitic fluid volume at the second study. The most probable explanation of this phenomenon is in the transfer of fluid from the edematous splanchnic organs into the peritoneal cavity in the early phase of ascites mobilization.

Biopsy of the peritoneum in decompensated cirrhosis of the liver.

Fifteen patients with noninfectious chronic ascites due to liver cirrhosis were investigated by laparoscopy and/or peritoneal biopsy. Laparoscopic inspection revealed thickening of the peritoneum, diffuse patchy redness and diffusely increased small vascular injection. Biopsies of the parietal peritoneum showed cuboidal transformation and hyperplasia of the mesothelial cells, fibrinoid depositions, fibroblastic proliferation and mononuclear cell infiltration. Probable pathogenesis of the parietal chronic nonspecific peritonitis in ascites of liver cirrhosis is the presence of irritating substances in the ascitic fluid. Diffuse small vascular injection of the peritoneum reflects most likely the inflammatory nature of the peritoneal process and not a direct influence of portal hypertension.

Permeability of the diaphragm and fluid resorption from the peritoneal cavity in the rat.

The ability to remove fluid from the peritoneal cavity is greatly impaired in rats after sealing the diaphragm (abrading such that fibrous tissue forms). The in vivo resorptive capacity of rats with sealed diaphragms was significantly reduced from 12.3 +/- 1.77% . hr-1 in controls to 5.05 +/- 2.53% . hr-1 in rats with sealed diaphragms. The in vitro permeability of isolated diaphragms for mannitol, inulin, and dextrans of mol wt 16,000 and 75,000 was 4.69 +/- 0.74, 1.16 +/- 0.22, 0.54 +/- 0.11, and 0.22 +/- 0.04 cm . sec-1 . 10(-6) for controls, and 0.54 +/- 0.24, 0.19 +/- 0.19, 0.09 +/- 0.03, and 0.08 +/- 0.02 cm . sec-1 . 10(-6) for sealed diaphragms, respectively. The reduction in the permeability of the fibrosed diaphragm to larger molecules could account for the reduced resorptive capacity.

[Diminished peritoneal pain perception in patients with liver cirrhosis and ascites]. / Verminderte peritoneale Schmerzempfindung bei Patienten mit Lebrzirrhose und Aszites.

Complete loss of parietal peritoneal sensitivity observed in a patient with long-standing ascites secondary to cirrhosis of the liver prompted an investigation of peritoneal sensitivity in 22 patients with the same condition. In all of them a decrease of the peritoneal sensitivity to needle perforation was found. All perceived peritoneal perforation as less painful than perforation of the abdominal skin by the same needle. In 8 control patients perforation of the peritoneum caused more discomfort than the perforation of the skin. In 7 cirrhotic patients where a histologic examination of the parietal peritoneum was available a chronic fibrotic peritonitis was present. Peritoneal insensitivity may partly account for mild abdominal symptoms in cirrhotics developing bacterial peritonitis.

Resistant ascites in alcoholic liver cirrhosis: course and prognosis.

A group of 29 patients with decompensated cirrhosis of the liver who retained a large amount of ascites under a hospital regimen during two months or longer was identified. The prognosis for this selected group of patients, while grave [during continuous hospitalization 11 out of 29 patients (= 38%) died], is not without hope: 18 patients (62%) improved and could be discharged from the hospital. Their further course was influenced by resumption of alcohol usage. Five of 11 (45.4%) who resumed drinking died due to hepatic causes within 10 months. Of the remaining six only one lost his ascites. Those who abstained (7 patients) remained alive for an average follow-up of 33 months and all lost their ascites. Alcohol resumption significantly decreased both survival (P less than 0.05) and ascites resorption (P less than 0.0015). Continued abstinence from alcohol may thus obviate the need for surgical measures to relieve ascites in these patients.

Histology of the intestinal peritoneum in patients with cirrhosis of the liver and ascites.

Portal hypertension and hypoalbuminemia are usually incriminated in the development of ascites in liver cirrhosis, and altered peritoneal permeability is considered only as a hypothetical possibility. Jejunal postmortem specimens were studied in 15 control patients and 16 patients dying with cirrhosis of the liver and ascites. In decompensated cirrhosis a fibrous thickening of the peritoneum was found, 159.0 +/- 96.4 micrometer (mean +/- SD) compared to 24.5 +/- 10.6 micrometer in controls (P less than 0.001). An increase in the size and number of blood vessels, lymphangiectasiae, and mononuclear cell infiltration were invariably present. These histological changes are consistent with a nonspecific chronic peritonitis. The findings indicate there is increased blood perfusion and lymph flow within the intestinal peritoneum in patients with decompensated cirrhosis of the liver and support the existence of an intestinal peritoneal factor in the pathogenesis of cirrhotic ascites.