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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ascites is the most common complication in cirrhotic patients. The presence of ascites predisposes the cirrhotic patients to complications that significantly increase their morbidity and mortality. These include spontaneous bacterial peritonitis and the hepato-renal syndrome. The ascitic process has different stages, from the diuretic responsive ascites through the unresponsive ascites to the development of the hepato-renal syndrome. Until a few years ago there was a controversy regarding the pathophysiology of ascites in portal hypertension. Nowadays, the peripheral vasodilatation theory is accepted as the mechanism responsible for the development of the ascites. This theory proposes that elevated blood levels of vasodilators cause a systemic vasodilatation, that leads to the development of a hyperdynamic circulation. This vasodilatation causes activation of compensatory vasoconstrictive mechanisms. The vasoconstrictors cause functional kidney damage, which leads to the retention of sodium and water, and thus to the development of ascites.
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PMID:[The pathophysiology of ascites formation in cirrhosis of the liver]. 1222 38

Renal function abnormalities and ascites in cirrhosis are the final consequence of a circulatory dysfunction characterized by marked splanchnic arterial vasodilation. This causes a reduction in effective arterial blood volume and the homoeostatic activation of vasoconstrictor and sodium-retaining systems. Albumin is very effective in preventing renal failure associated with large-volume paracentesis and spontaneous bacterial peritonitis, conditions that are known to cause an impairment of circulatory function in patients with cirrhosis and ascites. Moreover, albumin administration improves survival in patients with spontaneous bacterial peritonitis. In patients with hepatorenal syndrome the administration of vasoconstrictor drugs in combination with albumin improves circulatory and renal function markedly and survival slightly. By contrast, the administration of albumin without vasoconstrictors has marginal or no effects on renal function in this setting.
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PMID:Review article: albumin for circulatory support in patients with cirrhosis. 1242 50

Ascites accumulation is the product of a complex process involving hepatic, renal, systemic, hemodynamic, and neurohormonal factors. The main pathophysiologic theories of ascites formation include the "underfill," "overflow," and peripheral arterial vasodilation hypotheses. These theories are not necessarily mutually exclusive and are linked at some level by a common pathophysiologic thread: The body senses a decreased effective arterial blood volume, leading to stimulation of the sympathetic nervous system, arginine-vasopressin feedback loops, and the renin-angiotensin-aldosterone system. Cornerstones of ascites management include dietary sodium restriction and diuretics. Spironolactone is generally tried initially, with furosemide added if clinical response is suboptimal. More refractory patients require large-volume paracentesis (LVP) accompanied by volume expansion with albumin. Placement of a transjugular intrahepatic portosystemic shunt is reserved for individuals with compensated liver function who require very frequent sessions of LVP. Peritoneovenous shunts are not used in contemporary ascites management. Liver transplantation remains the definitive therapy for refractory ascites. Although treatment of ascites fails to improve survival, it benefits quality of life and limits the development of such complications as spontaneous bacterial peritonitis.
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PMID:Pathophysiology and management of pediatric ascites. 1273 47

A decreased effective arterial blood volume is the principal haemodynamic disturbance in cirrhosis, leading to activation of the renin angiotensin aldosterone and the sympathetic nervous systems, sodium and water retention and renal impairment. Albumin is a plasma expander that could be used in clinical settings in cirrhosis in which plasma expansion would reverse some of the decreased effective arterial blood volume, or prevent its iatrogenic (i.e., paracenteses) or spontaneous worsening (spontaneous bacterial peritonitis). However, apart from the issue of transmission of prion agents, which may become an important issue in clinical risk management of the use of albumin in the future, the problem with albumin is its expense. Every effort must thus be made to definitely prove albumin is always the best colloid for all clinical settings in cirrhosis. Further randomized trials are justified.
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PMID:Is the use of albumin of value in cirrhosis? The case not so in favour, or is there an alternative? 1456 92

Pharmacologic studies suggest that the release of nitric oxide (NO) by endothelial NO synthase (eNOS) contributes to functional alterations of the peritoneal membrane (PM) induced by acute peritonitis. In this study, peritoneal permeability parameters in a mouse model of peritoneal dialysis were characterized, and the effects of eNOS deletion on the PM structure and permeability at baseline and after catheter-induced bacterial peritonitis were examined. Exposure of C57BL/6 mice to standard dialysate yielded a transport of urea and glucose, a sodium sieving, and a net ultrafiltration that were remarkably similar to the values obtained in rats. In comparison with controls, mice with catheter-induced peritonitis were characterized by structural changes in the PM (mononuclear cells infiltrate, vascular proliferation), upregulation of endothelial and inducible NOS, increased permeability for urea and glucose, decreased ultrafiltration, and increased protein loss in the dialysate. Comparison of eNOS wild-type and knockout mice revealed that the permeability modifications and structural changes induced by acute peritonitis were significantly reversed in eNOS knockout mice, resulting in a net increase in ultrafiltration. In contrast, the deletion of eNOS in mouse peritoneum was not reflected by permeability modifications or structural changes at baseline. These results are the first to take advantage of a knockout mouse model to demonstrate directly the crucial importance of eNOS in the permeability and structural modifications caused by acute peritonitis. The characterization of this mouse model suggests that genetically modified mice represent useful tools to investigate the molecular bases of the peritoneal changes during peritoneal dialysis.
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PMID:Mice that lack endothelial nitric oxide synthase are protected against functional and structural modifications induced by acute peritonitis. 1463 19

Complications of liver cirrhosis are usually confined to advanced stages of the disease. Bleeding from esophageal or gastric varices may be prevented by treatment with beta-blockers or by endoscopic band ligation in case of large varices and intolerance for beta-blockers. Treatment of an acute bleeding episode from varices can efficiently be treated by endoscopic procedures, potentially in combination with drug therapy. In case of bleeding uncontrolled by endoscopy, TIPS is an effective alternative in selected patients. Treatment of ascites consists of reduction of sodium intake, aldosterone antagonists, and loop diuretics as needed. TIPS or repeated paracentesis may be necessary in refractory ascites. Spontanous bacterial peritonitis (SBP) must be sought and treated with antibiotics in conjunction with albumin administration in order to reduce mortality. Hepatorenal syndrome is characterized by a poor prognosis. Therefore, liver transplantation should be considered in appropriate patients.
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PMID:[Therapy of complications of hepatic cirrhosis]. 1593 84

Spontaneous bacterial peritonitis is a major cause of mortality after liver cirrhosis. Altered permeability of the mucosa and deficiencies in host immune defenses through bacterial translocation from the intestine due to intestinal bacterial overgrowth have been implicated in the development of this complication. Molecular mechanisms underlying the process are not well known. In order to understand mechanisms involved in translocation of bacteria, this study explored the role of oxidative stress in mediating changes in intestinal mucosal glycosylation and luminal bacterial content during cirrhosis. CCl4-induced cirrhosis in rats led to prolonged oxidative stress in the intestine, accompanied by increased sugar content of both intestinal brush border and surfactant layers. This was accompanied by changes in bacterial flora in the gut, which showed increased hydrophobicity and adherence to the mucosa. Inhibition of xanthine oxidase using sodium tungstate or antioxidant supplementation using vitamin E reversed the oxidative stress, changes in brush border membrane sugar content, and bacterial adherence. In conclusion, oxidative stress in the intestine during cirrhosis alters mucosal glycosylation, accompanied by an increased hydrophobicity of luminal bacteria, enabling increased bacterial adherence onto epithelial cells. This might facilitate translocation across the mucosa, resulting in complications such as spontaneous bacterial peritonitis.
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PMID:Intestinal mucosal alterations in rats with carbon tetrachloride-induced cirrhosis: changes in glycosylation and luminal bacteria. 1655 55

Hepatorenal syndrome (HRS), a feared complication of advanced cirrhosis, is characterized by functional renal failure, secondary to renal vasoconstriction in the absence of underlying kidney pathology. Extreme underfilling of the arterial circulation, caused by arterial vasodilation of the splanchnic circulation, activates vasoconstrictor systems, which lead to intense renal vasoconstriction and HRS. Factors predictive for the development of HRS include intense urinary sodium retention, dilutional hyponatremia, low blood pressure, decreased cardiac output, and increased activity of systemic vasoconstrictors. The prognosis for patients with HRS is extremely poor, especially for those with the acute, progressive (type 1) form. Liver transplantation is the best treatment for suitable candidates and should always be the management option considered first. Pharmacologic therapies are aimed at improving renal function to enable patients to survive until transplantation is possible. These therapies are based on plasma expansion with albumin, combined with the use of either vasopressin analogs or alpha-adrenergic agonists. Other nonpharmacologic therapies, such as transjugular intrahepatic portosystemic shunts and albumin dialysis show promise, but experience with these treatments is limited. For prevention of HRS, albumin infusion is recommended in patients with spontaneous bacterial peritonitis, and pentoxifylline treatment is recommended in patients with acute alcoholic hepatitis.
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PMID:Therapy insight: Management of hepatorenal syndrome. 1674 53

Major complications of cirrhosis include ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal hypertension, variceal bleeding, and hepatorenal syndrome. Diagnostic studies on ascitic fluid should include a differential leukocyte count, total protein level, a serum-ascites albumin gradient, and fluid cultures. Therapy consists of sodium restriction, diuretics, and complete abstention from alcohol. Patients with ascitic fluid polymorphonuclear leukocyte counts of 250 cells per mm3 or greater should receive empiric prophylaxis against spontaneous bacterial peritonitis with cefotaxime and albumin. Patients who survive an episode of spontaneous bacterial peritonitis should receive long-term prophylaxis with norfloxacin or trimethoprim/sulfamethoxazole. Patients with gastrointestinal hemorrhage and cirrhosis should receive norfloxacin or trimethoprim/sulfamethoxazole twice daily for seven days. Treatment of hepatic encephalopathy is directed toward improving mental status levels with lactulose; protein restriction is no longer recommended. Patients with cirrhosis and evidence of gastrointestinal bleeding should undergo upper endoscopy to evaluate for varices. Endoscopic banding is the standard treatment, but sclerotherapy with vasoconstrictors (e.g., octreotide) also may be used. Prophylaxis with propranolol is recommended in patients with cirrhosis once varices have been identified. Transjugular intrahepatic portosystemic shunt has been effective in reducing portal hypertension and improving symptoms of hepatorenal syndrome, and can reduce gastrointestinal bleeding in patients with refractory variceal hemorrhage. When medical therapy for treatment of cirrhosis has failed, liver transplantation should be considered. Survival rates in transplant recipients have improved as a result of advances in immunosuppression and proper risk stratification using the Model for End-Stage Liver Disease and Child-Turcotte-Pugh scoring systems.
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PMID:Cirrhosis and chronic liver failure: part II. Complications and treatment. 1697 21

Ascites is a common clinical problem in children with liver disease. The peripheral arterial vasodilation hypothesis is mostly accepted as the pathophysiological basis of ascites. The most important complication is spontaneous ascitic fluid infection in the form of spontaneous bacterial peritonitis (SBP) and its variants. Aerobic gram-negative bacteria, primarily Escherichia coli, are the most common isolates. Diagnostic paracentesis is done in patients with ascites when diagnosed first time and at the beginning of each admission to hospital. Ascitic fluid is evaluated for cell count with differential, albumin level, total protein and culture. Serum-ascites albumin gradient (SAAG) is the best single test for classifying ascites into portal hypertensive (SAAG> 1.1 g/dL) and non-portal hypertensive (SAAG < 1.1 g/dL) causes. In patients with tense ascites LVP should be performed. A neutrophil count of > 250 cells/mm3 is highly suggestive of bacterial peritonitis. Intravenous cefotaxime is the empiric antibiotic of choice. Long-term administration of oral norfloxacin 5-7.5 mg/Kg once a day in cirrhotic patients with ascitic fluid protein content of < 1g/dL or prior episode of SBP is recommended for prevention of SBP. Oral dual diuretic therapy of single morning dose of spironolactone along with furosemide in the ratio of 5:2 is recommended. While obtaining satisfactory diuretic response dual diuretic therapy can be changed over to monotherapy with spironolactone. Patients should be on sodium restricted diet. Management of ascites might ultimately require liver transplantation.
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PMID:Ascites in childhood liver disease. 1700 42


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