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

Portal hypertension is one of the main consequences of cirrhosis. It results from a combination of increased intrahepatic vascular resistance and increased blood flow through the portal venous system. The condition leads to the formation of portosystemic collateral veins. Esophagogastric varices have the greatest clinical impact, with a risk of bleeding as high as 30% within 2 years of medium or large varices developing. Ascites, another important complication of advanced cirrhosis and severe portal hypertension, is sometimes refractory to treatment and is complicated by spontaneous bacterial peritonitis and hepatorenal syndrome. We describe the pathophysiology of portal hypertension and the current management of its complications, with emphasis on the prophylaxis and treatment of variceal bleeding and ascites.
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PMID:Current management of the complications of portal hypertension: variceal bleeding and ascites. 1668 12

Hepatorenal syndrome is a particular form of functional renal failure which may develop in patients with liver cirrhosis. On a clinical standpoint, precise diagnostic criteria have been established to clearly define this entity, whereas recent advances in the understanding of the biology of vasoactive mediators and the physiology of microcirculation have allowed to better anticipate its pathophysiological mechanisms. During the course of cirrhosis, sinusoidal portal hypertension leads to splanchnic and systemic vasodilation, responsible for a reduction of effective arterial blood volume. As a result, a state of intense renal vasoconstriction develops, leading to renal failure in the absence of any organic renal disease. At this stage, liver transplantation is the only definitive therapy able to reverse renal dysfunction. In recent years, innovative therapies have shown promise to prolong survival in patients with hepatorenal syndrome, including the administration of analogs of vasopressin (mainly terlipressin), the insertion of transjugular intrahepatic portosystemic shunts and the use of novel techniques of dialysis. On a preventive viewpoint, several simple measures have been shown to reduce the risk of hepatorenal syndrome in cirrhotic patients, including the appropriate use of diuretics, the avoidance of nephrotoxic drugs, the prophylaxis of spontaneous bacterial peritonitis and optimal fluid management in patients undergoing large volume paracentesis.
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PMID:[Hepatorenal syndrome in patients with liver cirrhosis]. 1689 84

Cirrhosis and chronic liver failure are leading causes of morbidity and mortality in the United States, with the majority of preventable cases attributed to excessive alcohol consumption, viral hepatitis, or nonalcoholic fatty liver disease. Cirrhosis often is an indolent disease; most patients remain asymptomatic until the occurrence of decompensation, characterized by ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, or variceal bleeding from portal hypertension. Physical examination of patients with cirrhosis may reveal a variety of findings that necessitate a hepatic- or gastrointestinal-based work-up to determine the etiology. Some patients already may have had laboratory or radiographic tests that incidentally uncovered signs of cirrhosis and its comorbidities. No serologic or radiographic test can accurately diagnose cirrhosis. A significant correlation has been demonstrated between persistently elevated liver function tests and biopsy-proven underlying hepatic disease; thus, a more targeted serologic work-up is indicated in patients whose liver function test results are persistently abnormal. Unnecessary medications and surgical procedures should be avoided in patients with cirrhosis. Referral for liver biopsy should be considered only after a thorough, non-invasive serologic and radiographic evaluation has failed to confirm a diagnosis of cirrhosis; the benefit of biopsy outweighs the risk; and it is postulated that biopsy will have a favorable impact on the treatment of chronic liver disease.
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PMID:Cirrhosis and chronic liver failure: part I. Diagnosis and evaluation. 1739 87

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

The purpose of this study was to provide evidence-based approaches to detect ascites, perform paracentesis, order tests, and interpret the results. A Medline search was performed to identify relevant articles. Of 731 identified articles, 50 articles were used. The most sensitive findings for ascites detection are ankle edema (93%), increased abdominal girth (87%), flank dullness (84%), and bulging flanks (81%). Paracentesis is safe, with bleeding rates and leakage of <1%. An ascitic fluid polymorphonuclear cell count >or=250 cells/mm(3) is the most sensitive test (86%-100%) to diagnose spontaneous bacterial peritonitis. The serum-ascites albumin gradient is the most useful test in identifying portal hypertension-related ascites. Large-volume paracentesis is effective in the treatment of refractory ascites. We conclude that paracentesis is a safe and vital procedure in patients with new-onset ascites. Once detected, an algorithmic approach to ordering tests and their interpretation is useful to determine etiology and direct further management.
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PMID:An evidence-based manual for abdominal paracentesis. 1739 12

Intestinal microflora plays an important role in the pathogenesis of hepatic cirrhosis (HC) complications. These patients are at a high risk of bacterial infections, mainly spontaneous ascitis infection or spontaneous bacterial peritonitis, pneumonia, or pleural empyema. Other HC complications, such as varicose vein hemorrhage, gastropathy, hepatorenal and hepatopulmonary syndromes, and portopulmonary hypertension, develop mainly due to portal hypertension. Portal hypertension is primarily caused by increased intrahepatic resistance, while after the forming of collateral circulation high portal pressure is maintained by increased splanchnic blood inflow secondary to vasodilatation. Itraorganic vasodilatation initiates hyperdynamic circulatory status, which exacerbates HC complications. Intestinal microflora plays a role in the development of both infectious complications and hyperdynamic circulatory status in HC. The article contains evidence of the influence of intestinal microflora on the development of HC complications.
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PMID:[The role of intestinal microflora in the development of complications of hepatic cirrhosis-associated portal hypertension]. 1792 83

Cirrhosis is the terminal phase of hepatic fibrosis, that leads to impaired hepatic function and blood flow. Liver cirrhosis is the final stage of many hepatic diseases characterized by chronic cellular destruction. The complications of liver cirrosis are the result of the hepatocellular lesion and portal hypertension. The most frequent complications are ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, gastroesophageal varices, portal hypertensive gastropathy, hypersplenism, hepatocellular carcinoma, methabolic disorders, hepatorenal syndrome and hepatopulmonary syndrome. We review the current approach of cirrhosis and its complications in order to improve the prevention and therapeutics of this frequent disease.
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PMID:[Chronic viral hepatitis: protocol proposal for the management of cirrhosis]. 1862 97

The two most widely used experimental models of advanced liver disease are the administration of carbon tetrachloride, and common bile duct ligation (BDL), however, neither has been systematically evaluated as a model of hepatorenal syndrome (HRS). The BDL model in rats, studied at diverse time points, induced a progressive renal dysfunction without structural changes in the kidney. The authors concluded that BDL is a good model for further studies of HRS and its treatment. However, the renal impairment observed at the acute phase of the BDL model is based on a different pathophysiology than that of HRS. Specifically, in acute obstructive jaundice, cholemia predominates over parenchymal liver disease (reversible at this stage without portal hypertension or cirrhosis) and independently induces negative inotropic and chronotropic effects on the heart, impaired sympathetic vasoconstriction response and profound natriuresis and diuresis that might lead to volume depletion. In addition, systemic endotoxemia contributes to the prerenal etiology of renal impairment and promotes direct nephrotoxicity and acute tubular necrosis. On the other hand, the renal failure observed in the chronic BDL model (with development of biliary cirrhosis, portal hypertension and ascites) shares pathophysiological similarities with HRS, but the accordance of the chronic BDL model to the diagnostic criteria of HRS (e.g. absence of spontaneous bacterial peritonitis, no renal function improvement after plasma volume expansion) should have been confirmed. In conclusion, we think that the BDL model is not suitable for the study of the natural history of HRS, but the chronic BDL model might be valid for the study of established HRS and its potential therapies.
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PMID:Bile duct ligation in rats: a reliable model of hepatorenal syndrome? 1868 Feb 30

A patient with alcoholic cirrhosis of the liver, portal hypertension with hepatic encephalopathy and spontaneous bacterial peritonitis (SBP) was admitted in an obtunded condition. Attempts at delineating the aetiology of the SBP using conventional cultures as well as automated systems were not successful. The use of non-anionic surfactant agents such as Tween 80-incorporated blood agar and Triton X treatment of the specimens facilitated the growth of Klebsiella pneumoniae from the ascitic fluid, which otherwise would have been concluded to represent culture-negative neutrocytic ascites. Thus, the use of the aforementioned agents could be explored in elucidating the aetiology of body cavity infections when conventional methods fail.
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PMID:Diagnosis of spontaneous bacterial peritonitis: Role of tween 80 and triton X in ascitic fluid cultures. 1938 43

Ascites is a classic complication of advanced cirrhosis and it often marks the first sign of hepatic decompensation. Ascites occurs in more than 50% of patients with cirrhosis, worsens the course of the disease, and reduces survival substantially. Portal hypertension, splanchnic vasodilatation, liver insufficiency, and cardiovascular dysfunction are major pathophysiological hallmarks. Modern treatment of ascites is based on this recognition and includes modest salt restriction and stepwise diuretic therapy with spironolactone and loop-diuretics. Tense and refractory ascites should be treated with large volume paracentesis followed by plasma volume expansion or transjugular intrahepatic portosystemic shunt. Ascites complicated by spontaneous bacterial peritonitis requires adequate treatment with antibiotics. New potential treatment strategies include the use of vasopressin V(2)-receptor antagonists and vasoconstrictors. Since formation of ascites is associated with a poor prognosis, and treatment of fluid retention does not substantially improve survival, such patients should always be considered for liver transplantation.
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PMID:Ascites: pathogenesis and therapeutic principles. 1947 32


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