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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 manifestation in cirrhotic patients, and is associated with a reduced survival rate. Management of ascites is primarily focused on sodium restriction and diuretic treatment to which most patients respond appropriately. For the small group of patients who do not respond sufficiently, interventions such as large volume paracentesis and transjugular intrahepatic portosystemic shunt placement should be considered. Most important in the management of cirrhotic patients with ascites is prevention of complications. Spontaneous bacterial peritonitis and hepatorenal syndrome are severe complications with a poor prognosis when not detected and treated in an early stage. In all hospitalised patients with ascites, an infection of the ascitic fluid should be ruled out. For those patients at risk of developing spontaneous bacterial peritonitis, in particular patients after a first episode and patients with gastrointestinal bleeding, antibiotic prophylaxis should be given. To prevent the hepatorenal syndrome, substitution with albumin is essential, both in patients who experience an episode of spontaneous bacterial peritonitis and in patients treated with large volume paracentesis. For those patients unresponsive to standard treatment regimens, liver transplantation may be the only suitable treatment option.
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PMID:Ascites in cirrhosis: a review of management and complications. 1842 69

Hepatorenal syndrome (HRS) is a severe complication in patients with cirrhosis and ascites. Renal insufficiency is functional and is caused by renal vasoconstriction. HRS occurs in 10% of patients with advanced cirrhosis. Diagnosis of HRS is based on ruling out other causes of renal insufficiency. There are two types of HRS: type 1 has rapid onset and progressive course and a mean survival of 15 days without treatment, while type 2 is less severe and progressive, with a mean survival of 6 months. Definitive treatment of HRS is liver transplantation. However, in the last few years administration of vasoconstrictive drugs or placement of portosystemic shunts have been shown to be effective in reversing HRS. Therefore, these measures may be used as a bridge before liver transplantation is performed. Finally, the risk of developing HRS in the context of spontaneous bacterial peritonitis can be prevented by administering albumin together with the corresponding antibiotics. In cases of severe acute alcoholic hepatitis, pentoxifylline can be administered.
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PMID:[Hepatorenal syndrome]. 1798 Jan 34

Accumulation of fluid as ascites is the most common complication of cirrhosis. This is occurring in about 50% of patients within 10 years of the diagnosis of cirrhosis. It is a prognostic sign with 1-year and 5-year survival of 85% and 56%, respectively. The most acceptable theory for ascites formation is peripheral arterial vasodilation leading to underfilling of circulatory volume. This triggers the baroreceptor-mediated activation of renin-angiotensin-aldosterone system, sympathetic nervous system and nonosmotic release of vasopressin to restore circulatory integrity. The result is an avid sodium and water retention, identified as a preascitic state. This condition will evolve in overt fluid retention and ascites, as the liver disease progresses. Once ascites is present, most therapeutic modalities are directed on maintaining negative sodium balance, including salt restriction, bed rest and diuretics. Paracentesis and albumin infusion is applied to tense ascites. Transjugular intrahepatic portosystemic shunt is considered for refractory ascites. With worsening of liver disease, fluid retention is associated with other complications; such as spontaneous bacterial peritonitis. This is a primary infection of ascitic fluid caused by organisms originating from large intestinal normal flora. Diagnostic paracentesis and antibiotic therapy plus prophylactic regimen are mandatory. Hepatorenal syndrome is a state of functional renal failure in the setting of low cardiac output and impaired renal perfusion. Its management is based on drugs that restore normal renal blood flow through peripheral arterial and splanchnic vasoconstriction, renal vasodilation and/or plasma volume expansion. However, the definitive treatment is liver transplantation.
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PMID:Fluid retention in cirrhosis: pathophysiology and management. 1818 68

Hepatorenal syndrome (HRS) is a functional renal failure that frequently develops in patients with advanced cirrhosis and severe impairment in systemic circulatory function. Traditionally it has been considered to be the consequence of a progression of the splanchnic arterial vasodilation occurring in these patients. However, recent data indicate that a reduction in cardiac output also plays a significant role. There are two different types of HRS. Type-2 HRS consists of a moderate and steady or slowly progressive renal failure. It represents the extreme expression of the circulatory dysfunction that spontaneously develops in patients with cirrhosis. The main clinical problem in these patients is refractory ascites. Type-1 HRS is a rapidly progressive acute renal failure that frequently develops in closed temporal relationship with a precipitating event, commonly spontaneous bacterial peritonitis. In addition to renal failure, patients with type-1 HRS present deterioration in the function of other organs, including the heart, brain, liver, and adrenal glands. Type-1 HRS is the complication of cirrhosis associated with the worst prognosis. However, effective treatments of HRS (vasoconstrictors associated with intravenous albumin, transjugular intrahepatic portacaval shunt, albumin dialysis) that can improve survival have recently been introduced.
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PMID:Pathogenesis and treatment of hepatorenal syndrome. 1829 79

In recent years, there have been important advances in the clinical management of ascites and its related complications, such as hyponatremia, hepatorenal syndrome (HRS), and spontaneous bacterial peritonitis (SBP). Moreover, new drugs are currently being investigated for their potential usefulness in managing these complications. This article is not intended to comprehensively review all the literature published in recent years; rather, the authors discuss only studies they believe represent a potentially significant advance in this field. The following review is divided into two parts; the first discusses ascites and renal function abnormalities, including hyponatremia and HRS, and the second discusses SBP management.
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PMID:What's new in the treatment of ascites and spontaneous bacterial peritonitis. 1841 37

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 detection of bacterial DNA in serum and ascitic fluid (AF) from patients with liver cirrhosis and ascites is interpreted as molecular evidence of intestinal bacterial translocation (BT) and considered sufficient to activate the cellular immune response leading to greater cytokine synthesis. We studied 34 patients with liver cirrhosis and culture-negative, non-neutrocytic ascites [22 patients without bacterial DNA (group I) and 12 patients with bacterial DNA (group II)]. History and clinical examination were done with the following investigations at first admission and followed up for 24 weeks: serum and AF tumour necrosis factor-alpha (TNF-alpha), AF polymorphonuclear leukocytes, AF cultivation and detection of blood and AF bacterial DNA. Serum and AF TNF-alpha were significantly higher in patients with bacterial DNA compared to those without bacterial DNA at first admission [54.5+/-22.56 vs 35.2+/-17.97 pg ml(-1) (P=0.02) and 123.2+/-49.32 vs 82.6+/-29.58 pg ml(-1) (P <0.005), respectively]. These changes became highly significant at the end of follow-up of both groups [119.3+/-27.19 vs 40.2+/-16.08 pg ml(-1) (P <0.001) and 518.8+/-91.11 vs 97.6+/-17.81 pg ml(-1) (P <0.001), respectively]. In group II, there was a significant increase in serum and AF TNF-alpha at the end of follow-up compared to at first admission (P <0.001). The relative risk of death, hepatorenal syndrome (HRS) and spontaneous bacterial peritonitis (SBP) was higher in patients with bacterial DNA compared to those without bacterial DNA. We conclude that cirrhotic patients with culture-negative, non-neutrocytic ascites and bacterial DNA have a significantly higher level of serum and AF TNF-alpha and higher risk of HRS, SBP and mortality compared to those without bacterial DNA, suggesting that bacterial DNA and TNF-alpha are implicated in these complications of liver cirrhosis.
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PMID:Bacterial DNA and its consequences in patients with cirrhosis and culture-negative, non-neutrocytic ascites. 1901 26

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

The coagulopathy of liver disease is complex and often unpredictable. Despite clear evidence of an increased tendency for bleeding in patients who have cirrhosis, many circumstances also promote local and systemic hypercoagulable states. The consequences of hypercoagulability include the obvious morbidity and mortality of portal vein thrombosis, deep vein thrombosis, and pulmonary embolism, but possibly also include other end-organ syndromes, such as portopulmonary hypertension, hepatorenal syndrome, and spontaneous bacterial peritonitis. A more subtle contribution also could be responsible for progression of early fibrosis to decompensated cirrhosis. Future research is needed to elucidate specific mechanistic pathways that might lead to local hypercoagulation and the clinical interventions that might prevent morbidity and mortality related to hypercoagulation in patients who have cirrhosis.
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PMID:Hypercoagulation in liver disease. 1915 Mar 15

Cirrhosis represents the end stage of any chronic liver disease. Hepatitis C and alcohol are currently the main causes of cirrhosis in the United States. Although initially cirrhosis is compensated, it eventually becomes decompensated, as defined by the presence of ascites, variceal hemorrhage, encephalopathy, and/or jaundice. These management recommendations are divided according to the status, compensated or decompensated, of the cirrhotic patient, with a separate section for the screening, diagnosis, and management of hepatocellular carcinoma (HCC), as this applies to patients with both compensated and decompensated cirrhosis. In the compensated patient, the main objective is to prevent variceal hemorrhage and any practice that could lead to decompensation. In the decompensated patient, acute variceal hemorrhage and spontaneous bacterial peritonitis are severe complications that require hospitalization. Hepatorenal syndrome is also a severe complication of cirrhosis but one that usually occurs in patients who are already in the hospital and, as it represents an extreme of the hemodynamic alterations that lead to ascites formation, it is placed under treatment of ascites. Recent advances in the pathophysiology of the complications of cirrhosis have allowed for a more rational management of cirrhosis and also for the stratification of patients into different risk groups that require different management. These recommendations are based on evidence in the literature, mainly from randomized clinical trials and meta-analyses of these trials. When few or no data exist from well-designed prospective trials, emphasis is given to results from large series and consensus conferences with involvement of recognized experts. A rational management of cirrhosis will result in improvements in quality of life, treatment adherence, and, ultimately, in outcomes.
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PMID:Management and treatment of patients with cirrhosis and portal hypertension: recommendations from the Department of Veterans Affairs Hepatitis C Resource Center Program and the National Hepatitis C Program. 2013 82


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