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

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

Renal failure in patients with liver disease is mostly none-organic: prerenal failure or hepatorenal syndrome (HRS). In addition there is organic renal failure, mostly acute tubular necrosis (ATN). In order to avoid functional renal failure cautious diuretic treatment as well as intravenous albumin substitution following paracentesis are pivotal. For prophylaxis of HRS patients with spontaneous bacterial peritonitis shall be given albumin infusions in addition to antibiotic treatment. Patients with HRS type I exhibit a very poor prognosis. Liver transplantation is the only established therapy with long-term success. To bridge the time to transplantation TIPS or terlipressin and albumin can be used.
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PMID:[Renal impairment in liver diseases]. 1704 10

Liver cirrhosis is associated with a wide range of cardiovascular abnormalities. These abnormalities include hyperdynamic circulation characterized by an increase in cardiac output and a decrease in peripheral vascular resistance. Despite the increased cardiac output, impaired ventricular contractility in response to both physiological and pharmacological stimuli has been described. Other cardiac abnormalities include structural changes including enlargement or hypertrophy of different cardiac chambers and electrophysiological changes such as QT prolongation. This constellation of cardiac abnormalities is termed cirrhotic cardiomyopathy. The pathogenic mechanisms of cirrhotic cardiomyopathy are multifactorial and include cardiomyocyte plasma membrane physico-chemical changes, attenuated stimulatory pathways, and enhanced activity of inhibitory systems. Accumulating evidence suggests that cirrhotic cardiomyopathy plays a major role in the pathogenesis of cardiac dysfunction following liver transplantation or transjugular intrahepatic portosystemic shunt placement. Recent research also strongly suggests that cirrhotic cardiomyopathy contributes to the pathogenesis of hepatorenal syndrome, especially following infections such as spontaneous bacterial peritonitis. Treatment of this syndrome remains largely empirical. Successful liver transplantation is thought to improve all the organ-related hemodynamic dysfunctions, including hepatopulmonary syndrome, cerebral hypoperfusion, hepatorenal syndrome, and cirrhotic cardiomyopathy. The prolonged QT interval normalizes following liver transplantation. Thus, liver transplantation appears to be the ultimate treatment for the cardiovascular complications of cirrhosis.
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PMID:Cirrhotic cardiomyopathy. 1706 Aug 68

In 1996, the International Ascites Club defined "refractory ascites" as ascites that cannot be mobilized by medical therapy or that recurs early after initial mobilization despite continued treatment. Of all patients with ascites, 5% to 10% will become refractory to medical therapy. Management of refractory ascites should attempt to control fluid accumulation, reduce the likelihood of developing complications such as spontaneous bacterial peritonitis (SBP) and the hepatorenal syndrome, and improve the patient's nutritional status and overall well-being. Measures to control ascites accumulation include documenting medication and dietary compliance and eliminating potentially nephrotoxic agents that promote sodium retention. Large volume paracentesis is an effective first step in managing these patients and can be performed routinely in an outpatient setting. When more than 5 L of fluid are removed during a paracentesis, intravenous albumin should be infused to reduce the likelihood of the patient developing postparacentesis circulatory dysfunction. Transjugular intrahepatic portosystemic shunt (TIPS) placement effectively eliminates ascites; however, there is no convincing evidence that the shunt improves mortality. Furthermore, it is associated with frequent complications of encephalopathy and shunt malfunction. We feel TIPS should be reserved for patients requiring extremely frequent paracentesis, those who develop significant postparacentesis circulatory dysfunction, or those with hepatic hydrothorax. Patients who have evidence of SBP should be treated with antibiotics and intravenous albumin infusion. Patients who have had a previous episode of SBP or an ascitic fluid protein level of less than 1.0 should receive prophylactic antibiotics. Overall, the prognosis for patients with refractory ascites remains grim, and liver transplantation is the only definitive therapy. Appropriate candidates should be identified promptly and referred for transplant evaluation.
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PMID:Treatment of refractory ascites. 1708 86

Low serum sodium concentration is an independent predictor of mortality in patients with cirrhosis, but its prevalence and clinical significance is unclear. To evaluate prospectively the prevalence of low serum sodium concentration and the association between serum sodium levels and severity of ascites and complications of cirrhosis, prospective data were collected on 997 consecutive patients from 28 centers in Europe, North and South America, and Asia for a period of 28 days. The prevalence of low serum sodium concentration as defined by a serum sodium concentration < or =135 mmol/L, < or =130 mmol/L, < or =125 mmol/L, and < or =120 mmol/L was 49.4%, 21.6%, 5.7%, and 1.2%, respectively. The prevalence of low serum sodium levels (<135 mmol/L) was high in both inpatients and outpatients (57% and 40%, respectively). The existence of serum sodium <135 mmol/L was associated with severe ascites, as indicated by high prevalence of refractory ascites, large fluid accumulation rate, frequent use of large-volume paracentesis, and impaired renal function, compared with normal serum sodium levels. Moreover, low serum sodium levels were also associated with greater frequency of hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome, but not gastrointestinal bleeding. Patients with serum sodium <130 mmol/L had the greatest frequency of these complications, but the frequency was also increased in patients with mild reduction in serum sodium levels (131-135 mmol/L). In conclusion, low serum sodium levels in cirrhosis are associated with severe ascites and high frequency of hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome.
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PMID:Hyponatremia in cirrhosis: Results of a patient population survey. 1713 58

Albumin is the most abundant protein in the circulation. Its main physiologic function is to maintain colloid osmotic pressure. Better understanding of albumin's other physiologic functions has expanded its application beyond maintenance of intravascular volume. In patients with cirrhosis, albumin has been used as an adjunct to diuretics to improve the diuretic response. It has also been used to prevent circulatory dysfunction developing after large-volume paracentesis. Newer indications in cirrhotic patients include preventing hepatorenal syndrome in those with spontaneous bacterial peritonitis, and treating established hepatorenal syndrome in conjunction with vasoconstrictor therapies. The use of albumin for many of these indications is controversial, mostly because of the paucity of well-designed, randomized, controlled trials. The cost of albumin infusions, lack of clear-cut benefits for survival, and fear of transmitting unknown viruses add to the controversy. The latest indication for albumin use in cirrhotic patients is extracorporeal albumin dialysis, which has shown promise for the treatment of hepatic encephalopathy; its role in hepatorenal syndrome or acute on chronic liver failure has not been established. Efforts should be made to define the indications for albumin use, dose of albumin required and predictors of response, so that patients gain the maximum benefit from its administration.
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PMID:Drug insight: the role of albumin in the management of chronic liver disease. 1720 88

Cirrhosis is known to be associated with numerous cardiovascular abnormalities. These include increased cardiac output and decreased arterial pressure and total peripheral resistance. Despite this increased baseline cardiac output, patients with cirrhosis show an attenuated systolic and diastolic function in the face of pharmacological, physiological and surgical stresses, as well as cardiac electrical abnormalities such as QT prolongation. These abnormalities have been termed cirrhotic cardiomyopathy. The pathogenic mechanisms that underlie this syndrome include impairment of the beta-adrenergic receptor signalling, cardiomyocyte plasma membrane function, intracellular calcium kinetics, and humoral factors such as endogenous cannabinoids, nitric oxide and carbon monoxide. Cirrhotic cardiomyopathy is believed to contribute to the cardiac dysfunction that can be observed in patients with transjugular intrahepatic portosystemic stent-shunt insertion and liver transplantation. Insufficient cardiac contractile function may also play a role in the pathogenesis of hepatorenal syndrome precipitated by spontaneous bacterial peritonitis. In this review, the clinical features, pathogenic mechanisms, clinical consequences and management options for cirrhotic cardiomyopathy are discussed.
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PMID:Cardiac dysfunction in cirrhosis. 1722 1

Hepatorenal syndrome is complication of the advanced cirrhosis characterized by functional renal failure and changes of systemic blood pressure due to increased activity of endogenous vasoactive systems. Functional renal failure is due to severe renal cortical ischemia and reduction of glomerular filtration rate (GFR) developing in the late stages of cirrhosis. The pathogenesis of hepatorenal syndrome is the result of an extreme underfilling of the arterial circulation secondary to arterial vasodilatation located in the splanchnic circulation. Reduced effective arterial blood volume triggers a compensatory response with activation of systemic and renal vasoconstrictor systems. At the same time, the ascites becomes refractory in some patients, as it is no longer responsive to diuretic treatment. These changes result from combination of deteriorating liver function and increasing portal pressure, further splanchnic vasodilatation, increase of circulating vasoconstrictors, and decrease of renal blood flow and GFR. Hepatorenal syndrome can be precipitated by shock, infection, nephrotoxic drugs, bleeding, surgery or large volume paracentesis. Renal failure may be rapidly progressive (type I HRS) or may develop more slowly (type II HRS), which is usually associated with refractory ascites. The diagnosis of HRS is based on established diagnostic criteria aimed at excluding the nonfunctional causes of renal failure. The prognosis of patients with HRS is very poor. Liver transplantation remains the only curative treatment for the time being. Pharmacological therapies based on the use of vasoconstrictor drugs may serve as a bridge to liver transplantation. Prevention of HRS by albumin infusion is recommended in patients with spontaneous bacterial peritonitis and by pentoxifylline in patients with the acute alcoholic hepatitis.
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PMID:[Hepatorenal syndrome]. 1750 77

Refractory ascites indicates advanced chronic liver disease and represents a therapeutic challenge. It may be triggered by spontaneous bacterial peritonitis and denotes poor prognosis. While liver transplantation is the ultimate treatment, for the relief of ascites therapeutic paracentesis with iv-administration of albumin and/or transjugular intrahepatic portosystemic shunt (TIPS) are well established. With rapid deterioration of renal function patients can develop hepatorenal syndrome. There is increasing evidence that these patients can be bridged to transplantation with vasopressin analogs (terlipressin) and albumin.
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PMID:The patient with refractory ascites. 1754 17

HIV coinfection is associated with faster progression of liver disease resulting from hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. Thus, liver complications have become a major cause of illness and death in coinfected patients. Controlling HIV through highly active antiretroviral therapy may slow disease progression to nearly the rate of HIV-negative persons. Several antiretroviral regimens have been associated with drug-induced liver injury, however, which is more common in patients coinfected with hepatitis B or C. After development of cirrhosis and decompensation, survival is shorter in coinfected patients. Diagnosis and management of cirrhosis should be the same for coinfected and monoinfected HBV/HCV patients. The main complications of cirrhosis are ascites, spontaneous bacterial peritonitis, bleeding esophageal varices, hepatic encephalopathy, the hepatorenal syndrome, and hepatocellular carcinoma. Liver transplantation is feasible in patients with HIV infection, and early evaluation for this option is crucial because of the accelerated course of complications in HIV coinfection.
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PMID:Diagnosis and management of cirrhosis in coinfected patients. 1770 91


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