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

Hepatorenal syndrome (HRS) is a common complication of advanced cirrhosis, characterised by renal failure and major disturbances in circulatory function. Renal failure is caused by intense vasoconstriction of the renal circulation. The syndrome is probably the final consequence of extreme underfilling of the arterial circulation secondary to arterial vasodilatation in the splanchnic vascular bed. As well as the renal circulation, most extrasplanchnic vascular beds are vasoconstricted. The diagnosis of HRS is currently based on the exclusion of other causes of renal failure. The prognosis is very poor, particularly when there is rapidly progressive renal failure (type 1). Liver transplantation is the best option in patients without contraindications to the procedure, but it is not always possible owing to the short survival expectancy. Therapies introduced during the past few years, such as vasoconstrictor drugs (vasopressin analogues, alpha-adrenergic agonists) or the transjugular intrahepatic portosystemic shunt, are effective in improving renal function. Nevertheless, liver transplantation should still be done in suitable patients even after improvement of renal function because the outcome of HRS is poor. Finally, recent findings suggest that the risk of developing HRS in the setting of spontaneous bacterial peritonitis may be reduced by the administration of albumin together with antibiotic therapy, and that of HRS occurring in severe alcoholic hepatitis can be lowered by administration of pentoxifylline. Although these findings need to be confirmed, these two strategies represent innovative approaches to lower the frequency of HRS in clinical practice.
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PMID:Hepatorenal syndrome. 1465 22

Hepatorenal syndrome is complication of advanced cirrhosis characterized by renal failure, changes in systemic blood pressure, and increased activity of endogenous vasoactive systems. Renal failure is due to severe renal vasoconstriction 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 an arterial vasodilation located in the splanchnic circulation. This underfilling triggers a compensatory response with activation of vasoconstrictor systems. The diagnosis of hepatorenal syndrome is based on established diagnostic criteria aimed at excluding nonfunctional causes of renal failure. The prognosis of patients with hepatorenal syndrome is very poor. Liver transplantation is the best option in selected patients, but it is not always applicable due to the short survival expectancy and donor shortage. Pharmacological therapies based on the use of vasoconstrictor drugs (terlipressin, midodrine, octreotide or noradrenline) are the most promising in aims of successfully offering a bridge to liver transplantation. Prevention of hepatorenal syndrome with albumin infusion is recommended in patients with spontaneous bacterial peritonitis and with pentoxifylline in patients with acute alcoholic hepatitis.
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PMID:Hepatorenal syndrome. 1509 2

Hepatorenal syndrome (HRS) is a complex syndrome. In addition to severe reduction of renal function due to renal vasoconstriction, there is impairment in systemic haemodynamics, activation of the renin-angiotensin and sympathetic nervous systems and antidiuretic hormone, vasoconstriction of the brain, muscle and skin, and dilutional hyponatraemia. Treatment in patients with type 2 HRS, the most frequent form of HRS, is directed towards managing refractory ascites. Paracentesis is the treatment of choice. TIPS is also effective but is more expensive, is associated with higher incidence of hepatic encephalopathy, and does not increase survival. Although a rapidly progressive renal failure is the most characteristic manifestation of type 1 HRS, there is failure in other organs such as the liver and the brain. A decrease in cardiac output develops in these patients, associated with a decrease in cardiopulmonary pressures. Since type 1 HRS mainly occurs in patients with spontaneous bacterial peritonitis and massive release of cytokines within the peritoneal cavity, it may be considered as a special form of multiorgan failure of circulatory origin. Not surprisingly, the treatment of choice in type 1 HRS is the combination of vasoconstrictors to reduce arterial vasodilation and plasma volume expansion with albumin to increase cardiac preload. TIPS is also effective in these patients and the combination of pharmacological treatment followed by TIPS may be the most effective approach.
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PMID:Review article: hepatorenal syndrome--how to assess response to treatment and nonpharmacological therapy. 1533 2

In the past few years, there have been important advances in the field of pathogenesis and management of ascites and spontaneous bacterial peritonitis in cirrhosis. A new pathogenic theory of ascites and renal dysfunction in cirrhosis has been presented, and previously ill-defined conditions, such as refractory ascites and hepatorenal syndrome, have been defined precisely. The reintroduction of therapeutic paracentesis has modified markedly the way in which patients hospitalized for ascites are treated. The use of potent and safe antibiotics has improved the resolution rate and survival of patients with spontaneous bacterial peritonitis, and the use of oral antibiotics will simplify the management of this condition in the near future. Finally, prophylactic antibiotic regimens represent a major step forward in the prevention of spontaneous bacterial peritonitis in subsets of cirrhotic patients with a great risk of developing this complication.
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PMID:Pathophysiology, complications, and treatment of ascites. 1556 74

Sequential diuretic treatment of ascites with spironolactone and furosemide is equivalent to initial combination therapy. Orally applicable vasopressin-V2-receptor antagonists are an interesting novel therapeutic approach for the elimination of free water. The therapeutic efficacy for patients with cirrhosis and ascites is currently being investigated in phase II trials. Following paracentesis of up to 6 liters volume, infusion of 3.5 % saline is as effective as 20 % albumin. Another trial confirms the superiority of TIPS for the treatment of massive ascites, also demonstrating survival benefit. Determination of leukocyte esterase activity with a simple stix method may be helpful for the rapid and easy diagnosis of spontaneous bacterial peritonitis. Patients with hepatorenal syndrome seem to benefit from a combination of terlipressin and albumin whereas the effect of albumin dialysis on survival remains to be proven.
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PMID:[Advances in therapy for ascites and hepatorenal syndrome]. 1565 Sep 69

Hepatorenal syndrome is the dreaded complication of end-stage liver disease characterized by functional renal failure due to renal vasoconstriction in the absence of underlying kidney pathology. The pathogenesis of hepatorenal syndrome is the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in the splanchnic circulation. This underfilling triggers a compensatory response with activation of vasoconstrictor systems leading to intense renal vasoconstriction. The diagnosis is based on established diagnostic criteria aimed at excluding nonfunctional causes of renal failure. The prognosis of patients with hepatorenal syndrome is extremely poor especially in those who have a rapidly progressive course. Liver transplantation is the best option in suitable candidates, but it is not always applicable due to the short survival expectancy and donor shortage. Pharmacological therapies based on the use of vasoconstrictor drugs (terlipressin, midodrine, octreotide, or noradrenline) are the most promising in the aim of successfully offering a bridge to liver transplantation. Other treatments such as transjugular intrahepatic portosystemic shunts and albumin dialysis are effective but experience is very limited. Although there is limited information on the prevention of hepatorenal syndrome, intravenous albumin infusion in patients with spontaneous bacterial peritonitis and with oral pentoxifylline in patients with acute alcoholic hepatitis seems to effectively prevent hepatorenal syndrome in these two settings.
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PMID:Hepatorenal syndrome: a dreaded complication of end-stage liver disease. 1566 8

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

The administration of albumin improves circulatory function, prevents hepatorenal syndrome, and reduces hospital mortality in patients with cirrhosis and spontaneous bacterial peritonitis. This randomized unblinded pilot study compared the effect of albumin (10 patients) and the synthetic plasma expander hydroxyethyl starch 200/0.5 (10 patients) on the systemic hemodynamics of patients with spontaneous bacterial peritonitis. Baseline measurements were performed within 12 hours after diagnosis of infection. Patients then received 2 doses of the volume expander (1.5 g/kg body weight after baseline measurements and 1 g/kg body weight on day 3). Measurements were repeated after infection resolution. Treatment with albumin was associated with a significant increase in arterial pressure and a suppression of plasma renin activity, indicating an improvement in circulatory function. This occurred in the setting of a significant expansion of central blood volume (increase in cardiopulmonary pressures and atrial natriuretic factor) and an increase in systolic volume and systemic vascular resistance. In contrast, no significant changes were observed in these parameters in patients treated with hydroxyethyl starch. Von Willebrand-related antigen plasma levels significantly decreased in patients treated with albumin but not in those treated with hydroxyethyl starch. Serum nitrates and nitrites increased in patients treated with hydroxyethyl starch but not in those treated with albumin. These data suggest an effect of albumin on endothelial function. In conclusion, albumin but not hydroxyethyl starch improves systemic hemodynamics in patients with spontaneous bacterial peritonitis. This effect is due not only to volume expansion but also to an action on the peripheral arterial circulation.
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PMID:A randomized unblinded pilot study comparing albumin versus hydroxyethyl starch in spontaneous bacterial peritonitis. 1611 26

In patients with recent onset renal insufficiency, the decision to perform combined kidney/liver transplantation (CKLT) vs. orthotopic liver transplantation alone (OLTa) can be difficult. We hypothesized that duration of renal dysfunction may correlate with creatinine elevation after liver transplantation. We retrospectively identified 69 liver transplantation patients with pretransplantation creatinine > or =1.5 mg/dL (53 OLTa, 13 CKLT). Variables analyzed were presence of hepatorenal syndrome, creatinine, Model for End-Stage Liver Disease score, albumin, age, race, gender, cause of liver disease, diabetes mellitus, hypertension, and history of ascites, spontaneous bacterial peritonitis, variceal bleeding, hepatic encephalopathy, renal replacement therapy (RRT), and transjugular intrahepatic portosystemic shunting. Duration of pretransplantation renal dysfunction was predictive of 6- and 12-month creatinine post-OLTa. Area under the receiver operating characteristic (ROC) curve for prediction of 12-month renal insufficiency by renal dysfunction duration was 0.71; optimal duration cutoff was 3.6 weeks. We applied a multivariable model, derived from OLTa patients, to CKLT subjects with definite or possible hepatorenal syndrome. Predicted 12-month creatinine without renal transplantation was >2.0 mg/dL for each patient. CKLT patients as opposed to OLTa patients had longer duration of renal dysfunction (median, 18.1 vs. 2.7 weeks, P < 0.001), higher creatinine (median 4.0 versus 1.7 mg/dL, P < 0.001), and higher rate of pretransplantation RRT (62% vs. 7%, P < 0.001). Adjusting for baseline characteristics, CKLT patients had lower creatinine than OLTa patients at 6 months (P =0.15) and 12 months (P =0.01) after transplantation. In conclusion, duration, but not cause, of renal dysfunction predicts renal outcome in OLTa recipients. Prospective studies may use duration of renal dysfunction to help identify CKLT candidates.
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PMID:Renal function after orthotopic liver transplantation is predicted by duration of pretransplantation creatinine elevation. 1612 56

Onset of ascites in cirrhosis of the liver is associated with worsened quality of life, increased risk of spontaneous bacterial peritonitis, and renal failure. Portal hypertension produces splanchnic vasodilation that triggers the cascade of events leading to release of Na retentive vasoconstrictor hormones. Management of ascites caused by cirrhosis is based on improving the Na excretion with diuretics and Na restriction in diet. Refractory ascites and hepatorenal syndrome are the complications of ascites that carry a very high mortality. Large volume paracentesis and transjugular intrahepatic porto-systemic shunts are useful in managing patients with refractory ascites. Liver transplant is the only way to improve survival in ascites caused by cirrhosis.
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PMID:Management of ascites in cirrhosis. 1620 72


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