Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Repeated large-volume paracentesis (4-6 L/day) is an effective and safe therapy of ascites in patients with cirrhosis provided albumin is infused intravenously. To investigate whether ascites can be safely mobilized in only one paracentesis session ("total paracentesis"), 38 cirrhotic patients with tense ascites were treated with total paracentesis plus intravenous albumin (6-8 g/L ascites removed). Standard liver tests and renal function tests, glomerular filtration rate, free water clearance, plasma volume, plasma renin activity, and plasma aldosterone and norepinephrine concentrations were measured before and after treatment. Total paracentesis was effective in mobilizing ascites in all but 1 patient and did not impair any of the parameters studied. The volume of ascitic fluid removed and the duration of the procedure were 10.7 +/- 0.5 L (mean +/- SEM) and 60 +/- 3 min, respectively. Five of the 38 patients (13%) developed complications during the first hospital stay (hepatic encephalopathy and gastrointestinal hemorrhage in 2 patients each and culture-negative bacterial peritonitis in 1). No patient developed renal impairment. This complication rate, as well as the clinical course of the disease during follow-up, estimated by the probability of readmission to hospital, causes of readmission, and survival probability after treatment, was similar to that reported in patients treated with repeated large-volume paracentesis. These results indicate that total paracentesis associated with intravenous albumin can be safely performed in cirrhotic patients with tense ascites and suggest that these patients could be treated in a single-day hospitalization regime.
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PMID:Total paracentesis associated with intravenous albumin management of patients with cirrhosis and ascites. 229 73

A new method for ascites recirculation, consisting of a cellulose diacetate filter to remove substances with molecular weight > or = 300,000, cell debris and bacteria, followed by the concentration of ascitic fluid prior to i.v. infusion, was used 24 times in 19 patients with cirrhosis and massive or refractory ascites. The amount of ascites removed was 7.67 +/- 0.49 l, which was reduced to 407 +/- 37 ml. The procedure took 367 +/- 22 min to complete. No statistically significant changes in liver function tests, coagulative parameters, platelet count or natremia were found. The activity of coagulation and fibrinolytic systems was further assessed in six patients. No changes suggesting an activation of intravascular coagulation and/or primary fibrinolysis were disclosed. An asymptomatic fall in mean arterial pressure (from 88.6 +/- 2.6 to 80.3 +/- 3.0 mmHg; p = 0.02) occurred after paracentesis and was still present 48 h after ascites reinfusion. Plasma renin activity significantly decreased at the end of the procedure, but was not associated with a proportional reduction of plasma aldosterone concentrations. Both variables returned to baseline values 48 h later. A significant increase in the glomerular filtration rate occurred just after the end of the procedure (from 50.4 +/- 9.1 to 73.1 +/- 23.5 ml/min; p < 0.05) and subsided 48 h later. In contrast, no significant changes in diuresis and renal sodium excretion were found. Complications due to volume overload and sepsis did not occur; in one case, spontaneous bacterial peritonitis developed 3 days after the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ascites apheresis, concentration and reinfusion for the treatment of massive or refractory ascites in cirrhosis. 800 9

Ascites is a common complication of chronic liver disease. Treatment of the underlying liver disease with modalities such as abstinence from alcohol in Laennec's cirrhosis, phlebotomy in hemochromatosis, copper removal in Wilson's disease, and steroids in autoimmune liver disease, can improve survival in many patients. In addition, therapy of ascites alleviates the symptoms and improves the quality of life of the patients, and probably decreases the incidence of life-threatening conditions including spontaneous bacterial peritonitis and hepatorenal syndrome. The mean survival rate at 2 years is approximately 50%. Precipitating factors such as gastrointestinal bleeding, nonsteroidal anti-inflammatory drugs and infections, should be identified, since most of them can be corrected. Most cirrhotics with ascites can be managed with a 'step-by-step' approach, including dietary salt restrictions, aldosterone antagonists, and loop diuretics. When tense or refractory ascites is present, large-volume paracentesis is safe and effective. Peritoneovenous shunting (i.e. Denver, LeVeen) is less frequently used because of perioperative morbidity and mortality, and thrombotic complications with occlusion of the stent. Reinfusion of concentrated ascites is of potential benefit and has been used in Europe. Transjugular intrahepatic portosystemic shunt (TIPS) is an alternative procedure performed by interventional radiologists that allows decompression of portal hypertension. In many cases, ascites is improved after TIPS, but long-term randomized trials for tense or refractory ascites comparing TIPS with standard therapy are not conclusive. Liver transplantation is the ultimate step for the treatment of ascites, providing the cure for the underlying liver disease as well. Transplantation is indicated when quality of life of the patient is impaired due to recurrent episodes of ascites, or in the presence of spontaneous bacterial peritonitis and hepatorenal syndrome.
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PMID:Treatment of ascites: old and new remedies. 886 22

The pathophysiology of circulatory and renal dysfunction in cirrhosis and the treatment of ascites and related conditions (hepatorenal syndrome and spontaneous bacterial peritonitis) have been research topics of major interest during the last two decades. However, many aspects of these problem remain unclear and will constitute major areas of investigation in the next millennium. The pathogenesis of sodium retention, the most prevalent renal function abnormality of cirrhosis, is only partially known. In approximately one third of patients with ascites, sodium retention occurs despite normal activity of the renin-aldosterone and sympathetic nervous systems and increased circulating plasma levels of natriuretic peptides and activity of the so-called natriuretic hormone. These patients present an impairment in circulatory function which, although less intense, is similar to that of patients with increased activity of the renin-aldosterone and sympathetic nervous systems, suggesting that antinatriuretic factors more sensitive to changes in circulatory function that these systems may be important in the pathogenesis of sodium retention in cirrhosis. The development of drugs that inhibit the tubular effect of antidiuretic hormone and increase renal water excretion without affecting urine solute excretion has opened a field of great interest for the management of water retention and dilutional hyponatremia in cirrhosis. Two families of drugs, the V2 vasopressin receptor antagonists and the kappa-opioid agonists, have been shown to improve free water clearance and correct dilutional hyponatremia in human and experimental cirrhosis with ascites. The first type of drugs blocks the tubular effect of antidiuretic hormone and the second inhibits antidiuretic hormone secretion by the neurohypophysis. On the other hand, two new treatments have also been proved to reverse hepatorenal syndrome in cirrhosis. The most interesting one is that based on the simultaneous administration of plasma volume expansion and vasoconstrictors. The second is transjugular intrahepatic porto-systemic shunt. The long-term administration (1-3 weeks) of analogs of vasopressin (ornipressin or terlipressin) or other vasoconstrictors together with plasma volume expansion with albumin is associated with a dramatic improvement in circulatory function and normalization of serum creatinine concentration in patients with severe hepatorenal syndrome. Of interest is the observation that in many of these patients, hepatorenal syndrome does not recur following discontinuation of the treatment, thus raising important questions about the mechanism by which hepatorenal syndrome follows a progressive course in most untreated cases. The pathogenesis of circulatory dysfunction in cirrhosis and the role of local mechanisms in the development of the splanchnic arteriolar vasodilation associated with portal hypertension will continue as important topics in clinical and basic research in Hepatology. Of special interest is the study of the mechanism by which circulatory function further deteriorates following complications such as severe bacterial infection or therapeutic interventions such as therapeutic paracentesis, and the adverse consequences of the impairment in circulatory function on renal and hepatic hemodynamics. Finally, although major advances have been made concerning the treatment and secondary prophylaxis of spontaneous bacterial peritonitis in cirrhosis, many aspects of the pathogenesis of this infection remain unclear. The mechanism of bacterial translocation and of the colonization of bacteria in the ascitic fluid are particularly important to design adequate measures for primary prophylaxis of this severe bacterial infection.
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PMID:Complications of cirrhosis. II. Renal and circulatory dysfunction. Lights and shadows in an important clinical problem. 1072 2

In cirrhosis of the liver, according to the peripheral arterial vasodilation hypothesis, relative underfilling of the arterial tree triggers a neurohumoral response (activation of renin-angiotensin-aldosterone system, sympathetic nervous system, nonosmotic release of vasopressin) aimed at restoring circulatory integrity by promoting renal sodium and water retention. Evidence has accumulated for a major role of increased vascular production of nitric oxide as the primary cause of arterial vasodilation in cirrhosis. Ascites is a common complication in cirrhosis. Treatment of ascites consists of a low salt diet with diuretics, and paracentesis together with plasma volume expanders in diuretic-resistant patients. Progression of cirrhosis may result in hepatorenal syndrome, a state of functional renal failure that carries an ominous prognosis. Orthotopic liver transplantation has remained the only curative treatment for patients with advanced liver disease; other modalities such as transjugular intrahepatic portosystemic shunt or vasopressin analogues may serve as a bridge to transplantation. Another complication of decompensated cirrhosis is spontaneous bacterial peritonitis, the incidence of which can be reduced by primary or secondary antibiotic prophylaxis by using orally active antibiotics.
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PMID:Update on peripheral arterial vasodilation, ascites and hepatorenal syndrome in cirrhosis. 1111 Jun 23

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

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

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

Ascites formation in patients with cirrhosis, portal hypertension, or both usually results from hyperdynamic circulatory dysfunction, where the retention of sodium and water is associated with the activation of the sympathetic and renin-angiotensin-aldosterone systems. The presence of ascites indicates the development of liver decompensation. Furthermore, complications seen in conjunction with ascites such as spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatic hydrothorax may result in increased morbidity and mortality. Although nonpharmacological, pharmacological, and surgical approaches have been introduced and clinically practiced, their therapeutic effects are still suboptimal or limited by their potential side effects, such as large-volume paracentesis-induced postparacentesis circulatory dysfunction. Herein, we discuss strategies to prevent and properly manage ascites-related complications, including a review of the literature and controlled studies that assess these strategies.
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PMID:Management of ascites in patients with liver cirrhosis: recent evidence and controversies. 2349 63


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