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

A cirrhotic patient with ascites was apparently well managed with diuretics and salt and water restriction for 9 months. A spontaneous bacterial peritonitis (SBP) developed and the patient finally died following septic shock. There were enough findings indicating that SBP in this case had been existing silently for some time. During this period the only apparent manifestation of this complication was a cutaneous pigmentation on the abdomen. It is suggested that pigmentation may be incuded among other presentations of this frequently silent process.
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PMID:Cutaneous pigmentation: a probable sign of spontaneous bacterial peritonitis. 699 87

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

Hepatic hydrothorax is the accumulation of ascitic fluid in the pleural space and requires the same treatment as ascites: salt restriction, diuretics, and paracentesis. Refractory hydrothorax appears when there is no response to those measures and its management is not well established. Videothoracoscopy is a promising therapy that permits the detection and closure of diaphragmatic defects, and when used with pleurodesis resulted in long-lasting control of hydrothorax in six of eight patients without appreciable morbidity. The transjugular intrahepatic portosystemic shunt is an effective therapy in more than 75% of refractory hydrothorax cases. Hepatic encephalopathy and worsening of liver function in some patients are the main adverse effects. Spontaneous bacterial empyema, the infection of a hydrothorax, was reported in 13% of 120 cirrhotic patients with hydrothorax. Forty percent of the episodes of spontaneous bacterial empyema were not associated with spontaneous bacterial peritonitis. The sensibility of pleural fluid culture improves inoculating pleural fluid into a blood culture bottle at the bedside. Patients with refractory hydrothorax or those having an episode of spontaneous bacterial empyema should be considered candidates for liver transplantation.
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PMID:Hepatic hydrothorax. 1081 41

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

Several age-related changes occur in the structure and functions of the liver. The volume of the liver decreases, despite an increase in the size of hepatocytes, suggesting loss of liver cells. There are decreases in hepatic blood flow, the synthesis of urea and cholesterol, and the metabolism of drugs. Moreover, the regenerative capacity of liver becomes less efficient. Certain caveats are important when treating older patients with liver disease. Strict dietary restrictions, such as a low protein diet, should be avoided in the elderly (unless the patient is encephalopathic) because these patients are often undernourished to start with. Similarly, strict salt restriction should be enforced with caution, since it makes food less palatable and may take away what little desire such patients have to eat. Diuretic doses should be adjusted carefully because of greater risks of azotaemia and electrolyte disturbances in the elderly. Extra vigilance should be exercised in the early detection of infections that are more likely to occur in patients with cirrhosis. For example, spontaneous bacterial peritonitis can be missed in the elderly because of poor systemic (fever, abdominal tenderness) and laboratory responses (leucocytosis). In patients presenting with acute variceal bleeding, it is better to err on the side of underhydration than overhydration because of the risk of congestive heart failure. Vasopressin should be avoided in the elderly, since this drug has a high probability of precipitating an ischaemic event. Older patients do not tolerate beta-blockers as well as younger individuals and may require other treatment strategies for the prevention of variceal rebleeding episodes. Hepatic encephalopathy, especially the milder form, needs careful assessment because it can be easily confused with senile dementia syndromes. Cirrhosis is a premalignant condition and patients are at increased risk of developing hepatocellular carcinoma (HCC), a tumour seen predominantly in the elderly. All patients with cirrhosis should be maintained on a lifelong screening programme consisting of a 6-monthly assessment of alpha-fetoprotein and an imaging study, since early detection provides the only hope for cure of HCC. The only definitive treatment of cirrhosis is liver transplantation. Advanced age is not a contraindication to transplantation, and survival in older patients (aged >60 years) is comparable to that in younger individuals.
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PMID:Drug treatment of the complications of cirrhosis in the older adult. 1158 44

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 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

Ascites is one of the major complications of liver cirrhosis and is associated with a poor prognosis. It is important to distinguish noncirrhotic from cirrhotic causes of ascites to guide therapy in patients with noncirrhotic ascites. Mild to moderate ascites is treated by salt restriction and diuretic therapy. The diuretic of choice is spironolactone. A combination treatment with furosemide might be necessary in patients who do not respond to spironolactone alone. Tense ascites is treated by paracentesis, followed by albumin infusion and diuretic therapy. Treatment options for refractory ascites include repeated paracentesis and transjugular intrahepatic portosystemic shunt placement in patients with a preserved liver function. Potential complications of ascites are spontaneous bacterial peritonitis (SBP) and hepatorenal syndrome (HRS). SBP is diagnosed by an ascitic neutrophil count > 250 cells/mm(3) and is treated with antibiotics. Patients who survive a first episode of SBP or with a low protein concentration in the ascitic fluid require an antibiotic prophylaxis. The prognosis of untreated HRS type 1 is grave. Treatment consists of a combination of terlipressin and albumin. Hemodialysis might serve in selected patients as a bridging therapy to liver transplantation. Liver transplantation should be considered in all patients with ascites and liver cirrhosis.
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PMID:Diagnosis and therapy of ascites in liver cirrhosis. 2252 2

Cirrhosis is the 12th leading cause of death in the United States. It accounted for 29,165 deaths in 2007, with a mortality rate of 9.7 per 100,000 persons. Alcohol abuse and viral hepatitis are the most common causes of cirrhosis, although nonalcoholic fatty liver disease is emerging as an increasingly important cause. Primary care physicians share responsibility with specialists in managing the most common complications of the disease, screening for hepatocellular carcinoma, and preparing patients for referral to a transplant center. Patients with cirrhosis should be screened for hepatocellular carcinoma with imaging studies every six to 12 months. Causes of hepatic encephalopathy include constipation, infection, gastrointestinal bleeding, certain medications, electrolyte imbalances, and noncompliance with medical therapy. These should be sought and managed before instituting the use of lactulose or rifaximin, which is aimed at reducing serum ammonia levels. Ascites should be treated initially with salt restriction and diuresis. Patients with acute episodes of gastrointestinal bleeding should be monitored in an intensive care unit, and should have endoscopy performed within 24 hours. Physicians should also be vigilant for spontaneous bacterial peritonitis. Treating alcohol abuse, screening for viral hepatitis, and controlling risk factors for nonalcoholic fatty liver disease are mechanisms by which the primary care physician can reduce the incidence of cirrhosis.
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PMID:Cirrhosis: diagnosis, management, and prevention. 2223 Feb 70

Ascites is a common complication of liver cirrhosis and is associated with a poor prognosis. The main pathophysiology is an increased portal pressure with compensatory activation of neurohumoral systems. A patient history, proper physical exam and adequate examination of ascitic fluid will reveal the aetiology in most cases. Complications such as spontaneous bacterial peritonitis and thrombosis of hepatic vessel should be excluded in cases of first episode of ascites or deterioration of ascites. A moderate salt restriction and treatment with diuretics is the mainstay of treatment. Potentially nephrotoxic drugs such as NSAID and ACE inhibitors should be avoided in patients with cirrhosis.
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PMID:[Ascites is usually caused by an underlying liver cirrhosis. Salt restriction and diuretics is the basis for treatment]. 2697 10


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