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

Infectious complications in cirrhotic patients can cause severe morbidity and mortality. Bacterial infections are estimated to cause up to 25% of deaths in cirrhotic patients. The most frequent are urinary tract infection, spontaneous bacterial peritonitis, respiratory tract infection, and bacteremia. It has been said that cirrhosis is the most common form of acquired immunodeficiency, exceeding even AIDS. The specific risk factors for infection in cirrhotic patients are low serum albumin, gastrointestinal bleeding, intensive care unit admission for any cause, and therapeutic endoscopy. Certain infectious agents are more virulent and more common in patients with liver disease. These include Vibrio, Campylobacter, Yersinia, Plesiomonas, Enterococcus, Aeromonas, Capnocytophaga, and Listeria species, as well as organisms from other species. Spontaneous bacterial peritonitis is a frequent, severe, life-threatening complication of patients with ascites. Current observations and recommendations regarding treatment and prophylaxis are reviewed. A brief synopsis of miscellaneous infections encountered in cirrhotic patients is also included.
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PMID:Infectious complications of cirrhosis. 1146 97

Our article concentrates on two acute states, which develop less dramatically but their after-effects may be very serious: Spontaneous bacterial peritonitis and Ogilvie's syndrome. Spontaneous bacterial peritonitis is a bacterial infection of the ascitic fluid without any intraperitoneal source of infection. Ascites is a condition of the disease but need not be clinically manifested. Spontaneous bacterial peritonitis comes usually during heavy hepatic impairment. Diagnosis can be set according: 1. Positive cultivation of ascitic fluid, 2. PMN levels higher than 250/mm3, 3. No infection, which may require a surgical intervention is apparent. Liver disease, which brings about the spontaneous bacterial peritonitis can be: 1. Chronic (e.g. alcoholic cirrhosis), 2. Subacute (e.g. alcoholic hepatitis), 3. Acute (e.g. fulminant hepatic failure). Mortality of this form of peritonitis can reach up to 46%. The most frequent etiological factor is alcohol and viral hepatitis, the most frequent agents are E. coli and Klebsiella pneumoniae. The disease is most effectively cured by cefalosporins of the third generation. With inadequate treatment, prognosis may be poor. Intestinal pseudoobstruction syndrome has clinical symptomatology of a serious impairment with ileus without signs of any mechanical intestinal obstruction. Syndrome can be classified according to its development: 1. Acute form--acute intestinal pseudoobstruction syndrome--Ogilvie's syndrome, 2. Chronic form--chronic intestinal pseudoobstruction syndrome. Pathogenic mechanism of the syndrome is not known. The disease is related to immobility, administration of some drugs, electrolyte imbalance and concomitant diseases (most frequently malignant tumors). Clinical symptomatology dominates nausea, vomiting, diffuse abdominal pain, constipation or diarrhoea. For diagnostics the first step should be termination of all medication, which could have causing affects, then taking native abdominal X-ray picture where gaseous intestinal distension can be prominent (coecum distended up to 9-12 cm). Identification of fluid surfaces is not usual. Endoscopic examination can exclude obstruction in the distal part of gut minimally. The most frequent complication is perforation of coecum. Pharmacological treatment relays on prokinetics. The basic intervention remains decompression by a rectal catheter or an effective coloscopic decompression with subsequent introduction of a cannula. Mortality of the disease fluctuates between 43 and 46%.
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PMID:[Acute states in gastroenterology: spontaneous bacterial peritonitis and the acute intestinal pseudoobstruction syndrome]. 1150 91

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

This report describes a case of spontaneous bacterial peritonitis in a patient with end stage liver disease in whom Leuconostoc spp. was isolated from blood and ascitic fluid. In common with several previously described patients with cultures positive for Leuconostoc from other body sites, this patient had recently received vancomycin. The antibiotic susceptibilities and mechanism of vancomycin resistance of this Gram-positive bacteria are reviewed.
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PMID:Spontaneous bacterial peritonitis and bacteremia due to Leuconostoc species in a patient with end-stage liver disease: a case report. 1167 26

Hepatocellular carcinoma is a primary tumor complicating liver disease, associated with cirrhosis in 80-90% of the cases. A kidney transplant recipient with chronic B and C viral hepatitis was admitted because of general malaise, renal function impairment and positive AST, ALT and alkaline phosphatase tests, and very high alpha-fetoprotein levels. Ascites, spontaneous bacterial peritonitis and renal failure developed. A CT showed multiple liver masses. Renal failure required hemodialysis. The patient died 17 days after the initial symptoms with hepatic encephalopathy. A postmortem liver biopsy confirmed the diagnosis of cirrhosis and hepatocellular carcinoma (HCC). This report, as well as a few others, shows the accelerated evolution of chronic viral hepatitis in kidney transplant patients and questions the convenience of kidney transplantation and the adequate follow up in chronic viral hepatitis.
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PMID:[Fatal acute hepatic failure with hepatocarcinoma presentation in a patient with renal transplant with asymptomatic chronic B and C hepatitis]. 1172 27

Spontaneous bacterial peritonitis is a serious complication of cirrhotic ascites, arising most frequently in those with advanced liver disease. Its development leads to a further reduction in the effective arterial blood volume, and it has a mortality rate equivalent to that of a variceal bleed. However, problems remain with regard to the identification and optimal treatment of spontaneous bacterial peritonitis. Several important studies and consensus documents on the condition have recently been published which aid in the identification of patients at risk and help to guide therapy. In this review, we discuss these publications and address the issues of diagnosis, treatment and both primary and secondary prophylaxis of spontaneous bacterial peritonitis in the light of recent data.
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PMID:Review article: spontaneous bacterial peritonitis--diagnosis, treatment and prevention. 1173 14

Ascites is the most common of the major complications of cirrhosis. The initial evaluation of a patient with ascites should include a history, physical evaluation and some investigations. Treatment should consist of treating the underlying liver disease, sodium restricted diet (2 g of Na+/day) and diuretics. This regimen is effective in 90% of patients. The treatment options for the diuretic resistant patients include serial therapeutic paracentesis, peritoneovenous shunting, TIPS and liver transplantation. The treatment and prophylaxis of spontaneous bacterial peritonitis which is a frequent and severe complication in cirrhotic patients with ascites is also important. The differential diagnosis with secondary bacterial peritonitis is essential because the latter usually does not resolve unless patients are surgically treated.
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PMID:[How I treat ... ascites]. 1182 32

BACKGROUND: The aim of the present study was to assess the clinical and laboratory characteristics, the course, and the factors influencing the hospital mortality and relapse rate of spontaneous bacterial peritonitis (SBP) in cirrhotic patients admitted in a single University Hospital in Greece. METHODS: The study comprises the evaluation of 81 cirrhotic patients who developed SBP during a 30-month period. RESULTS: The occurrence of SBP was independent of the etiology of liver disease and was symptomatic in 66/81 patients (82%). Encephalopathy, as presenting symptom, occurred mainly in Child C patients. Ascitic fluid culture was positive in 20 patients (25%); E. coli (60%) and Enterococcus faecalis (14%) were the most common bacteria isolated. Empirical treatment was effective in 94% of patients. Renal impairment was observed in 21 patients (26%), six of whom developed hepatorenal syndrome. Total mortality was 10% and was related to the existence of symptoms (P<0.01), ascetic fluid polymorphonuclear cell count (P<0.05), bilirubin levels (P<0.01), and kidney function at the beginning of the episode (P<0.01). The relapse rate was 24.6% and was related to the Child stage (P<0.01). CONCLUSIONS: SBP was asymptomatic in a substantial number of patients. Deterioration of renal function was frequently observed and was the main cause of death. The low (10%) in-hospital mortality seems to be related to earlier diagnosis and treatment. Relapse was associated with the severity of liver disease.
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PMID:Spontaneous bacterial peritonitis (SBP): clinical, laboratory, and prognostic features. A single-center experience. 1202 Jun 28

The hepatorenal syndrome is defined as functional renal failure in advanced chronic or acute liver disease with portal hypertension. Morphologic abnormalities of the kidneys are frequently absent and tubular function is preserved. Patients with the hepatorenal syndrome are characterized by progressive splanchnic and systemic vasodilation and decreased effective arterial blood volume. Compensatory activation of vasoconstrictory systems maintains systemic hemodynamic stability but causes progressive afferent renal vasoconstriction, leading to reduction of glomerular filtration rate. Renal failure may be rapidly progressive (type I hepatorenal syndrome, frequently associated with spontaneous bacterial peritonitis) or may develop more slowly (type II). Orthotopic liver transplantation is the best current treatment and leads to a gradual recovery of renal function in the vast majority of patients. Because mortality of type I hepatorenal syndrome is excessive, supportive treatment by vasoconstrictor drugs, transjugular intrahepatic portosystemic shunt, and renal replacement therapy has been investigated to achieve stability until transplantation. The definite role of these promising developments, however, is still uncertain, emphasizing the need for large prospective multicentric investigations.
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PMID:Hepatorenal syndrome. 1211 94

296 patients with first clinical symptoms of alcoholic liver disease were hospitalized in Probationary-Infectious Diseases Department in Kielce, between 1994-2000. In 52 (17.6%) of them, acute hepatic failure was diagnosed by detection of hepatic encephalopathy. Initial laboratory data of those patients who died (6.1%), and those who survived (11.5%) was compared. No statistically significant differences in analyzed parameters were found, except for significantly higher bilirubin concentration in the group of deceased. In both groups of patients, the frequency of hepatic failure complications, present at the admission to the hospital or those developed in the course of the disease, was also analyzed. The following complications were observed significantly more often in deceased: ascites, hepatorenal syndrome (HRS), spontaneous bacterial peritonitis (SBP), and gastrointestinal haemorrhage (GIH), while sepsis was similarly frequent in both groups.
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PMID:Acute hepatic failure in alcoholic liver disease. 1221 30


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