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

We analyzed the clinical and bacteriologic features of 12 episodes of spontaneous bacterial peritonitis (SBP) in 11 children (four boys, median age 5.5 years) with chronic liver disease. All patients had cirrhosis and ascites; four had hypersplenism, and one was asplenic. Symptoms included increasing abdominal distention, pyrexia, abdominal pain, gastrointestinal disturbance, and encephalopathy. Nine had rebound tenderness on abdominal palpation, and 12 had reduced bowel sounds. The most frequent organisms isolated from culture of ascitic fluid were Streptococcus pneumoniae (nine). Klebsiella (two), and Haemophilus influenzae (one); blood cultures grew identical organisms in nine. Seven patients died despite intensive antibiotic therapy. In the 3 months prior to onset of SBP, defective yeast opsonization and reduced serum concentration of C4 were found in all nine children tested; eight had reduced concentration of C3. Functional deficiency of all complement components was present in four tested within 1 to 5 months of the onset. In contrast, only eight of 59 cirrhotic children without SBP had low C3, and eight had defective yeast opsonization, although 35 had low C4 values. Four of the patients with SBP and low C3 and C4 concentrations had normal concentrations at the time of diagnosis of liver disease 2 to 5 years previously. Opsonization of type III pneumococci was reduced in sera from three patients who subsequently developed pneumococcal peritonitis. The incidence of SBP in children with chronic liver disease is similar to that in adults, as are the clinical features. Our observations suggest that complement deficiency induced by chronic liver disease may be important in the pathogenesis of SBP.
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PMID:Spontaneous bacterial peritonitis in children with chronic liver disease: clinical features and etiologic factors. 399 46

TIPSS is a new therapeutic modality for decompressing the portal tree and its use has broadened in the last five years. From February 1993 to August 1994 a prospective study was performed to evaluate its efficacy and safety. Nineteen cirrhotic patients (Child A-5, B-10, and C-4) with a TIPSS placed were included. The mean follow-up was 7.2 months. The indication was therapy of esophageal variceal bleeding in 18 patients (acutely in 8 and elective in 10 patients) and refractory ascites in one. In all cases could the "stent" be placed and the portocaval gradient decreased from 22.8 +/- 3.71 to 9.3 +/- 2.27 mmHg. In the first thirty days the mortality rate was 10.5%, with the following complications: two portal thromboses, two acute non-lithiasic cholecystitis, one hemoperitoneum, one spontaneous bacterial peritonitis, and one hepatic encephalopathy. During the follow-up period two patients developed hemorrhagic relapses and two additional patients subclinical encephalopathy. TIPSS dysfunction was observed in 57.8%.
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PMID:[The clinical efficacy and complications of the transjugular intrahepatic portosystemic shunt-stent]. 748 Oct 3

The spectrum of liver disease is extremely wide, with many of the underlying disorders having acute and chronic presentations. Most of the underlying pathogenetic mechanisms are accounted for by autoimmune disease, viral infection and toxic insult. The management strategy of any liver disease is a combination of treating the symptoms and complications that arise, as well as drug therapies relevant to the specific underlying diagnosis. Encephalopathy, ascites, spontaneous bacterial peritonitis, variceal bleeding and pruritus are the main complications at which drug therapy is directed, although in some cases it represents only 1 aspect of the overall management. Drug therapy per se is largely ineffective in acute liver failure with the possible exception of acetylcysteine, but many drugs are used in the management of the constituent components of this complex medical emergency. Treatments for specific liver conditions are expanding, especially in the areas of autoimmune and viral disease. The increasing availability and success of liver transplantation has tended to change the emphasis of management, and it is often not appropriate to exhaust the treatment options before referring the patient for transplantation. A comprehensive review of all liver disease is beyond the scope of this article, but hopefully the important principles of management and commonly occurring clinical decisions are discussed.
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PMID:Hepatic disorders. Features and appropriate management. 770 18

Almost 10% of patients with cirrhosis and ascites develop intractable ascites. When large-volume paracentesis fails to relieve ascites, patients may be submitted to one of the three following surgical options: portosystemic shunting, peritoneovenous shunting, or liver transplantation. Portosystemic shunting is efficient in clearing ascites, but it is associated with a high rate of encephalopathy and liver failure. The indications for portosystemic shunting are therefore limited for treatment of intractable ascites and should be performed only in patients with good liver function in whom all other treatments failed. Peritoneovenous shunting has been associated with a high rate of early complications and valve obstruction. Improvements in perioperative care and in the material used have greatly reduced the operative risks and increased the patency rate. Mortality remains high in patients with severe liver failure or with a history of spontaneous bacterial peritonitis or variceal bleeding. Peritoneovenous shunting should not be done when these risk factors are present. In the absence of such risk factors, peritoneovenous shunting is a good procedure and may provide definitive relief of ascites and long-term survival in more than 50% of the operated patients. In patients with poor risk factors liver transplantation may be preferable, and the onset of intractable ascites in a patient with a severely compromised liver should trigger the indication of liver replacement.
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PMID:Role of surgical therapy in management of intractable ascites. 804 29

Ascites is a manifestation of cirrhosis-induced portal hypertension. Pathogenesis is the result of a complex interaction of mechanical, humoral and neural events. Impaired excretion of sodium by the kidney is a hallmark of ascites, which is addressed by many of the available treatment options. Ascites contributes significantly to the morbidity and mortality rates of cirrhosis by increasing the likelihood of such fatal complications as variceal bleeding, hepatorenal syndrome and spontaneous bacterial peritonitis. Most ascitic patients respond to conservative or medical treatment. Five to 10 percent of the patients are refractory and may be candidates for surgical treatment. Peritoneovenous shunting is effective, and while safety is improved by following certain guidelines, its impact on survival is not clear. Portacaval shunting is also safe and effective. The use is accompanied by a prohibitively high morbidity rate because of encephalopathy, which limits its application despite what seems to be a significant impact on survival.
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PMID:Pathophysiologic factors and management of ascites. 842 10

Seven patients with decompensated posthepatitis B cirrhosis were treated with low doses of interferon alpha. The initial plasma level of HBV-DNA ranged from 3.0 to 189.3 pg/ml, and that of ALT from 37 to 156 IU/l. Liver biopsies demonstrated ongoing piecemeal necrosis. In sera of all but one patient, HBV-DNA became undetectable by hybridisation techniques within 10 to 28 weeks. Plasma HBeAg became negative in four and HBe-antibodies positive in three patients. Serum transaminase levels showed a marked initial rise 3 to 13 weeks after onset of therapy; they dropped to normal values later in all except one patient. Therapy was initiated at 1 MU (million units) three times a week for 2 weeks and was increased to 2.5 MU for 16 weeks. Later, this dosage was raised to 5 MU three times a week in some patients. Complications included variceal haemorrhage, aggravation of ascites or of encephalopathy, development of pneumonia, recurrence of spontaneous bacterial peritonitis or of gastric ulcer bleeding. One year after stopping the therapy, three patients are well and without any feature of liver decompensation. Three patients died before they could undergo a liver transplantation. In one patient treatment was interrupted because of marked exacerbation of liver cell necrosis. It thus seems possible to suppress HBeAg and HBV-DNA in patients with decompensated cirrhosis. This is important to prepare them for possible liver transplantation. Interferon should be initiated at low doses and the patients be very carefully monitored. Prophylactic therapy for bacterial peritonitis and for variceal haemorrhage is warranted.
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PMID:Treatment of decompensated viral hepatitis B-induced cirrhosis with low doses of interferon alpha. 845 21

Twenty two patients of subacute hepatic failure (SAHF), diagnosed when jaundice progressed for more than 8 weeks with appearance of ascites, with or without encephalopathy, along with biochemical evidence of hepatocellular damage, were studied. The male and female ratio was 4.5:1 and majority (45.4%) of cases were between the age group of 41-50. The mean biochemical values were: S.bilirubin; 9.2 +/- 3.8 mg/dl SGOT; 94.4 +/- 25.0 I.U./lit., SGPT; 107.8 +/- 32.7 I.U./lit., S.Protein; 5.2 +/- 3.5 secs. Ascitic fluid analysis showed transudate in 16 (72.7%) and exudate in 6 (27.2%) patients. Bacterial peritonitis was found in 5 (22.7%) patients. Liver biopsy showed bridging and submassive necrosis. The complications developed in the hospital were: renal failure (36.3%), infection (27.2%), G.I. bleeding (18.1%) and encephalopathy (13.6%). The mortality was (86.3%). Out of 3 (13.6%) patients who survived, only two recovered completely and one had biochemical evidence of hepatocellular necrosis after 6 months of follow up.
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PMID:Clinicopathological profile of subacute hepatic failure. 928 51

Cirrhosis of the liver results from a variety of mechanisms that cause progressive hepatic injury. It is the sixth leading cause of death in all patients between the ages of 35 and 55. This study attempts to correlate the morbidity and mortality of spontaneous bacterial peritonitis in liver failure patients to numerous etiologic and clinical variables. A retrospective review of 26 patients with spontaneous bacterial peritonitis associated with chronic liver disease was performed in a university hospital. Demographics (age and gender), clinical variables (etiology of liver failure, Child's classification, prior history of ascites, fever, abdominal pain, encephalopathy, and upper gastrointestinal hemorrhage), and laboratory variables (ascitic polymorphonuclearcyte count and cultures, serum albumin, bilirubin, creatinine, and prothrombin time) were studied. All of the patients had Child's C liver disease. Mortality rate was 46 per cent. Alcohol (46%) and hepatitis (30%) were the most common etiologies. Escherichia coli and Klebsiella pneumoniae were the most common culture isolates. All of the infections were monomicrobial. The only significant predictor of mortality (P < 0.05) in this study was the peritoneal fluid polymorphonuclear (PMN) cell count. PMN count >1000 PMN/mm3 was associated with a mortality of 88 per cent. Few patients with spontaneous bacterial peritonitis are ultimately transplanted.
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PMID:Spontaneous bacterial peritonitis in liver failure. 984 34

Subacute hepatitis and liver failure occurred in a 40-yr-old woman following a 1-month course of treatment with the nonsteroidal anti-inflammatory drug bromfenac. Serologies for hepatitis A, B, and C were negative, as were antinuclear antibodies and ceruloplasmin. A transjugular liver biopsy demonstrated submassive hepatic necrosis. The clinical course was complicated by encephalopathy, fluid retention, and spontaneous bacterial peritonitis, prompting consideration for liver transplantation. With supportive measures, jaundice and fluid retention resolved over a 3-month period. We conclude that prolonged use of bromfenac was the etiological agent in this case, and that this drug can cause severe hepatotoxicity resulting in liver failure.
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PMID:Severe hepatotoxicity associated with bromfenac sodium. 1023 25

Increased intestinal permeability has for many years been implicated as a possible contributory factor in the development of encephalopathy and spontaneous bacterial peritonitis (SBP) seen in patients with cirrhosis. The majority of studies indicate that there is an increase in small intestinal permeability in cirrhotic patients and there is also evidence of an increase in patients with acute liver failure. The cause of these changes is unknown and whether they are related to the development of SBP and encephalopathy is unclear.
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PMID:Intestinal permeability and liver disease. 1032 58


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