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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Occurrence of fever in a patient with liver cirrhosis should suggest the following: 1. Endotoxemia. Endotoxins are normally present in portal blood; in hepatic cirrhosis they are insufficiently cleared by the liver and their presence can be demonstrated in the systemic circulation by the "limulus test". Fever is one of the many consequences ascribed to the presence of endotoxins in the blood. 2. Infections. Cirrhosis and alcoholism (which often accompanies it) impair host defenses against bacteria and other organisms. Thus, infections are actually more frequent in hepatic cirrhosis as is shown by the example of bacterial endocarditis. Spontaneous bacterial peritonitis must be searched for carefully when ascites is present. 3. Alcoholic hepatitis. This diagnosis is established histologically. The usual symptoms, occurring with variable incidence, include anorexia, nausea and vomiting, abdominal pain, fever and jaundice in the presence of hepatomegaly, leukocytosis and an elevated SGOT. Differential diagnosis from obstructive jaundice and a severe prognosis without alcohol abstinence make early diagnosis mandatory. Its evolution in cirrhosis can be astonishingly rapid. In the absence of hepatic encephalopathy, corticosteroids do not appear to be recommended. 4. Hepatoma.
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PMID:[Fever and liver cirrhosis]. 22 38

The Budd-Chiari syndrome caused by occlusion of the major hepatic veins, often of unknown etiology, is typically characterized by massive ascites, hepatomegaly and abdominal pain due to intense congestion of the liver. The outcome has almost always been fatal. This report describes an evaluation of side-to-side portacaval shunt in dogs with experimental Budd-Chiari syndrome and in six patients with hepatic vein thrombosis. In the animal studies, side-to-side portacaval shunt was very effective in relieving massive ascites, hepatomegaly, hepatic congestion and portal hypertension produced by ligation of the hepatic veins. Only one of 24 dogs with side-to-side anastomosis reformed ascites, 67% of the animals survived until the study was concluded after one year, and liver biopsies showed reversal of the severe pathologic abnormalities. In contrast, all 20 control dogs subjected to a sham laparotomy, and all 20 dogs that underwent end-to-side portacaval shunt reformed massive ascites and died within six months with continued hepatic congestion and necrosis. All six patients with the Budd-Chiari syndrome due to hepatic vein occlusion had massive ascites (4.4-15.9 l), hepatomegaly, abdominal pain and disturbed liver function. In all six, angiography demonstrated occlusion of the hepatic veins with a patent inferior vena cava (IVC) and a normal IVC pressure, and liver biopsy showed intense centrilobular congestion and necrosis. The most valuable diagnostic study was angiography of the IVC and hepatic veins with pressure measurements. Side-to-side portacaval shunt was performed from four to 14 weeks after the onset of symptoms, and produced dramatic and sustained relief of ascites in five of the six patients during follow-up periods of from eight months to seven years. Liver function returned to normal, hepatosplenomegaly disappeared, none of the survivors developed portal-systemic encephalopathy, and follow-up liver biopsies showed disappearance of congestion and necrosis, but mild to moderate fibrosis. One patient died following an emergency IVC thrombectomy and portacaval shunt, which was undertaken when, during the course of his workup, his condition deteriorated suddenly because the thrombotic process extended from the hepatic veins into the IVC. The everpresent risk of this complication, and the dangers associated with delaying operation were emphasized by this case. It is concluded that side-to-side portacaval shunt, which decompresses the liver by converting the portal vein into an outflow tract, provides effective treatment of the Budd-Chiari syndrome when the occlusive process is confined to the hepatic veins.
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PMID:Treatment of Budd-Chiari syndrome by side-to-side portacaval shunt: experimental and clinical results. 69 34

Forty cirrhotic patients with non-advanced hepatic encephalopathy were randomly allocated into groups which were given orally either two capsules three times daily of a preparation of Enterococcus lactic acid bacteria strain SF68 or 30 ml lactulose four times daily. The patients were evaluated over a 10-day course of treatment and for 10 days post-treatment. The Enterococcus SF68 preparation proved to be as effective as lactulose in lowering blood ammonia, and in improving mental state and psychometric performance. Moreover, the effects of Enterococcus SF68, contrary to that of lactulose, persisted longer after treatment withdrawal. Some patients reported diarrhoea and abdominal pain with lactulose. Lactulose is a standard therapy in the treatment of patients with hepatic encephalopathy. In this study, however, the use of the Enterococcus SF68 preparation was shown to offer advantages over lactulose in these patients.
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PMID:Enterococcus lactic acid bacteria strain SF68 and lactulose in hepatic encephalopathy: a controlled study. 312 77

During a two-year period, 30 patients with spontaneous bacterial peritonitis were documented. All patients had ascites and 70% were alcoholic cirrhosis. Fever and abdominal pain were the most frequent presenting manifestations (96.66% and 76.66% respectively). Triads of fever, abdominal pain and rebound tenderness were found in 40%. A third had hepatic encephalopathy and decreased bowel sound. Ascitic fluid was transudate. Positive ascitic fluid culture and blood culture were obtained in 40% and 59% respectively, and three quarters were due to gram negative enteric bacilli. There was no significant statistic correlation among the result of ascitic fluid gram's stain and ascitic fluid culture, and of ascitic fluid culture and blood culture. The clinical and laboratory findings of patients with positive and negative ascitic fluid culture were similar. Significant increased mortality was found in patients who had hepatic encephalopathy, hypotension, increased bilirubin level and serum creatinine. The over all mortality was 33.33%. We recommend abdominal paracentesis in every cirrhotic patients with ascites who were admitted into hospital.
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PMID:Spontaneous bacterial peritonitis in cirrhotics: clinical and ascitic fluid findings. 353 Jan 6

The authors analyse 115 cases of acute fatty liver of pregnancy, proven histologically. Characteristics of the condition is the finding of central nuclei in the hepatocytes containing microvesicular droplets. The disease occurs more frequently in primiparous women (54 per cent) and usually occurs in the third trimester of the pregnancy. A pre-icteric phase usually precedes the jaundice and during that time there is usually vomiting and/or nausa with abdominal pain or anarexia. In 92 per cent of case there is transient loss of consciousness with hepatic encephalopathy. Further tests show that there is more defective liver function than would be expected from the extent of cell lysis; and there is defective renal function. The worst complications are intestinal haemorrhages (48 per cent of cases)--genital bleeding (43 per cent of cases)--shock--diffuse intravascular coagulation and complications associated with coma. Maternal mortality at present runs at 25 per cent and fetal mortality at 60 per cent. The condition does not recur. Early evacuation of the uterus is recommended by most authors and does probably improve the outlook. The various hypotheses concerning the aetiology are discussed.
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PMID:[Acute fatty liver of pregnancy]. 354 2

Acute fatty liver of pregnancy is a rare clinical entity unique to pregnancy that can lead to hepatic failure and encephalopathy and, if the diagnosis is delayed, to death for the baby and the mother. The characteristic histological picture demonstrates microvesicular fatty infiltration of hepatocytes. Acute fatty liver of pregnancy is a disease of the third trimester of pregnancy. The most significant clinical findings are nausea or vomiting, abdominal pain, jaundice, hepatic encephalopathy, increased transaminase levels, decreased platelet count, increased prothrombin time, and renal failure. Hypertension and proteinuria are common. Liver biopsy is not always necessary for diagnosis but may be useful in atypical cases. The primary therapy is early delivery and supportive care. Both the obstetric team and the medical consultants must have a high index of suspicion for this disease because early delivery is lifesaving and has transformed the prognosis for the mother and the baby. Collaboration between obstetricians and gastroenterologists is necessary to make the diagnosis and also to improve our understanding of this disease of unknown etiology.
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PMID:Acute fatty liver of pregnancy: the hepatologist's view. 805 22

Budd Chiari syndrome is a rare disorder resulting from occlusion of hepatic venous drainage by hepatic vein thrombosis or by a membranous web in the inferior vena cava. In western countries the commonest causes are myeloproliferative disorders and hypercoagulable states. Presentation may be acute with rapid accumulation of ascites and hepatic failure, or subacute with symptoms developing over a few months. A chronic progressive form has also been described. On presentation there is usually abdominal pain, ascites, and hepatosplenomegaly; hepatic encephalopathy is found in about a third. Noninvasive, ultrasound-Doppler is recommended in diagnosis, and has a high correlation with hepatic venography. Liver biopsy is required for therapeutic decisions. Those with advanced hepatic failure or severe fibrosis on liver biopsy are referred for hepatic transplantation. When biopsy shows only hepatic congestion and inflammatory infiltrates, portosystemic shunting is recommended. We present a 61-year-old woman with ascites and hepatosplenomegaly that had developed over the courses of a few months. Budd-Chiari syndrome with chronic myelofibrosis and congenital protein C deficiency were diagnosed. Portosystemic shunt was performed but death from sepsis followed shortly.
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PMID:[Budd-Chiari syndrome]. 933 72

The clinicopathological features of 50 cases of equine hepatic disease were reviewed. There was a wide range of clinical signs and at least 50 per cent of the animals exhibited either dull demeanour, anorexia, abdominal pain, cerebral dysfunction and/or weight loss. Life-threatening complications of hepatic failure recorded were: gastric impaction in 10 cases, bilateral laryngeal paralysis in seven cases and coagulopathy in five cases. All the cases had high activities of gamma-glutamyl transferase (GGT) and most had high activities of glutamate dehydrogenase (GLDH) and high concentrations of bile acids. Fewer of the horses had abnormal concentrations of bilirubin, albumin and globulin. The horses that were euthanased or died had significantly higher concentrations of GGT, GLDH and bile acids than the survivors. There were biochemical data for 18 cases with signs of hepatic encephalopathy, all of them had plasma ammonia levels greater than 90 micromol/litre but this was not significantly correlated with the clinical severity of the condition. Half of the cases with hepatic encephalopathy were hyperglycaemic, none was hypoglycaemic, and none had abnormally low levels of plasma urea.
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PMID:Clinicopathological features of equine primary hepatic disease: a review of 50 cases. 1046 31

We reviewed the current techniques and published results of balloon-occluded retrograde transvenous obliteration (B-RTO) for gastric varices (GV) and hepatic encephalopathy. The portal hemodynamics of gastric varices were classified into three types according to their feeding vessels, and the development of collateral veins under balloon occlusion of gastro-renal shunt was classified into five grades. The main draining veins of gastric varices were gastro-renal and gastro-inferior phrenic shunts. Preprocedural diagnosis of portal hemodynamics is important in selecting the technique for B-RTO. The rate of disappearance or marked reduction of GV was 98%, and the rate of recurrence of GV was 2%. Hepatic encephalopathy due to gastro-renal shunt improved markedly. In contrast, esophageal varices were aggravated at rates of 10% to 62.5% by the post-procedural elevation of portal pressure. Common adverse effects were hemoglobinuria, abdominal pain, and low-grade fever, but ascites and pleural effusion were also reported. Severe complications such as cardiogenic shock, atrial fibrillation, and pulmonary embolism were reported. We await technical improvements and further indications for this procedure.
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PMID:[Balloon-occluded retrograde transvenous obliteration (B-RTO) for portal hypertension]. 1092 Dec 94

Hospitalized patients with cirrhosis are at increased risk of developing bacterial infections, the most common being spontaneous bacterial peritonitis (SBP) and urinary tract infections. Independent predictors of the development of bacterial infections in hospitalized cirrhotic patients are poor liver synthetic function and admission for gastrointestinal hemorrhage. Short term (seven-day) prophylaxis with norfloxacin reduces the rate of infections and improves survival and should therefore be administered to all patients with cirrhosis and variceal hemorrhage. Cirrhotic patients who develop abdominal pain, tenderness, fever, renal failure or hepatic encephalopathy should undergo diagnostic paracentesis, and those who meet the criterion for SBP (eg, an ascites neutrophil count greater than 250/mm3) should receive antibiotics, preferably a third-generation cephalosporin. In addition to antibiotic therapy, albumin infusions have been shown to reduce the risk of renal failure and mortality in patients with SBP, particularly in those with renal dysfunction and hyperbilirubinemia at the time of diagnosis. Patients who recover from an episode of SBP should be given long term prophylaxis with norfloxacin and should be assessed for liver transplantation.
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PMID:Bacterial infections in cirrhosis. 1519 Mar 98


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