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

Patients with liver cirrhosis and ascites suffer from spontaneous bacterial peritonitis (SBP) in up to 25%. The typical clinical signs are abdominal pain with tenderness and fever. 30% have no signs of peritonitis. Then clinical worsening, encephalopathy, rising serum creatinine levels, and therapy resistant ascites may be the only clinical features. SBP must be differentiated from bacterascites and culture negative neutrocytic ascites by the polymorphonuclear neutrophil (PMN) count in the ascites and the presence of positive culture results, which has prognostic implications. Gram negative rods from the colon play an important etiological role in SBP. Gastrointestinal bleeding, lack of serum complement, a low ascites protein and the extent of intrahepatic shunts predispose to SBP. Then, prophylaxis with the comparable drugs neomycin and norfloxacin is indicated. Coexisting encephalopathy has to be treated by the therefore effective neomycin. Otherwise, norfloxacin is the drug of choice because of better acceptance and lower costs. Chemical parameters of the ascites (pH value less than 7.4; LDH and lactate greater than serum levels; glucose less than 50 mg%) help to assess the severity of peritonitis. The course of ascitic PMN under therapy and the time of persisting positive cultures can discriminate SBP from secondary peritonitis. Antibiotics of choice are amoxicillin-clavulanic acid and cefotaxime. Short course therapy (5 days) is a effective as long course therapy (10 days). Today SBP is no more life-threatening because diagnosis, prophylaxis and therapy have improved. However, complication rate of patients with liver cirrhosis and ascites has not changed.
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PMID:[Spontaneous bacterial peritonitis]. 141 38

To assess the prevalence of spontaneous bacterial peritonitis (SBP), ascitic fluid cell count, and ascitic fluid culture by conventional method and by bedside inoculation in blood culture bottles were performed in 31 consecutive patients of liver cirrhosis. Seven (22.58%) patients had ascitic fluid polymorphonuclear count (PMN) more than 500/mm. Ascitic fluid culture by conventional method was negative in all the patients, while in 4 patients culture was positive by bedside inoculation method. Six of 7 patients with SBP or its variant were in Child class C. Clinical features in these patients were abdominal pain (5 patients), fever (4) and encephalopathy (2); serum bilirubin level was 6.8 +/- 5.5 mg/dl, serum albumin 1.98 +/- 0.2 g/dl, prothrombin index 59.8 +/- 12.2%, ascitic fluid protein 0.78 +/- 0.24 g/dl. Three of 7 patients with SBP or its variant expired during hospital stay; the other 4 patients recovered after appropriate antibiotic therapy. We conclude that SBP is a serious complication in patients of liver cirrhosis with ascites. Ascitic fluid PMN count and bedside inoculation of blood culture bottles with ascitic fluid are sensitive indicators of SBP. Hence they should be performed routinely for early detection of SBP.
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PMID:Prevalence of spontaneous bacterial peritonitis. 145 29

This is a retrospective study of 35 patients with spontaneous bacterial peritonitis and liver cirrhosis identified between 1981 and 1989. The mean age of all patients was 44 years, with a range of 16 to 68. Criteria for spontaneous bacterial peritonitis included either a positive ascites culture with a polymorphonuclear cell concentration greater than 250 cells per mm3 (18 cases) or a negative ascitic fluid culture with a polymorphonuclear cell count greater than 500 cells per mm3 and no evident intra-abdominal source of infection (17 cases). Twenty-one patients were male and 14 female. The most frequent presenting symptoms were abdominal pain and fever, noted in 20 (57%) and 19 (54%) patients, respectively, while 5 patients (14%) were completely asymptomatic. The overall mortality in this series was 54% (19 of 35 patients). The presence of encephalopathy or renal insufficiency was associated with a high mortality rate (73% and 87%, respectively). Encephalopathy was present in 67% of the non-survivors, but in only 25% of the survivors (p < 0.0025); likewise, renal failure was observed in 68% of the non-survivors, but in only 12.5% of those who survived (p < 0.001). The use of newer-generation cephalosporins and penicillins led to a diminished mortality (42%) as compared with that (64%) observed in patients treated with conventional antibiotic regimens.
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PMID:Spontaneous bacterial peritonitis in cirrhosis: clinical and laboratory features, survival and prognostic indicators. 148 64

Twenty-four cases of dengue haemorrhagic fever/dengue shock syndrome were studied in Delhi in the months of September and October, 1988. The majority of these cases were boys aged 6-10 years. Classical symptoms of dengue (fever, headache, aesthesia, myalgia) occurred in all the patients. Digestive symptoms (nausea, vomiting, anorexia, abdominal pain and hepatomegaly) were also common. Haemorrhagic manifestations were present in 41.7% of the cases. Of these, 90% had gastrointestinal haemorrhages. Shock occurred in 17 cases (70.8%). Thrombocytopenia and prolongation of coagulation profile were found in 62.5% of cases. Three patients (12.5%) who presented with encephalopathy died. The other 21 patients recovered after an average period of 2-8 days.
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PMID:An epidemic of dengue haemorrhagic fever and dengue shock syndrome in Delhi: a clinical study. 170 58

An outbreak of food poisoning resulting in 13 deaths in children occurred in Malaysia during the Chinese Festival of the Nine-Emperor Gods in 1988. The offending food was a Chinese noodle called 'Loh See Fun' (LSF). The source was traced to a factory where a banned food preservative was added to make the LSF. The food poisoning was attributable to aflatoxins and boric acid. The clinical features included vomiting, pyrexia, diarrhoea, abdominal pain, anorexia, giddiness, seizures, and eventual coma. Initially, many presented with a Reye-like syndrome. Eleven post-mortem examinations were performed. The pathological findings included extensive coagulative necrosis of the liver with proliferative 'ductal/ductular metaplasia of the hepatocytes'. Giant cell formation, central vein sclerosis, bile stasis, and steatosis were also noted. There was presence of acute tubular necrosis, superficial upper gastrointestinal erosions, and ensuing encephalopathy. The eventual cause of death is acute hepatic and renal failure.
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PMID:An outbreak of aflatoxicosis and boric acid poisoning in Malaysia: a clinicopathological study. 189 May 47

We report a 14-year-old boy with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) who presented repeated episodes of abdominal pain and vomiting since the age of 8 years. In addition, he developed strokelike episodes with myoclonic seizures and transient hemiplegia on three occasions. At the age of 14-1/12-years, he also developed epilepsia partialis continua persisting for 10 days, which was associated with myoclonic seizures synchronized with spike discharges at the right central area. Laboratory examination disclosed increased levels of lactate and pyruvate in serum and CSF and low density areas in the bilateral temporal regions on CT scan. Muscle biopsy showed scattered ragged-red fibers. The enzyme activities (pyruvate dehydrogenase complex, pyruvate carboxylase, phosphoenol pyruvate carboxykinase, and cytochrome c oxidase) and the rates of decarboxylation of [3-14C]pyruvate in cultured skin fibroblasts were within normal ranges.
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PMID:[A case with MELAS associated with epilepsia partialis continua]. 189 96

Spontaneous bacterial peritonitis rarely complicates high-protein (greater than 2.5 g/dl) ascites. The relatively high endogenous antimicrobial (opsonic) activity of the ascitic fluid in this setting appears to protect the patient from infection. We report two patients with high-protein, noncirrhotic ascites complicated by spontaneous peritonitis due to Salmonella species. One patient had ascites due to heart failure, whereas the other patient's ascites was due to peritoneal carcinomatosis. The ascitic fluid total protein concentrations were 3.1 and 3.3 g/dl, respectively, and the opsonic activity of the ascitic fluid specimens were 2.03 and 2.00 log kill, respectively, indicating a high degree of bacterial killing. We hypothesize that the virulence of the Salmonella species was able to overcome the high opsonic activity in the ascitic fluid, resulting in infection in these two patients. Fever, abdominal pain, or encephalopathy in a patient with high-protein ascites may suggest the presence of an unusual organism causing spontaneous bacterial peritonitis.
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PMID:Spontaneous Salmonella infection of high-protein noncirrhotic ascites. 220 53

Biliary hemorrhage may occur in a variety of clinical settings, but spontaneous hemobilia has not been reported from a cirrhotic liver. We describe a case of major hepatic hemobilia in a patient with cirrhosis and no history of trauma. A 50-year-old woman had abdominal pain, melena, and profound anemia. An extensive workup did not show the site of bleeding but did show a mass in the gallbladder. Cholecystectomy was performed, and at operation the patient was found to have cirrhosis and portal hypertension. The gallbladder "mass" was simply an organized clot, and hemorrhage recurred postoperatively. On reoperation, bleeding from the ampulla of Vater was observed, confirming the diagnosis of hemobilia. She was treated with angiographic interruption of hepatic arterial flow, at which time bleeding ceased. Her total transfusion requirements included 46 units of blood. Through 16 months of follow-up the patient has had no recurrent bleeding and no evidence of encephalopathy. This case demonstrates that spontaneous hemobilia may indeed arise from a cirrhotic liver. Proximal interruption of arterial flow is usually not recommended for hemobilia, especially in the presence of portal hypertension and cirrhosis, but may be life-saving in selected patients.
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PMID:Atraumatic hemobilia arising from a cirrhotic liver. 266 59

We recently saw a 12-year-old black boy with known sickle cell disease who had been seen many times for abdominal pain thought to be secondary to a vasoocclusive crisis. The patient eventually was admitted, after a seizure and the onset of obtundation. The etiology of his acute encephalopathy remained unclear until bone films of his knees fortuitously revealed "lead lines." The patient was treated and did well subsequently. This case emphasizes the importance of considering other diagnoses when a sickle cell patient presents with a crisis.
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PMID:Lead toxicity masquerading as sickle cell crisis. 308 61

Acute fatty liver of pregnancy, with a case history where an early diagnosis could have been made, and a review of the French literature. Acute fatty liver of pregnancy, or Sheehan's syndrome is a rare but very serious complication of pregnancy. The disease is demonstrated by vomiting, abdominal pain and a high level of uric acid in the blood before jaundice is noted. Within a few days the triad of jaundice, pruritus and encephalopathy occur. These are often associated with toxaemia of pregnancy and with polyuria and polydipsia. A raised white blood count and a high level of bilirubinemia are almost always present. The outlook is very serious when haemorrhage appears. This malignant form of the disease is characterised by liver and kidney failure. Liver biopsy confirms the diagnosis. The prognosis is related to an early diagnosis and is good when labour is induced or caesarean section performed. Acute fatty liver of pregnancy is an emergency from the diagnostic as well as the therapeutic angles.
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PMID:[Acute fatty liver of pregnancy. Diagnostic value of hyperuricemia in the pre-jaundice stage]. 322 Oct 52


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