Cases reported "Ascites"

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1/40. Fetal meconium peritonitis after maternal hepatitis A.

    hepatitis a virus has rarely been implicated in congenital infections. After maternal hepatitis A at 13 weeks' gestation, ultrasonographic examinations revealed fetal ascites (20 weeks) and meconium peritonitis (33 weeks). After delivery, a perforated distal ileum was resected. Elevated levels of hepatitis A immunoglobulin g persisted in the infant 6 months after delivery.
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2/40. hepatic veno-occlusive disease in ataxia-telangiectasia.

    Existing descriptions of liver abnormalities in ataxia-telangiectasia have been associated with co-existent hepatitis virus infection. Here we report veno-occlusive disease of the liver in 2 patients with ataxia telangiectasia that is not attributable to bone marrow transplantation or coincidental hepatitis infection.
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3/40. laparoscopy extends the indications for liver resection in patients with cirrhosis.

    BACKGROUND: Clinical or biological evidence of liver failure is usually considered a contraindication to open liver surgery as it is associated with a prohibitive risk of postoperative death. methods: This report describes three patients who had resection of a superficial hepatocellular carcinoma suspected either to be ruptured, or at high risk of rupture, using the laparoscopic approach. All three patients had intractable ascites, in two superimposed on active hepatitis. Surgery was per- formed under continuous carbon dioxide pneumoperitoneum with intermittent clamping of the hepatic pedicle. RESULTS: Intraoperative blood loss was between 100 and 400 ml; no blood transfusion was required. The postoperative course was uneventful except for a transient leak of ascites through the trocar wounds. Duration of in-hospital stay was 6-10 days. liver function tests had returned to preoperative values within 1 month of surgery in all patients. CONCLUSION: The laparoscopic approach may enable liver resection in patients with cirrhosis and evidence of liver failure that would contraindicate open surgery.
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4/40. CA-125 tumor-associated antigen in a patient with tuberculous peritonitis.

    A 64-year-old woman with a history of chronic hepatitis B had abdominal pain and ascites, a serum albumin ascitic gradient (SAAG) of 0.8, and an elevated serum CA-125 value. Exploratory laparotomy revealed ascites and obliteration of the abdominal cavity by advanced adhesive disease consistent with carcinomatosis. Surgical biopsy revealed noncaseating granulomas. She responded well to antituberculous therapy and is presently asymptomatic.
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5/40. Multi-system cytomegalovirus fetopathy by recurrent infection in a pregnant woman with hepatitis B.

    A pregnant woman with acute hepatitis b virus (HBV) infection had her second pregnancy terminated at 25 weeks' gestation because of fetal ascites and ventriculitis. meconium peritonitis was also found at autopsy. No HBV dna but cytomegalovirus (CMV) dna was detected in the fetal liver and ascitic fluid. Recurrent maternal CMV infection was demonstrated by pre-existing CMV IgG antibodies, high IgG avidity and low IgM levels. After abortion, the patient developed chronic active hepatitis. Nevertheless, having become pregnant again with a new partner, she had an uneventful third pregnancy and gave birth to a healthy boy.
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6/40. Hepatic decompensation in patients with cirrhosis during infection with influenza A.

    BACKGROUND: patients with chronic liver disease can develop hepatic decompensation during systemic infections. Although gram-negative and gram-positive bacteria are well recognized as causes of decompensation, the effect of influenza virus infection on patients with chronic liver disease is poorly documented. methods: Retrospective analysis of patients with positive viral cultures who were seen at a liver transplantation clinic in a tertiary care referral center during the 1997-1998 influenza A (H3N2) epidemic in San Diego, Calif. RESULTS: Three patients with end-stage liver disease (1 with Wilson disease and 2 with alcoholic liver disease) developed hepatic decompensation and required hospitalization during infection with influenza A. Two patients had biochemical and clinical evidence of hepatic decompensation, including ascites, hepatic encephalopathy, and peripheral edema, and the third had acute hepatocellular damage, with elevated levels of aminotransferases. Viral hepatitis serologic test results, acetaminophen levels, drug and alcohol screening findings, and bacterial and fungal cultures were negative in all 3 patients. Hepatic decompensation resolved without the need for transplantation in the 2 patients with liver failure, and all patients recovered to their baseline liver function levels within 1 month of onset of acute illness. CONCLUSIONS: Influenza A infection can cause hepatic decompensation and hospitalization in patients having cirrhosis or who are awaiting liver transplantation. Effective prevention with vaccination and early recognition and treatment of influenza are strongly recommended in these individuals.
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7/40. Case studies in orthotopic liver transplantation for hepatitis B: a panel discussion.

    Five cases that were referred to the Division of Transplantation at NYU School of medicine for consideration for liver transplantation were discussed among a panel of hepatitis B and liver transplant experts. Opinions were obtained on the management at every stage of treatment of patients with the following initial information: Case one: young Asian woman in stage IV hepatic coma; intubated; prothrombin time (PT): 30 s; serum glutamic oxaloacetic transaminase (SGOT): 8,000 IU; total bilirubin: 25 mg/dL; hepatitis B surface antigen (HBsAg) positive. Case two: 70-yr-old woman, native of greece; decompensated cirrhosis with encephalopathy; child-Pugh Class C; HBsAg positive; hepatitis B surface antibody (HBsAb) negative; hepatitis B e antigen (HBeAg) positive; hepatitis B e antibody (HBeAb) negative; hepatitis b virus (HBV) dna titer: 10,000. Case three: Muscular detective working full-time; cirrhosis; child Pugh Class B; ascites controlled with spironolactone and furosemide; PT: 19s; HBsAg positive; HBsAb negative; HBV dna titer: 50,000; low platelet count. Case four: 45-yr-old baker; cirrhosis and resectable 4-cm hepatoma; child-Pugh Class B; PT: 16 s; Blood type O; United Network for Organ Sharing (UNOS) 2B; HBV dna titer: 3,000. Case five: 40-yr-old Indian man; 300 pounds with massive ascites; child Pugh Class C; PT: 17 s; HBsAg positive; HBV dna titer: 22,000; transplanted with intra-operative hypotension; tacrolimus; graft functioning; HBIg 10,000 IU intra-operative and around the clock during the first post-operative week; required huge doses of hepatitis B immune globulin (HBIg) to maintain adequate HBsAb level; daily loss of 5 6 L of ascites fluid; post-operative day 8: anuric, blood urea nitrogen (BUN) 127, creatinine 3, mental status changes.
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keywords = hepatitis
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8/40. Three cases of severe acute hepatitis after parenteral administration of amiodarone: the active ingredient is not the only agent responsible for hepatotoxicity.

    amiodarone is one of the most effective antiarrhythmic drugs available and is widely prescribed despite several potentially life-threatening side-effects. Hepatotoxicity is the most frequent one during long-term oral therapy: occasionally acute hepatitis necessitates the suspension of treatment but monitoring of a transient increase in serum aminotransferases is usually sufficient; the clinical-morphological pictures of liver cirrhosis have also been reported. Fulminant hepatitis soon after a parenteral load of the drug is far less well described in the literature. Most published cases were reversible after the suspension of treatment. A negative challenge after oral amiodarone exposure suggested that polysorbate 80, a solvent added to the intravenous infusion and already implied in the pathogenesis of a similar syndrome observed in infants, is a more likely cause of this complication. The occurrence of acute hepatitis complicating parenteral amiodarone treatment does not preclude subsequent oral use of the drug: an evidence-based therapeutic behavior now definitively consolidated. Because of the rarity of this diagnosis, we report 3 cases of short-term hepatotoxicity secondary to amiodarone treatment for supraventricular tachyarrhythmias: in 2 male patients with dilated cardiomyopathy and in a female with liver disease. The diagnosis was presumptive and based on a thorough drug history, the temporal relationship, the time-course of liver dysfunction, the exclusion of other causes and on the rapid improvement observed after parenteral amiodarone withdrawal in 2 cases; in no case could we find any other explanation for the liver damage. Since amiodarone is sometimes still an irreplaceable antiarrhythmic drug, we raise the question of whether careful and continuous vigilance should be mandatory in patients receiving the drug or whether it is possible to introduce a pharmaceutical preparation not containing the vehicle that induces acute liver toxicity.
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9/40. ethacrynic acid can be effective for refractory congestive heart failure and ascites.

    ethacrynic acid is a loop diuretic little used today because of its side-effect profile and the availability of multiple alternative agents. However, in our clinical experience, ethacrynic acid can alleviate acute congestive heart failure and ascites resistant to other diuretics. Two patients aged 89 and 94 in life-threatening pulmonary edema were stabilized by ethacrynic acid after furosemide proved ineffective. A third patient, aged 83, with a pleural effusion and ascites secondary to end-stage hepatitis B and C, responded to ethacrynic acid when spironolactone and furosemide produced little urine output. Ethacrynic acid may have a unique niche as a diuretic of last resort, especially in geriatric practice.
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keywords = hepatitis
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10/40. Hepatic hydropericardium.

    A 41-year-old man with chronic hepatitis c and cirrhosis presented with pericardial effusion and tamponade requiring pericardiocentesis. Nine liters of pericardial fluid was drained with complete resolution of his ascites. He represented with recurrent pericardial effusions despite salt restriction and diuretic therapy. Subsequent radionuclide scans demonstrated a direct connection between the peritoneal and pericardial spaces. A pericardial window was formed but despite this there was recurrence of pericardial effusion and pleural effusion. The patient underwent orthotopic liver transplantation 7 months later and no recurrence of pleural or pericardial effusion was observed following transplantation. We believe this is the first case report of pericardial effusion secondary to cirrhotic ascites and a communication between the peritoneal and pericardial cavities.
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