Cases reported "Ascites"

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1/39. ascites and weight loss in a child: due to congenital division of the right atrium.

    Congenital division of an atrial chamber is a very rare congenital malformation that more commonly affects the left atrium but which may, in rare circumstances, involve the right atrium. Such a divided right atrium may present with symptoms consistent with increased portal venous pressure. Reported is a case with unusual clinical presentation. The patient underwent resection of the dividing shelf with good postoperative results.
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2/39. pharmacokinetics of gemcitabine and 2',2'-difluorodeoxyuridine in a patient with ascites.

    Gemcitabine (dFdC) is a prodrug that undergoes metabolism by cytidine deaminase to form an inactive metabolite, 2',2'-difluorodeoxyuridine (dFdU). The pharmacokinetics of dFdC and dFdU have been studied; however, their disposition has never been evaluated in a patient with ascites. A patient with pancreatic cancer and malignant ascites was treated with dFdC 1,500 mg/m2 over 150 minutes weekly for 3 weeks, repeated every 4 weeks. Serial plasma and ascites samples were obtained on weeks 1 and 2 of cycle 2. High-pressure liquid chromatography was used to quantify dFdC and dFdU in plasma and ascites. The systemic dispositions of dFdC and dFdU were similar to those reported in patients without ascites. The concentration of dFdC in ascites approached 1 mg/ml. ascitic fluid did not serve as a depot for dFdC, and the agent's concentration in ascites approached that at which its phosphorylation is saturated.
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3/39. Massive right pleural effusion and ascites caused by a primary constrictive pericardial band.

    A previously healthy 57-year-old woman with peripheral edema and exertional dyspnea had diminished right breath sounds and edema of both legs. Chest radiography showed massive right pleural effusion, and abdominal computed tomography showed ascites. During cardiac catheterization, pressure curves of both ventricles showed "dip-and-plateau" patterns. We diagnosed constrictive pericarditis and conducted pericardiectomy. During surgery, we found a thick fibrous pericardium surrounding the entire heart and a band of calcium in the atrioventricular groove. Histological examination of excised pericardial tissue showed fibrosis, hyalinization, and calcification, with thickening of < or = 18 mm. Cases of localized pericardial thickening, including constricting bands in the atrioventricular groove, are rare and many such complications occur postoperatively. We report a rare case of primary constrictive pericardial band resulting in massive right pleural effusion and ascites.
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4/39. Transjugular intrahepatic portosystemic shunt for intractable posthepatectomy ascites.

    We report two cases of transjugular intrahepatic portosystemic shunt for control of intractable ascites after resection of cirrhotic livers. The first case was a 46-year-old male who had undergone right lobectomy of the liver for a small hepatocellular carcinoma. His liver function had recovered within a week after the operation, but ascites drainage of 1-4 L/day persisted for more than a month despite vigorous medical therapy. We performed transjugular intrahepatic portosystemic shunt on the 49th postoperative day and the pressure gradient between the right atrium and the left portal vein was reduced to from 21 mmHg to 6 mmHg. Thereafter, ascites became responsive to diuretic therapy and was well controlled without complication. Second case of a 54-year-old male patient who had undergone left lateral segmentectomy due to a small hepatocellular carcinoma presented intractable ascites of 1-3 L/day, which was also effectively controlled after transjugular intrahepatic portosystemic shunt performed on the 34th postoperative day, though there was an episode of hepatic encephalopathy stage 1. Based on our limited experience, hepatectomized patients suffering from prolonged intractable ascites despite a favorable profile of liver function may be candidates for transjugular intrahepatic portosystemic shunt with an acceptable risk of hepatic failure and procedure-related complication.
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5/39. Massive ascites in severe pre-eclampsia: a rare complication.

    We report three rare cases of massive maternal ascites complicating severe pre-eclamptic toxemia seen in the last 18 months. This complication developed in association with the rise of blood pressure to 160/110 mmHg or more, worsening of proteinuria and hyperuricemia. The onset of massive ascites caused respiratory compromise in all these patients, thus necessitating immediate termination of pregnancy.
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6/39. pancreatitis-induced extrahepatic portal vein stenosis treated by percutaneous transhepatic stent placement.

    One month after onset of an acute biliary pancreatitis, a 75-year-old man developed refractory ascites. Duplex ultrasound and CT scan revealed a focal stenosis of the extrahepatic portal vein as confirmed by transhepatic direct portography. In the same session, this stenosis, responsible for symptomatic prehepatic portal hypertension, was successfully dilated and stented and afterwards a residual pressure gradient of 1 mmHg over the stented segment was measured. One week after the stenting procedure the patient was free of ascites and control physical and biochemical examination one year later is completely normal.
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7/39. A patient with myelofibrosis complicated by refractory ascites and portal hypertension: to tips or not to tips? A case report with discussion of the mechanism of ascites formation.

    In patients with myelofibrosis, clinically significant portal hypertension is known to be predominantly presinusoidal; however, the exact mechanisms are still controversial. The pathophysiology is particularly enigmatic in those patients without histological and angiographic evidence of significant intra- or extrahepatic obstruction to portal blood flow, respectively. Moreover, ascites formation has been reported in such cases, but in general is rare in presinusoidal portal hypertension. Here we present such a patient in which ascites developed even in the presence of unchanged serum protein levels (oncotic pressure) and was refractory to sodium restricted diet and high-dose diuretic treatment. A discussion on the parameters influencing fluid exchange and ascites formation particularly emphasizing the potential importance of the hyperdynamic circulation in this case is given. Finally, the patient was treated by implanting a transjugular intrahepatic shunt (TIPS), exerting a diuretic effect sufficient enough to avoid re-formation of ascites for several months. However, ascites re-accumulated potentially due to the appearance of ectopic peritoneal myeloid metaplasia and the patient died soon afterwards. In conclusion, TIPS may be considered as rescue management for refractory ascites secondary to portal hypertension, but caution in respect to the presence and/or development of peritoneal or other ectopic haematopoesis has to be taken.
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8/39. Massive fetal ascites causing increased middle cerebral artery systolic velocity.

    BACKGROUND: An elevated peak systolic velocity in the middle cerebral artery, assessed by Doppler ultrasonography, is commonly associated with fetal anemia. Other fetal abnormalities associated with a high middle cerebral artery velocity have rarely been reported. CASE: A fetus with increasing ascites was found to have an elevated middle cerebral artery peak systolic velocity. Following paracentesis, the peak systolic velocity normalized. Peak systolic velocity continued to correlate with the level of ascites, falling to normal ranges when large-volume amniocentesis and paracentesis were performed. At birth, the infant was found to have a normal hematocrit. CONCLUSION: An elevated middle cerebral artery peak systolic velocity may result from massive fetal ascites without anemia. We hypothesize that the massive ascites led to increased afterload of the heart, with relatively preserved preload, leading to an increased systolic blood pressure and an elevated middle cerebral artery peak systolic velocity.
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9/39. ascites reinfusion dialysis (ARD) for renal failure with refractory ascites.

    BACKGROUND: dialysis is difficult for patients who have simultaneous liver and kidney failure. Effective mobilization of ascites is rare, and hypotension is common. Combining repeated paracentesis with continuous renal replacement therapy can achieve effective volume removal with hemodynamic stability, but requires intensive care unit resources. Large amounts of albumin are lost from the body in the drained ascites. Combining ascites reinfusion with hemodialysis is a potential alternative therapy. methods: Eight treatments were undertaken in 3 patients with refractory ascites in the setting of acute onset renal failure. Hemodialysis was unsuccessful due to hypotension in each case. Two patients were treated twice, and 1 patient was treated 4 times. Each patient underwent hemodialysis with reinfusion of ascites directly into the blood inlet of the dialysis machine. Weight, blood urea nitrogen, albumin and platelet counts were measured before and after treatment. Hemodynamic tolerance was assessed, and patients were observed for the development ofencephalopathy, disseminated intravascular coagulation, infection and hemodynamic decompensation. RESULTS: All patients survived. There was 1 episode of transient hemoperitoneum, but no encephalopathy, GI bleeding or infection. One patient recovered renal function, and the other 2 were discharged ambulatory to chronic hemodialysis programs. blood pressure was supported easily during therapy, despite removal of 3-8 kg of fluid. Platelet counts decreased by 27,000 /- 13,000, and albumin increased by 0.5 /- 0.2 g/dl. All values returned to baseline over the next 1-4 days. CONCLUSIONS: ascites recirculation with dialysis is a safe and effective therapy for patients with refractory ascites and severe renal failure, which can be carried out in routine inpatient and outpatient settings. Hemodynamic tolerance was good and thrombocytopenia was modest.
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10/39. Outflow block secondary to stenosis of the inferior vena cava following living-donor liver transplantation?

    Although it is well known that outflow block is caused by stenosis or occlusion of hepatic vein anastomoses following living donor liver transplantation (LDLT), there have been few reports on inferior vena cava (IVC) stenosis following LDLT. In this paper, we report two cases of IVC stenosis and hepatic vein outflow block following right hepatic LDLT in the absence of stenosis of any of the anastomoses. Both patients presented with liver dysfunction, an ascitic fluid volume of approximately 2000 mL, and congestion in their biopsy specimens, and venocavography demonstrated IVC stenosis with gradients of more than 10 mmHg in patients with a dominant inferior right hepatic vein (IRHV) anastomosis. After a Gianturco expandable metallic stent successfully implanted in the IVC, the patient's liver function recovered and the volume of ascitic fluid decreased. The pathogenesis of hepatic vein outflow block secondary to IVC stenosis following LDLT may involve the anastomosis with the IRHV, which is the dominant draining vein of the graft and larger than the RHV, caudal to the IVC stenosis and a significant IVC pressure gradient that results in increased IRHV pressure. In conclusion, it is important to include hepatic vein outflow block in the differential diagnosis when patients who have undergone right hepatic LDLT in which anastomosis of the large IRHV has been performed develop manifestations of liver dysfunction.
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