[Circulatory pressure in normal infants and its changes due to dehydration].
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Biomedical subjects
Publications and source records attributed to J Quiroga.
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Percutaneous transhepatic treatment of portal vein thrombosis after liver transplantation in a patient with a preexisting high volume spontaneous splenorenal shunt is presented. Local thrombolysis with urokinase and balloon angioplasty of the main portal vein stenosis were performed followed by shunt embolization to restore hepatopetal portal blood flow.
Posttransplant lymphoproliferative disorders are infrequent tumors related to chronic immunosuppressive therapy. We present a liver transplant recipient who developed such a tumor in the porta hepatis that provoked obstruction of the entire portal triad. Treatment consisted of systemic chemotherapy, percutaneous dilatation, and placement of Wallstent endoprostheses across both biliary and portal vein stenoses. The patient died 3 weeks later of pneumonia and sepsis. At necropsy, the tumor was completely necrosed and the prostheses in both the common bile duct and the portal vein were patent.
Liver transplantation preserving the retrohepatic inferior vena cava, the so-called piggyback technique, is becoming more frequently used because it avoids caval cross-clamping during the anhepatic phase of surgery. However, hepatic venous outflow blockade causing ascites seems to be less infrequent after piggyback than with cavo-caval anastomosis. We report a 62-year-old patient who underwent liver transplantation using the piggyback technique and developed a stenosis in the anastomosis between the hepatic veins and the inferior vena cava leading to severe postoperative ascites. Ascites was unresponsive to diuretic therapy and was associated with renal function impairment. Since the etiology of the stenosis was mechanical (torsion), percutaneous transluminal angioplasty was unsuccessful. Finally, an autoexpandable prosthesis was placed across the anastomosis resulting in rapid and permanent (3 years of follow-up) resolution of ascites.
Abnormal cytokine levels have been described in patients with chronic liver disease, but studies correlating cytokine homeostasis with abnormalities in coagulation and fibrinolysis are lacking. In order to establish a link between cytokines and the hemostatic changes the following parameters were determined in 44 patients with cirrhosis (alcoholic = 15, postnecrotic = 22, others = 7): TNF-alpha, IL-6, thrombin-antithrombin (TAT) complexes, prothrombin fragment 1 + 2 (F1 + 2) and t-PA by using enzyme-linked immunosorbent assays, and PAI-1, plasminogen and alpha 2-antiplasmin (alpha 2-AP) by using chromogenic substrates. All patients were at stages B and C of Child's classification when entering the study. Mean cytokine concentrations were significantly higher in cirrhotic patients as compared to age- and sex-matched controls (p < 0.009). There was a significant increase of TAT (p < 0.02) and F1 + 2 (p < 0.001) in the patients groups, suggesting a grade of intravascular coagulation. A hyperfibrinolytic state as demonstrated by an increase of t-PA and decrease of plasminogen and alpha 2-AP was also observed (p < 0.001). We could define a subgroup of patients with cytokine values higher than 20 pg/ml. Interestingly, in this group there was a significant increase of TAT (p < 0.04) and t-PA (p < 0.02) levels and a decrease of plasminogen and alpha 2-AP (p < 0.02) as compared to values observed in patients with cytokines lower than 20 pg/ml. We conclude that high levels of TNF-alpha and IL-6 may contribute to hyperfibrinolysis and intravascular coagulation in patients with liver cirrhosis, as assessed by the increase of TAT and t-PA levels and the reduction of plasminogen and alpha 2-AP.
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Amiodarone is useful for the treatment of ventricular and supraventricular arrhythmias, but it has been associated with several adverse effects. Amiodarone-induced hepatotoxicity is a frequent complication and often consist in a mild and asymptomatic elevation of liver function tests, although severe cases have been described. A case of severe amiodarone-induced hepatotoxicity slowly resolving after discontinuation of the drug and in which liver biopsy was crucial for diagnosis is reported. Although there are no pathognomonic histopathological findings, phospholipidosis is the morphologic hallmark of amiodarone hepatotoxicity.
We studied the effects of intravenous flecainide acetate, given as a single dose of 2 mg/kg in no less than 15 minutes, on 31 patients with supraventricular tachyarrhythmias. Fourteen (87%) of the 16 patients with paroxysmal atrial fibrillation converted to sinus node rhythm. All 7 (100%) of the patients with paroxysmal supraventricular tachycardia converted to sinus node rhythm. Five (60%) of the 8 patients with paroxysmal atrial flutter converted to sinus node rhythm. The average time of conversion, after completion of drug administration, was 15 +/- 20 minutes. The QRS was prolonged an average of 82 to 91 milliseconds; in those cases who converted, the PR interval duration was 180 milliseconds average; QT was prolonged an average of 425-450 milliseconds. There were no changes in the JT interval, and we observed no hemodynamic untoward effects.
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