1/39. Long-term extracorporeal bilirubin elimination: A case report on cascade resin plasmaperfusion.Acute hepatic failure develops as a disease entity of rather diverse origin. With disease progression, toxic bilirubin levels may cause severe complications which include AV-nodal blockage, cardiac arrhythmia, impaired consciousness, generalized seizures, and status epilepticus. Treatment choices to prevent clinical deterioration comprise of costly and limited available orthotopic liver transplantation, utilization of extracorporeal bioartificial liver support devices and haemoperfusion/plasmaperfusion treatment with activated charcoal/anion exchange filters. Here, we present a patient with acute drug-induced cholestatic hepatitis. Excessively elevated bilirubin levels were accompanied by cardiac and cerebral complications. Extracorporeal resin perfusion treatment (Plasorba, BR-350) was successfully performed over a 50-day period without activation of the coagulation system or side effects. bilirubin levels were lowered to a minimum of 225 micromol/l, with concurrent clinical improvement. In conclusion, extracorporeal anion exchange plasmaperfusion may be a viable long-term treatment for hyperbilirubinaemic side effects in overt cholestatic hepatitis.- - - - - - - - - - ranking = 1keywords = cardiac (Clic here for more details about this article) |
2/39. Autonomic dysfunction in end-stage liver disease manifested as defecation syncope: impact of orthotopic liver transplantation.patients with end-stage liver disease (ESLD) may be at increased risk for syncopal episodes based on their circulatory physiological state. Although a definitive cause for this is not known, several mechanisms have been proposed. In patients with ESLD, defecation syncope may result from a failure of short-term neurocirculatory adaptation to the valsalva maneuver in the face of a hyperdynamic circulatory state and a decreased effective intravascular volume. We describe 2 patients with ESLD who had repeated episodes of defecation syncope before orthotopic liver transplantation (OLT). The most effective treatment of these syncopal episodes appears to be fluid administration and the use of a pressor agent, such as dopamine, to help maintain both an effective heart rate and intravascular volume. Correction of this altered circulatory physiological state through OLT prevented further syncopal episodes in both patients. A search of the literature failed to show previous reports associating ESLD and defecation syncope. Possible mechanisms favoring this association are reviewed.- - - - - - - - - - ranking = 1.927884549082keywords = heart (Clic here for more details about this article) |
3/39. Peripheral arterial coil embolization for hepatic arteriovenous malformation in Osler-Weber-Rendu disease; useful for controlling high output heart failure, but harmful to the liver.A 55-year-old Japanese housewife, who had Osler-Weber-Rendu disease, was admitted to our hospital because of frequent epistaxis and worsening exertional dyspnea. The computed tomography and hepatic arteriography revealed large hepatic arteriovenous malformation, which was considered to be the leading cause of her high output heart failure. Two series of hepatic arterial coil embolization procedures were performed to reduce hepatic shunt flow. They temporarily improved her cardiac condition, but gradually induced progressive hepatic failure due to intrahepatic cholangitis. Hepatic dysfunction restricted her quality of life and lead to a fatal clinical course one year after the second coil embolization.- - - - - - - - - - ranking = 22.703860358509keywords = heart failure, heart, cardiac (Clic here for more details about this article) |
4/39. Hepatic failure in a patient taking rosiglitazone.BACKGROUND: Rosiglitazone maleate is the second approved oral hypoglycemic agent of the thiazolidinedione class. The first, troglitazone, has been associated with liver failure, occasionally resulting in liver transplantation or death. There have been no reports to date of rosiglitazone-associated elevations in the alanine aminotransferase level or hepatotoxicity. OBJECTIVE: To report the clinical characteristics of liver failure developing in a patient receiving rosiglitazone. DESIGN: Case report. SETTING: University hospital. PATIENT: 69-year-old man taking rosiglitazone, 4 mg/d. INTERVENTION: Discontinuation of rosiglitazone therapy and treatment with lactulose, vitamin k, fresh frozen plasma, ventilatory assistance, and intensive care unit support. MEASUREMENTS: blood test monitoring, including toxicology screening, liver function tests, coagulation studies, serum chemistries, and complete blood counts. RESULTS: After 21 days of rosiglitazone therapy, hepatic failure developed. Other causes of hepatic failure, such as viruses and toxins, were excluded, although it is possible that congestive heart failure was also a causative factor. The patient recovered fully with supportive care. CONCLUSION: Rosiglitazone may be associated with hepatic failure.- - - - - - - - - - ranking = 4.4407720717018keywords = heart failure, heart (Clic here for more details about this article) |
5/39. Neonatal repair of Ebstein's anomaly: indications, surgical technique, and medium-term follow-up.BACKGROUND: Ebstein's anomaly in the severely symptomatic neonate is usually fatal. Because the mortality for various surgical interventions has been prohibitively high, the indications for operation in these critically ill neonates are unclear. methods: We reviewed our results with biventricular repair of three consecutive severely symptomatic neonates (2.8 to 3.2 kg) at our institution since 1994. Each had associated complex cardiac pathology, including multiple muscular ventricular septal defects (n = 1), pulmonary stenosis with functional pulmonary atresia (n = 1), and anatomic pulmonary atresia (n = 1). Preoperatively, all infants had severe tricuspid regurgitation, Great Ormond Street Ebstein echocardiogram scores greater than 1.3:1 (grade 3 or 4) and cardiothoracic ratio greater than 0.85. Two patients were severely cyanotic. Hepatic and renal insufficiency with diffuse coagulopathy was present preoperatively in two patients. Surgical repair consisted of (1) reconstruction of a competent monocuspid tricuspid valve, (2) right ventriculorrhaphy, (3) subtotal closure of atrial septal defect (ASD), (4) aggressive reduction atrioplasty, and (5) repair of all associated cardiac defects. RESULTS: There were no early or late deaths. All patients are currently asymptomatic, without medications, and in sinus rhythm. At 5-year follow-up, trivial tricuspid regurgitation is present in 1 and mild regurgitation in 2 patients. On the basis of these results and review of the current literature, we propose new indications for surgical repair in the neonate with Ebstein's anomaly. CONCLUSIONS: Biventricular repair of Ebstein's anomaly in the critically ill neonate is feasible and medium-term durability of the repair is excellent. Therefore, conventional management of these patients should be revised and early surgical repair encouraged.- - - - - - - - - - ranking = 1keywords = cardiac (Clic here for more details about this article) |
6/39. Use of aerosolized inhaled epoprostenol in the treatment of portopulmonary hypertension.BACKGROUND: Portopulmonary hypertension is a known complication in the liver transplant candidate. Intravenous epoprostenol has been demonstrated to decrease pulmonary artery pressures and possibly remodel right ventricle geometry. methods: In this report, we document the efficacy of inhaled aerosolized epoprostenol in a patient with portopulmonary hypertension. The effect was of rapid onset and offset. RESULTS: After 10 min of delivery, mean pulmonary artery pressure decreased 26%; cardiac output increased by 22%; pulmonary vascular resistance decreased by 42%; and the transpulmonary gradient decreased by 29%. There were no untoward side effects. CONCLUSION: The inhaled route of delivery of epoprostenol is potential alternative for the acute therapy of portpulmonary hypertension.- - - - - - - - - - ranking = 0.5keywords = cardiac (Clic here for more details about this article) |
7/39. Cardiac perforation and tamponade during transjugular intrahepatic portosystemic shunt placement.A patient developed acute severe hemodynamic compromise during a transjugular intrahepatic portosystemic shunt (TIPS) procedure for intractable ascites. Rapid clinical and radiographic evaluation of the patient disclosed pericardial blood and cardiac tamponade as the cause, probably due to right heart perforation from guidewire and catheter manipulation. The tamponade was successfully treated percutaneously, and the patient survived. cardiac tamponade should be considered in the differential diagnosis of patients who develop hypotension during TIPS placement.- - - - - - - - - - ranking = 2.427884549082keywords = heart, cardiac (Clic here for more details about this article) |
8/39. Fulminant hepatic failure caused by diffuse intrasinusoidal metastatic liver disease: a case report.A 53-year-old woman experienced rapidly progressing liver failure four years after a quadrantectomy for a breast carcinoma. She had received adjuvant chemotherapy and radiotherapy, and second-line chemotherapy for bone metastasis one year earlier. The hepatic failure manifested with ascites, jaundice, elevation of serum bilirubin and hepatic enzyme levels and hypoalbuminemia. Imaging studies showed an enlarged liver without metastatic lesions. The patient died of hepatic decompensation within two weeks. Liver examination at autopsy revealed massive neoplastic infiltration consistent with a primary breast carcinoma. It is important to realize that this unusual pattern of liver metastasis cannot be demonstrated even with the most advanced techniques of instrumental diagnosis (CT scan, ultrasonography and magnetic resonance imaging), and should be taken into account in the differential diagnosis of rapidly progressing liver failure.- - - - - - - - - - ranking = 204.25081605205keywords = decompensation (Clic here for more details about this article) |
9/39. Rejection of pig liver xenografts in patients with liver failure: implications for xenotransplantation.The pathophysiological state of rejection in liver xenotransplantation is poorly understood. Data from clinical pig liver perfusion suggest that pig livers might be rejected less vigorously than pig hearts or kidneys. Pig livers used in clinical xenoperfusions were exposed to blood from patients with liver failure. We have shown in an animal model that transplant recipients with liver failure are less capable of initiating hyperacute rejection of a xenografted liver than a healthy transplant recipient. The goal of this report is to examine the pathological characteristics of pig livers used in 2 clinical pig liver perfusions and combine this information with in vitro studies of pig-to-human liver xenotransplantation to determine whether the findings in the perfused pig livers could be explained in part by the diminished capacity of the patient with liver failure to respond to xenogeneic tissue. Pathological analysis of the perfused pig livers showed immunoglobulin m deposition in the sinusoids with little evidence of complement activation. Our in vitro studies showed that serum from patients with liver failure caused less injury to pig liver endothelium than serum from healthy subjects. serum from patients with liver failure had similar levels of xenoreactive antibodies as serum from healthy humans. Incubation of serum from patients with liver failure with pig hepatic endothelial cells generated less iC3b, Bb fragment, and C5b-9 than serum from healthy subjects. We conclude that the altered injury in the perfused pig livers can be attributed to the relative complement deficiency that accompanies liver failure.- - - - - - - - - - ranking = 1.927884549082keywords = heart (Clic here for more details about this article) |
10/39. Fatal hepatic decompensation in a patient with hepatitis B cirrhosis following famciclovir withdrawal.hepatitis b virus (HBV) infection is a major cause of chronic liver disease worldwide. Famciclovir is a nucleoside analogue with potent antiviral activity that appears promising in the management of patients with HBV infection. No data exist regarding the safety of nucleoside analogue withdrawal in patients treated for HBV cirrhosis. The authors describe a 41-year-old man with compensated HBV cirrhosis who developed fatal hepatic decompensation due to a rebound in viral replication within six weeks of discontinuing famciclovir therapy. Although several mutations in the HBV dna polymerase gene have been documented, none has been associated with famciclovir resistance or adverse clinical outcomes. Clinicians should consider the risk of inducing serious flares in hepatic inflammation as a result of abrupt nucleoside analogue withdrawal. Until further data are available regarding the safety of withdrawal of these agents, indefinite treatment may be required in patients with established cirrhosis.- - - - - - - - - - ranking = 1021.2540802603keywords = decompensation (Clic here for more details about this article) |
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