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At least 415 records · Page 23Linked to original sources
PubMed1993

Revascularization technique for reduced-size liver transplantation for infants weighing less than 10 kg.

Reduced-size liver transplantation has been recognized as a powerful modality in alleviating the global donor shortage in pediatric liver transplantation. We describe, for the first time, a technique for revascularizing reduced-size grafts which has not been patterned after adult revascularization techniques. This revascularization method for reduced-size liver transplantation is particularly suitable for infants weighing < 10 kg. This technique differs from adult revascularization techniques in that the supraceliac aorta is always used as the origin for graft arterialization, and that the anastomoses are always performed in the following order: end-to-side donor celiac artery to supraceliac aorta anastomoses first, followed by the suprahepatic vena caval anastomoses, infrahepatic vena caval anastomoses, and then portal vein anastomoses. Hepatic artery thrombosis in infants weighing < 10 kg has occurred in 4 of 32 nonreduced versus 0 of 21 reduced transplantations (P = .05616, Z test, one tail). Adult revascularization was primarily used in the nonreduced group, whereas our proposed revascularization method was primarily used in the reduced group. We conclude that, for infants weighing < 10 kg receiving reduced grafts, this proposed technique should be used to decrease hepatic artery thrombosis.

Adult↗
PubMed2000

[Management of post liver transplantation complications].

Survival rate of liver transplanted patients is depending on management of postoperative complications. These complications include technical problems related to the operation, dysfunction of the allograft, and variety of medical complications. Differentiating and appropriately managing these diverse complications is a formidable challenge. Given the complexity of liver transplantation, it is not surprising that a variety of technical complication can occur following the operation. The most prominent of these include intraabdominal bleeding, hepatic artery thrombosis, portal vein thrombosis, and obstruction of or leak from the biliary anastomosis. In addition to these technical complications, each of which can result in dysfunction of the graft, there are a number of intrahepatic causes of graft dysfunction. The most common of these are allograft rejection, viral hepatitis and non-specific postoperative jaundice. In living related liver transplantation, primary graft non-function is rare. Accurate diagnosis and management of the various causes of graft dysfunction, whether intrahepatic or extrahepatic in origin, is very important.

Blood Loss, Surgical↗
PubMed1996

Resolution of Budd-Chiari syndrome following bone marrow transplantation for paroxysmal nocturnal haemoglobinuria.

Thrombosis of the hepatic veins (Budd-Chiari syndrome) is a life-threatening thrombotic complication which can occur in patients with paroxysmal nocturnal haemoglobinuria (PNH). Despite aggressive medical and surgical therapy, mortality from Budd-Chiari syndrome remains high. We report a boy with PNH who developed Budd-Chiari syndrome and underwent syngeneic bone marrow transplantation (BMT). Now, 3 years following BMT, he has had dramatic clinical and radiographic evidence of resolution of the thrombosis. We suggest that BMT for PNH can successfully correct life-threatening thrombosis in patients with PNH.

Bone Marrow Transplantation↗
PubMed2005

[A case of multiple hepatocellular carcinoma with rapidly progressing bilateral portal vein tumor thrombosis--a complete remission achieved with dual treatment of reductive surgery plus percutaneous isolated hepatic perfusion].

We herein report a case of multiple advanced hepatocellular carcinoma (HCC) with rapidly progressing portal vein tumor thrombosis (PVTT). All of the hepatic tumors have completely disappeared for more than two years by a dual treatment with reductive surgery plus percutaneous isolated hepatic perfusion (PIHP). A 55-year-old man was referred to our institution on June 30, 2003. The abdominal CT scan demonstrated multiple massive HCC in the entire liver with PVTT reaching the portal trunk (Vp4). Two weeks later, the PVTT rapidly progressed to the umbilical portion of the left portal vein, and to the confluence of the superior mesenteric vein and to the splenic vein. Thus, we semi electively performed an extended right hepatectomy together with thrombectomy of the PVTT. Subsequently, he underwent a repeated PIHP (1st; doxorubicin 90 mg/m2, 2nd doxorubicin 65 mg/m2). This treatment produced complete tumor clearance of all of the residual tumors in the left liver. In March 2005, he underwent partial pneumonectomy for a metastatic lung. This again resulted in normalization of serum AFP and PIVKA-II levels. Dual treatment is considered to be the strongest therapeutic modality for multiple advanced HCC with severe PVTT. In addition, a close follow-up is required because in such far advanced cases, metastatic lesions most likely recur in the liver but also in the distant organs.

Carcinoma, Hepatocellular↗
PubMed1999

Successful recanalization of late portal vein thrombosis after liver transplantation using systemic low-dose recombinant tissue plasminogen activator.

Portal vein thrombosis (PVT) is an infrequent complication following hepatic transplantation. However, deterioration of liver function and accompanying complications may be life threatening. Several attempts of surgical or percutaneous transhepatic procedures have been described. In some cases high dose fibrinolytic regimens have been successful. We describe the case of a male liver recipient with recurrent liver fibrosis due to hepatitis B reinfection and late portal vein thrombosis 45 months after transplantation. Complete recanalization was achieved using systemic low dose recombinant tissue plasminogen activator (rt-PA).

Fibrinolytic Agents↗
PubMed1994

Hepatic venous outflow obstruction in autosomal dominant polycystic kidney disease.

To discuss the clinical presentation, diagnosis, and treatment of hepatic venous outflow obstruction as a complication of polycystic liver disease, four cases diagnosed and treated at our institution have been reviewed and the information from six previously published case reports has been summarized. Eight of the 10 patients were women. All presented with severe ascites. Nine had polycystic kidneys. Three had moderate-to-advanced renal insufficiency, four were on hemodialysis, and one had a renal allograft. Possible predisposing factors were identified in seven patients; the most common was recent abdominal surgery, which, in three cases, was a bilateral nephrectomy. All patients had extrinsic compression of the hepatic veins and the inferior vena cava by hepatic cysts, and four had proven superimposed thrombosis of the inferior vena cava and/or hepatic veins. In the patients seen in this institution, magnetic resonance imaging was helpful in determining the level of obstruction in the inferior vena cava and the patency of the hepatic and portal veins. The outcome was worse in the patients with thrombosis; one recovered after a portocaval shunt, and the remaining three patients died. On the other hand, five of the six patients without thrombosis recovered after alcohol sclerosis of a large dominant cyst (one patient) or after hepatic resection and cyst fenestration (four patients). Hepatic venous outflow obstruction probably has been underrecognized as a cause of portal hypertension, ascites, and liver dysfunction in polycystic liver disease. The diagnosis can be reliably established with current imaging techniques, especially magnetic resonance imaging.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1980

Noncirrhotic portal vein thrombosis. Physiology before and after shunts.

Controversy exists concerning the proper therapy for bleeding gastroesophageal varices secondary to noncirrhotic portal vein thrombosis. Disparity of opinion exists regarding the significance of hepatic portal blood flow and the consequences of total portal-systemic shunts in this condition. One patient is presented who developed severe, crippling encephalopathy 20 years after a central splenorenal shunt. This was associated with loss of portal flow to the liver and marked nitrogen intolerance. Closure of the shunt resulted in restoration of hepatic portal flow via collateral veins (HPI 0.36), clearance of encephalopathy and return to near normal protein tolerance. An additional patient was studied with hyperammonemia and early suggestive signs of encephalopathy eight years following a mesocaval shunt. Four patients were evaluated before and after selective distal splenorenal shunts. All had "cavernous transformation" of the portal vein with angiographic evidence of portal flow to the liver. Postoperative angiograms revealed continued hepatic portal perfusion and a patent shunt in each patient. Radionuclide imaging postoperatively gave an estimated portal fraction of total hepatic blood flow (HPI) of .39 and .60 in two of the four patients. We conclude that 1) there is significant hepatic portal perfusion in noncirrhotic portal vein thrombosis (cavernous transformation), 2) loss of this hepatic portal flow following total shunts can lead to severe encephalopathy, 3) the selective distal splenorenal shunt maintains hepatic portal perfusion and is the procedure of choice when there is a patent splenic vein and surgical intervention is indicated.

Adolescent↗
PubMed1993

Late presentation of portal vein thrombosis as a complication of appendicitis.

A case of appendicitis which resulted in portal pyaemia, hepatic and splenic abscesses, presumed portal vein thrombosis and subsequent portal hypertension is described. It confirms the merit of ultrasonic imaging in monitoring abscess resolution but questions the ability of the technique to recognise acute suppurative portal endophlebitis.

Abscess↗
PubMed1994

Emergency oesophageal transection for uncontrolled variceal haemorrhage.

Continued haemorrhage from oesophageal varices despite adequate injection sclerotherapy and tamponade has a high mortality rate. Such patients are usually referred for surgery. Over a 10-year period, 30 patients (21 men and nine women of median age 52 (range 21-70) years) with acute variceal haemorrhage uncontrolled by initial treatment underwent early emergency oesophageal transection. Portal hypertension was caused by alcoholic cirrhosis in 22 patients; other forms of cirrhosis were present in seven and portal vein thrombosis in one. Hepatic function immediately before operation was Pugh grade A in two patients, B in six and C in 22. Deterioration between admission and transection from grade A to B occurred in one patient and from B to C in five. Oesophageal transection stopped variceal haemorrhage in 29 of the 30 patients. Rebleeding from gastric varices within 35 days of surgery occurred in five patients. Postoperative haemorrhage also occurred from perioesophageal vessels (two patients), a gastrotomy (one) and oesophageal ulceration (two). Hepatic failure developed in seven patients, renal failure in five and both hepatic and renal failure in four. Mortality at 30 days occurred in neither of the two patients with liver function of grade A, in one of six of grade B and in 18 of 22 of grade C. The overall 30-day mortality rate was thus 63 per cent. Mortality was related to the preoperative Pugh grade (hazard ratio 3.95 per grade; P = 0.013) and preoperative blood transfusion (hazard ratio 1.37 per unit; P = 0.035). Four of six patients with grade B liver function died within 3 months and 21 of 22 with grade C disease within 1 year. Oesophageal transection is effective at stopping variceal bleeding but does not modify the underlying disease. Caution is urged for patients with grade C hepatocellular impairment proceeding to acute oesophageal transection after initial sclerotherapy. Such patients may benefit more from treatment with somatostatin or an intrahepatic porta-systemic stent shunt while awaiting definitive therapy.

Adult↗
PubMed1993

Balloon dilatation of inferior vena cava obstruction in Budd-Chiari syndrome.

Budd-Chiari syndrome is a well described entity which can easily be confused with congestive hepatomegaly. The syndrome usually is caused by thrombosis of the hepatic veins, however it also can be caused by congenital fibrous webs that occlude hepatic vessels in the inferior vena cava. It leads to an enlarged liver with ascites, peripheral edema, and portal hypertension.

Budd-Chiari Syndrome↗
PubMed1994

Budd-Chiari syndrome and Epstein-Barr virus (EBV) associated plasmacytoma in a patient with chronic active EBV infection.

A 42-year-old Japanese man with chronic active Epstein-Barr virus (EBV) infection initially responded to treatment with interleukin-2 (IL-2). Six months later he developed thrombosis in the hepatic veins, and Budd-Chiari syndrome associated with severe hepatic damage was diagnosed. He also developed a solitary EBV-positive plasmacytoma in the right femur. Since these rare complications occurred after long-term IL-2 therapy, the possibility that long-term IL-2 therapy might cause Budd-Chiari syndrome and liver damage as well as EBV-associated plasmacytoma is discussed.

Adult↗
PubMed1979

Hepatic failure in a patient treated with dacarbazine (DTIC) for malignant melanoma.

A 55-year-old white woman received chemotherapy with DTIC after surgery for malignant melanoma (stage I, SSM IV, depth of invasion 12 mm). She died suddenly during the second treatment cycle. Autopsy revealed massive necrosis of the liver and thrombosis of the hepatic veins. The cause of the fatal outcome is attributed to the adverse toxic effects of DTIC.

Budd-Chiari Syndrome↗
PubMed1993

Meso-atrial shunt for Budd-Chiari syndrome: evaluation of patency by magnetic resonance angiography, with color Doppler ultrasound and angiographic correlation.

We report the case of a boy with Budd-Chiari syndrome. At 3 years of age a meso-atrial shunt was inserted for thrombosis of the hepatic veins with associated inferior vena cava occlusion by an enlarged caudate lobe. Seven uneventful years later, the patient was reassessed because of concern about insufficient length of the synthetic shunt. Ultrasound with color Doppler imaging (CDI) and magnetic resonance imaging (MRI) with magnetic resonance angiography (MRA) clearly depicted a patent graft, without kinking, stenosis or other sign of graft dysfunction. Conventional selective angiography confirmed the patency of the shunt. MRI with MRA and CDI are less invasive and less expensive than conventional angiography and might replace this technique for assessment of meso-atrial shunt patency.

Angiography, Digital Subtraction↗