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PubMedDate not supplied

Surgical considerations of extracardiac total cavopulmonary connection.

Extracardiac total cavopulmonary connection has been proposed as a rational alternative to the lateral intra-atrial tunnel for complex congenital cyanotic heart diseases undergoing univentricular repair. In five patients, aged 4 1/2 years to 27 years, an extracardiac lateral conduit was used for total cavopulmonary connection at our Institute. Extracardiac lateral conduits were constructed in all the five patients using polytetrafluoroethylene tube grafts. One child required reoperation because of graft thrombosis and an aortic homograft was used in him on the second occasion. Aortic cross clamp was completely avoided in all including reoperation. The results showed no early or late mortality. One child developed persistent hypoxemia and progressive hepatomegaly. Reoperation on 5th post-operative day revealed graft thrombosis with technically unrestricted anastomosis which was replaced by an aortic homograft. He also required embolectomy for inferior vena cava and hepatic veins thrombosis. Post-operative follow-up (range 3 months to 14 months) revealed all patients in functional class I and in normal sinus rhythm. Doppler echocardiography, magnetic resonance imaging and angiocardiography revealed unrestricted anastomoses and unobstructed pulmonary blood flow across the conduit. The technical advantages and haemodynamic benefits of this operation are encouraging. However, the lone incidence of graft thrombosis raises concern about the routine usage of synthetic grafts in extracardiac total pulmonary connection. Other inherent weakness appears to be the lack of growth potential of the synthetic tube.

Adolescent↗
PubMedDate not supplied

MR imaging findings in a patient with hepatic veno-occlusive disease.

We report the MRI findings in a 31-year-old woman with veno-occlusive disease. MRI demonstrated patent hepatic veins and patchy signal enhancement of the liver after gadolinium chelate injection. This enhancement was compatible with sinusoidal congestion. The diagnosis of veno-occlusive disease was confirmed by histological examination of liver biopsy. The diagnosis of veno-occlusive disease should be evoked when patchy liver enhancement suggestive of sinusoidal congestion is observed in the absence of hepatic vein thrombosis and congestive heart failure.

Adult↗
PubMedDate not supplied

Late retransplantation of the liver: a single-centre experience.

Liver retransplantation is considered to carry a higher risk than primary transplantation. The aim of this study was to analyse a single-center experience with late liver retransplantation. The overall rate of primary retransplantation was 11% (30 re-OLT out of 272 primary OLT). fiftten of these (50%) had retransplantation more than 3 months after the first transplant and were analyzed by reviewing their medical records. Causes of primary graft failure leading to retransplantation were chronic hepatic artery thrombosis in 6 cases (40%), HCV cirrhotic recurrence in 4 cases (28%), chronic rejection in 2 cases (14%), veno-occlusive disease, hepatic vein thrombosis and idiopathic graft failure in 1 case each (6%). UNOS status at re-OLT was 2A in all cases. All patients were hospitalised, and three of them were in intensive care. One- and two-year patient and graft survival rates were 80% and 66% and 66% and 59%, respectively. Death occurred in 5 patients, including 2 of the 3 admitted to the intensive care unit at the time of retransplantation, who died after a mean interval of 15 +/- 9 days from retransplantation. Retransplantation should be considered a very efficient way of saving lives, especially when the optimal timing for its execution is defined.

Adult↗
PubMed1990

Ultrasound-Doppler diagnosis of Budd-Chiari syndrome.

We report a case of apparently idiopathic Budd-Chiari syndrome, diagnosed by ultrasound and Doppler sonography, in a patient with latent myeloproliferative disease. This case proves that Doppler sonography shows in the hepatic veins a flow pattern suggestive of partial thrombotic obstruction. Moreover, we suggest that the search for a latent myeloproliferative disorder, by means of the spontaneous erythroid colonies formation in culture of bone marrow or blood mononuclear cells, should be routinely included in the diagnostic evaluation of each case of hepatic vein thrombosis without other recognizable causes.

Blood Flow Velocity↗
PubMed1990

In vitro colony culture and chromosomal studies in hepatic and portal vein thrombosis--possible evidence of an occult myeloproliferative state.

We have studied the prevalence of an underlying myeloproliferative state in 20 patients with either hepatic or portal vein thrombosis. Using conventional clinical and laboratory criteria, an underlying myeloproliferative state was identified as the cause of the thrombosis in five patients (25%). A further 10 of the remaining 15 cases were found to have characteristic in vitro bone marrow culture studies and cytogenetic abnormalities suggestive of an underlying myeloproliferative disorder. Although none of these 10 cases have developed overt clinical and laboratory features of such a myeloproliferative disorder after a median observation period of two years, the presence of clonal karyotypic abnormalities in three cases, increased megakaryocyte colony growth in three cases and endogenous erythropoietin independent colony growth of the marrow erythroid progenitors in seven cases, argues strongly in favour of a primary haematological disorder. This has important therapeutic implications, particularly in cases being considered for orthotopic liver transplantation.

Adolescent↗
PubMed2000

Clinical features and etiology of hepatocellular carcinoma arising in patients with membranous obstruction of the inferior vena cava: in reference to hepatitis viral infection.

BACKGROUND AND AIMS: Budd-Chiari syndrome (BCS) comprises hepatic vein thrombosis and inferior vena cava (IVC) obstruction known as membranous obstruction of the IVC (MOVC). The latter is frequently complicated by hepatocellular carcinoma (HCC). The etiology of MOVC-associated HCC in relation to hepatitis viral infection is not known. In this study, we investigated the clinical features and etiology of HCC in MOVC. METHODS: Membranous obstruction of IVC and HCC were diagnosed and studied by using imaging techniques. Sera from patients with MOVC, complicated by HCC, were examined for hepatitis viral antigens and antibodies (hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs), antibody to hepatitis B core antigen (anti-HBc) and third generation antibody to hepatitis C virus (anti-HCV)) and for hepatitis viral nucleic acids (hepatitis B virus (HBV)-DNA, hepatitis C virus (HCV)-RNA, hepatitis G virus (HGV)-RNA and TT virus DNA). RESULTS: We studied 12 patients with BCS who were seen between April 1968 and February 1999. All of them had MOVC. Hepatocellular carcinoma developed in three (25%) of them. There were no obvious differences in the clinical features and imaging findings concerning MOVC between patients with and without HCC. Hepatocellular carcinoma in these three patients showed no clear trend in clinical features and imaging findings. Of the hepatitis viral markers examined, HBsAg, anti-HBc and HBV-DNA were positive in only one of three patients with HCC and all of the viral markers were negative in the other two patients. CONCLUSIONS: Chronic congestion in the liver, caused by an outflow block of hepatic veins and subsequent histopathologic change, must have led to HCC in two patients without any hepatitis viral markers. Patients with MOVC should be followed closely as a high-risk group for HCC.

Adult↗
PubMed2006

Anagrelide: a review of its use in the management of essential thrombocythaemia.

Anagrelide (Agrylin, Xagrid) is an oral imidazoquinazoline agent which is indicated in Europe for the reduction of elevated platelet counts in at-risk patients with essential thrombocythaemia who are intolerant of or refractory to their current therapy, and in the US for the reduction of elevated platelet counts and the amelioration of thrombohaemorrhagic events in patients with thrombocythaemia associated with myeloproliferative disorders. Anagrelide is well established as an effective platelet-lowering agent in most patients with essential thrombocythaemia, including both treatment-naive patients and those refractory to other cytoreductive therapy. Results of the only randomised trial to date (the Primary Thrombocythaemia 1 [PT1] study) indicated that the composite primary endpoint (arterial or venous thrombosis, serious haemorrhage or death from vascular causes) occurred more often in recipients of anagrelide plus aspirin than in those receiving hydroxycarbamide (hydroxyurea) plus aspirin. This trial also indicated that the incidence of the secondary endpoints transient ischaemic attack and gastrointestinal bleeding favoured hydroxycarbamide plus aspirin, while the incidence of venous thrombosis favoured anagrelide plus aspirin. There were no differences between the groups in the incidence of secondary endpoints myocardial infarction, stroke, unstable angina, pulmonary embolism, hepatic-vein thrombosis, other serious haemorrhage or related deaths. The design of the PT1 study has been queried with respect to the heterogeneous nature of the study population (possible inclusion of patients with early myelofibrotic disease) and the concomitant use of aspirin (interaction with anagrelide causing increased bleeding events). Further data are therefore required before the role of anagrelide in essential thrombocythaemia can be finalized. In the meantime, when considering treatment options for patients with this disorder, anagrelide's positive effects on platelet function, lack of mutagenicity and lack of association with leukaemia or angiogenesis must be balanced against its comparative expense and positive inotropic effects. Thus, the role of anagrelide in the management of high-risk patients with essential thrombocythaemia will ultimately depend on individual patient assessment and future clarification of the potential leukaemogenicity of hydroxycarbamide.

Blood Platelets↗
PubMed2002

Maintenance of the celiac trunk with the left-sided liver allograft for in situ split-liver transplantation.

BACKGROUND: It has been shown that in situ split-liver transplantation (SLT) expands the cadaveric donor pool, decreases recipient waiting time, and decreases pretransplant morbidity. However, the technique as previously described requires a microvascular left hepatic artery anastomosis. In an attempt to decrease the incidence of hepatic artery thrombosis and to increase collaboration among transplant teams, in the current report, we describe a modification of the in situ SLT technique that maintains the celiac trunk with the left-sided liver allograft. METHODS: Twelve in situ split-liver procurements resulted in 24 segmental liver allografts; 11 right trisegments, 11 left lateral segments, 1 right lobe, and 1 left lobe. The common bile duct and main portal vein were maintained with the right-sided liver allograft in all cases. The right hepatic artery was divided, and the celiac trunk was maintained with the left-sided liver allograft in nine cases. In one case the left hepatic artery was divided and the celiac trunk was maintained with the right-sided allograft. Two of the 12 donors had a completely replaced left hepatic artery originating from the left gastric artery, which was divided at its origin from the celiac trunk. When the celiac trunk was maintained with the left-sided allografts, arterial reconstruction of the right-sided allograft was performed with an external iliac arterial interposition graft. Nineteen of the 24 split-liver allografts were transplanted at our center. The remaining five liver allografts were shared with regional liver transplant centers. RESULTS: In this series, 1-year actuarial patient and allograft survival rates are 100% and 96%, respectively. Hepatic artery thrombosis (HAT) did not occur in any patient receiving a left-sided split allograft in which the celiac trunk or left gastric artery was maintained; in addition, HAT did not occur in any of the right-sided allografts. HAT did occur immediately after transplantation in the one patient who was transplanted with a left lateral segment without the celiac trunk. This allograft was salvaged by early thrombectomy and interposition grafting. One patient required retransplantation, owing to portal vein thrombosis. Hepatic venous outflow obstruction did not occur in any of the patients. Two patients required reexploration in the posttransplant period because of arterial anastomotic site bleeding, and one of the left lateral segment allograft recipients had a cut-surface bile leak, which was managed nonoperatively. All of the patients are alive and well, including the five patients who received their transplants at other centers, with a median follow-up of 10 months (range, 1-27 months). CONCLUSIONS: In summary, our data demonstrate that maintaining the celiac trunk with the left-sided allograft in SLT provides excellent early survival results with low complication rates. This technical modification obviates the need for a left hepatic artery microvascular anastomosis and should lower the incidence of hepatic artery thrombosis in the small-caliber left hepatic artery. We have also shown that this technique allows sharing among liver transplant centers without compromise in patient or allograft survival rates. It is hoped that this modification in SLT will increase the number of livers split, and will promote sharing among transplant centers to truly optimize the number of liver allografts available from the cadaveric pool.

Adolescent↗
PubMed1986

Hepatic vein occlusion: morphologic features on computed tomography and ultrasonography.

Hepatic vein occlusion causes morphologic changes that can be demonstrated by computed tomography (CT) and ultrasound. In this study the imaging findings of acute, subacute, and chronic occlusion of the hepatic veins were analyzed retrospectively in 9 patients and correlated with the histopathologic changes. The CT findings were focal or scattered hypodense parenchymal lesions of the liver before and a patchy enhancement after intravenous bolus injection of contrast material. In none of the cases could the hepatic veins be identified. Hepatomegaly with relative enlargement of the caudate lobe was almost always observed. Ultrasonography demonstrated solid material within the major hepatic veins, intrahepatic venous collaterals, and focal parenchymal lesions, which varied with the stage of the disease: a hypoechogenic area was observed in acute hepatic vein thrombosis with subsequent hemorrhagic infarction; hyperechogenic lesions corresponded with fibrotic zones in chronic disease. Ascites was shown by both methods in all patients.

Adult↗
PubMed1988

Response to steroids in Budd-Chiari syndrome caused by idiopathic granulomatous venulitis.

A 31-yr-old man presented with the Budd-Chiari syndrome. A liver biopsy specimen demonstrated noncaseating centrilobular granulomas and an idiopathic necrotizing granulomatous venulitis involving hepatic vein radicles with superimposed thrombotic occlusion. High-dose prednisone therapy produced dramatic clinical improvement with resolution of the hepatomegaly, ascites, and portal hypertension and normalization of the hepatic venous angiogram. A repeat liver biopsy specimen showed resolution of the venulitis and disappearance of the hepatic vein thrombosis. Idiopathic granulomatous venulitis that is reversible with prednisone therapy should be considered in the differential diagnosis of the Budd-Chiari syndrome.

Adult↗
PubMed1997

[Budd-Chiari syndrome].

Budd Chiari syndrome is a rare disorder resulting from occlusion of hepatic venous drainage by hepatic vein thrombosis or by a membranous web in the inferior vena cava. In western countries the commonest causes are myeloproliferative disorders and hypercoagulable states. Presentation may be acute with rapid accumulation of ascites and hepatic failure, or subacute with symptoms developing over a few months. A chronic progressive form has also been described. On presentation there is usually abdominal pain, ascites, and hepatosplenomegaly; hepatic encephalopathy is found in about a third. Noninvasive, ultrasound-Doppler is recommended in diagnosis, and has a high correlation with hepatic venography. Liver biopsy is required for therapeutic decisions. Those with advanced hepatic failure or severe fibrosis on liver biopsy are referred for hepatic transplantation. When biopsy shows only hepatic congestion and inflammatory infiltrates, portosystemic shunting is recommended. We present a 61-year-old woman with ascites and hepatosplenomegaly that had developed over the courses of a few months. Budd-Chiari syndrome with chronic myelofibrosis and congenital protein C deficiency were diagnosed. Portosystemic shunt was performed but death from sepsis followed shortly.

Budd-Chiari Syndrome↗
PubMed1991

Vascular complications after orthotopic liver transplantation.

Over a 57-month period, we performed 430 orthotopic liver transplants in 372 patients. A total of 38 vascular complications were identified including hepatic artery thrombosis (n = 24), portal vein thrombosis (n = 6), combined hepatic artery thrombosis/portal vein thrombosis (n = 3), and hepatic artery rupture (n = 5). A number of potential risk factors for the development of vascular thrombosis were evaluated with only children, weight less than 10 kg, and cold ischemia time found to be significant. The clinical presentation included fulminant hepatic failure, allograft dysfunction, biliary sepsis, and screening ultrasound. Duplex ultrasonography was diagnostic in nearly all cases. Therapeutic modalities included revascularization, revascularization followed by retransplantation, retransplantation alone, and observation. Five cases of hepatic artery rupture occurred in four patients. Infectious arteritis was present in four patients. The 6-month actuarial survival in patients with vascular complications was 70%. Early diagnosis is critical for graft salvage, with surgical intervention the mainstay of therapy.

Adult↗
PubMed1983

Budd-Chiari syndrome and renal failure in Behcet disease. Report of a case and review of the literature.

A case of Behcet syndrome associated with three rare complications is presented. The patient initially presented with asymmetric polyarticular arthritis, subcutaneous nodules, conjunctivitis, and episcleritis. Necrotizing vasculitis and renal failure subsequently evolved. Despite immunosuppressive therapy, Budd-Chiari syndrome with high grade hepatic obstruction developed. A Denver shunt procedure failed to alter the terminal course. At postmortem examination, skin lesions, carditis, hepatic vein thrombosis, gastric ulcerations, and focal proliferative glomerulonephritis were found. The immunoglobulins and complement present in skin and renal tissue suggest an immune complex pathogenesis.

Adult↗
PubMed1994

Preparation of aminated fucoidan and its evaluation as an antithrombotic and antilipemic agent.

Fucoidan, a sulfated poly(L-fucopyranose), is an effective anticoagulant in vitro and in vivo. In the present study, an aminated derivative of fucoidan was prepared and examined for its fibrinolytic and anticoagulant activities. The aminated derivative was more potent than native fucoidan as a stimulator of tissue plasminogen activator-induced plasma clot lysis, and its effectiveness was comparable to that of oversulfated fucoidan reported previously. Furthermore, the ability of aminated fucoidan to accelerate heparin cofactor II-mediated thrombin inhibition was 2.3 times more potent than that of native fucoidan. Aminated fucoidan effectively prevented endotoxin-induced hepatic vein thrombosis in hyperlipemic rats and decreased the elevated levels of serum cholesterol and triglyceride. The present results that the anticoagulant and antilipemic potency of fucoidan can be improved by charge modification may provide useful clues for the development of an ideal anticoagulant and antilipemic drug.

Amines↗
PubMed2005

Unusual thromboses associated with protein S deficiency in patients with acquired immunodeficiency syndrome: case reports and review of the literature.

Recent reports indicate that patients infected with HIV are at increased risk for the development of thrombosis. Among other possibilities, an acquired deficiency of protein S (PS), one of the plasma's natural anticoagulants, might explain this tendency. PS deficiency can be classified in three types depending on the levels of total and free protein (antigenic assays) as well as anticoagulant activity (functional assay). Although the prevalence of inherited PS deficiency is not known because of its rarity, several conditions can lead to acquired forms of the disease. We report two AIDS patients with coexistent type III PS deficiency and thrombosis. Our first patient presented with bilateral chronic leg ulcers and a skin biopsy revealed dermal microthromboses. On laboratory evaluation he had PS deficiency and was started on anticoagulation, but was lost to follow-up. The second patient presented with hepatic vein thrombosis (Budd-Chiari syndrome) and was also PS deficient. On long-term anticoagulation, she experienced resolution of the thrombosis. Neither patient had prior personal or family history of venous thrombosis, nor acquired risk factors such as immobility, acute infection, recent surgery, or hormonal therapy. The literature contains a few reports of skin ulcers and Budd-Chiari syndrome associated with PS deficiency, although none in AIDS patients. While a larger number of studies describe an association between PS deficiency and HIV infection, the causal effect of this deficiency on the thrombophilic tendency in AIDS has not been established. We propose that awareness of the increased risk for thrombosis in HIV infection is important to the understanding of disease pathophysiology and management of these patients.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Hepatic artery chemoembolization or embolization for primary and metastatic liver tumors: post-treatment management and complications.

This paper describes complications and patient management issues associated with hepatic arterial chemoembolization (HACE) and embolization (HAE) used to treat liver malignancies and characterizes patient survival based on histologic tumor type. We performed a retrospective review of all patients treated with HACE or HAE between January 1, 1988 and December 31, 1990. During the study period, 314 HACEs and HAEs were performed in 121 patients. Ninety-six of the patients (79%) were treated for neoplasms metastatic to the liver. The morbidity rate following HACE and HAE in this study was 5.1%. The major complications included portal vein thrombosis, hepatic abscess, and liver failure. The treatment-related mortality rate was 4.1%. Fever and ileus were the most common management problems following HACE or HAE. Median survival for patients with liver metastases varied according to histologic type, and median survival for patients with hepatocellular cancer was 306 days. Morbidity and mortality from HACE and HAE to treat liver tumors can be minimized by proper selection and careful management of patients. HACE or HAE alone was not curative in any of these 121 patients. An understanding of treatment-related side effects is necessary to aid in the management of patients following HACE or HAE.

Adult↗
PubMed1995

Sonographic diagnosis of hepatic vascular disorders.

Perhaps the most valuable application of duplex sonography in the abdomen is in the diagnosis of vascular disorders of the liver. Duplex sonography provides an accurate assessment of the portal and hepatic venous systems that is both noninvasive and convenient, because the examination can be conducted at the bedside. In this article, the normal features of portal and hepatic venous flow are considered as well as the sonographic manifestations of pathological conditions, including: (1) portal hypertension; (2) portosystemic collaterals; (3) portal vein thrombosis; and (4) hepatic vein thrombosis (Budd-Chiari syndrome).

Budd-Chiari Syndrome↗