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PubMed2006

Therapeutic approach to "downhill" esophageal varices bleeding due to superior vena cava syndrome in Behcet's disease: a case report.

BACKGROUND: One of the rare presentations of superior vena cava syndrome is bleeding of "downhill" esophageal varices (DEV) and different approaches have been used to control it. This is a case report whose DEV was eradicated by band ligation for the first time. CASE PRESENTATION: We report a 42-year-old man who is a known case of Behcet's disease. The patient's first presentation was superior vena cava syndrome due to thrombosis followed by bipolar ulcers and arthralgia. He received warfarin, prednisolone and azathioprine. The clinical course of the patient was complicated by one episode of hematemesis without abdominal pain when the patient's PT was in therapeutic range. After resuscitation and correction of PT with fresh frozen plasma transfusion, upper gastrointestinal endoscopy was done. Prominent varices were seen in the upper third of the esophagus, tapering to the middle part without acute bleeding. Stomach and duodenum were normal. Color ultrasonography evaluation of the portal, hepatic and splenic veins was negative for thrombosis. Band ligation was done and the patient's bleeding did not recur. CONCLUSION: Band ligation is a safe and effective method for controlling DEV bleeding in patients with uncorrectable underlying disorders.

Adult↗
PubMed1993

[Resurgence of a forgotten pathology: pylephlebitis caused by tuberculous adenopathies].

The incidence of abdominal tuberculosis represents less than 1% of all forms of tuberculosis. We report the case of a portal vein thrombosis associated with tuberculous adenopathy of the hepatic hilum discovered in a young woman free of symptoms, without any risk factors, who had recovered from a cavity pulmonary tuberculosis after a classical anti-tuberculous treatment. This case suggests that abdominal tuberculosis often remains undiagnosed. Reemergence of tuberculosis is likely because of the increase in the incidence of the acquired immunodeficiency syndrome.

Adult↗
PubMed1997

Factors affecting survival after orthotopic liver transplantation in infants.

The technical and medical management of small infants requiring orthotopic liver transplantation remains a challenge. The present study examined 117 orthotopic liver transplantations performed in 101 infants from <1 to 23 months of age between March 1988 and February 1995 to determine factors that influence patient and graft outcome. Factors analyzed included etiology of liver disease, recipient and donor age and weight, United Network for Organ Sharing (UNOS) status, retransplantation, ABO-compatibility, full-size (FS) versus reduced-size grafts, vascular thrombosis (VT), including hepatic artery and portal vein (PVT), and the presence of lymphoproliferative disease (LPD). UNOS status 1, fulminant hepatic failure, and the development of Epstein-Barr virus-associated LPD were each associated with 10-20% lower patient and graft survival rates. Of 101 infants, 11 (11%) developed LPD with an associated 36% mortality. VT occurred in 10 (9 hepatic artery and 1 portal vein) of 117 orthotopic liver transplantations (9%), all less than 1 year of age, and was associated with significantly poorer 1-year (50% vs. 85% no VT, P<0.01) and 5-year patient survival rates (50% vs. 83% no VT, P<0.01). One-year graft survival rates for FS grafts in recipients <12 months versus 12-23 months were 67% vs. 94% (P<0.01); the patient survival rate was also significantly lower in FS graft recipients <12 months (76% vs. 100%, P<0.05). Recipients <5 months of age had the worst survival rates: 1-year and 5-year patient survival rates were 65% and 46% for recipients 0-4 months (n=17) versus 82% and 82% for recipients 5-11 months (n=56), and 93% and 93% for recipients age 12-23 months (n=28; P<0.05). In summary, factors associated with reduced survival rates include recipient age <5 months, recipient age <12 months who received FS grafts, development of VT and donor weight <6 kg. There was a trend for UNOS status 1, fulminant hepatic failure, and presence of LPD to be associated with reduced survival rates.

Aging↗
PubMed1979

The pathology and pathogenesis of fatal hepatic amoebiasis--A study based on 79 autopsy cases.

The present study is based on a retrospective analysis of 79 autopsy cases of hepatic amoebiasis. An attempt has been made to reconstruct the sequence of events starting from intestinal infection to invasion and transport of amoebae along the radicles of the portal veins, the formation of early Zahn's infarct and the proliferation of amoebae in such foci leading to the formation of small abscesses. The coalescence of small abscesses gives rise to the apparently large abscesses. Apart from direct contiguity, more distant extension leading to a satellite abscess is due to involvement of the hepatic and/or portal venous radicles. It seems that obstruction of the hepatic vein contributes substantially towards the enlargement of the liver and its exaggerated nutmeg appearance. Signs and symptoms of hepatic vein obstruction sometimes overshadow the abscess pathology. Thrombosis or pressure of a neighbouring abscess over the portal vein obstruction sometimes overshadow the abscess pathology. Thrombosis or pressure of a neighbouring abscess over the portal vein and bile-duct lead to development of portal hypertension and jaundice. Both cell-mediated and humoral immunity are depressed in fatal cases of hepatic amoebiasis.

Budd-Chiari Syndrome↗
PubMed2000

Combined hepatic artery and segmental portal vein occlusion in antiphospholipid syndrome.

Antiphospholipid syndrome can have various clinical presentations, two of the most common being arterial and venous thrombosis. It is, however, unusual for them to occur in combination. We report here a case of combined hepatic artery and segmental portal venous occlusion in a 32-year-old patient who was shown to have a lupus anticoagulant. There have been no previous reports of thrombosis occurring simultaneously in the coeliac axis and the portal vein. Computerised tomography, Doppler ultrasound scanning and selective visceral angiography were used to demonstrate the anatomical lesions. The patient was treated medically with unfractionated heparin leading to a favourable clinical outcome. The diagnosis and management of this case is discussed with reference to the current literature on visceral thrombosis and antiphospholipid antibody syndrome.

Adult↗
PubMed1989

[Oral contraceptives and blood diseases are the most common causes of Budd-Chiari syndrome].

Two cases of young patients with the chronic form of Budd-Chiari syndrome are reported. The first concerns a 22-year-old woman with a 6-month history of hepatomegaly, who had used oral contraceptives almost continuously during the five years preceding diagnosis. In a thorough diagnostic work-up, thromboses were detected in all but one of the hepatic veins, and a possible non-occluding thrombosis in the retrohepatic portion of the inferior vena cava. In the blood and bone marrow, findings were compatible with polycythaemia rubra vera, and a high anti-cardiolipin antibody titre was found. The second case concerns a 25-year-old male smoker with normal bone marrow, who had thromboses in at least two of the hepatic veins, though the inferior vena cava was not occluded. In both cases a mesocaval shunt was interposed with synthetic grafts, and postoperatively the patients are doing well--at sixteen and five months, respectively. Both are maintained on anticoagulants, and even without diuretics there has been no recurrence of ascites. The woman takes a small dose of hydroxy-urea to control her hypercoagulability. To our knowledge, hers is the first case to be reported of Budd-Chiari syndrome with hypercoagulability due to the concomitant presence of oral contraceptives, polycythaemia rubra vera and anti-phospholipid antibodies.

Adult↗
PubMed1994

Maintaining long-term central venous access by repetitive hepatic vein cannulation.

Long-term central venous access has become a critical issue in the treatment of pediatric patients. Exhaustion of access sites can lead to superior and inferior vena cava thrombosis, limiting the choices for central line placement. Under such circumstances, hepatic vein cannulation is a viable option. We present the cases of two patients who, combined, have undergone five hepatic vein catheterizations. One patient has received four consecutive central lines via a hepatic vein. This experience suggests that the hepatic vein is a reusable site of cannulation in patients with no other alternative for venous access.

Catheterization, Central Venous↗
PubMed1976

[Obliterative disease of liver veins: clinical, diagnostic, therapeutic and pathogenetic aspects of Budd-Chiari syndrome (author's transl)].

Both external and internal factors have to be thought of as causes of obliterative disease of liver veins. Pathogenetically, thrombosis or proliferative vascular disease (endophlebitis hepatica obliterans) may affect either large veins (with occlusion of the ostia) or small ones. Veno-occlusive disease, caused by pyrrolizidine derivatives, is a special form. Injection of contrast medium to the inferior vena cava and (or) the liver veins is the most important diagnostic method. In two personal cases there was secondary occlusion of the liver veins as a result of IVC thrombosis, while in a third case there was non-thrombotic proliferative disease of the wall of the small hepatic veins, closely similar to veno-occlusive disease. In a 19-year-old girl in whom thrombosis of the vena cava (with signs of liver-vein occlusion) occurred after pregnancy, revascularisation was achieved by fibrinolytic treatment.

Adult↗
PubMed1992

The incidence of portal vein thrombosis at liver transplantation.

The incidence of portal vein thrombosis was examined in 885 patients who received orthotopic liver transplantations for various end-stage liver diseases between 1989 and 1990. The thrombosis was classified into four grades. Grade 1 was thrombosis of intrahepatic portal vein branches, grade 2 was thrombosis of the right or left portal branch or at the bifurcation, grade 3 was partial obstruction of the portal vein trunk, and grade 4 was complete obstruction of the portal vein trunk. Among the 849 patients without previous portosystemic shunt, 14 patients (1.6%) had grade 1, 27 patients (3.2%) had grade 2, 27 patients (3.2%) had grade 3 and 49 patients (5.8%) had grade 4 portal vein thrombosis. The incidence of portal vein thrombosis was highest (34.8%) in the patients with hepatic malignancy in the cirrhotic liver, followed by those with Budd-Chiari syndrome (22.2%) and postnecrotic cirrhosis of various causes (15.7%). The patients with encephalopathy, ascites, variceal bleeding, previous splenectomy and small liver had significantly higher incidences of portal vein thrombosis than the others. The total incidence of portal vein thrombosis among the 36 patients with previous portosystemic shunt was 38.9%, which was significantly higher than that (13.8%) of those without shunt.

Adolescent↗
PubMed1998

Characteristics of hepatocellular carcinoma presenting with variceal bleeding.

Patients with hepatocellular carcinoma may present with variceal bleeding as the initial symptoms. The aims of this study is to investigate the characteristics of such patients. A total of 1046 hepatocellular carcinoma cases were retrospectively retrieved from our computer records between 1980 and 1993. The medical records and image studies were reviewed. The status of each patient was assessed at the time of presentation. A total of 14 (about 1 %) patients with hepatocellular carcinoma presented with variceal bleeding. Five (36%) did not have past history of liver disease. The tumour size ranged from 2.5 to 11.3 cm. Compared with hepatocellular carcinoma patients not presenting with variceal bleeding, these patients had a higher percentage of portal vein thrombosis (57.1 vs 19.4%). In two patients, the hepatic tumours were missed in the initial abdominal sonography. The average survival time was 71 days. Seven patients died within 2 months mainly due to variceal bleeding (41.6%). Variceal bleeding might be a clue to the presence of hepatocellular carcinoma with portal vein thrombosis even in patients without a previous history of liver disease. The tumours in such patients might be the infiltrative type, and thus the portal vein should be carefully worked-up. Overall, these patients have an extremely poor prognosis. In the management of patients with variceal bleeding, the possibility of hepatocellular carcinoma with portal vein thrombosis should not be overlooked, especially in areas where this cancer is prevalent.

Carcinoma, Hepatocellular↗
PubMed2005

Liver transplant with portocaval hemitransposition: blood supply with only hepatic artery is possible?

We present herein a case of orthotopic liver transplantation (OLT) with portocaval hemitransposition. The patient underwent OLT for hepatocellular carcinoma with diffused portomesenteric vein thrombosis. The unique feature of this case was that 6 months after the operation, because of recurrent carcinoma, the hepatic vein was occluded and the portal vein became the drainage vein and the hepatic artery was the only vessel that supplied the liver. Yet the patient survived. Regarding the unique hemodynamic changes of the patient, could we let the portal vein alone in case of diffuse portomesenteric thrombosis in OLT?

Adult↗
PubMed2003

A 25-year clinical history of portopulmonary hypertension associated with latent myeloproliferative disorder.

Pulmonary hypertension associated with increased pulmonary vascular resistance occurring in the setting of portal hypertension, referred to as "portopulmonary hypertension", is a complication of chronic liver disease, and occurs in 2% to 3% of patients with portal hypertension. Portal hypertension is a relatively common finding in patients with chronic myeloproliferative disorder (CMPD). Pulmonary hypertension is also an occasional finding in CMPD patients. Latent myeloproliferative disorder, on the other hand does not fulfill the diagnostic criteria of classical CMPD and is characterized by younger age of onset, slow disease progression, a high risk of thrombosis, platelet dysfunction, and normal or increased platelet count in spite of the presence of splenomegaly. We report findings in a 50-year-old woman with portal hypertension for which there were three major etiological findings-increased splenic blood flow, infiltration of hematopoietic cells in the liver, and thrombosis in the portal or hepatic vein-over a 25-year clinical course, during which there was also reversible stenosis of the portal vein. Twenty-three years after her first admission, her condition was diagnosed as latent myeloproliferative disorder, and she developed pulmonary hypertension. Her clinical history and data indicated that the portopulmonary hypertension was due to the latent myeloproliferative disorder.

Constriction, Pathologic↗
PubMedDate not supplied

Living donor liver transplantation in adult patients: our experience.

INTRODUCTION: Living donation in adult liver transplantation (LDLTx) is an important resource because of the waiting list growth. We started a living donor program to overcome the shortage of cadaveric sources. PATIENTS: From May 2001 to May 2003, 36 patients underwent LDLTx: 27 received a right lobe, 8 received a left lobe, and 1 received segments II and III. RESULTS: The 1-year actuarial survival rate was 77.7%, with a mean follow-up, in survivors, of 754 +/- 248 days. Eleven of 27 (40.7%) right lobe recipients died. Among left graft recipients, 3 patients died (33%). We undertook retransplantation in 4 cases, because of 2 "small for size" syndrome, 1 late hepatic artery thrombosis, and 1 early portal vein thrombosis. After a period of 797 days, all 36 donors returned to a normal social and working life. Two donors, who underwent right lobe donation, experienced major complications: 1 case of biliary stenosis, treated by stenting, and 1 case of biliary leak from the cut surface of the liver, requiring laparotomy and abscess drainage. Left lobe donors developed no complications. CONCLUSIONS: LDLTx has a learning curve for experienced liver transplantation surgeons. Our last 18 cases showed better survivals than the first 18 (9 deaths vs 5), even if, in the latter group, we transplanted 8 left livers. In our experience, LDLTx of a left liver graft has an increased risk of "small for size syndrome," but patients, both donors and recipients, report improved outcomes.

Actuarial Analysis↗
PubMed2003

Cholangiocarcinoma in liver cirrhosis.

BACKGROUND AND AIM: Hepatocellular carcinoma (HCC) is usually associated with chronic liver diseases and liver cirrhosis, while conversely, cholangiocarcinoma (CC) usually occurs in a non-cirrhotic liver. The purpose of the present study was to evaluate CC in liver cirrhosis. METHODS: Between January 1998 and December 1999, 26 patients with CC were retrospectively reviewed. The occurrence of CC in chronic hepatitis B infection-related liver cirrhosis, portal vein thrombosis (PVT) and survival were analyzed. RESULTS: Twenty-six patients with CC (19 with a non-cirrhotic liver and seven with chronic hepatitis B infection-related liver cirrhosis) were included in the present study. All cases of CC in the cirrhotic group were incidentally discovered during routine screening for HCC. The mean age (+/- SD) was 58.8 +/- 14 years in the cirrhotic group and 73.2 +/- 15.9 years (P = 0.001) in the non-cirrhotic group. When compared to the cirrhotic group, the non-cirrhotic group had a higher median level of albumin (42 compared to 30 g/L, P = 0.005), bilirubin (117.5 compared to 18 micro mol/L, P = 0.01), alkaline phosphatase (291.5 compared to 100 U/L, P = 0.001) and gamma glutamyl transpeptidases (215.5 compared to 31 U/L, P = 0.001). In contrast, the cirrhotic group had a higher median prothrombin time (PT) compared to the non-cirrhotic group (18.2 compared to 12 s, P = 0.05). In the non-cirrhotic group, only one patient (5.3%) showed evidence of PVT on a computerized tomography and Doppler ultrasound, while in the cirrhotic group six patients (85.7%) had PVT (P < 0.001). The median survival period in the cirrhotic group was six months (range 2-24 months) compared to 16 months (range 6-41 months) in the non-cirrhotic group (P = 0.036). CONCLUSION: CC in cirrhotic liver presented at a younger age and patients who developed CC were prone to PVT. The survival period was also shorter in comparison to that of non-cirrhotic liver patients.

Adult↗
PubMed2000

Erythematous plaques due to platelet plugging: a clue to underlying myeloproliferative disorder.

We report a syndrome in a middle-aged woman characterized by tender erythematous plaques with histologic evidence of dramatic dermal vessel occlusion. These cutaneous findings occurred in association with progressive inferior vena cava and portal vein thrombosis while on coumarin anticoagulation, following hepatic transplantation for Budd-Chiari syndrome. The material occluding dermal vessels was proven by immunohistochemical staining to be platelet plugs. These findings led to the diagnosis of an underlying myeloproliferative disorder explaining both her cutaneous and liver abnormalities and institution of appropriate platelet directed anticoagulation with aspirin.

Bone Marrow↗
PubMed1998

Pediatric liver transplantation.

Liver transplantation is accepted therapy for acute or chronic liver failure. Advances in preoperative and postoperative management and surgical techniques have extended the indications for transplantation and refined selection, particularly for fulminant hepatic failure. Radiologic techniques, such as magnetic resonance imaging and placement of transjugular intrahepatic portosystemic shunts, have improved preoperative assessment and management. Successful split liver and living related transplantation may reduce waiting list deaths and relieve the organ donor shortage. Auxiliary liver transplantation, although technically difficult, is now accepted management for Crigler-Najjar type I disease but remains controversial for the treatment of organic acidemias and fulminant hepatic failure. Microsurgical techniques have reduced the incidence of postoperative hepatic thrombosis, and radiologic management of portal vein thrombosis and stenosis has decreased operative intervention and improved survival. Immunosuppressive drugs such as cyclosporine microemulsion and tacrolimus have the potential to improve rejection rates and reduce sepsis in the future. There are now good data confirming that long-term survival is achieved with nutritional rehabilitation and good quality of life.

Child↗
PubMed2001

Factor V Leiden related Budd-Chiari syndrome.

BACKGROUND: The role of factor V Leiden as a cause of Budd-Chiari syndrome has only recently been described. AIMS: To assess the specific features of factor V Leiden related Budd-Chiari syndrome. PATIENTS: Sixty three consecutive patients with hepatic vein or terminal inferior vena cava thrombosis. METHODS: Standardised chart review. RESULTS: Factor V Leiden was found in 20 patients (31% (95% CI 20-43)). In the subgroup of patients with, compared with the subgroup without, factor V Leiden, a combination of prothrombotic states was more common (70% (95% CI 50-90) v 14% (95% CI 3-24)); inferior vena cava thrombosis was more frequent (40% (95% CI 19-61) v 7% (95% CI 0-14)); and distribution of initial alanine aminotransferase values was bimodal (almost normal or extremely increased) versus unimodal (p=0.003). Factor V Leiden accounted for four of five cases of massive ischaemic necrosis (transaminases >50-fold the upper limit of normal values) (p=0.014), and also for all three cases developing during pregnancy. Patients with and without factor V Leiden did not differ with regard to mortality, portosytemic shunting, or listing for liver transplantation. Hepatocellular carcinoma developed in two patients; both had factor V Leiden and indolent obstruction of the inferior vena cava. CONCLUSIONS: In patients with Budd-Chiari syndrome, factor V Leiden (a) is common; (b) precipitates thrombosis mostly when combined with another risk factor; (c) is associated with one of two contrasting clinical pictures: indolent thrombosis-particularly of the inferior vena cava-or massive ischaemic necrosis; and (d) is a major cofactor of Budd-Chiari syndrome developing during pregnancy.

Adult↗