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PubMed1999

Portal vein thrombosis in paroxysmal nocturnal haemoglobinuria.

A 28-year-old man was hospitalized with nausea, vomiting, abdominal pain and low-grade fever. He had a 6-month history of paroxysmal nocturnal haemoglobinuria (PNH), and laboratory data showed anaemia and liver dysfunction. An abdominal ultrasonography showed ascites and portal vein thrombosis. After receiving antithrombotic treatment, the portal vein thrombosis did not extend. Portal vein thrombosis is very rare but should be considered when we encounter liver dysfunction associated with PNH as well as hepatic vein thrombosis. Ultrasonography is very useful in detecting portal vein thrombosis and facilitating early diagnosis. Warfarin is very effective in preventing exacerbation of portal vein thrombosis in PNH.

Adult↗
PubMedDate not supplied

Evaluation of hemodynamics and hepatic mitochondrial function on extrahepatic portal obstruction in the rat.

An animal model resembling clinical cases with extrahepatic portal vein obstruction was developed. The changes in hepatic mitochondrial function and the hepatic hemodynamics including hepatic regional blood flow, portal venous pressure, and portogram were evaluated to assess the effect of portal vein obstruction in the model. Portal vein ligation in this model was a simple and easy maneuver and could produce collateral veins to the liver--cavernomatous transformation--which were obviously seen in clinical patients with extrahepatic portal obstruction. Hepatic blood flow was significantly decreased until 5 days after portal vein ligation; however, hepatic blood flow was gradually increased and reached the normal value at 3 weeks after portal vein ligation due to the formation of the collateral veins to the liver. Respiratory parameters of mitochondria were gradually decreased and reached the lowest levels at 5 days after portal vein ligation, while they recovered to normal values in accordance with increasing hepatic blood flow at 3 weeks after portal vein ligation. In extrahepatic portal obstruction, although the liver is temporarily deteriorated by portal vein obstruction such as portal vein thrombosis, hepatic blood flow and the liver functions are to be normally improved with the formation of collateral veins to the liver.

Animals↗
PubMed1989

Thrombosis in particular organ veins.

Renal vein thrombosis in early infancy is a complication of dehydration and prolonged hypotension. The onset is usually acute and the most common clinical signs are uni- or bilateral frank masses, hematuria, proteinuria and thrombocytopenia. In most cases, with conservative management, the late outcome is favorable. In the adult, renal vein thrombosis is often a silent complication of the nephrotic syndrome, the hypercoagulability of which may be an important factor in the pathogenesis of the thrombosis. Clinically, the presentation of a sudden complete occlusion is that of severe abdominal and lumbar pain with hematuria and loss of function of the kidney that suffers hemorrhagic infarction. Physical examination often reveals an enlarged kidney. With gradual occlusion, renal function is preserved. The initial diagnostic approach is with ultrasound studies and computed tomography; definitive diagnosis is established by renal venography or by selective renal arteriography. In general, a conservative approach including the use of anticoagulant treatment is preferred to surgical intervention. Priapism is a persistent painful penile erection due to ischemic or non-ischemic causes; therapeutic intracavernosal injection of papaverine is becoming the most common cause. In early and mild stages, aspiration of blood from the corpora cavernosa supplemented with intracavernosal irrigation with alpha-stimulating agents is the procedure of first choice; in late and severe ischemia, a shunt procedure may become necessary. Hepatic vein thrombosis occurs in association with a number of conditions considered predisposing factors including the use of oral contraceptives. The clinical picture may be that of an acute illness with abdominal pain, hepatomegaly, ascites and hepatic failure as well as early death. More often, the onset is insidious with slowly developing ascites and wasting. For the diagnosis, hepatic scintigraphy may be helpful but, at present, ultrasonography, computed tomography and magnetic resonance scanning are procedures of choice. There is, as yet, no adequate treatment. A fatal outcome may be prevented by surgical decompression of the congested liver and, in recent years, liver transplantation has been employed. Portal vein thrombosis, in children, is usually considered a complication of umbilical sepsis or a result of a congenital abnormality of the portal vein. In adults, the most frequent causes are hepatic cirrhosis and neoplasia. Clinically, there may be a sudden appearance of ascites with resolution in a symptom-free interval until the onset of other features of portal hypertension occur. Currently, ultrasound real-time imaging supplemented with Doppler capability, computed tomography and magnetic resonance scanning provide the necessary diagnostic information. Variceal hemorrhage is often the first major complication requiring treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Budd-Chiari Syndrome↗
PubMed1995

Postpartum thrombotic thrombocytopenic purpura complicated by Budd-Chiari syndrome.

BACKGROUND: Thrombotic thrombocytopenic purpura is an infrequent but devastating complication of pregnancy, often difficult to differentiate from severe preeclampsia and the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP). To our knowledge, the combination of thrombotic thrombocytopenic purpura and hepatic vein thrombosis has not been reported previously in pregnancy. CASE: A 33-year-old woman, a multigravida, was delivered at 36 weeks' gestation because of pregnancy-induced hypertension and HELLP syndrome. Postpartum, the patient became obtunded, disoriented, and anuric. Her laboratory values revealed a Coombs-negative, microangiopathic hemolytic anemia, modestly abnormal coagulation studies, and thrombocytopenia. She also had elevated liver enzymes, lactate dehydrogenase, and creatinine. The largest plasma von Willebrand factor multimeric forms were relatively decreased in her ethylenediaminetetra-acetic acid-platelet-poor plasma. A diagnosis of thrombotic thrombocytopenic purpura was made. The patient received plasma exchange, hemodialysis, blood transfusion, and glucocorticoids. She responded to therapy, but was later noted to have increasing hepatosplenomegaly, rising levels of bilirubin, and elevated alkaline phosphatase. A Doppler study and magnetic resonance imaging demonstrated the absence of flow in the middle and left hepatic veins, secondary to thrombosis (Budd-Chiari syndrome). She was maintained on warfarin therapy and was discharged on postpartum day 50. CONCLUSION: The early recognition of thrombotic thrombocytopenic purpura is crucial for the initiation of appropriate treatment as soon as possible. The avoidance of platelet transfusion and early plasma-exchange therapy may be lifesaving.

Adult↗
PubMed1989

Occlusion of small hepatic veins associated with systemic lupus erythematosus with the lupus anticoagulant and anti-cardiolipin antibody.

We report the case of a woman with lupus anticoagulant-positive systemic lupus erythematosus who developed small hepatic vein occlusion. Since the age of 34, she had been known to have hepatomegaly. A definitive diagnosis of systematic lupus erythematosus was made eight years later. Histological evaluation of the liver biopsy specimen was not fully diagnostic of prominent hepatomegaly during this period. Occlusion of the small hepatic veins was confirmed by hepatic venography, but the lumen of the large hepatic veins showed a smooth appearance. The lupus anticoagulant and anti-cardiolipin antibody were both positive. Since a high incidence of thromboembolic diseases in patients with the lupus anticoagulant or anti-cardiolipin antibody has been reported, the presence of this type of anticoagulant may provide an explanation for hypercoagulability and subsequent development of hepatic vein thrombosis in this patient. This is the first report of a patient with systemic lupus erythematosus who developed an occlusion of small hepatic veins attributable to the lupus anticoagulant and anticardiolipin antibody. This case suggested that a systematic search for hepatic vein occlusion should be made in patients with systemic lupus erythematosus who have developed inexplicable hepatomegaly, especially in those with positive tests for the lupus anticoagulant and/or anti-cardiolipin antibody.

Adult↗
PubMedDate not supplied

Carcinogenicity of heptachlor and heptachlor epoxide.

Heptachlor and its metabolite heptachlor epoxide are unequivocally carcinogenic in rats and mice. The chemicals induced carcinomas of the liver, which were highly significant. There were neoplasms at other sites in rats. Neoplasms at all sites, as well as malignant tumors, were increased in heptachlor-treated male rats. There were similar increases in benign and malignant neoplasms of endocrine organs, particularly in female rats. Neoplasms of the thyroid and pituitary were increased in male rats and neoplasms of the reproductive system, including the ovary and uterus, in female rats given heptachlor. Mice also developed hepatic vein thrombosis and thrombosis of the atria of the heart. Nephritis, myocarditis, encephalitis, hepatitis, polyarteritis and atrophy of the testes were observed in rats.

Animals↗
PubMed1978

Treatment of Budd-Chiari syndrome by side-to-side portacaval shunt: experimental and clinical results.

The Budd-Chiari syndrome caused by occlusion of the major hepatic veins, often of unknown etiology, is typically characterized by massive ascites, hepatomegaly and abdominal pain due to intense congestion of the liver. The outcome has almost always been fatal. This report describes an evaluation of side-to-side portacaval shunt in dogs with experimental Budd-Chiari syndrome and in six patients with hepatic vein thrombosis. In the animal studies, side-to-side portacaval shunt was very effective in relieving massive ascites, hepatomegaly, hepatic congestion and portal hypertension produced by ligation of the hepatic veins. Only one of 24 dogs with side-to-side anastomosis reformed ascites, 67% of the animals survived until the study was concluded after one year, and liver biopsies showed reversal of the severe pathologic abnormalities. In contrast, all 20 control dogs subjected to a sham laparotomy, and all 20 dogs that underwent end-to-side portacaval shunt reformed massive ascites and died within six months with continued hepatic congestion and necrosis. All six patients with the Budd-Chiari syndrome due to hepatic vein occlusion had massive ascites (4.4-15.9 l), hepatomegaly, abdominal pain and disturbed liver function. In all six, angiography demonstrated occlusion of the hepatic veins with a patent inferior vena cava (IVC) and a normal IVC pressure, and liver biopsy showed intense centrilobular congestion and necrosis. The most valuable diagnostic study was angiography of the IVC and hepatic veins with pressure measurements. Side-to-side portacaval shunt was performed from four to 14 weeks after the onset of symptoms, and produced dramatic and sustained relief of ascites in five of the six patients during follow-up periods of from eight months to seven years. Liver function returned to normal, hepatosplenomegaly disappeared, none of the survivors developed portal-systemic encephalopathy, and follow-up liver biopsies showed disappearance of congestion and necrosis, but mild to moderate fibrosis. One patient died following an emergency IVC thrombectomy and portacaval shunt, which was undertaken when, during the course of his workup, his condition deteriorated suddenly because the thrombotic process extended from the hepatic veins into the IVC. The everpresent risk of this complication, and the dangers associated with delaying operation were emphasized by this case. It is concluded that side-to-side portacaval shunt, which decompresses the liver by converting the portal vein into an outflow tract, provides effective treatment of the Budd-Chiari syndrome when the occlusive process is confined to the hepatic veins.

Adult↗
PubMed1979

[Liver and ovulation inhibitors. Effects on liver function of estrogen-progestagen containing steroid oral contraceptives].

Since introduction of oral contraceptive steroids a variety of physiologic-adaptive and toxic side effects have been reported. -a review is given. The study reports also four cases of hepatic vein thrombosis (Budd-Chiari-Syndrome--Venoocclusive disease) and three cases of benign hepatic tumors (liver cell adenoma and focal nodular hyperplasia) in young women following 2- to 5-year treatment with oral contraceptive steroids.

Adenoma↗
PubMed2004

Simultaneous hepatic artery and portal vein thrombosis after living donor liver transplantation.

Simultaneous hepatic artery and portal vein thrombosis rarely occurs after liver transplantation. The etiology is unknown. Of 213 patients (72 children and 141 adults) that underwent living donor liver transplantation (LDLT) from January 1996 to March 2003, 4 (2%) developed simultaneous thrombosis at 3 hours to 7 days (median, 4 days) after the operation. Emergent thrombectomy was performed in three patients; the remaining patient was registered in the Japan organ transplant network. All of the patients died due to hepatic failure (range, 18 hours to 6 days after the diagnosis; median, 2 days). Portal vein, hepatic artery, and hepatic vein velocity in the liver graft were measured every 12 hours by Doppler ultrasonography for 2 weeks after liver transplantation. These parameters were stable until just before the simultaneous thrombosis. These findings indicate that protocol Doppler ultrasonography can diagnose, but not predict, this fatal complication.

Adolescent↗
PubMed1976

Anemic infarction of the liver resulting from hepatic and portal vein thrombosis.

True anemic infarction of the liver is a rare lesion. Most of the reported cases are due to occlusion of the hepatic artery. Whether venous occlusion can result in such anemic infarcts has been disputed although few authentic cases have been reported. A case of polycytheia vera complicated by hepatic and portal vein thrombosis with anemic infarction of a large segment of the liver is presented. The case illustrates that anemic infarcts of the liver can result from venous occlusion. The intense congestion secondary to hepatic vein occlusion may cause secondary arterial hypoperfusion unless the portal vein is available as an outflow tract.

Adult↗
PubMed1978

Drug-induced liver disease.

The large number of chemical agents administered for therapeutic or diagnostic purposes can produce various types of hepatic injury by several mechanism. Acute injury may be cytotoxic, cholestatic or mixed. Cytotoxic injury may consist of necrosis or steatosis. Cholestatic injury may be cholangiolitic (hepatocanalicular) or bland (canalicular). Chronic hepatic lesions caused by medicinal agents include chronic active hepatitis, steatosis, cirrhosis, fibrosis, hepatoportal sclerosis (non-cirrhotic portal hypertension), hepatic vein thrombosis, peliosis hepatis, adenoma, carcinoma, and angiosarcoma. There is a useful relationship between the type of hepatic injury and the chemical setting in which the drugs are employed. Some agents produce the liver damage because they are intrinsic (true, predictable) hepatotoxins. Other (non-predictable "hepatotoxins"), produce hepatic injury only in the rare and unusually susceptible individual (idiosyncratic injury). Hepatotoxic agents can be recognised by their dose-dependent and experimental reproducibility, properties which are not shared by agents which produce hepatic injury only in idiosyncratic hosts. Intrinsic hepatotoxins may be categorised as direct or indirect. Direct hepatotoxins injure the hepatocyte by direct physiochemical alteration and as a consequence produce metabolic defects. Indirect hepatotoxins selectively block metabolic pathways and, by producing a precise biochemical lesion, lead to structural changes. They may lead to hepatic steatosis or necrosis (cytotoxic indirect hepatotoxins) or block bile flow (cholestatic indirect hepatotoxins). Direct hepatotoxins are rarely encountered as drugs. Overdoses of some drugs and antineoplastic agents appear to be indirect cytotoxic hepatotoxins, and the C-17 alkylated anabolic and contraceptive steroids are indirect, cholestatic hepatotoxins. Idiosyncracy of the host is the mechanism for most types of drug-induced hepatic injury. It may reflect allergy to the drug or a metabolic aberration of the host permitting the production of hepatotoxic metabolites.

Chemical and Drug Induced Liver Injury↗
PubMed1997

Living related partial liver transplantation in biliary atresia: 11 cases of experience.

Eleven children, 4 males and 7 females, with biliary atresia receiving living related liver graft were studied. The mean age was 1.8 years and the mean body weight was 10.3 kg. The donors were 4 fathers and 7 mothers. The graft was the lateral segment or left lobe. ABO blood group matching was compatible in 9 and incompatible in 2. All patients except one were crossmatch negative. Immunosuppression at induction was triple therapy (cyclosporine, azathioprine and steroid) or FK506 plus steroid. Acute rejection episodes were treated with pulse steroids. When the signs of rejection persisted despite steroid pulse therapy, 15-deoxyspergualin (DSG) was added. The survival rate of the patients was 73%. Three patients died of portal vein thrombosis, hepatic artery thrombosis and sepsis respectively. Other major complications included hyperbilirubinemia, bile duct stenosis, bile leakage and portal vein anastomosis narrowing. Complications of the donor were sepsis in one, and liver dysfunction in two. Although there are some complications related to graft size mismatch and operative procedure, living related partial liver transplantation is an effective therapy in countries where donor source is restricted.

ABO Blood-Group System↗
PubMed2003

Multiple telangiectatic focal nodular hyperplasia: vascular abnormalities.

The aim of this study was to look for vascular abnormalities in the liver of patients with multiple telangiectatic focal nodular hyperplasia. Four patients, all women on oral contraceptives, were included in this study. In none of the cases was the diagnosis of multiple telangiectatic focal nodular hyperplasia made preoperatively. In the nodules, the pathological aspect was quite characteristic with dilated sinusoidal areas surrounding compact areas. Compact areas comprised portal tract-like structures with vessels, mainly thickened arteries, usually amidst an inflammatory reaction. A ductular reaction of varied intensity was present in three cases. The non-nodular liver was grossly normal. However, in rare areas, there were obvious or minor vascular abnormalities looking like minimal abnormalities seen inside telangiectatic nodules. These results seem to support the concept that multiple telangiectatic focal nodular hyperplasia is a non-specific reaction to focal ischemia induced by various mechanisms such as hepatic vein thrombosis induced, perhaps, by oral contraceptives.

Adult↗
PubMed1991

Budd-Chiari syndrome in association with Behçet's disease.

Budd-Chiari syndrome developed in 3 patients with preexisting Behçet's disease. Benign intracranial hypertension was the chief presenting complaint in one patient, who later suffered extensive inferior vena caval and hepatic vein thrombosis, with manifestations of Budd-Chiari syndrome. She did not respond to treatment and subsequently died of hepatic coma. In the other 2 patients, Budd-Chiari syndrome was confirmed by liver biopsy. Both patients made a good recovery and remain well at the time of this report.

Adult↗
PubMed2006

Vascular reconstruction and complications in living donor liver transplantation in infants weighing less than 6 kilograms: the Kyoto experience.

Smaller-size infants undergoing living-donor liver transplantation (LDLT) are at increased risks of vascular complications because of their smaller vascular structures in addition to vascular pedicles of insufficient length for reconstruction. Out of 585 child patients transplanted between June 1990 and March 2005, 64 (10%) weighing less than 6 kg underwent 65 LDLTs. Median age and weight were 6.9 months (range: 1-16 months) and 5 kg (range: 2.8-5.9 kg), respectively. Forty-five lateral segment, 12 monosegment, and 8 reduced monosegment grafts were adopted, and median graft-to-recipient weight ratio was 4.4% (range: 2.3-9.7). Outflow obstruction occurred in only 1 patient (1.5%). Portal vein complication occurred in 9 (14%) including 5 with portal vein thrombosis. Hepatic artery thrombosis (HAT) occurred in 5 (7.7%). Patient and graft survivals were 73% and 72% at 1 yr, and 69% and 68% at 5 yr after LDLT, respectively. Thirteen of 22 grafts (58%) lost during the follow-up period occurred within the first 3 months posttransplantation. Overall graft survival in patients with and without portal vein complication was 67% and 65%, respectively (P = 0.54). Overall graft survival in patients with and without HAT was 40% and 67%, respectively. HAT significantly affected graft survival (P = 0.04). In conclusion, our surgical technique for smaller-size recipients resulted in an acceptable rate of vascular complications. Overcoming early posttransplantation complications will further improve outcomes in infantile LDLT.

Anastomosis, Surgical↗
PubMed2005

Single pretransplant bolus of recombinant activated factor VII ameliorates influence of risk factors for blood loss during orthotopic liver transplantation.

Large blood loss and transfusions during liver transplantation (LTx) may lead to serious complications and have a negative impact on post-transplant mortality and morbidity. In the retrospective study we compared two groups of recipients of primary cadaveric liver transplantation: group I (study group), consisted of 28 patients with preoperative risk of high intraoperative blood loss, including severe uncorrected coagulopathy. This group was given a bolus of recombinant activated factor VII (rFVIIa) just before LTx. Group II (control group) included 61 patients without a particular risk for increased intraoperative blood loss. These patients were not given rFVIIa. We analyzed both groups for: coagulation parameters before, during and after surgery (INR, APTT, factor VII activity), blood and FFP transfusions, operative time, postoperative complications (vascular thrombosis, reoperation for bleeding), postoperative ICU stay, post-transplant hospitalization time and mortality. Patients from the study group (I) had significantly worse coagulation parameters than patients in the control group (II) at the start of the surgical procedure; however, after administration of a bolus of rFVIIa there was immediate correction of coagulation in all recipients. No significant differences in intraoperative blood transfusions were observed between study and control groups (1980 +/- 311.4 mL vs. 1527 +/- 154.2 mL, respectively), operating time (8.7 h vs. 8.9 h) or ICU and hospital stay (7.03 days vs. 6.15 days and 40.89 days vs. 41.1 days). Re-exploration because of bleeding was performed in three patients from group I (10.7%) and in seven patients (11.5%) from group II. No single case of vascular thrombosis was observed in the study group, while in the control group there were three hepatic artery thromboses, two portal vein thromboses and one hepatic vein thrombosis. We conclude that rFVIIa given preoperatively to liver transplant recipients with several risk factors for high intraoperative bleeding adjusts these patients to a normal risk group, without an increased risk for thrombotic complications.

Adolescent↗
PubMedDate not supplied

Surgical and interventional radiological treatment of Budd-Chiari syndrome: report of nine cases.

BACKGROUND/AIMS: The authors present the methods and results of treatment of patients with Budd-Chiari syndrome. METHODOLOGY: From a group of 15 patients with Budd-Chiari syndrome, treated in our department from January 1996 to September 2001, nine patients (6 females and 3 males, aged from 23 to 45 years) were qualified for surgical or radiological treatment. In 3 of them the hepatic vein thrombosis resulted from untreated polycythemia. In the remaining 6 cases the etiology of thrombosis remained unknown. In four patients with dominating portal hypertension symptoms, a meso-caval H-type graft was created. Four patients with severe liver insufficiency were qualified for orthotopic liver transplantation; all of them were transplanted. In 1 patient a balloon dilatation of the right and middle hepatic veins orifices was performed during the diagnostic cavography. The follow-up period ranged from 4 months to 5 years. RESULTS: In 2 patients with Budd-Chiari syndrome of unknown etiology, the "H"-shunt remained patent, and the patients were free of ascites and splenomegaly. During the period of follow-up (more than 5 years) they remained free of symptoms and demonstrated acceptable liver function parameters. Doppler sonography revealed the partial recanalization of the venous system. In 2 polycythemic patients, the shunt thrombosed, which was the indication for orthotopic liver transplantation in one of them. The transplantation was performed, but was unsuccessful because of hepatic graft artery thrombosis. The retransplantation in this case was also unsuccessful. The remaining 3 patients transplanted for cryptogenic Budd-Chiari syndrome are alive and well, 4, 5 and 11 months after orthotopic liver transplantation. In the patient subjected to interventional radiological hepatic veins dilation, the vessels remain patent 26 months post-procedure. The patient is free from ascites. CONCLUSIONS: Shunt surgery and liver transplantation are the valuable methods of treatment in selected cases of Budd-Chiari syndrome. In patients with polycythemia, however, thrombotic complications may occur in spite of anticoagulant and chemotherapeutic treatment. Balloon dilatation may appear an alternative to surgical treatment, but it seems that its indications should be limited to a highly selected group of patients.

Adult↗