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PubMed1996

Pathologic and radiographic studies of intrahepatic metastasis in hepatocellular carcinoma; the role of efferent vessels.

The efferent vessel of hepatocellular carcinoma (HCC) and the mechanism and pathogenesis of the high frequency of intrahepatic metastasis in HCC has not yet been clarified. Three hundred ninety-three resected specimens of HCC were examined for tumor thrombosis in the portal vein and the hepatic vein: 231 tumors < or = 5 cm in diameter were examined for the relationship between mode of tumor spread and tumor size. Efferent vessels in HCC were identified by direct injection of radiopaque material into the tumor in 23 resected liver specimens and by percutaneous infusion of radiopaque media into tumor nodules in 8 patients. The mode of tumor spread in HCC progressed from capsular invasion to extracapsular invasion, then to vascular invasion, and finally to intrahepatic metastasis. There was a strong statistical correlation between the presence of intrahepatic metastasis and portal vein thrombosis (p < 0.05, R = 0.998). Radiopaque material injected directly into 23 resected tumors entered only the portal vein in 17 tumors and into both the portal and hepatic veins in 6 tumors. In all 8 patients with unresectable lesions, radiopaque media injected percutaneously into tumor nodules flowed only into the portal vein. These findings suggest that intrahepatic invasion by HCC may occur through the portal vein as an efferent tumor vessel.

Aged↗
PubMed2005

Hepatocavopathy and isolated splenic vein thrombosis due to hypercoagulability state.

We report a patient with protein C and protein S deficiency and factor V Leiden mutation presenting with splenic vein thrombosis and with a web between the hepatic venous confluence and vena cava inferior. These two findings were thought to be due to the hypercoagulable state of the patient. Interestingly, there was no need for invasive procedures as the inferior accessory hepatic vein was patent. Hepatic venous flow was being maintained by the inferior accessory hepatic vein or a dominant collateral vein.

Anticoagulants↗
PubMed1995

Early fulminant graft failure in orthotopic liver transplantation with massive haemorrhagic necrosis.

Early fulminant liver allograft failure is a post-transplant syndrome presenting as massive haemorrhagic necrosis of the graft. A single organ Shwartzman reaction has previously been suggested as a cause. We report on a patient who lost her liver graft due to fulminant graft failure ten days after orthotopic liver transplantation (OLT), the liver showing massive haemorrhagic necrosis. Fresh thrombosis was noted in the portal and hepatic veins. As a Shwartzman reaction could be expected to lead to complement deposition in vessel walls, tissue was analyzed for the presence of complement components. However, even though protein-rich and fibrinogen-containing deposits were detected within the vessel walls, these deposits were not immunoreactive for complement (C3 and Clq). These findings suggest that pathogenesis of fulminant liver allograft failure differs from that of a complement-mediated Shwartzman reaction, or of a hyperacute rejection, where IgM and Clq had previously been detected in hepatic veins and arteries.

Adult↗
PubMed1997

Infected false hepatic artery aneurysm after orthotopic liver transplantation treated by resection and reno-hepatic vein graft.

Vascular complications after liver transplantation are relatively rare. Thrombosis of the host-transplant arterial anastomosis is the most frequently encountered vascular complication whereas only a few observations of infected anastomotic aneurysms, often leading to death by massive bleeding or loss of the transplant, have been reported. We report herein the case of a patient with an infected false anastomotic aneurysm of the hepatic artery associated with dissection of the celiac artery following orthotopic liver transplantation in a 35-year-old man who had received a liver transplantation for end-stage liver disease secondary to posthepatitis cirrhosis in March 1989. Starting at day 30, he had signs of infection associated with hemocultures positive for Staphylococcus aureus. A subhepatic collection was found on sonography and CT scan and also cultured positive for the same germ. Arteriograms demonstrated a celiac artery dissection associated with a false anastomotic aneurysm of the hepatic artery. Surgical treatment consisted of arterial reconstruction using a saphenous vein graft between the right renal artery and the hepatic artery of the transplant, followed by resection of the hepatic artery aneurysm and the celiac artery. Hepatic ischemia was 12 min. The immediate postoperative course was uneventful and postoperative angiograms showed that the reconstruction was patent at 5 years.

Adult↗
PubMed1985

Hyperbilirubinemia following distal splenorenal shunt.

To assess the incidence, pathogenesis, and associated morbidity and mortality of hyperbilirubinemia following the distal splenorenal shunt, hepatic hemodynamics, liver function, and clinical course were evaluated before and after this procedure in 78 cirrhotic patients. Individuals with a peak postoperative bilirubin level greater than 5 mg/dL had a higher preoperative bilirubin concentration, worse Child's score, longer hospital stay, and higher mortality than patients with a peak postoperative bilirubin level less than 5 mg/dL. Mean preoperative and postoperative hepatic portal perfusion and sinusoidal pressure were similar in both groups. When only patients with minimally elevated preoperative bilirubin levels (less than 2 mg/dL) were analyzed, 83% of individuals who developed postoperative hyperbilirubinemia (level, greater than 5 mg/dL) had a major alteration in hepatic hemodynamics as manifested by either complete portal vein thrombosis or a marked change in sinusoidal pressure (greater than 4 mm Hg). Although preoperative hepatic functional reserve is the major determinant of postoperative bilirubin concentration, alterations in hepatic hemodynamics secondary to the distal splenorenal shunt may also play a role.

Hemodynamics↗
PubMedDate not supplied

Transjugular intrahepatic portocaval shunt (TIPS) and hepatic vein-to-caval stenting as salvage treatment of portal hypertension secondary to neoplasm.

A percutaneous transjugular intrahepatic portocaval shunt (TIPS) was successfully performed using Wallstents in a 53-year-old man with neoplastic disease causing portal hypertension and life-threatening variceal hemorrhage. Shortly afterwards, recurrent hemorrhage was investigated by shunt venography which showed that extrinsic narrowing of the hepatic vein and hepatic vena cava was causing shunt thrombosis. Shunt thrombosis was cleared by balloon occlusion of the shunt and forceful retrograde flushing of thrombus into the portal circulation. The compressed hepatic vein and vena cava were then dilated and stented using Gianturco "Z" stents. Bleeding recurred 3 months later due to focal narrowing within the shunt which possibly was due to intimal proliferation. Repeat dilatation and placement of a coaxial Palmaz stent again relieved portal hypertension. Creation of a TIPS for portal hypertension secondary to neoplasm can produce valuable palliation. Complete assessment of hepatic vein and vena cava patency is required to ensure shunt function.

Angiography, Digital Subtraction↗
PubMedDate not supplied

Endovascular treatment of acute portal vein thrombosis after liver transplantation in a child.

Although operative techniques in hepatic transplantation have reduced the time and mortality on waiting lists, the rate of vascular complications associated with these techniques has increased. Stenosis or thrombosis of the portal vein is an infrequent complication, and if present, surgical treatment is considered the traditional management. This article describes a case of acute portal vein thrombosis after liver transplantation from a living donor to a child managed by percutaneous techniques.

Acute Disease↗
PubMed1987

Porta hepatis: duplex Doppler US with angiographic correlation.

Duplex Doppler ultrasonography (US) and panhepatic angiography were performed and interpreted independently in 20 patients with suspected portal hypertension to assess the accuracy of duplex US in the porta hepatis. Hepatic arterial resistive indexes were correlated with corrected sinusoidal pressures. The results of duplex US agreed with those of angiography in 16 patients with a normal portal vein (including three with hepatofugal flow) and two with total thrombosis. One angiographically normal portal vein appeared thrombosed on an initial sonogram, but a second scan was normal. One case of partial thrombosis was not diagnosed with duplex US. Sensitivity and specificity for main portal vein disorders were 83% and 93%, respectively. Two patients had portal vein branch occlusions that were found by angiography but not by US. Portal vein echogenicity was neither sensitive nor specific for thrombosis. The resistive index of the hepatic artery was specific for portal hypertension when above .78, but it was not sensitive. Duplex US is accurate in prospectively assessing the direction of flow and the presence of total thrombosis in the portal vein, but partial thrombosis may not be detected on sonograms.

Adolescent↗
PubMed2003

Vascular liver diseases.

This article reviews the primary circulatory liver diseases, which include Budd-Chiari syndrome, obstruction of the hepatic portion of the inferior vena cava, portal vein thrombosis, sinusoidal obstruction syndrome (veno-occlusive disease), nodular regenerative hyperplasia, and peliosis hepatis. In addition, two systemic cardiovascular diseases that impair hepatic circulation, ischemic hepatitis and congestive hepatopathy, are briefly discussed. A characteristic of the primary circulatory liver diseases is that portal hypertension usually precedes liver dysfunction; however, this is not the case with the primary parenchymal liver diseases, in which liver dysfunction always progresses before portal hypertension is manifested. Significant overlap exists among the diseases and risk factors that predispose patients to the primary circulatory liver diseases, though the pathogenesis of individual diseases varies.

Budd-Chiari Syndrome↗
PubMed2003

Portal vein thrombosis.

Portal vein thrombosis (PVT) is a complication of hepatic disease and a potentially lethal complication of splenectomy. The reported incidence of this complication is low (approximately 1%). However, its true incidence may have been underestimated due to difficulty in making the diagnosis. Herein we report the case of a 19 year-old woman who presented with a 2-year history of idiopathic thrombocytopenic purpura (ITP). Because she had become refractory to medical therapy, she underwent laparoscopic splenectomy. She was discharged on postoperative day 2 after an uncomplicated procedure. She did well, complaining only of mild backache, until postoperative day 21, when she presented with nausea, vomiting, and leukocytosis. CT showed PVT and superior mesenteric vein thrombosis. Despite heparin and fluid administration, her condition worsened. At laparotomy, she had diffuse small bowel edema and congestion. At a second-look procedure 24 h later, nearly all her jejunum and ileum were necrotic. After three procedures, she was left with 45 cm of proximal and 10 cm of distal small bowel. Bowel continuity was restored 8 weeks later. She continued on warfarin anticoagulation therapy for 1 year. Postsplenectomy PVT is most often seen following splenectomy for myeloproliferative disorders and almost never after trauma. The large splenic vein stump and the hypercoagulable state in patients with splenomegaly are thought to be contributory. The presentation of PVT is vague, without defining signs or symptoms. Color-flow Doppler and contrast-enhanced CT scans are the best methods for the nonoperative diagnosis of PVT. Aggressive thrombolysis offers the best hope for clot lysis and maintenance of bowel viability. Even vague symptoms must be considered seriously following splenectomy.

Adult↗
PubMed1991

Four patients in Singapore with anti-Golgi antibodies.

Serum specimens for anti-nuclear fluorescence tests are routinely received in our laboratory. Four specimens were spotted to be negative for anti-nuclear fluorescence but positive for fluorescence characteristic of that caused by anti-golgi antibodies. (a) Patient A had acute glomerulonephritis; (b) Patient B had acute viral hepatitis; (c) Patient C had deep vein thrombosis; and (d) Patient D had non-Hodgkin's lymphoma. The relevance and possible aetiology of anti-golgi antibodies are also discussed.

Acute Disease↗
PubMed2000

Pediatric recipients of three or more hepatic allografts: results and technical challenges.

BACKGROUND/PURPOSE: Children who require a liver transplant at an early age risk chronic allograft rejection (CAR) and other causes of allograft loss. Multiple retransplants may be required for long-term patient survival. The authors evaluate this approach based on our results and technical difficulties. METHODS: Charts of 7 children who received 3 or more liver transplants from 1989 to the present were reviewed retrospectively. RESULTS: A total of 151 children required liver transplantation at our institution since 1989. Of these, 4 boys and 3 girls (mean age, 6.2 years; range, 3 to 14 years) have received 3 or more allografts. The etiology of liver failure for the penultimate allograft was CAR (n = 6) and hepatic artery thrombosis (HAT; n = 1). Five cases required modification of portal vein or hepatic artery anastomoses. Two patients with vena caval strictures required supradiaphragmatic vena caval reconstruction. The original Roux-en-Y limb was adequate for biliary reconstruction in all cases. Five children currently are alive (survival rate, 71%) with good graft function having had a mean follow-up of 23 months (range, 2 to 48 mos.). CONCLUSIONS: The operative procedure for the multiple hepatic transplant child is challenging. The transplant team must be prepared for intraoperative issues such as extended organ ischemia time during hepatectomy, extensive blood loss, and potential need for creative organ revascularization techniques. Overall, multiple retransplant results are good and justify the use of multiple allografts.

Adolescent↗
PubMed1963

Infarction of the human liver.

The rarity of hepatic infarction in the human being is commonly explained as due to the double blood supply via the hepatic artery and the portal vein. This explanation cannot be accepted, because, if the arterial blood supply alone is arrested the portal blood supply does not protect the liver from infarction. The factor of importance is that the arterial blood supply comes by three different routes and it is difficult to obstruct these collateral supplies simultaneously. Infarction of the liver can be caused by thrombosis or ligation of the main hepatic artery between the origin of the right gastric artery and the hilum of the liver, but the more common causes are infected emboli or polyarteritis nodosa; these presumably interfere not only with the main arterial supply but also with some of the collateral arterial supply.

Arteries↗
PubMed1990

Effect of hepatic artery ligation in rats with chronic extrahepatic cholestasis.

Because of the liver's dependence on arterial blood to exert its metabolic functions in cirrhosis of the liver, with or without thrombosis of the portal vein, the interruption of hepatic arterial flow for the palliative treatment of malignant tumors of the liver is counterindicated. However, the effects of arterial devascularization on the cholestatic liver are not fully understood. The objective of the present study was to investigate hepatic alterations due to hepatic artery ligation in rats with chronic extrahepatic cholestasis. Serum alkaline phosphatase, bilirubin and alanine aminotransferase were measured in rats 3 h after sham operation (group A, N = 29) or ligation of the hepatic artery (group B, N = 29). Alanine aminotransferase activity was significantly higher (P less than 0.05) in group B, demonstrating acute hepatocellular damage in animals with chronic extrahepatic cholestasis.

Alanine Transaminase↗
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↗