Portal vein occlusion

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. 

Interventional treatment of children with portal hypertension secondary to portal vein occlusion. Eur J Pediatr Surg 13 312-218... 

Chemoembolization and Portal Vein Occlusion In the presence of portal vein invasion, the risks of hepatic complications following chemoembolization are increased and the survival rates are decreased. In a series of 110 patients with HCC invading major portal branches, Chung et al. (1995) reported 1-, 2-, and 3-year survival rates of 30%, 18%, and 9%, respectively. Complete or partial response (22/33) and survival times (22 months) were significantly longer in those patients with disease limited to one or two hepatic segments. In 77 patients with more extensive hepatic involvement, the mean survival time was 5 months. Ten patients in this latter group developed hepatic insufficiency and three deaths occurred within 1 month after treatment. 

Collateral hepatic circulation (cirrhosis, portal vein thrombosis, occlusion of hepatic vein, etc)... 

Scintigraphic proof of cirrhosis is based on (i.) enlarged rectangular liver, (2.) reduced and patchy uptake of radioactivity by the hepatic RES ( mottled liver ), (3.) shift in the maximum activity from the right to the left lobe of liver, and (4.) increased uptake by the spleen and bone RES. The recorded scintigraphic findings permit assessment of the course of liver cirrhosis and provide information on focal complications such as .) occlusion of the branches of the portal vein with locally impaired perfusion and (2.) development of hepatocellular carcinoma. 

Tc-DTPA Arterial perfusion accounts for 20%-40% of the circulation in portal hypertension, cirrhosis causes arterial perfusion to increase to over 60%. In portal vein thrombosis, only an arterial curve is visible. Liver metastasis usually displays relatively high arterial perfusion. In (rare) occlusions of the hepatic artery, only a portal venous curve is visible. When a bolus injection of 400 MBq "Tc-diethylenetriamine pentaacetic acid (DTPA) is applied, scintigraphy is able to reveal a bi-phasic time-activity curve. The initial increase of activity is produced by the arterial influence and the second peak by the portal venous inflow. Both curves can be evaluated quantitatively. (36) Perfusion scintigraphy may be useful in the case of liver trauma, TIPS, hyper-vascularized hepatic tumours and partial liver resection as well as after liver transplantation. 

Prehepatic (non-parenchymatous) portal hypertension develops (i.) as a result of an increase in the portal blood supply in the form of hyperkinetic hypertension or (2.) due to occlusion of the portal vein or its trunks. The frequency is 10—20%. The liver is morphologically normal, but is diminished in size. Its function is not impaired. The reduced afferent portovenous flow is compensated by arterial perfusion of the liver. Ascites occurs only rarely. 

The Cruveilhier-von Baumgarten disease develops when postnatal occlusion of the umbilical vein is absent (P. VON Baumgarten, 1907). An open, dilated umbilical vein connects the left portal vein with the systemic venous circulation in the navel area. This collateral vein has a diameter of >3 mm and a hepatofugal flow of >5 cm/... 

Liver involvement in Osier-Vaquez disease is rare or not detectable at all. There is, however, evidence of hepato-splenomegaly due to extramedullary haemopoiesis. Of importance here is the association with Budd-Chiari syndrome and veno-occlusive disease. Polycythaemia vera should be considered in cases of aetiologically unclarified portal vein thrombosis. 

Occlusion of the hepatic artery is responsible for a 50% reduction in oxygen supply. Even if an unimpaired oxygen supply via the portal vein is guaranteed, arterial occlusion usually causes ischaemic infarction. The clinical and morphological pictures are characterized (1.) by the speed with which an occlusion develops and (2.) by the presence of variants that can be used as a bypass or of collaterals that have already been established in gradual vascular occlusion. This results in a broad clinical spectrum, which may range from a symptom-free condition to liver hypoxia, including infarction up to hepatic coma. 

Matsumoto, T., Kuwabara, N., Abe, H., Fnkuda, Y., Suyama, M., Fuji , D., Kojima, K., Futagawa, S. Zahn infarct of the liver resulting from occlusive phlebitis in portal vein radicles. Amer. J. Gastroenterol. 1992 87 356-368... 

Hg, Portal hypertension occurs when there is obstruction to portal flow anywhere along its course. The causes of obstruction leading to portal hypertension are classified by site (1) presinusoidal, (2) sinusoidal, and (3) postsinusoidal. Pre-sinusoidal portal hypertension is most commonly caused by portal vein thrombosis or schistosomiasis but may also occur with increased portal flow, such as occurs with Felty syndrome (a combination of chronic rheumatoid arthritis, splenomegaly, leukopenia, pigmented spots on the lower extremities, and sometimes other evidence of hyper-splenism, such as anemia and thrombocytopenia). Sinusoidal hypertension is most commonly caused by cirrhosis but may occur transiently with acute and chronic hepatitis or acute fatty liver. The most important cause of postsinusoidal hypertension is hepatic vein occlusion or Budd-Chiari syndrome, in which sudden obstruction or occlusion of the... 

Hepatic arterial bland and chemo-embolization have also been utilized. This therapy is based on the anatomic vascular distribution of the blood supply for hepatic tumors. The hepatic artery serves tumors in the liver almost exclusively while the portal vein serves normal hepatic parenchyma. There is some crossover but it is only approximately 10%. Bland embolization uses particles placed in the hepatic artery only while chemoembolization mixes these particles with a variety of chemotherapeutic agents and lipiodol, an iodinated poppy seed oil, which has been shown to increase the uptake into the cell via a pump in the cell wall. This therapy has been utilized for the last 20 years but eventual re-growth and recurrence have also uniformly occurred. Repeated embolizations are necessary to keep the disease in check and to palliate the patient s symptoms. The mean response to embolization is approximately 12-18 months with eventual occlusion of the hepatic arterial supply to the tumor after multiple embolizations. Response to embolotherapy has been dramatic for palliation of symptoms, with 63% of patients reporting a reduction in symptoms and an objective response seen on CT to be 76% either partial or minimal response, with an additional 16% reporting stable disease [4]. The embolotherapy will rid the patient of much of their tumor burden but isolated islets of viable tumor will remain after the procedure, accounting for the resurgence of disease. 

There is one further indication for thrombin occlusion of pancreatitis associated visceral aneurysms. Where the portal vein has occluded as a complication and the patient has a proximal splenic or gastroduodenal aneurysm, the proximal and distal coil embolization of which could compromise the hepatic arterial supply to the liver causing liver infarction, thrombin injection maybe a safer technique [29]. 

An insufficient remnant liver volume, calculated pre-operatively, might lead to the performance of iatrogenic occlusion of the right or left portal vein in order to determine a lobar liver hypertrophy, making the resection feasible. Software for calculation of liver volume is under continuous improvement. From completely manual software - where... 

Evidence of toxicity may not become apparent until some time after the alkaloid is ingested. The acute illness has been compared to the most common pro-thrombotic disorders that lead to Budd-Chiari syndrome, portal vein thrombosis, and sinusoidal obstruction syndrome, previously known as hepatic veno-occlusive disease of... 

Thijs WJ, de Groot EH, Hofstra LS. Portal and splenic vein occlusion complicating Histoacryl injection therapy in bleeding gastric varices. Endoscopy 2008 40(Suppl 2) E187. 

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