Clinical Investigation Of The Etiology And Treatment Of Portal Vein Thrombosis

Objective: To study the etiology,pathogenesis,diagnosis and treatmentof portal vein thrombosis(PVT ).Methods: 44 cases of PVT in our hospital from January 2002 to October2005 were retrospectively analyzed . The persons which had the highestincidence of PVT, were the cases following splenectomy and devascularizationof portal hypertension. So we analyzed the risk factors of these casesespecially.21 cases of PVT following the operation were enrolled in this study,and 40 cases following splenectomy and devascularization of portalhypertension without PVT were chosen randomly as control group. Carrying ona statistical analysis to the data .Results: The statistical analysis shows that the average width of mainportal vein (MPV),the average width of splenic vein, and the increase of bloodplatelets following splenectomy were the risk factors to inducting PVT ,whilesex ,liver function ,depth of spleen ,time operation used , blood losing and bloodtransfusion during the operations ,PT, may not be related to the formation ofPVT . Some cases showed that use coagulant too much maybe a risk factor ofPVT .27 cases were given medication for thrombolysis, restraining bloodplatelet conglomeration and anticoagulating. 10 cases were given interventionaltreatment. 7 cases were operated .The mortality was 0. The prognosis of onecase was not well, because the necrotic intestine was too long ,and remanentintestine was less than 1 metre. The prognoses of other cases weresatisfying .Discussion and Conclusion: The etiologies of PVT are multifarious,include:liver cirrhosis with portal hypertension, operations and trauma inabdominal, inflammation and infection in abdominal, myeloproliferativedisorder, deficiency of natural anticoagulant proteins gene mutation andhepatocellular carcinoma. Liver cirrhosis with portal hypertension and thesplenectomy and devascularization of portal hypertension are the most frequentcauses of portal vein thrombosis. PVT just as the other deep veinthrombosis ,are related to increased blood coagulability,venous stasis fromdecrease flow and trauma to the vein well. We consider that the pathogenesis ofPVT following splenectomy and devascularization of portal hypertension is asfollow: â‘ Influence of the primary affection: When Liver cirrhosis and portalhypertension occurred ,blood flowed slowly in portal vein. Average width ofmain portal vein augmented. Blood stream changed. The wall of portal veinbecame incrassation and scleroses. Endothelium was injured. Prothrombin andplatelet was activated locally. Synthesizing function of liver weakened,antlthrombin synthesized reduced, for example, antlthrombin â…¢(AT â…¢)andtissue factor passby inhibitor (TFPI) were lower than normal. â‘¡ Influence ofthe operations: Quantity and speed of blood flow in portal vein increased afteroperations, homodynamic changed that could cause turbulent flow in portal vein.The blood in remnant splenic vein flowed slowly after splenectomy, that couldcause thrombosis. The surface/ cubage of red blood cell increased, thetransmutative ability of red blood cell descended. That could cause bloodviscosity increase. The destruct of platelets descended after splenectomy. Theplatelet count increased. The level of AT â…¢ was lower than before operation.â‘¢ The management was improper after operation: Given coagulant too muchor given liquid not enough, that could increase blood coagulability.The clinical manifestations of PVT are multifarious. Chronic portal veinthrombosis may have no syndrome, may be windy, may have diarrhea,abdominal pain, splenomegaly and hypersplenism. Acute portal vein thrombosismay cause abdominal pain, gastrointestinal bleeding, and ascites. It lack oftypical symptom and signs at early. And some of they follow a different naturalhistory to those with portal hypertension related to cirrhosis. So some patientsmight be diagnosed until peritonitis, intestines necrotize and exploratorylaparotomy. As the diversity of its clinical manifestations, misdiagnosis iscommon if we do not bear PVT in mind during differential diagnosis. When thepatients who have the risk factors occur diarrhea, abdominal pain, we shouldthink of the possibility of PVT. Color Doppler sonography should be performedin time for filtration. If further information is required, magnetic resonanceangiography or contrast-enhanced computed tomography is the next step, and ifthese tests are unsatisfactory, digital subtraction angiography (DSA) should beperformed.The patients of PVT should be given property treatments in time.Therapeutical options are different to different patients. Chronical PVT cananticoagulate alone, it can prevent further extension of the thrombus. Acute PVTshould given systemic anticoagulation and thrombolytic therapy, beforeperitonitis and intestine necrobiosis occur. Preferred anticoagulation drugs areheparin and low molecular weight heparins(LMWH).If heparin is not effective,dicoumarol and warfarin sodium can be used. Preferred thrombolytic drug isurokinase. Maintain the PT at 1.5-2.5 times normal, and keep internationalnormalized ratio (INR) between 2 to 3. If there is a major contraindication tosystemic thrombolytic, for example, gastrointestinal bleeding or operation inshort time, intervational therapy should be used. The route via femoral artery,superior mesentery artery (MSA) is used often, given local thrombolytic. Thisapproach is easy and safe. The concentration of thrombolytic in local is higher.But this approach exists shortages contrasting with puncture portal vein direct.The thrombolytic can be diluted and decomposed during the circulation. Theeffect may be not satisfying. And if the portal vein was obturated completely, itmay increase the probability of intestines bleeding.When the portal vein wasobturated completely, we can percutaneous puncture splenic vein, givemechanical thrombolysis and local thrombolytic. Inject urokinase into thethrombus in PV and SMV, it can reduce the dosage of urokinase, so thecomplication of bleeding may cut down. There are shortages of this approach. Itmay cause celiac bleeding, and it can not be used for the patient with ascites.Reported that via a percutaneous transhepatic route and via a transjugularintrahepatic portosystimic shunt (TIPS) approach also could be used. Thepatients who are taken bad acutely, with abdominal pain, gastrointestinalbleeding or signs of peritonitis, should operate decidedly. The operationsinclude combination of portal vein embolectomy and local fibrinolysis or partialresection of small intestine. The key is the estimation whether intestinesnecrotizes occurred and the range of intestines necrotized.During portal vein embolectomy, we needn't separate the main portal veinconstrainedly, because it is too short and too deep. We can take out thethrombus through the embranchment of portal vein with 4F Fogarty duct.Anticoagulation therapy should keep for 3-6 months, or even more time.Prevention PVT is more important than treatment. The patients with riskfactors of PVT, should perform color Doppler sonography termly, and assayplatelet count and blood viscosity termly. And give anticoagulant treatment ifnecessary.