Portal vein thrombosis

Portal vein thrombosis

Thrombosis of the portal vein is the process of thrombus formation up to complete occlusion of the lumen of the vessel draining the bed of the gastrointestinal tract. The occurrence of the disease, as well as other venous thrombosis, can be explained by the Virchow triad, which includes the following elements:

    • Injury to the vein wall during surgery.
    • Decreased portal venous blood flow in:
    • Compression of the vessel from the outside by a tumor, scars, echinococcal cyst, alveococcus
    • Chronic heart failure
    • Constrictive pericarditis
    • Budd-Chiari syndrome (thrombosis of the hepatic veins).
    • Increased blood clotting or a change in the ratio of its cellular elements
    • In the postoperative period, especially in oncological


    • In inflammatory processes Purulent pylephlebitis (thrombophlebitis of the portal vein), most often occurring as a complication of acute appendicitis. Less commonly, pylephlebitis occurs with purulent cholangitis and lymphadenitis of the hepatoduodenal ligament or ulcerative colitis.
    • Pancreatic necrosis
    • Umbilical infection in the neonatal period (neo-natal septicemia, omphalitis, infection during catheterization of the umbilical vein for exchange transfusion).
    • With complications of pregnancy (in particular, eclampsia).
    • With some hematological diseases that cause an increase in blood clotting (for example, Banti’s pseudosyndrome with visceral leishmaniasis). The frequency of postoperative thrombosis of the portal vein in patients suffering from cancer of the liver or other organs, cirrhosis of the liver, is 17.7%.

The clinical picture depends on the location and extent of portal vein thrombosis, the speed of its development and the nature of the predisposing liver disease. The most severe manifestation of the disease is liver infarction or atrophy of its segment. The combination of portal vein thrombosis with mesenteric vein thrombosis in most cases is lethal. However, in one third of cases, thrombosis forms slowly, as a result of which collateral blood flow develops, and the portal vein eventually rectifies (cavernous transformation of the portal vein occurs). Nevertheless, even with a relatively favorable course, portal hypertension develops.

    • Clinical manifestations depend on the predisposing disease.
    • Thrombosis of the portal vein is manifested by bleeding from varicose veins of the esophagus. Bleeding is relatively well tolerated, because. in many patients, the functions of hepatocytes are preserved.
    • Enlargement of the spleen is characteristic, especially in children.
    • Violations of blood flow through the mesenteric veins cause paralytic ileus (abdominal pain, bloating, lack of peristalsis). The result of mesenteric thrombosis can be intestinal infarction and subsequent purulent peritonitis.
    • With purulent pylephlebitis, signs of liver abscesses appear (repeated stunning chills, pain on palpation of the enlarged liver, on the plane of which nodes are felt – abscesses).
    • Ascites (not typical for pylephlebitis).
    • Subicteric sclera.
    • Encephalopathy and other signs of liver failure.
    • Postoperative portal vein thrombosis most often occurs during the period of hypercoagulability (3-8 days).

Special Studies

    • Portal vein thrombosis should be suspected in any case of portal hypertension associated with normal liver biopsy findings.
    • Coagulogram: increase

fibrinogen content, the appearance of activated fibrinogen B, an increase in PTI, a decrease in blood clotting time

    • Ultrasound and CT: ulcers in the liver with pylephlebitis
    • Angiography (the method of final confirmation of the diagnosis), in particular splenoportography or images taken in the venous phase of the superior mesenteric arteriography.

Treatment: Drug Therapy

    • Anticoagulants
    • Emergency therapy: heparin 40,000-60,000 IU intravenously for 4-6 hours, then 40,000 IU / day (from 1 to 8-10 days) intravenously. The dose of the product is selected according to the time of blood clotting, plasma tolerance to heparin and the results of thromboelastography.
    • Maintenance therapy: 1-3 days before the end of heparin administration, indirect anticoagulants (phenylin, neodicoumarin, sincumar) are prescribed, the dose is selected individually (reduction of IPT to 40%). For example, doses of phenylin: on day 1 – 0.12-0.18 g / day (in 3-4 doses), on day 2 – 0.09-0.06 g / day, on subsequent days – 0.03 -0.06 g/day (depending on PTI).
    • Contraindications to prescribing anticoagulants
    • Absolute contraindications: severe bleeding, recent (within 1 month) neurosurgical operations, pregnancy, intolerance reactions
    • Relative contraindications: recent severe bleeding, surgery (except neurosurgery), a history of peptic ulcer or a recent stroke (not associated with embolism).
    • Possible drug interactions
    • The action of anticoagulants is enhanced by alcohol, allopurinol, amiodarone, anabolic steroids, androgens, many antimicrobials, cimetidine, ranitidine, chloral hydrate, disulfiram, all NSAIDs, sulfinpyrazone, tamoxifen, thyroid hormones, vitamin E
    • The action of anticoagulants is reduced by aminoglutethimide, antacids, barbiturates, carbamazepine, cholestyramine, diuretics, griseofulvin, rifampin, oral contraceptives.
    • Thrombolytic products, for example fibrinolysin (20,000-40,000 units with the addition of heparin, 10,000 units per 20,000 units of fibrinolysin) intravenously for 3-4 hours, streptokinase, streptodecase.
    • Reopoliglyukin reogluman (in / in 400-800 ml / day for 3-5 days).
    • With pylephlebitis – broad-spectrum antibiotics, for example, thienam up to 4 g / day / in 3-4 doses.


    • Conservative therapy
    • Application of the Sengstaken-Blackmoor probe. After inserting the probe into the stomach, air is injected into the cuffs, pressing the veins of the cardia and the lower third of the esophagus. In order to avoid bedsores, the balloons are freed from air for 5-10 minutes after 5-6 hours. The total duration of the probe should not exceed 48 hours
    • Injection sclerosing therapy: during esophagoscopy, a sclerosing product decylate (thrombovar) is injected into the varicose veins of the esophagus, leading to their thrombosis.
    • Surgical treatment is used when conservative treatment fails.
    • While maintaining the patency of the splenic vein, the operation of choice is the imposition of a splenorenal anastomosis
    • Otherwise, a mesenteric-caval anastomosis is created using a large-diameter vascular prosthesis (16–18 mm) between the superior mesenteric and inferior vena cava
    • With ongoing esophageal bleeding, esophageal varicose veins can be sutured, for example, the Tanner operation (transverse section of the stomach in the cardial region, followed by end-to-end stitching of its walls)
    • With pylephlebitis, opening and drainage of liver abscesses.


    • OPN
    • Intestinal infarction
    • Subhepatic or subdiaphragmatic abscess
    • Diffuse purulent peritonitis
    • Massive bleeding.

See also Bacterial liver abscess, Subdiaphragmatic abscess, Portal hypertension, Intestinal obstruction, ICD hepatorenal syndrome. 181 Portal vein thrombosis

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