Splenic vein thrombosis is a blockage of the vessel lumen by a thrombus, which is accompanied by an increase in the spleen and an expansion of the network of collaterals. Acute thrombosis is manifested by abdominal pain, bloody vomiting and intestinal bleeding. The chronic variant is characterized by discomfort and heaviness in the left hypochondrium, periodic bleeding from the nose and gastrointestinal tract, anemia. Diagnostics includes invasive (splenoportography, endoscopic ultrasound, laparoscopy) and non-invasive studies (CT or MRI of the abdominal cavity, ultrasound Dopplerography). Conservative treatment or surgical intervention (bypass surgery, splenectomy) is indicated.
ICD 10
I82.8 Embolism and thrombosis of other specified veins
Meaning
Splenic vein thrombosis is one of the variants of prehepatic portal hypertension, which accounts for about 5-10% of all pathologies of the portal vein system. The prevalence in the population is approximately 0.5%. The danger of vascular damage lies in hemorrhagic complications and the development of hypersplenism. Most often, thrombosis of the veins of the spleen is detected in patients with cirrhosis of the liver (up to 25%). There were no significant age and gender differences among patients.
Causes
Venous thrombosis is considered a polyethological disease, since its occurrence is influenced by local and systemic factors. In half of the patients, the exact cause of the pathology cannot be established even after a thorough instrumental examination. The most well—known etiological factor is cirrhosis of the liver, which is accompanied by secondary changes in the splenic vein. In practical phlebology , other causes of thrombosis are distinguished:
- Intraabdominal factors. The most extensive category of causes, which causes up to 70% of cases of the disease. Chronic pancreatitis and pancreatic necrosis, cysts and pseudocysts of the pancreas lead to obstruction of the splenic vein. Thrombosis is promoted by inflammatory processes in the intestine, viral hepatitis.
- Innate prerequisites. Thrombosis in the lumen of the veins of the spleen is observed in people with genetically determined thrombophilia, hypercoagulation conditions. The predisposing factor of thrombosis is structural abnormalities of the splenic and portal veins, which contribute to the delay of platelet masses.
- Malignant neoplasms. The disease occurs with tumors of the head of the pancreas or hepatocellular carcinoma and is associated with mechanical compression of venous vessels. In 3% of patients, thrombosis is the first manifestation of myeloproliferative disease.
- Systemic venous lesions. Recurrent splenic vein thrombosis is a frequent companion of migratory thrombophlebitis. The inflammatory process in the venous wall is combined with an increased influx and aggregation of platelets. Some cases of thrombosis are caused by obliterating thrombangiitis (Burger’s disease).
- Mechanical damage. The appearance of thrombosis is expected after a blunt abdominal injury, a blow to the lumbar region. Extremely rarely, blockage of the splenic vein occurs as an iatrogenic complication — during surgical interventions on the liver or pancreas.
Risk factors
Among the risk factors, researchers identify systemic or local infectious processes (endocarditis, sepsis, tuberculosis), which are accompanied by an increase in blood clotting activity. The likelihood of obstruction increases in women during pregnancy and in the postpartum period, in patients who take oral contraceptives. The frequency of thrombosis increases with prolonged adherence to strict bed rest, during the rehabilitation period after extensive surgical interventions.
Pathogenesis
The development of the disease is based on Virchow’s triad: hypercoagulation, destruction of vascular endothelial cells and local slowing of blood flow. At the same time, favorable conditions arise for the accumulation of platelets in the vein, which then attach to the damaged venous wall. Red blood clots form in the splenic veins, which consist of platelets, fibrin and erythrocytes.
Under favorable conditions, aseptic autolysis or recanalization of a thrombus with partial restoration of blood flow in the splenic vein is possible. More often there is a gradual growth of a blood clot and progressive hemodynamic disorders in the portal vein system. At the same time, a network of collateral venous vessels is activated. In acute thrombosis, collaterals do not have time to form.
Classification
By localization, there are thrombotic processes that affect small veins extending from the spleen, as well as splenic vein thrombosis formed by the fusion of small venous vessels. Thrombi are divided into parietal, in which part of the venous lumen is free, and obstructing. The obstruction of the splenic vein is systematized according to the nature of the course, according to which 2 types of thrombosis are distinguished:
- Acute. Clinical manifestations manifest within a few hours or days. It is characterized by a serious condition and a high risk of complications.
- Chronic. The disease develops for 2-3 years or more, proceeds with little symptoms. According to etiology, chronic thrombosis can be primary, when the pathological process is immediately localized in the vein of the spleen, and secondary.
Symptoms
Acute thrombosis
The course of acute thrombosis resembles surgical diseases of the abdominal organs. Suddenly there is a sharp pain in the abdomen, which is localized on the left in the hypochondrium or in the epigastrium. The pain is not associated with eating or physical activity. Simultaneously with the pain syndrome, vomiting appears. Admixtures of scarlet blood are found in the vomit. After bloody vomiting, patients feel relieved. After a few hours, the tar-like stool departs.
Chronic thrombosis
Chronic splenic vein thrombosis is asymptomatic or low-symptomatic for a long time. The first sign is a feeling of heaviness and discomfort in the left abdomen. With awkward movements, sharp turns in the left hypochondrium, dull pains bother. When the inflammatory process is joined, episodes of an increase in body temperature occur, combined with intense pain syndrome.
A few years after the manifestation of thrombosis, nasal or gastrointestinal bleeding (vomiting with blood, black feces) appears. There is a periodic increase in abdominal volume due to ascites. Ascites is characterized by rapid progression and self-resorption. Anemia develops due to repeated bleeding. Patients complain of dizziness, weakness, intolerance to physical exertion.
Complications
A typical consequence of thrombosis, which occurs in 90% of patients, is profuse bleeding from the gastrointestinal tract. Blood clots in the veins of the spleen are characterized by damage to the vessels of the stomach, and not the lower third of the esophagus, as in classical portal hypertension. The differences in the localization of bleeding are due to the peculiarities of anastomosis of the vessels of the spleen. In the absence of medical care, massive bleeding ends in death.
In the chronic variant of pathology, blood clots spread to mesenteric veins and intestinal arcades. The blood supply to the small intestine is disrupted, reflex spasm of arterioles occurs. Intestinal ischemia occurs, which in 5% of cases ends with an intestinal infarction. With compensatory expansion of venous collaterals, compression of extrahepatic bile ducts occurs, which causes mechanical jaundice and cholangitis.
Diagnostics
The diagnosis of splenic vein thrombosis is more often performed by surgeons, less often by gastroenterologists or highly specialized hepatologists. Physical data do not differ from those in classical forms of portal hypertension. The patient is prescribed a complex of laboratory and instrumental studies:
- Blood test. The clinical analysis reveals anemia or pancytopenia, which is characteristic of hypersplenism. A coagulogram is performed to exclude congenital coagulopathies. In patients with cirrhosis of the liver, a decrease in the prothrombin index is detected.
- Abdominal ultrasound. Classical percutaneous sonography is not informative enough, therefore endoscopic ultrasound with 99% specificity is recommended. The method reveals the presence of blood clots in the lumen of the splenic vein, splenorenal and portosystemic shunts. Ultrasound Dopplerography is performed to assess blood flow.
- Abdominal CT. It is used not only to detect a blood clot, but also to verify the causes of thrombosis. CT with contrast is more often used. An alternative to the X-ray method is an MRI of the abdominal organs, in which there is no radiation load.
- Splenoportography. Invasive examination of the vessels of the portal vein basin is indicated at the stage of preparation for surgical correction of the disease. Using the radiopaque method, all venous vessels and their collaterals are visualized, the size, extent and localization of thrombosis are determined.
- Laparoscopy. Modern minimally invasive technique is recommended to identify the etiology of the disease. When the splenic vessels are affected, surgeons see an unchanged or cirrhotic liver against a background of well-developed collaterals and a sharply enlarged spleen.
Treatment
Conservative therapy
Therapeutic tactics for thrombosis involves the elimination of blood flow obstruction and compensation for the resulting disorders. Due to the high risk of bleeding, treatment is carried out in a hospital. With continued bleeding, hemostatics are administered, endoscopic vascular coagulation is performed. Basic therapy includes 3 groups of drugs:
- Thrombolytics. Enzyme drugs that destroy blood clots are used only in the case of acute thrombosis, since the appearance of which no more than 5 days have passed. For targeted administration of drugs, an intravenous or catheter method is chosen.
- Anticoagulants. Low molecular weight heparins are indicated to prevent the spread of a blood clot. Modern drugs are safe and do not require constant monitoring of the coagulogram. Indirect anticoagulants are added a week after the start of heparin therapy.
- Disaggregants. Drugs are prescribed for long-term use. Their action is mainly aimed at preventing secondary thrombosis, if it is not possible to eliminate etiological factors. Instead of acetylsalicylic acid, thienopyridine derivatives are preferred.
To prevent pileflebitis, parenteral antibacterial therapy in combination with an antifungal drug is necessary. According to the indications, patients take painkillers — analgesics from the group of nonsteroidal anti-inflammatory drugs, antispasmodics. To improve the rheological properties and electrolyte composition of the blood, infusion therapy is performed. Further treatment is selected taking into account the cause of thrombosis.
Surgical treatment
Splenorenal or mesocaval bypass surgery is common among surgical interventions, which is designed to relieve the venous network and prevent bleeding from dilated veins. If it is impossible to create vascular anastomoses, splenectomy is recommended. Removal of the spleen solves the problem of hypersplenism and pancytopenia, but is an independent risk factor for recurrent thrombosis.
Prognosis and prevention
In 90-95% of patients with splenic vein thrombosis, conservative methods allow to stop exacerbation and normalize venous blood flow. For a complete cure, elimination of the cause of thrombosis is required, therefore, in oncological processes, the prognosis is doubtful. Prevention consists in the timely treatment of liver and pancreatic diseases, the appointment of disaggregants to patients with hypercoagulation disorders.
Literature
- Al Mofleh I. A. Does Helicobacter pylori affect portal hypertensive gastropathy? // Saudi J Gastroenterol. — 2007. — № 2. — Р. 95–97.
- Hashizume M., Tanaka K., Inokuchi K. Morphology of gastric microcirculation in cirrhosis // Hepatology. — 1993. — № 6. — Р. 1008–1012.
- Hino S., Kakutani H., Ikeda K., Uchiyama Y. et al. Hemodynamic assessment of the left gastric vein in patients with esophageal varices with color Doppler EUS: Factors affecting development of esophageal varices // Gastrointest. Endosc. — 2002. — № 4. — Р. 512–517.
- Kiyono S., Maruyama H., Kondo T. et al. Hemodynamic effect of the left gastric artery on esophageal varices in patients with cirrhosis // J. Gastroenterol. — 2016. — № 9. — Р. 900–909.
- Snady H., Feinman L. Prediction of variceal hemorrhage: A prospective study // Am J Gastroentrol. — 1988. — № 5. — Р. 519–525.
- The Veterans Affairs Cooperative Variceal Sclerotherapy Group. Prophylactic sclerotherapy for esophageal varices in men with alcoholic liver disease. A randomized, single-blind, multicenter clinical trial // N Engl J Med. — 1991. — № 25. — Р. 1779–1784.
