Vein Obstruction

Etiology

Venous thromboembolism (VTE) is a multifactorial disorder which can be due to inherited or acquired risk factors.

• Inherited: Factor V Leiden is the most common condition. This condition might not cause blood clots on its own, only when combined with 1 or more other risk factors.[1]
• Prolonged immobilization: Decreased activity of the soleus pump increase the risk of stasis and lead to thromboembolism formation. This is seen after prolonged bed rest, long plane flights, and intensive care unite (ICU) hospitalizations.
• Direct or indirect injury to veins or from surgical procedures can increase the risk of clot formation.
• Pregnancy can increase the risk by 2 mechanisms: Increase hypercoagulability as the concentration of clotting factors are affected these include fibrinogen, which can rise 3-times its normal value, thrombin levels increase, and Protein S, an anticoagulant, decreases.[2]
• Birth control pills (oral contraceptives) or hormone replacement therapy: Oral contraceptives cause significant increases in fibrinogen levels.[3]
• Obesity has been shown to be associated with an increased risk of venous thromboembolism.[4]
• Smoking: Factor XIII, which stabilizes fibrin clots, is increased in smokers and exposure to nicotine may also increase plasminogen activator inhibitor-1 (a major regulator of fibrinolysis). Quantitative exposure to passive smoke has been positively correlated with blood coagulation activity.[3]
• Cancer: Some forms of cancer increase substances that cause blood to clot. Certain cancer treatments also increase the risk of blood clots.
• Heart failure: Decreased function leads to increased venous pooling and increased stasis.
• Inflammatory bowel diseases including Crohn disease or ulcerative colitis increase the risk of deep vein thrombosis (DVT).

Epidemiology

Each year, there are about 4,000,000 surgical patients and 8,000,000 medical patients who are hospitalized in the United States at moderate or high risk for VTE.[5] In a global cross-sectional study, a large proportion of hospitalized patients were also at moderate or high risk for VTE, more specifically, 42% of medical patients and 64% of surgical patients.[6] Among hospitalized medical patients, the 4 risk factors most predictive of VTE in the Intermountain Healthcare database were: (1) previous VTE, (2) bed rest, (3) peripherally inserted central venous catheter, and 4) cancer.[7] Of particular importance is VTE in the outpatient setting. In a community study in Worcester, about three-fourths of patients developed VTE as outpatients. More than half had undergone surgery or had been hospitalized within the prior 3 months.[8] Cancer, severe infection, or congestive heart failure increased the likelihood of a poor outcome from VTE in the community setting.[9] In a population-based study in Norway, the incidence rate for all first VTE events was 1.43 per 1000 person-years. For DVT it was 0.93 per 1000 person-years with a 30-day case-fatality rate was 4.6% for DVT.  Incidence rates increased exponentially with age and were slightly higher in women than men.

Pathophysiology

Venous thrombosis pathogenesis is based on the triad of Virchow proposed in 1865. The triad includes venous stasis, changes in the vessel wall, and/or changes in the blood leading to a hypercoagulability state which can increase the risk of obstruction.[10]

History and Physical

Venous obstruction is most commonly seen in the form of deep venous thrombosis (DVT). Patients present with unilateral or bilateral leg swelling after prolonged stasis, for example, plane travel or another long period of inactivity. Other symptoms include leg pain, which can occur in 50% of patients and is aggravated by dorsiflexion. Edema, if present, is one of the most specific symptoms of DVT. There is no correlation to the pain and tenderness to the size of the thrombus.

Finding are usually confined to the affected limb. These include tenderness to the calf with a positive Homans sign which is a pain with passive dorsiflexion). Leg swelling of 2 centimeters or more in the affected limb is suggestive of DVT, and a positive D-dimer test shows the highest correlation to DVT.[11]

Symptoms of portal vein thrombosis include right upper quadrant pain, nausea, and/or fever. Patients may have progressive ascites and ischemia of intestine due to microthrombi propagation of blood vessels. Intestinal suffusion secondary to acute portal hypertension can also be present.

Evaluation

Evaluation of DVT includes blood tests to help stratify patients with the risk for deep venous thrombosis (DVT) include D-dimer assay; levels of antithrombin III (ATIII), N-terminal pro-brain natriuretic peptide (NT-proBNP), and C-reactive protein (CRP); and erythrocyte sedimentation rate (ESR). Studies have shown all patient presenting with a positive D-dimer and leg swelling have confirmed DVT on evaluation.[11]

Radiologic investigations include an ultrasound of the affected leg and pelvis. It may require additional evaluation in some patients with either CT (computed tomography) scan or MRI (magnetic resonance imaging).

Investigation for portal vein thrombosis includes laboratory test: coagulation studies to rule out inherited coagulation disorders, liver function test, and radiographic imaging. Ultrasound is the first line modality, and this can be done endoscopically. Further imaging modalities are MRI or MRA and possible CT scan.

Treatment / Management

Management of VTE is to prevent further extension of DVT proximally and the prevention of pulmonary embolism. Treatment is divided into an initial active treatment phase of 3 months and a subsequent secondary phase.[12] Anticoagulation during the initial treatment shows a reduction in the risk of embolization in patients with proximal DVT or PE and reduces the risk of death in patients with PE.[13]

Initial treatment consists of the administration of an anticoagulant. Anticoagulants include low molecular weight heparin (LMWH) or fondaparinux or unfractionated heparin (UFH) for a minimum of 5 days, with early administration of a vitamin-K antagonist (VKA) like warfarin.[14] An international normalized ratio (INR) of at least 2 is achieved on 2 consecutive days, because of the slow onset of action of the antithrombotic effect of VKAs.[15] After the first 3 months, management is based on the risk of bleeding compared to the risk of recurrent thrombosis. Thrombectomy of venous obstruction is less frequently performed, and often, an IVC filter is placed in patients in whom anticoagulation is contraindicated.(A1)

Treatment for portal venous obstruction includes thrombolysis using tissue-type plasminogen activator (tPA) through the transhepatic route, followed by prolonged anticoagulation therapy with warfarin for at least 3 months.

Differential Diagnosis

• Venous thromboembolism: Trauma, edema, cellulitis
• Portal vein obstruction: Cirrhosis, Budd-Chiari, sarcoidosis

Prognosis

If treated appropriately, the overall prognosis of VTE is good. 

The overall mortality has been reported to be less than 10% in chronic pulmonary vein thrombosis.[16]

Complications

Complication of VTE is pulmonary embolism of the pulmonary artery which can lead to death. 

Portal vein thrombosis complications include splenomegaly, esophageal- and gastric varices with or without bleeding, portal hypertensive gastropathy, and ascites.