Venous thromboembolism

Learning objectives

Describe the mechanisms and risk factors for venous thromboembolism
Prevent perioperative venous thromboembolism
Diagnose and manage venous thromboembolism

Background

Venous thromboembolism (VTE) is a major cause of morbidity and mortality in both hospital and community settings
Most preventable cause of mortality in hospitalized patients
Encompasses deep vein thrombosis (DVT) and pulmonary embolism (PE)
DVT occurs when red blood cells, fibrin, platelets, and leucocytes form a mass within an intact deep vein
Signs & symptoms are nonspecific and only occur in up to 50% of patients
PE occurs in about a third of patients with a DVT
Adequate perioperative thromboprophylaxis is essential to prevent perioperative VTE

Risk factors

Three main factors that cause thrombosis:
- Alterations in blood flow (stasis and turbulence)
- Vascular endothelial injury
- Alterations in the blood coagulability
Risk factors:

Stasis–endothelial injury	Thrombophilias	Medical conditions	Medications	Other
Indwelling venous device	Activated protein C resistance	Malignancy (solid tumour and myeloproliferative disorders)	Oral contraceptive use (combined only)	Increasing age
Surgery (abdominal, pelvic, orthopedic most commonly)	Factor V Leiden	Pregnancy, postpartum	Hormone replacement therapy	Smoking
Major trauma, burns	Prothrombin gene mutation G20210A	Myocardial infarction	Chemotherapy (including tamoxifen)
Prolonged travel	Hyperhomocysteinemia	Congestive heart failure
Paralysis (including anesthesia for >30 min)	Anticardiolipin antibodies	Obesity
Varicose veins	Lupus anticoagulant	Inflammatory bowel disease
	Elevated factor VIII level	Nephrotic syndrome
	Protein C deficiency	History of VTE
	Protein S deficiency	Heparin-induced thrombocytopenia
	Dysfibrinogenemia	Paroxysmal nocturnal hemoglobinuria
	Dysplasminogenemia
	Antithrombin deficiency

Pathophysiology

Venous thrombi typically develop at a site of vascular trauma, around intravascular catheters, or in areas of reduced blood flow (e.g., venous valves)
Accumulation of fibrin and platelets causes rapid growth in the direction of blood flow
Endogenous fibrinolysis results in partial or complete resolution of the thrombus
Any residual thrombus may result in incomplete recanalization of the vein, potentially narrowing the lumen and causing valve incompetence
Extensive collateral network may develop

Prevention

$venout thromboembolism, vte, mobility, bleeding, prophylaxis, anti-embolism stockings, vascular disease, arteriosclerosis, neuropathy, edema, heat failrue, stroke, pneumatic compression, foot impulse, neuraxial block, unfractionated heparin, low molecular weight heparin, LMWH, warfarin, factor xa, aspirin, danaparoid, fandaparinux, Lepirudin, thrombocytopenia, dextran, physiotherapy$

Diagnosis

DVT
- Duplex ultrasonography
- D-dimer blood test
- Contrast venography
- MRI
PE
- Computed tomographic pulmonary angiography
- Ventilation-perfusion scan
- Pulmonary angiography
- MRI

Management

Preferred DVT treatment: Low molecular weight heparins
Maintain anticoagulation for 3-6 months for VTE secondary to transient risk factors and >12 months for recurrent VTE
Thrombolytics in severe cases
When anticoagulation fails: Inferior vena cava filter
Thrombectomy/embolectomy (rarely required)