Virchow's Triad
Applied
Type
AdditionConfidence
90%
Created
Mar 19, 2026
Evidence
3 sources
Rationale
The section was updated to include modern mechanistic insights (venous valve hypoxia) and contemporary acquired hypercoagulable states (VITT/TTS). Additionally, the risk associated with specific traumatic injuries (spine fractures) was added to the endothelial injury/stasis section to provide more clinical specificity. All abbreviations were expanded on first use as per instructions.
Evidence
Content Changes
removedadded
<!-- type: risk-factors --> **Virchow's triad** 1. **Venous stasis** (immobility, hospitalization, surgery, trauma, paralysis, long-distance travel, heart failure). Stasis-induced venous valve hypoxia is a recognized mechanism for thrombus initiation, even in the absence of overt vessel wall damage [@shaydakov2024]. 2. **Endothelial injury** (trauma, surgery, central venous catheters, prior thrombosis). High-energy trauma, such as traumatic spine fractures, significantly increases the risk of concomitant venous thromboembolism (VTE) through direct vessel damage and associated immobility [@murtada2024]. 3. **Hypercoagulability** - Inherited: factor V Leiden, prothrombin G20210A, antithrombin deficiency, protein C/S deficiency. - Acquired: malignancy, pregnancy/postpartum, estrogen therapy, antiphospholipid syndrome (APS), inflammatory states.states, and vaccine-induced immune thrombotic thrombocytopenia (VITT), also known as thrombosis with thrombocytopenia syndrome (TTS) [@waqar2026] [@heit2015_corrected] [@esvs2021vte][@esvs2021vte]. **Surgical venous thromboembolism (VTE) risk assessment** Validated risk assessment models (e.g., Caprini) help stratify perioperative VTE risk and guide prophylaxis intensity and duration in surgical patients. :::widget{type="calculator" id="caprini"} {} :::