SAIMSARA Journal

Machine Generated Science • ISSN 3054-3991

Deep Vein Thrombosis Risk Factors: Scoping Review with ☸️SAIMSARA.

Cardiac & Vascular Health icon

Cardiac & Vascular Health

Issue 1, Volume 1, 2026

DOI: 10.62487/saimsara05326f98

Editorial note
• Last update: 2026-05-02 09:45:09
What is this paper about
Deep vein thrombosis is not one disease trigger, but a convergence of risk: genes, cancer, surgery, catheters, hormones, infection, inflammation, and immobility can all push the body toward clot formation. This review maps where the strongest danger signals appear — from COVID-19 and oral contraceptives to cancer care and inherited thrombophilia — and shows why modern DVT prevention must be personalized rather than one-size-fits-all.
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Abstract: The aim of this review is to synthesize evidence regarding the multi-dimensional risk factors, diagnostic biomarkers, and prophylactic strategies for deep venous thrombosis (DVT) across surgical, medical, and genetic contexts. The review includes 107 cited references and is built on 105 original studies with 441130 total participants (topic-deduplicated ΣN). The mapped evidence indicates that DVT emerges from a convergence of inherited thrombophilia, acute systemic triggers, and iatrogenic exposures, with a particularly prominent signal for coronavirus disease 2019, where DVT was reported in 58% of an autopsy cohort, and for hormonal contraception, where current users showed an odds ratio of 5.0 versus non-users with further elevation for drospirenone-containing formulations. Cancer-associated thrombosis, major orthopedic surgery, critical illness, and central venous access devices recurred as dominant high-risk settings, with peripherally inserted central catheters causing substantially more catheter-related DVT than implanted ports (8% vs 1%). Inherited contributors including factor V Leiden, the prothrombin G20210A mutation, protein C deficiency, and elevated factors IX and XI were consistently associated with venous thrombosis risk, while mean platelet volume and D-dimer recurred as accessible hematological signals supporting risk stratification. Mechanistic studies highlight neutrophil extracellular traps, platelet–monocyte cooperation, and platelet-derived high-mobility group box 1 as biologically plausible drivers linking inflammation to thrombosis. Clinically, these signals support individualized prophylaxis decisions that integrate genetic background, contraceptive choice, device selection, and inflammatory context rather than relying on uniform protocols, while acknowledging that the heterogeneous and partly dated evidence base limits firm comparative conclusions. Future research should prioritize prospective, multi-ethnic studies that jointly evaluate genetic, inflammatory, and device-related risk factors and that clarify optimal prophylaxis in upper-extremity DVT, superficial-to-deep thrombosis progression, and coronavirus disease 2019–associated hypercoagulability.

Keywords: Deep venous thrombosis; Risk factors; Venous thromboembolism; COVID-19; Pulmonary embolism; D-dimer; Factor V Leiden; Post-thrombotic syndrome; Neutrophil extracellular traps; Thromboprophylaxis

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Reference Index (107)