Deep Vein Thrombosis and Pulmonary Embolism: Detection and Prevention
- Dec 3, 2019
- 7 min read
Updated: Oct 28
Deep vein thrombosis and pulmonary embolism arise from a complex interplay of genetic, hormonal, and environmental factors that disrupt normal blood flow. From vein injury and immobility to elevated estrogen levels and chronic medical conditions, the risk grows as these triggers converge. New data underscore how hospitalization, surgery, pregnancy, and obesity remain leading contributors, while early movement, hydration, and preventive screening can sharply reduce incidence and save lives.
Overview
What factors increase the risk of deep vein thrombosis and pulmonary embolism?
Anyone can develop a deep vein thrombosis (DVT) or pulmonary embolism (PE), but certain conditions and lifestyle factors significantly increase the likelihood. The risk rises sharply when multiple factors are present at the same time, as each one compounds the effects of impaired circulation, vessel injury, or abnormal blood clotting.
Vein Injury
How does damage to a vein’s inner lining trigger blood clot formation?
Damage to the inner lining of a vein, known as the endothelium, activates the body’s coagulation cascade, prompting platelets to adhere to the injured site and form a clot. This process, while protective during injury, can become pathologic when trauma or surgical intervention disrupts normal vessel function. Endothelial injury represents one component of Virchow’s triad, the foundational model for understanding thrombosis, alongside venous stasis and hypercoagulability.
Clinical research has consistently shown that trauma and surgical procedures greatly increase the risk of venous thromboembolism (VTE). A large meta-analysis published in The BMJ (2020) found that major orthopedic surgeries, such as hip or knee replacement, carry one of the highest postoperative VTE risks, with incidence rates ranging from 1–2% even with preventive anticoagulation. Fractures, especially of the pelvis or lower extremities, can disrupt local venous structures and release tissue factors that amplify clot formation. Severe muscle injury or crush trauma also contributes to localized inflammation and endothelial dysfunction, further heightening the risk.
Common causes of vein injury include:
Fractures and Vascular Disruption
Bone fractures that rupture or compress adjacent blood vessels—most often in the pelvis, femur, or tibia—disrupt normal circulation and trigger the body’s clotting cascade.
Trauma-Induced Inflammation
Severe muscle trauma or crush injuries that release inflammatory cytokines and tissue factors, damaging the microvascular endothelium and promoting localized thrombus formation.
Surgical Manipulation and Immobility
Major surgical procedures, particularly those involving the abdomen, pelvis, hips, or legs, where direct vessel handling, anesthesia-related immobility, and postoperative inflammation collectively heighten the risk of venous thrombosis.
Reduced or Slowed Blood Flow
How does reduced circulation contribute to the development of blood clots?
Venous stasis, also referred to as slowed or stagnant blood flow, is another central mechanism of clot formation and a second element of Virchow’s triad. When circulation slows, platelets and clotting factors accumulate rather than being cleared, allowing spontaneous clot formation in the deep veins.
Studies have shown that immobility remains one of the strongest modifiable risk factors for deep vein thrombosis (DVT). According to the U.S. Centers for Disease Control and Prevention (CDC), individuals confined to bed for more than three days after surgery or illness experience a two- to fourfold increase in clot risk. Similarly, long-duration travel (over four hours) doubles the risk of DVT, particularly in individuals with additional risk factors such as obesity, recent surgery, or hormonal therapy.
Situations associated with reduced blood flow include:
Prolonged Bed Rest and Immobility
Extended confinement to bed due to illness, recovery, or postsurgical care limits calf muscle contraction—the primary mechanism driving venous return—allowing blood to pool and increasing the risk of clotting.
Paralysis or Mechanical Restriction
Paralysis or immobilization, including the use of a leg cast or brace, diminishes the natural pumping action of leg muscles, slowing deep venous circulation and predisposing to thrombosis.
Extended Sitting and Travel-Related Stasis
Long periods of sitting, particularly during air travel or road trips, compress the veins behind the knees and restrict movement, leading to stagnant blood flow and a higher likelihood of clot formation.
Research supports preventive movement and hydration as simple yet effective countermeasures. Studies published in Thrombosis Research and The Lancet Haematology highlight that leg exercises, walking breaks, and adequate fluid intake can significantly reduce stasis-related clot formation, especially during prolonged travel or recovery periods.
Increased Estrogen Levels
Why does elevated estrogen make the blood more likely to clot?
Estrogen directly influences the body’s coagulation system by increasing the production of clotting factors II, VII, IX, and X while simultaneously reducing natural anticoagulants such as protein S. This hormonal shift creates a hypercoagulable state, explaining why elevated estrogen levels, whether from medication or physiological changes, significantly increase the risk of venous thromboembolism (VTE).
Extensive research supports this association. A Lancet meta-analysis conducted in 2015 found that women using combined oral contraceptives containing estrogen and progestin were nearly four times more likely to develop a venous thromboembolism (VTE) compared to non-users, with risk varying based on dosage and hormone formulation. Hormone replacement therapy (HRT) also carries an elevated risk, particularly in postmenopausal women within the first year of treatment.
Pregnancy represents one of the most prothrombotic physiological states. Blood volume increases by about 40–50%, venous return from the legs slows due to uterine pressure, and estrogen surges to maintain placental function. The American Society of Hematology (ASH) estimates that pregnancy and the postpartum period, up to 12 weeks after delivery. increase the risk of clotting by five to tenfold compared with non-pregnant women of similar age.
Higher-risk situations involving elevated estrogen include:
Estrogen-Containing Contraceptives
Hormonal birth control methods that include estrogen—particularly those with higher-dose ethinyl estradiol—can increase clotting factor production and reduce natural anticoagulant activity, raising the risk of venous thrombosis.
Hormone Replacement Therapy (HRT)
Postmenopausal hormone therapy, especially oral estrogen formulations, elevates clotting risk by influencing liver synthesis of coagulation proteins. Transdermal patches generally present a lower risk due to reduced systemic estrogen exposure.
Pregnancy and the Postpartum Period
During pregnancy and recovery after childbirth, rising estrogen levels, venous compression from the growing uterus, and reduced mobility combine to promote venous stasis and a temporary hypercoagulable state.
Underlying Medical Conditions
How do chronic diseases increase the likelihood of developing a blood clot?
A range of chronic diseases can significantly heighten the risk of venous thromboembolism (VTE) by sustaining systemic inflammation, impairing vascular integrity, and promoting blood flow stagnation. These mechanisms increase thrombin generation and reduce the body’s natural anticoagulant defenses, with risk compounding when multiple conditions are present simultaneously.
Heart Disease
Reduced cardiac output slows venous return, leading to blood pooling in the extremities. At the same time, chronic inflammation and endothelial dysfunction create a prothrombotic environment that favors clot formation.
Chronic Lung Disease
Conditions such as COPD and pulmonary hypertension decrease oxygenation and induce vasoconstriction. This combination increases endothelial stress and platelet activation, both of which elevate clotting risk.
Cancer and Its Treatments
Malignancies release procoagulant substances, including tissue factor, which directly activate the coagulation cascade. Chemotherapy and central venous catheters further damage vessel walls. Research published in The Journal of Clinical Oncology (2021) reports that cancer patients have a sevenfold higher risk of developing VTE compared to the general population, with rates varying by tumor type and treatment regimen.
Inflammatory Bowel Disease (IBD)
Ongoing systemic inflammation in Crohn’s disease and ulcerative colitis activates coagulation pathways even during remission. Studies in Gastroenterology (2020) show a two- to threefold higher incidence of VTE among patients with IBD, likely driven by cytokine-mediated endothelial injury and impaired fibrinolysis.
Chronic diseases, therefore, represent a critical intersection between inflammation, vascular injury, and impaired circulation—three key contributors to thrombosis that warrant proactive prevention and monitoring.
Additional Contributing Factors
What other conditions or personal factors can increase clotting risk?
A variety of physiological, genetic, and lifestyle conditions can heighten the likelihood of venous thromboembolism (VTE) by impairing circulation, damaging the vascular endothelium, or altering the body’s natural balance between clot formation and breakdown.
History of DVT or PE
A prior episode of deep vein thrombosis (DVT) or pulmonary embolism (PE) is one of the strongest predictors of recurrence. Persistent endothelial injury and residual vein obstruction can sustain a prothrombotic state, particularly within the first few years after the initial event.
Inherited or Acquired Thrombophilias
Genetic and autoimmune clotting disorders, such as Factor V Leiden, prothrombin G20210A mutation, and antiphospholipid syndrome (APS), predispose individuals to abnormal coagulation. Studies in Blood (2022) confirm that carriers of these conditions face a two- to eightfold higher lifetime risk of venous thromboembolism (VTE), depending on genetic profile and environmental triggers.
Family History of VTE
A family history of blood clots often reflects both shared genetic vulnerabilities and common environmental or behavioral factors, including sedentary lifestyle and hormonal exposure. Having a first-degree relative with venous thromboembolism (VTE) can double an individual’s personal risk, even in the absence of a confirmed thrombophilia.
Advanced Age
With age, veins lose elasticity, and the calf muscle pump weakens, slowing venous return. This venous stasis, combined with increased comorbidities and reduced mobility, makes adults over 60 significantly more prone to clot formation.
Overweight or Obesity
Excess abdominal pressure restricts venous drainage from the pelvis and lower limbs. Research in The Lancet Haematology (2021) shows that obesity increases venous thromboembolism (VTE) risk by two to three times, and the effect compounds when combined with hormonal therapy or prolonged immobility.
Central Venous Catheters
Intravenous lines and ports, particularly those used for chemotherapy or long-term medication delivery, can injure the vessel wall or serve as a surface for thrombus formation. Catheter-associated DVT occurs in up to 20% of hospitalized or cancer patients, according to The Journal of Thrombosis and Haemostasis (2020).
Recognizing these intersecting risk factors allows for early, targeted intervention. Medical counseling, weight management, smoking cessation, and, when indicated, preventive anticoagulation can significantly lower the likelihood of recurrence and improve long-term vascular outcomes.
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