Blood Clots Can’t Be Ignored in the Dental Chair

Venous thromboembolism (VTE), and its clinical manifestations deep vein thrombosis (DVT) and pulmonary embolism (PE), are uniquely dangerous conditions due to the range of their presentation: from no symptoms at all to sudden death. Due to the prevalence of VTE, and the associated morbidity and mortality, as well as the bleeding risks associated with anticoagulant therapies, accurate diagnostic/prognostic and treatment strategies are essential to confirm these conditions.

The role of the oral health professional may be limited in the diagnosis of VTE and its clinical manifestations, but is critical in identifying risk factors based on patients’ medical/medication history. Moreover, knowledge of these conditions, their etiology and risk factors, prevention and treatment strategies as well as potential treatment complications, will lead to appropriate patient management and successful outcomes.

As many as 900,000 Americans are affected by VTE, with 25% experiencing sudden death as their first symptom.¹ This statistic is likely an underestimate due to underdiagnosis of these conditions.² Death from all causes of VTE is estimated at 60,000 to 100,000 annually. Risk factors include recent hospitalization, surgical procedures, cancer and cancer treatment, pregnancy, childbirth, and post-partum complications within 3 months of giving birth.

PE is among the most common causes of pregnancy-related death. Hospital-acquired VTE, defined as occurring during or within 3 months of a hospital stay, accounts for more than half of all VTE in the US population and globally.³ Additionally, VTE can recur within 10 years, and long-term complications of DVT can occur in the affected limb. Heritability of VTE estimated from family studies is 40% to 60%, with many confirmed genes related to coagulation/anticoagulation, platelets, immune system cells, erythrocytes, and yet unknown cells/pathways.⁴ Additionally, there is a risk for a repeated VTE following the initial occurrence once the anticoagulant treatment is stopped, which depends on whether the initial incident was due to identified risk factors or was without identified risk factors.⁵ A recent systematic review found that the highest risk of recurrence was in patients with unprovoked VTE (7.4% over 0 to 24 months after stopping anticoagulant therapy).⁶ This risk is approximately 2.5 times higher than for patients with VTE provoked by surgery or a nonsurgical trigger.

Pathophysiology

In 1856, German physician Rudolf Virchow described three factors that contribute to the formation of venous blood clots: slow or stagnant blood flow (venous stasis), damage to the blood vessel lining, and increased blood clotting (hypercoagulability). This concept, known as Virchow’s Triad, remains the foundation for understanding VTE. Virchow also demonstrated that clots typically form in the peripheral veins and can then travel to the lungs, rather than forming in the pulmonary arteries themselves.⁷

Venous stasis is an important risk factor, but stasis alone generally is not enough to cause a clot; at least two of the three factors in Virchow’s Triad are typically involved.^7,8 Clots often begin near venous valves, where blood moves more slowly. This can promote fibrin buildup, low oxygen levels, and an environment that favors clotting. A protein called tissue factor helps activate the blood-clotting process, ultimately leading to clot formation and possible blockage of the vessel.⁹ Inflammation can further increase this risk because inflammatory substances can promote both blood clotting and damage to the vessel lining.¹⁰

DVT and PE are the two manifestations of VTE: DVT, ranging from asymptomatic to life-threatening venous obstruction of the deep veins of the limbs/abdomen, and PE, an occlusion of one or more of the pulmonary arteries by the embolus (dislodged thrombus) are both nonspecific, and therefore often underdiagnosed and dangerous conditions.² An estimated 25% of patients with clinical symptoms of DVT and only 5% of patients with suspected PE actually have the condition. This very low specificity can be explained by the challenges of the differential diagnosis, ranging from chronic venous insufficiency and thrombophlebitis to heart failure, lymphedema, and cellulitis.²

Signs and symptoms of DVT include pain, swelling, warmth, discoloration/cyanosis of the lower extremity, which is usually unilateral and can be distal, involving the calf, or proximal involving calf or whole leg. Although lower-extremity DVT is most common, it may happen in other sites leading to upper-extremity DVT (most commonly catheter-associated, which composes approximately 5% to 10% of all DVT); splanchnic vein thrombosis (portal, mesenteric, and splenic veins); cerebral venous sinus thrombosis; and retinal vein occlusion associated with sudden unilateral vision loss, the most common retinal vascular disease after diabetic retinopathy.¹¹

Dyspnea (about 70% of cases) is the most common symptom of a PE, usually with a rapid onset. Pleuritic chest pain is also common (~66%), often presenting with a cough. Patients may experience unexplained syncope, which, particularly in the presence of sudden dyspnea, is indicative of PE. A massive PE may lead to hemodynamic instability, right heart failure, and obstructive shock.¹¹ If PE leads to chronic pulmonary hypertension, the condition can prevent blood from reaching the lungs, resulting in death.¹

Risk Factors

Several medical conditions are responsible for the majority of all VTE cases: undergoing a surgical procedure, hospitalization, the presence of cancer in the body and cancer treatment itself, and pregnancy and post-partum. Numerous preventive protocols, or thromboprophylaxis, have been developed to address these risks based on patient characteristics, genetic history, and disease characteristics. Implementation of routine comprehensive risk assessments have been encouraged by stakeholders, such as the American Heart Association, to reduce the burden of VTE for hospitalized patients.³

Hospital-acquired VTE is the leading cause of preventable hospital-associated death, despite conclusive evidence of the efficacy, safety, and cost-effectiveness of thromboprophylaxis for high-risk hospitalized medical and surgical patients.³ Thromboprophylaxis regimens for presurgical procedures and hospitalized patients as well as routine VTE risk assessments are still underutilized.^3,11

The necessity, method, and duration of VTE prophylaxis are determined by patient characteristics, risk assessments for both VTE and potential bleeding, and, if applicable, planned surgical procedure. Orthopedic surgical procedures present the highest risk for VTE events, with total hip and knee arthroplasty and hip or pelvic fractures on the high end, and procedures below the knee or upper extremities and arthroscopic procedures on the lower end of the risk continuum.¹¹ Thromboprophylaxis may include pharmacological and/or mechanical methods. Patients at low-risk who are not undergoing surgery may only require early ambulation or walking and use of mechanical compression or compression stockings. Conversely, patients deemed at high risk for bleeding events may also be prescribed mechanical prophylaxis, even if VTE risk is moderate to high.¹¹

Pharmacologic VTE prophylaxis for patients evaluated as moderate to high risk for VTE includes low-molecular-weight heparin (LMWH) or unfractionated heparin, and in some cases, direct oral anticoagulants (DOACs) such as dabigatran, apixaban, or rivaroxaban.^3,11 Patients generally discontinue pharmacologic prophylaxis upon discharge unless immobilized. Surgical patients may be required to extend this practice up to 2 weeks post-surgically, and those at highest risk, such as after abdominal or pelvic surgery for cancer and major orthopedic patients, may continue for as long as 35 days.¹¹

A variety of physiological processes involved in the invasion of cancer cells in the human body contribute to a prothrombotic state, which may directly and indirectly cause life-threatening thromboses. Patients with cancer have a six-fold risk of VTE compared to those without malignancies; cancer-associated thrombosis (CAT) is the second-leading cause of death after the cancer itself.¹² Among cancer patients, those who develop VTE have a mortality rate more than twice of those without this complication. For those with cancer, arterial embolism is an additional risk, potentially leading to stroke and myocardial infarction.¹³

Relative risk of VTE is highest among those with primary cancer sites in the brain, pancreas, stomach, and lungs as well as hematologic cancers. The risk is low in breast and prostate cancers.¹⁴ Risk of VTE actually increases dramatically among children and adolescents with cancer, and CAT among all age groups mostly occurs within the first 6 months of diagnosis.¹³ While VTE risk is also elevated among hospitalized patients receiving systemic chemotherapy, risk assessments and prophylactic anticoagulation therapies may be recommended based on patient-associated characteristics, and extended to post-surgical and outpatient treatment.¹²

Cancer can increase the risk of VTE in several ways, including when cancer cells enter the bloodstream and spread to other parts of the body. Cancer cells can also attach to blood vessel walls and release substances that activate platelets and fibrin, creating a hypercoagulable state that promotes blood clot formation.¹² This injury to the vessels, which may also include compression from a tumor mass, combined with hemostasis due to bed rest, and various systemic chemotherapies, recreate the classic triad of VTE risk in many cases.

Treatment of CAT includes the use of LMWH, while DOACs may be used for VTE prophylaxis or extended therapy.¹⁴ As the nature and duration of cancer treatment is highly variable, oral health professionals may encounter ambulatory patients seeking treatment for noncancer-related and routine dental care. Evaluation of treatment risks, especially bleeding and immune status, should be considered.

The risk of VTE during pregnancy is approximately five times higher than in the nonpregnant state and increases as delivery approaches.¹⁵ Additionally, this risk increases to nearly 60 times during the post-partum period, with a total worldwide incidence rate of 0.5 to two per 1,000 pregnancies and a mortality rate of one per 100,000 deliveries.¹⁵ These phenomena are attributed to what is known as the maternal hemostatic shift, a natural protective physiologic adaptation, which includes hypercoagulability and reduced fibrinolysis to prevent excessive hemorrhaging during delivery.¹⁵

During pregnancy, the growing fetus exerts pressure on the iliac veins, contributing to hemostasis, and late in gestation when maternal immobility is common, the situation meets the third risk factor of Virchow’s Triad. Endothelial trauma during delivery may add an additional risk, and VTE occurrence after a Caesarean birth is understandably greater. Individual factors that contribute to risk include maternal age, obesity, diabetes, thrombophilia, and family history of VTE. In recent years, clinical guidelines have added risk assessments for women with these predisposing factors. This has contributed to thromboprophylaxis strategies for pregnant women identified as high-risk.¹⁵ Anticoagulants used either for thromboprophylaxis during pregnancy and breastfeeding, or for women who develop VTE post-partum, include UFH and LMWH preferentially over warfarin and DOACs.¹⁵

Treatment

Risk evaluation, thromboprophylaxis, and treatment strategies are highly dependent on patient characteristics and history, followed by formalized predictive assessments and diagnostic testing for DVT and PE. Diagnostic testing may include blood assays, such as the D-dimer, which measures protein fragments from clot dissolution; ultrasonography; contrast venography to locate thrombi for DVT; and magnetic resonance pulmonary angiography, a nonradiation MRI with contrast dye for PE. Anticoagulant therapy is the mainstay of VTE treatment, and utilizes many of the same agents used for thromboprophylaxis: warfarin, DOACs, UFH, LMWH, and fondaparinux.^3,12,14–16 The duration of anticoagulant therapy following a VTE event is usually a minimum of 3 months, and 6 to 12 months for those with increased thrombosis burden, long-lasting risk factors, or significant PE events, and may be indefinite for unprovoked or recurrent VTE.¹¹

For all patients exhibiting symptoms, assessment and treatment become urgent. Diagnostic testing includes assessment of hemodynamic stability. If deemed hemodynamically unstable, anticoagulation therapy may be initiated before definitive diagnosis.³ Additionally, treatment for those with confirmed VTE in the highest risk categories or for whom drug therapy is ineffective, may go beyond standard anticoagulants and include pharmacological fibrinolysis to break down the clot, catheter-led or surgical embolectomy for clot removal, or more invasive treatment, such as intravascular filters.

In some situations, patients with VTE may benefit from a percutaneous insertion of inferior vena cava (IVC) filters, which are permanent or temporary medical devices.^17,18 The safety of IVC filters placement and removal has been continually improving, and currently, biocompatible and absorbable filters are being investigated. Nevertheless, this treatment is reserved only for specific situations where anticoagulation is absolutely contraindicated due to the type or trauma or very high bleeding risk.¹⁸ The current recommendation is to have the device removed when the risk of PE has subsided to prevent the adverse events associated with the IVC filters, including device migration, fracture, embolization, and perforation, as well as adverse outcomes of lower extremity DVT and IVC occlusion.¹⁹

In some instances, both DVT and PE may result in chronic complications. Post-DVT syndrome may produce ongoing pain and swelling primarily in the lower leg, managed by medications, therapy and exercise, but with symptoms that mimic recurrent DVT. PE may lead to chronic dyspnea or more serious pulmonary hypertension, where the damage to the pulmonary arteries interferes with effective transfer of oxygen and carbon dioxide, along with increased risk of heart failure.¹¹ For those who experience long-term complications, increased vigilance for VTE symptoms and anxiety over recurring thrombotic events has been shown to reduce quality of life measures in addition to the physical symptoms and limitations.²⁰

Dental Treatment Implications

The prevalence and severity of VTE events warrants the attention of all oral health professionals in examining patients’ medical and drug histories and determining and mitigating any risks while undergoing dental care. In most cases, these risks would primarily involve concerns for perioperative bleeding for those on continued anticoagulant agents for thromboprophylaxis as well as other cardiovascular concerns. Risks of discontinuation of anticoagulants most often outweighs the risk of bleeding events, except in cases of extensive oral maxillofacial procedures, multiple extractions, or surgery for head and neck cancers.²¹

Routine prophylaxis, scaling and root planing, and simple extractions would normally not require drug discontinuation, and a recent review suggests bleeding risk for dental implant surgery for patients on warfarin or DOACs does not result in significant bleeding when local hemostatic measures are used.²² In any case where discontinuation may be warranted, medical clearance from the prescribing physicians must be sought, and appropriate testing obtained. For heparin, medically supervised, short-term discontinuation may be advised for invasive procedures, and local hemostatic measures used for bleeding. For DOACs, consideration for dosage and peak blood level periods, or discontinuation should be coordinated with the advice of the prescribing physician.²¹

Oral health professionals’ awareness of the symptomatology of VTE, as well as treatment and associated risks and best practices, will ensure patients’ safety and successful outcomes of dental/dental hygiene treatment.

References

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19. FDA Updates Safety Communication on IVC Filter Retrieval. Endovascular Today. Available at evtoday.com/news/fda-updates-safety-communication-on-ivc-filter-retrieval. Accessed August 18, 2026.
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From Dimensions of Dental Hygiene. September/October 2026; 24(5):28-31