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doi: 10.3810/psm.2010.12.1836
The Physician and Sportsmedicine: Volume 38: No.4
Venous Thromboembolism Following Vigorous Deep Tissue Massage
Casey Crump, MD, PhD And Scott A. Paluska, MD, FACSM
Copyright 2010 All rights reserved. Cover and contents may not be reproduced in whole or in part without prior written permission. The Physician and Sportsmedicine is a registered trademark of JTE Multimedia, LLC. Sending and distribution of any document from this site is strictly prohibited either for free and or a service fee, and will be sited as a violation of copyright under the laws of THE UNITED STATES OF AMERICA

Abstract: Venous thromboembolism (VTE) is an increasing public health concern, in part because of lack of awareness among patients and physicians. Nonpenetrating trauma to the legs may be an under-recognized potential risk factor for VTE. We report a case of VTE following vigorous deep tissue massage in a previously healthy 67-year-old man with no other identifiable risk factors. The etiology, risk factors, and implications for the prevention and detection of VTE are reviewed. There are few other published reports of VTE associated with massage, but under-reporting seems likely. Vigorous massage or any equivalent trauma to the legs should be considered and evaluated as a possible risk factor for VTE, especially in older adults. Additional research is needed to clarify the risks associated with nonpenetrating trauma to the legs in older adults and other susceptible groups. Improved awareness of VTE, including its risk factors and symptoms, is an urgent priority for more effective prevention, detection, and treatment.

Keywords: massage; pulmonary embolism; venous thromboembolism; venous thrombosis

Introduction

Venous thromboembolism (VTE), which encompasses deep vein thrombosis (DVT) and pulmonary embolism (PE), is a relatively common, life-threatening condition, and is a major public health concern. The average annual incidence of 1 to 2 cases per 1000 persons1,2 results in > 350 000 cases and 100 000 deaths annually in the United States.3 One in 20 persons develops symptomatic DVT during his or her lifetime,4 and without treatment, more than one-third of these cases progress to PE.5 Despite some efforts at improved prevention, the incidence of VTE has remained relatively unchanged since 1980.1,6 Given that the incidence increases markedly with age,1 the public health impact is expected to increase further as the US population increases in average age, unless more effective prevention can be achieved.

A major hindrance to effective prevention and treatment of VTE is a general lack of awareness of the condition among patients and clinicians. A survey conducted by the American Public Health Association found that only 6% of Americans know what DVT is and that it can be prevented.7 Other studies have suggested that physicians are often either unaware of or fail to follow evidence-based guidelines for the prevention and treatment of VTE.8,9 In response to the prevalent lack of awareness, the US Surgeon General recently issued a Call to Action to Prevent Deep Vein Thrombosis and Pulmonary Embolism.3 In this article, we report on a presentation of VTE that is uncommon in the literature and may be unrecognized and under-reported. We review the etiology and risk factors for VTE and the implications for improving its prevention and detection.

Case History

A 67-year-old man presented to the emergency department after experiencing right upper thoracic pain in the 4 hours prior. His medical history was unremarkable except for glaucoma, and his only medications were carteolol and latanoprost eyedrops. He was physically active, was a nonsmoker, and had not traveled recently. On initial examination, he was afebrile, with a blood pressure of 156/104 mm Hg, heart rate of 85 bpm, respiratory rate of 20 breaths per minute, and oxygen saturation of 97%. His chest was clear to auscultation, and heart sounds were normal. A chest radiograph showed a small granuloma in the right lower lobe but was otherwise clear. His pain was suspected to be musculoskeletal, and he was discharged with instructions to return if his symptoms worsened.

Five days later, he visited his primary care physician for worsening right upper thoracic pain accompanied by mild dyspnea on exertion. On further questioning, he reported a history of right calf pain and swelling, which had preceded the onset of his back pain by 5 days. The right calf symptoms had begun the day after receiving a vigorous deep tissue massage (for nonmedical reasons), which had included the lower extremities. His calf symptoms had gradually improved over the next 5 days, at which time he developed the right upper thoracic pain that had prompted his initial visit to the emergency department. He had no history of leg injuries, surgeries, or VTE. The only relevant family history was that his father had had superficial phlebitis, which had resolved without treatment.

At his primary care physician’s office, his blood pressure, respiratory rate, and oxygen saturation were normal. His chest was clear to auscultation and heart sounds were normal. His right and left calves measured 43 cm and 40 cm, respectively, 10 cm below the tibial tuberosity. The D-dimer level was 3.2 μg/mL (reference range < 0.4 μg/mL). He was promptly hospitalized for further evaluation and treatment, at which time venous duplex ultrasonography identified a well-attached DVT of the right posterior tibial vein without proximal extension. Spiral computed tomography of the chest revealed multiple bilateral PEs within nearly all of the interlobar arteries and a large saddle embolus at the right main pulmonary artery bifurcation. Transthoracic echocardiography demonstrated borderline pulmonary hypertension with an estimated pulmonary systolic pressure of 30 mm Hg (normal range, 15–30 mm Hg) and mild right ventricular dilation with preserved left ventricular systolic function.

Anticoagulation therapy was initiated immediately with intravenous heparin and oral warfarin. Functional assays for proteins C and S were not obtained prior to initiation of warfarin, and were therefore uninterpretable. Other hypercoagulability studies, including factor V Leiden, prothrombin gene 20210A mutation, antithrombin III level, homocysteine level, lupus inhibitor, and an antiphospholipid panel (anti-β2-glycoprotein I immunoglobulin G [IgG]; anticardiolipin IgA, IgG, IgM) were normal.

The patient remained hemodynamically stable and had no additional complications. Despite the widespread extent of his PE, his symptoms remained relatively mild. After 4 days of hospitalization, he was discharged home in stable condition with anticipated long-term anticoagulation.

Discussion

In the reported case, the close temporal relationship of vigorous leg massage and the onset of symptoms, as well as the absence of other identifiable risk factors for VTE, strongly suggest a causal role by massage. The potential for vigorous massage to cause DVT is consistent with the known mechanisms of thrombogenesis. Shear stress to the venous wall may cause endothelial cell damage leading to platelet aggregation and thrombin-mediated formation of a fibrin clot.10 Damage to the endothelial lining has been demonstrated with manual lymph massage at an external pressure of 70 to 100 mm Hg for 10 minutes.11 Alternatively, massage therapy may dislodge a preexisting asymptomatic DVT, although this is less likely in the reported case, given the onset of new calf symptoms following massage and the absence of risk factors for preexisting DVT.

Other cases of VTE associated with massage have rarely been reported. A 53-year-old woman, who was subsequently diagnosed with stage I endometrial adenocarcinoma, developed DVT and PE after vigorous massage of her calves at a pedicure shop.12 Other reports include a 72-year-old woman who developed PE after vigorous massage of her leg (which was already affected by deep vein thrombophlebitis13 ) and a 59-year-old man who developed a left renal embolism caused by dislodgement of a thrombus in an aortofemoral bypass graft as a result of a massage performed by someone walking on his back.14 In general, other adverse events resulting from massage therapy are uncommon.15

Venous thromboembolism is caused by the interaction of factors described in Virchow’s triad: venous stasis, venous wall injury, and activation of coagulation factors. The major cause is venous stasis, due to bed rest, prolonged travel, pregnancy, congestive heart failure, or any circumstances that result in immobilization of the lower extremities.16 Stasis predisposes to thrombosis by disrupting normal laminar blood flow, allowing greater contact of platelets and procoagulants with the endothelium.10 Venous wall injury also carries a high risk of thrombosis and may occur because of penetrating trauma; major surgeries, especially orthopedic, abdominal, pelvic, or neurosurgery (also associated with immobilization); and central venous catheter or transvenous pacemaker placement.17 Vigorous nonpenetrating trauma is a plausible but less well-established risk factor. Hypercoagulability factors include inherited disorders (factor V Leiden, prothrombin 20210A mutation, protein C or S deficiency, antithrombin III deficiency) and other acquired or mixed conditions (malignancy, pregnancy, exogenous estrogen, hyperhomocysteinemia, antiphospholipid syndrome).16

Approximately 35% of patients with VTE have ≥ 1 genetic susceptibility factor.18 The most common is factor V Leiden, a point mutation that renders factor Va inaccessible to cleavage by activated protein C, increasing the risk of thrombosis by 3-to 8-fold in heterozygotes and 50- to 80-fold in homozygotes.19 Factor V Leiden is most common in Caucasians who have a 5% population prevalence20 and has been noted in 15% to 20% of patients with VTE.18 The prothrombin 20210A gene mutation is associated with increased prothrombin levels and is found in 2% to 3% of Caucasians and 6% of patients with VTE.21,22 Deficiencies of proteins C and S and antithrombin III are less prevalent, occurring in < 1% of the general population.16,23 Protein C and free protein S inactivate factors Va and VIIIa in the coagulation cascade, and protein C or S deficiency has been noted in approximately 3% of patients with a first VTE event.24,25 Antithrombin III deficiency decreases the inhibition of thrombin and clotting factors XIa, IXa, and Xa. It is found in 1 in 5000 persons in the general population and 4% of patients with VTE.23 In most cases, genetic susceptibility factors result in thrombus formation only when combined with other risk factors or a triggering event.

Diagnostic evaluation for DVT should begin with determination of pretest probability using an established prediction model, such as that based on the Wells score.26 D-dimer testing and venous ultrasound should be performed according to a well-tested diagnostic algorithm.27 If the pretest probability is unlikely, a negative D-dimer test has a negative predictive value of ≥ 99%, in which case ultrasound testing can be safely omitted.26,28 If the pretest probability is likely, however, the D-dimer test is not sufficient to exclude DVT, and ultrasound testing is essential.27 This prediction model and algorithm are appropriate only if DVT is a diagnostic possibility based on history and physical examination.27

Summary

Most episodes of VTE occur in the outpatient setting.29 Thus, primary care and sports medicine physicians play a critical role for early detection and treatment. Prompt recognition of pertinent risk factors and symptoms is essential. This case report suggests that nonpenetrating trauma to the legs, such as vigorous massage, is a potential risk factor that may be unrecognized and underreported. This report should not necessarily deter individuals without any known risk factors for VTE from receiving massage therapy. Additional research is needed to clarify the risks associated with nonpenetrating trauma to the legs, especially in older adults and other susceptible groups. Improved awareness among physicians and education of the public regarding the risk factors, symptoms, and prevention of VTE are an urgent priority for reducing morbidity and mortality.



Conflict of Interest Statement
Casey Crump, MD, PhD and Scott A. Paluska, MD, FACSM disclose no conflicts of interest.
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Casey Crump, MD, PhD 1
Scott A. Paluska, MD, FACSM 2

1Division of Family and Community Medicine, Department of Medicine, Stanford University, 211 Quarry Rd, Room N300, MC 5765, Palo Alto, CA 94304. [email protected] 2Department of Family Medicine, University of Illinois, Urbana, IL

Correspondence: Casey Crump, MD, PhD, Stanford Family Medicine, 211 Quarry Rd, Room N300, MC 5765, Palo Alto, CA 94304.
Tel: 650-575-7747,
Fax: 650-498-4430,
E-mail: [email protected]
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In an effort to provide information that is scientifically accurate and consistent with accepted standards of medical practice, the editors and publisher of The Physician and Sportsmedicine routinely consult sources believed to be reliable. However, readers are encouraged to confirm this information with other sources. For example and in particular, physicians are advised to consult the prescribing information in the manufacturer's package insert before prescribing any drug mentioned.




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