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Acute pulmonary thromboembolism from deep vein thrombosis induced by trauma to the popliteal vein with a tennis racket
Journal of Cardiology Cases 9 (2014) 162–164
Contents lists available at www.sciencedirect.com
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Acute pulmonary thromboembolism from deep vein thrombosis induced by trauma to the popliteal vein with a tennis racket Takayuki Ise (MD) a,∗ , Takashi Iwase (MD, FJCC) a , Shiho Masuda (MD) b , Shusuke Yagi (MD) a , Masashi Akaike (MD) c , Susumu Nishio (RMS) a , Toshiyuki Niki (MD) a , Koji Yamaguchi (MD) a , Yoshio Taketani (MD) a , Hirotsugu Yamada (MD) a , Takeshi Soeki (MD, FJCC) a , Tetsuzo Wakatsuki (MD) a , Masataka Sata (MD, FJCC) a a b c
Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan Post-graduate Education Center, Tokushima University Hospital, Tokushima, Japan Department of Medical Education, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan
a r t i c l e
i n f o
Article history: Received 11 July 2013 Received in revised form 23 December 2013 Accepted 6 January 2014 Keywords: Acute pulmonary thromboembolism Deep vein thrombosis Trauma
a b s t r a c t Acute pulmonary thromboembolism (PTE) is mainly caused by deep vein thrombosis (DVT) and sometimes leads to a fatal outcome. Few cases of sport-related lower extremity DVT, involving direct external trauma, have been reported. A 58-year-old man, without any risk factors for thromboembolism suffered acute PTE from DVT after playing tennis. A detailed history revealed that he had hit his popliteal vein with each swing of his tennis racket and the site of the trauma, at popliteal fossa, was exactly the same as the site of the DVT formation. Therefore, the cause of DVT was suspected to be the repeated trauma to the popliteal vein. The repeated external trauma to the popliteal vein may have caused vascular endothelial damage, leading to DVT. © 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
Introduction
Case report
Acute pulmonary thromboembolism (PTE) is mainly caused by deep venous thrombosis (DVT) of the lower extremity and may lead to a fatal outcome [1–4]. Abnormal congenital congealing fibrinogenolysis; drug use, including use of contraceptives and cocaine; immobilization, such as prolonged sitting; and malignant tumors are the most common causes of DVT [1–4]. Furthermore, a few cases of sport-related lower extremity DVT, involving direct external trauma, have been reported [5–7]; the mechanisms underlying sports-related injuries are unknown. Here, we report a case of PTE resulting from DVT that was presumably caused by repeated trauma to the popliteal vein caused by a tennis racket.
A 58-year-old man, without any risk factors for cardiovascular disease, developed dyspnea shortly after playing tennis for 6 h. He presented to the hospital shortly after onset of symptoms. The patient’s blood pressure was 120/62 mmHg, heart rate was 94 beats/min, body temperature was 36.5 ◦ C, and oxygen saturation on room air was 92%. In addition, the levels of d-dimer and fibrin degradation product were elevated to 32 g/mL and 74 g/mL, respectively. A 12-lead electrocardiogram revealed an incomplete right bundle branch block in the limb lead. Echocardiography showed a pressure overload in the right ventricle (maximal tricuspid regurgitation gradient, 42 mmHg). Contrastenhanced computed tomography (CT) showed large thrombi in the right and left segmental pulmonary artery branches and a thrombus in the left popliteal vein (Fig. 1). The patient was immediately hospitalized and received anticoagulant therapy with 15,000 units/day of heparin and warfarin, as his findings were consistent with a diagnosis of PTE due to DVT. The symptoms, the thrombi in the right and left pulmonary arteries, and the right ventricular pressure overload disappeared by the 10th day of hospitalization.
∗ Corresponding author at: Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan. Tel.: +81 88 633 7751; fax: +81 88 633 7894. E-mail addresses: [email protected], [email protected] (T. Ise).
1878-5409/$ – see front matter © 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jccase.2014.01.001
T. Ise et al. / Journal of Cardiology Cases 9 (2014) 162–164
163
Fig. 1. Contrast computed tomography (CT) image of the lower limbs. Deep vein thrombosis (indicated by the arrow) at the left popliteal region, which is consistent with the region where the patient experienced bruising from the tennis racket (A, sagittal plane; B, coronal section).
After optimal anticoagulation with 2 mg of warfarin (the prothrombin time-international normalized ratio was between 2.0 and 2.5), he was monitored as an outpatient, and no exacerbation of pulmonary arterial hypertension was noted. He did not have any risk factors for DVT or PTE, including abnormal congenital congealing fibrinogenolysis; however, a careful history taking revealed that he had hit his popliteal vein after each swing of his tennis racket (Fig. 2). The site of the tennis racket-induced trauma, at the popliteal fossa, was exactly the same as the site of DVT formation. Therefore, the cause of DVT may be the repeated trauma to the popliteal vein.
Discussion Virchow’s triad, including blood flow congestion, vascular endothelium injury, and hypercoagulability, is important in thrombus formation [8]. The soleal vein, which is easily congested; the superficial femoral vein, which may be compressed by a muscle or inguinal band tunnel; and the left iliac vein, which may be compressed by the right internal iliac artery, are common sites of DVT formation. In addition, the popliteal vein may also develop DVT because of lengthy periods of congestion by bending the knee joint. The popliteal vein may also be anatomically compressed by muscle; however, the present patient did not have a history of such knee activity, nor was there contrast-enhanced CT evidence of abnormalities in the popliteal muscle or vessel structures. Rather, he reported hitting his popliteal fossa after each swing of his racket because of the nature of his swing. The popliteal vein is easily damaged by external mechanical stress because it runs superficially under the popliteal fossa and is not covered by muscle. In addition, the bones just behind the popliteal vein enhanced the effects of compression by the external force. Repeated trauma to the popliteal vein may cause vascular endothelial damage, leading to DVT. Dehydration, following prolonged exertion, may also increase the chances of DVT formation by causing hypercoagulability. To prevent recurrence, the patient was encouraged to change his swing to avoid hitting the popliteal fossa or to wear a knee protector covering the popliteal fossa. Traumatic injuries may cause DVT because of vascular endothelial injury. Therefore, sports-injury-induced DVT must be considered as a differential diagnosis in patients without known risks or causes of DVT. Financial support None. Conflict of interest Authors declare no conflict of interest. References
Fig. 2. Photograph showing the situation in which the patient received the traumatic injury. The patient repeatedly hit the back of his knee with a tennis racket while playing tennis.
[1] Pollack CV, Schreiber D, Goldhaber SZ, Slattery D, Fanikos J, O’Neil BJ, Thompson JR, Hiestand B, Briese BA, Pendleton RC, Miller CD. Clinical characteristics, management, and outcomes of patients diagnosed with acute pulmonary embolism in the emergency department: initial report of EMPEROR (Multicenter
164
T. Ise et al. / Journal of Cardiology Cases 9 (2014) 162–164
Emergency Medicine Pulmonary Embolism in the Real World Registry). J Am Coll Cardiol 2011;57:700–6. [2] Goldhaber SZ. Risk factors for venous thromboembolism. J Am Coll Cardiol 2010;56:1–7. [3] Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper Jr KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK. Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med 2007;120:871–9. [4] Horlander KT, Mannino DM, Leeper KV. Pulmonary embolism mortality in the United States, 1979–1998: an analysis using multiple-cause mortality data. Arch Intern Med 2003;163:1711–7.
[5] Thompson TL, Robinson AK, Gilbert C. Deep vein thrombosis of the lower extremity in a football player: a case report. Clin J Sport Med 2006;16: 372–4. [6] Echlin PS, Upshur RE, McKeag DB, Jayatilake HP. Traumatic deep vein thrombosis in a soccer player: a case study. Thromb J 2004;2:8. [7] Watson AS, Gray D, Godfrey J, Muller A. Deep venous thrombosis following sports injury to the calf – a potentially dangerous complication. Sports Training Med Rehab 1991;2:273–8. [8] Bagot CN, Arya R. Virchow and his triad: a question of attribution. Br J Haematol 2008;143:180–90.
Contents lists available at www.sciencedirect.com
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Acute pulmonary thromboembolism from deep vein thrombosis induced by trauma to the popliteal vein with a tennis racket Takayuki Ise (MD) a,∗ , Takashi Iwase (MD, FJCC) a , Shiho Masuda (MD) b , Shusuke Yagi (MD) a , Masashi Akaike (MD) c , Susumu Nishio (RMS) a , Toshiyuki Niki (MD) a , Koji Yamaguchi (MD) a , Yoshio Taketani (MD) a , Hirotsugu Yamada (MD) a , Takeshi Soeki (MD, FJCC) a , Tetsuzo Wakatsuki (MD) a , Masataka Sata (MD, FJCC) a a b c
Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan Post-graduate Education Center, Tokushima University Hospital, Tokushima, Japan Department of Medical Education, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan
a r t i c l e
i n f o
Article history: Received 11 July 2013 Received in revised form 23 December 2013 Accepted 6 January 2014 Keywords: Acute pulmonary thromboembolism Deep vein thrombosis Trauma
a b s t r a c t Acute pulmonary thromboembolism (PTE) is mainly caused by deep vein thrombosis (DVT) and sometimes leads to a fatal outcome. Few cases of sport-related lower extremity DVT, involving direct external trauma, have been reported. A 58-year-old man, without any risk factors for thromboembolism suffered acute PTE from DVT after playing tennis. A detailed history revealed that he had hit his popliteal vein with each swing of his tennis racket and the site of the trauma, at popliteal fossa, was exactly the same as the site of the DVT formation. Therefore, the cause of DVT was suspected to be the repeated trauma to the popliteal vein. The repeated external trauma to the popliteal vein may have caused vascular endothelial damage, leading to DVT.
Introduction
Case report
Acute pulmonary thromboembolism (PTE) is mainly caused by deep venous thrombosis (DVT) of the lower extremity and may lead to a fatal outcome [1–4]. Abnormal congenital congealing fibrinogenolysis; drug use, including use of contraceptives and cocaine; immobilization, such as prolonged sitting; and malignant tumors are the most common causes of DVT [1–4]. Furthermore, a few cases of sport-related lower extremity DVT, involving direct external trauma, have been reported [5–7]; the mechanisms underlying sports-related injuries are unknown. Here, we report a case of PTE resulting from DVT that was presumably caused by repeated trauma to the popliteal vein caused by a tennis racket.
A 58-year-old man, without any risk factors for cardiovascular disease, developed dyspnea shortly after playing tennis for 6 h. He presented to the hospital shortly after onset of symptoms. The patient’s blood pressure was 120/62 mmHg, heart rate was 94 beats/min, body temperature was 36.5 ◦ C, and oxygen saturation on room air was 92%. In addition, the levels of d-dimer and fibrin degradation product were elevated to 32 g/mL and 74 g/mL, respectively. A 12-lead electrocardiogram revealed an incomplete right bundle branch block in the limb lead. Echocardiography showed a pressure overload in the right ventricle (maximal tricuspid regurgitation gradient, 42 mmHg). Contrastenhanced computed tomography (CT) showed large thrombi in the right and left segmental pulmonary artery branches and a thrombus in the left popliteal vein (Fig. 1). The patient was immediately hospitalized and received anticoagulant therapy with 15,000 units/day of heparin and warfarin, as his findings were consistent with a diagnosis of PTE due to DVT. The symptoms, the thrombi in the right and left pulmonary arteries, and the right ventricular pressure overload disappeared by the 10th day of hospitalization.
∗ Corresponding author at: Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan. Tel.: +81 88 633 7751; fax: +81 88 633 7894. E-mail addresses: [email protected], [email protected] (T. Ise).
1878-5409/$ – see front matter © 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jccase.2014.01.001
T. Ise et al. / Journal of Cardiology Cases 9 (2014) 162–164
163
Fig. 1. Contrast computed tomography (CT) image of the lower limbs. Deep vein thrombosis (indicated by the arrow) at the left popliteal region, which is consistent with the region where the patient experienced bruising from the tennis racket (A, sagittal plane; B, coronal section).
After optimal anticoagulation with 2 mg of warfarin (the prothrombin time-international normalized ratio was between 2.0 and 2.5), he was monitored as an outpatient, and no exacerbation of pulmonary arterial hypertension was noted. He did not have any risk factors for DVT or PTE, including abnormal congenital congealing fibrinogenolysis; however, a careful history taking revealed that he had hit his popliteal vein after each swing of his tennis racket (Fig. 2). The site of the tennis racket-induced trauma, at the popliteal fossa, was exactly the same as the site of DVT formation. Therefore, the cause of DVT may be the repeated trauma to the popliteal vein.
Discussion Virchow’s triad, including blood flow congestion, vascular endothelium injury, and hypercoagulability, is important in thrombus formation [8]. The soleal vein, which is easily congested; the superficial femoral vein, which may be compressed by a muscle or inguinal band tunnel; and the left iliac vein, which may be compressed by the right internal iliac artery, are common sites of DVT formation. In addition, the popliteal vein may also develop DVT because of lengthy periods of congestion by bending the knee joint. The popliteal vein may also be anatomically compressed by muscle; however, the present patient did not have a history of such knee activity, nor was there contrast-enhanced CT evidence of abnormalities in the popliteal muscle or vessel structures. Rather, he reported hitting his popliteal fossa after each swing of his racket because of the nature of his swing. The popliteal vein is easily damaged by external mechanical stress because it runs superficially under the popliteal fossa and is not covered by muscle. In addition, the bones just behind the popliteal vein enhanced the effects of compression by the external force. Repeated trauma to the popliteal vein may cause vascular endothelial damage, leading to DVT. Dehydration, following prolonged exertion, may also increase the chances of DVT formation by causing hypercoagulability. To prevent recurrence, the patient was encouraged to change his swing to avoid hitting the popliteal fossa or to wear a knee protector covering the popliteal fossa. Traumatic injuries may cause DVT because of vascular endothelial injury. Therefore, sports-injury-induced DVT must be considered as a differential diagnosis in patients without known risks or causes of DVT. Financial support None. Conflict of interest Authors declare no conflict of interest. References
Fig. 2. Photograph showing the situation in which the patient received the traumatic injury. The patient repeatedly hit the back of his knee with a tennis racket while playing tennis.
[1] Pollack CV, Schreiber D, Goldhaber SZ, Slattery D, Fanikos J, O’Neil BJ, Thompson JR, Hiestand B, Briese BA, Pendleton RC, Miller CD. Clinical characteristics, management, and outcomes of patients diagnosed with acute pulmonary embolism in the emergency department: initial report of EMPEROR (Multicenter
164
T. Ise et al. / Journal of Cardiology Cases 9 (2014) 162–164
Emergency Medicine Pulmonary Embolism in the Real World Registry). J Am Coll Cardiol 2011;57:700–6. [2] Goldhaber SZ. Risk factors for venous thromboembolism. J Am Coll Cardiol 2010;56:1–7. [3] Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper Jr KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK. Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med 2007;120:871–9. [4] Horlander KT, Mannino DM, Leeper KV. Pulmonary embolism mortality in the United States, 1979–1998: an analysis using multiple-cause mortality data. Arch Intern Med 2003;163:1711–7.
[5] Thompson TL, Robinson AK, Gilbert C. Deep vein thrombosis of the lower extremity in a football player: a case report. Clin J Sport Med 2006;16: 372–4. [6] Echlin PS, Upshur RE, McKeag DB, Jayatilake HP. Traumatic deep vein thrombosis in a soccer player: a case study. Thromb J 2004;2:8. [7] Watson AS, Gray D, Godfrey J, Muller A. Deep venous thrombosis following sports injury to the calf – a potentially dangerous complication. Sports Training Med Rehab 1991;2:273–8. [8] Bagot CN, Arya R. Virchow and his triad: a question of attribution. Br J Haematol 2008;143:180–90.