Does hypocalcemia trigger pulmonary embolism?

Does hypocalcemia trigger pulmonary embolism?

464 Acknowledgements We thank the editor of the journal and the anonymous reviewers for critical review of this manuscript. The financial supports ar...

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464

Acknowledgements We thank the editor of the journal and the anonymous reviewers for critical review of this manuscript. The financial supports are provided by funds from The Project-sponsored by SRF for ROCS, SEM, from a start-up grant of Northeast Agricultural University and from Hei Long Jiang Province Personnel Department Foundation (LBH-Z05025 and LBH-Q05028), China. The providers of these funds are fully acknowledged.

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Guangxing Li Jiechao Yin Xiaofeng Ren * College of Veterinary Medicine, Northeast Agricultural University, 59 Mucai Street, 150030 Harbin, PR China * Tel.: +86 451 55190385. E-mail address: [email protected] (X. Ren).

doi:10.1016/j.mehy.2006.08.002

Does hypocalcemia trigger pulmonary embolism? To the Editor, Total hip and knee arthroplasty have been made for approximately 50 years. While these operations are very successful, deep-vein thrombosis and pulmonary embolism (PE) have been significant complications. The reported prevalence of PE has been 1.2% after total hip arthroplasty [1,2]. So many inherited and acquired risk factors predispose susceptible individuals [3]. Herein, we report a case of pulmonary embolism after unilateral total hip replacement, possibly triggered by hypocalcemia. A 56-year-old female, who had dysplastic left hip secondary to coxartrhosis, underwent uncomplicated total hip replacement under spinal anesthesia. Her medical history was unremarkable. Preoperative, her physical examination and laboratory results revealed no significant abnormality. Postoperative, she was being in the intensive care unit and low-molecular-weight heparin was initiated for deep vein thrombosis prophylaxis. She did not appear to be in acute distress but 15 h later, suddenly she developed dyspne, tachycardia and hypotension. At the same time her gastrocnemius muscles were in spasm with severe pain

and the feet were in plantar flexion. Her blood pressure was 90/60 mmHg and pulse rate was 124/min. The electrocardiogram was showing sinus tachycardia. Her arterial blood gas levels were pH 7.46, pO2 60 mmHg, pCO2 24 mmHg, standard bicarbonate 19 mmol/L, oxygen saturation 90%. Other laboratory results were hematocrit 31.4, platelet 117000/mm3, serum albumin 3.8 g/dl, calcium 6 mg/dl, phosphate 4 mg/dl and D-dimer 8065 lg/L (ELISA assay). Spiral computed tomography of the thorax showed thrombus in the branches of the inferior segments of both pulmonary arteries and linear atelectasis in superior part of inferior lobe and posterobasal segment of the right lung. Duplex Doppler ultrasonography of her lower limbs showed no acute partial thrombosis. We did not order echocardiography. The diagnosis of PE was established. She was therapeutically anticoagulated with heparin. The patient had mild hypocalcemia and we thought PE secondary to lower extremity spasm triggered by hypocalcemia. Calcium gluconate was infused over 4 h. Then, the signs and symptoms improved. Warfarin was added to the therapy. She was discharged on the 8th postoperative day. No recurrent pulmonary emboli attack occurred during

Correspondence the follow-up period of 6 months with an international normalized ratio target of 2.0–3.0. Pulmonary embolism is a common, potentially life threatening cardiopulmonary illness. It is difficult to diagnose PE because patients present with a wide range of symptoms and sings. Venous thromboembolic disease is a common and serious complication after total hip and total knee arthroplasty [4]. Early recognition is important because prompt medical or surgical intervention can be life-saving. Yamada et al. [5] described the incidence of the trigger of PE. They found at least 41% of the patients had obvious triggers of PE. The common triggers of PE are toilet activities such as defecation, micturition, first ambulation from bedridden and positional change on the bed. In our patient, the specific origin of embolization remains uncertain but we may speculate that spasm of lower extremities secondary to hypocalcemia might be trigger of PE. Hence, measuring of serum calcium level preoperatively should be a part of preoperative management. To our knowledge, this is the first case of PE triggered by hypocalcemia. In conclusion, clinicians should be aware of hypocalcemia might be a trigger of PE in inpatients.

References [1] Mohr DN, Silverstein MD, Ilstrup DM, et al. VTE associated with hip and knee arthroplasty: current prophylactic practices and outcomes. Mayo Clin Proc 1992;67:861–70. [2] Warwick D, Williams MH, Bannister GC, et al. Death and thromboembolic disease after total hip replacement: a series of 1162 cases with no routine chemical prophylaxis. J Bone Joint Surg Br 1995;77:6–10. [3] Anderson Jr FA, Spencer FA. Risk factors for venous thromboembolism. Circulation 2003;107:I9–I16. [4] Clarke MT, Green JS, Harper WM, Gregg PJ. Screening for deep-venous thrombosis after hip and knee replacement without prophylaxis. J Bone Joint Surg Br 1997;79(5):787–91.

465 [5] Nakamura M, Sakuma M, Yamada N, Tanabe N, Nakanishi N, Miyahara Y, et al. JaSPER investigators. Risk factors of acute pulmonary thromboembolism in Japanese patients hospitalized for medical illness: results of a multicenter registry in the Japanese society of pulmonary embolism research. J Thromb Thrombolys 2006;21(2):131–5.

Burhanettin Usta Department of Anesthesiology and Reanimation, Fatih University, School of Medicine, Ankara, Turkey Muhammet Gozdemir Department of Anesthesiology and Reanimation, Fatih University, School of Medicine, Ankara, Turkey Faruk Turgut Department of Internal Medicine, Fatih University, School of Medicine, alpaslan turkes cad no 57 Emek, 06510 Ankara, Turkey E-mail address: [email protected] Huseyin Sert Department of Anesthesiology and Reanimation, Fatih University, School of Medicine, Ankara, Turkey Mehmet Kanbay Department of Anesthesiology and Reanimation, Fatih University, School of Medicine, Ankara, Turkey Ruveyda Irem Demircioglu Department of Anesthesiology and Reanimation, Fatih University, School of Medicine, Ankara, Turkey Ali Akcay Department of Internal Medicine, Fatih University, School of Medicine, alpaslan turkes cad no 57 Emek, 06510 Ankara, Turkey

doi:10.1016/j.mehy.2006.07.047

Injection of vitreous body to the Joint Space may be an Alternative Treatment for Degenerative Joint Disorders, New Idea Sir, Vitreous body is a gel-like structure including 99% water, fine collagen fibrils (chiefly type 2), hyaluronic acid and also cells termed hyalocytes which

probably represent modified histiocytes, glial cells or fibroblasts [1]. In recent years, several reports have contributed to a growing suspicion that the vitreous body has the ability to induce tolerance similar to the anterior chamber-associated im-