DVT Prophylaxis for Total Joint Arthroplasty

Michael J. Dunbar M.D., FRCSC, PhD
Dalhousie University

Heparin was discovered in 1916 and is one of the oldest drugs currently still in widespread clinical use. It was originally isolated from canine liver cells, hence its name (hepar is Greek for "liver"). Pharmaceutical grade Heparin is commonly derived from mucosal tissues of slaughtered meat animals such as porcine intestine or bovine lung.

Heparin binds to the enzyme inhibitor antithrombin III (AT-III) causing a conformational change which results in its active site being exposed. The activated AT-III then inactivates thrombin and other proteases involved in blood clotting. The rate of inactivation of these proteases by AT-III increases 1000-fold due to the binding of Heparin.

Heparin is given parenterally, as it is degraded when taken by mouth. It can be injected intravenously or subcutaneously (under the skin). Intramuscular injections (into muscle) are avoided because of the potential for forming hematomas. Because of its short biologic half-life of approximately one hour, Heparin must be given frequently or as a continuous infusion.

Heparin was one of the first tested thromboprophylaxis agents in hip arthroplasty. In 1974, Morris et al. conducted a prospective, controlled, randomized trial, to test the prophylactic value of small doses of Heparin (5000 units given subcutaneously twelve-hourly from the day of admission until the 10th postoperative day) in 59 patients undergoing total hip replacement1. The frequency of venous thrombosis was confirmed venographically in 50% in the control group of 32 patients and 11% in the treated group of 27 patients. Blood-loss during operation and postoperatively was not increased in the Heparin-treated patients.

Recently, in 2006, Senaran compared the efficacy and safety of standard Heparin to that of low-molecular-weight Heparin (Enoxaparin) in a randomized trial on 100 hip replacement patients2. Each treatment was continued until the patients were discharged from the hospital and each underwent lower extremity duplex ultrasonography for deep vein thrombosis before discharge. Two patients in the Heparin group developed DVT, which was detected by routine duplex ultrasonography at the end of hospitalisation, and two patients in the Enoxaparin group were detected with late DVT during the postoperative period of six weeks. Seven patients had minor and major bleeding in both groups. Six patients in the Heparin group were discontinued from medication because of hepatic and renal dysfunction, and serious discharge from the wound. This was hardly a ringing endorsement for Heparin.

Heparin is not commonly used as DVT prophylaxis for arthroplasty in Canada. From 2002-2005 the use of subcutaneous Heparin was between two and three percent of all hip and knee arthroplasty cases recorded on the Canadian Joint Replacement Registry3.


  1. Morris, G.K., A.P. Henry, and B.J. Preston, Prevention of deep-vein thrombosis by low-dose heparin in patients undergoing total hip replacement. Lancet, 1974. 2(7884): p. 797-800.
  2. Senaran, H., et al., Enoxaparin and heparin comparison of deep vein thrombosis prophylaxis in total hip replacement patients. Arch Orthop Trauma Surg, 2006. 126(1): p. 1-5.
  3. Canadian Institute for Health Information, Canadian Joint Replacement Registry (CJRR) 2006 Report - Hip and Total Knee Replacements in Canada. 2006, Canadian Institute for Health Information.

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