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Clinical Specialist, Department of Cardiology, Ataturk Training and Research Hospital, Bilkent, Ankara, Turkey
Clinical Specialist, Department of Cardiology, Ataturk Training and Research Hospital
Chief, Department of Cardiology, Ataturk Training and Research Hospital
Clinical Specialist, Department of Endocrinology and Metabolism, Ankara Numune Training and Research Hospital, Cigdem Sokak. 5/4, Aydinlikevler-Ankara-Turkey, Opera, Ankara, Turkey, fax 90 312 3093398, tuncay{at}delibasi.net
Published Online, October 24, 2006. www.theannals.com, DOI 10.1345/aph.1H115
Case Report. A 69-year-old man arrived at our outpatient clinic with progressive shortness of breath and pedal edema. His history was significant for rheumatic aortic stenosis, mitral stenosis, and severe tricuspid regurgitation; a cardiovascular surgeon had suggested surgery. The patient was not taking any medication, including anticoagulation therapy, prior to hospitalization.
Physical examination on admission revealed an irregular heart rate of 96 beats/min, consistent with atrial fibrillation, and pedal edema and palpable pulses in the lower extremities. An electrocardiogram showed atrial fibrillation and left ventricular hypertrophy. Comprehensive blood test results, including liver and renal function tests, were normal, with creatinine 1.2 mg/dL and creatinine clearance 95 mL/min. Baseline complete blood cell count was normal, including platelets 375 x 103/mm3, hematocrit 37%, and hemoglobin 12.1 mg/dL.
To treat the ascites and congestion, the patient was administered high doses of furosemide; diltiazem and digoxin were given for rate control of atrial fibrillation. To prevent thromboembolic complications of atrial fibrillation, the patient was treated with enoxaparin 80 mg subcutaneously twice daily. He did not receive any treatment for atrial fibrillation as an outpatient. On day 12 of treatment, the patient developed pain and swelling in his right knee. We consulted the orthopedics team, and, during arthrocentesis, 150 mL of defibrinated blood was drained from the patient's knee. After arthrocentesis, enoxaparin therapy was discontinued because no other identifiable cause was found for the bleeding. Fresh frozen plasma and local treatment of the knee were initiated for hemarthrosis. The patient's international normalized ratio and activated partial thromboplastin time were 1.1 and 31 seconds, respectively, at the time of hemarthrosis. There were no significant changes in these parameters after hemarthrosis. Total duration of enoxaparin therapy was 12 days.
Discussion. Enoxaparin, a low-molecular-weight heparin, can be an attractive alternative to unfractionated heparin (UFH). Enoxaparin is obtained from standard unfractionated porcine intestinal mucosal heparin by controlled depolymerization.1,2 Enoxaparin is rapidly gaining acceptance in outpatient therapy, and it appears that it will replace UFH for treatment of venous or arterial thromboembolism. Enoxaparin is often administered to patients who temporarily discontinue warfarin prior to undergoing invasive procedures. We used enoxaparin for anticoagulation before elective cardiac valve surgery.
In patients receiving enoxaparin, factors that increase the risk of bleeding are high doses, advanced age, renal impairment, and concomitant use of other drugs that affect hemostasis.3,4 In our patient, the standard enoxaparin dose (1 mg/kg) was used. The patient's renal function was within normal limits. No other drugs affecting hemostasis were used, including aspirin. At the beginning of and during the treatment, the platelet count and other coagulation parameters were within normal ranges. Therefore, the patient's age of 69 years appeared to be the only risk factor for bleeding during enoxaparin therapy. The patient experienced no physical trauma and was bedridden due to peripheral edema. According to the Naranjo probability scale, it is probable that the patient's hemarthrosis was caused by enoxaparin.5
Clinicians should be aware of the potential for enoxaparin to be the cause of hemarthrosis.
References
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