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Ann Thorac Surg 2007;84:1390-1391
© 2007 The Society of Thoracic Surgeons
Department of Anesthesiology, Perioperative and Pain Medicine, Division of Cardiac Surgery, Brigham and Woman’s Hospital, Boston, Massachusetts
Accepted for publication May 14, 2007.
* Address correspondence to Dr D’Ambra, Brigham and Women’s Hospital, Department of Anesthesiology, Perioperative, and Pain Medicine, Division of Cardiac Anesthesia, 75 Francis St, Boston, MA 02115 (Email: mdambra{at}partners.org).
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Introduction |
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A 75-year-old woman presented with severe aortic regurgitation and mild aortic stenosis. Her history was significant for multiple episodes of lower extremity deep vein thromboses, New York Heart Association functional class I congestive heart failure, hypertension, hypothyroidism, diverticulitis, and osteoporosis. She had been anticoagulated with warfarin for 30 years with a preoperative international normalized ratio of 1.8. Warfarin therapy had prevented the recurrence of deep vein thromboses. A hypercoagulability workup 3 years prior showed that she was heterozygous for the prothrombin 20210A mutation.
Warfarin was discontinued 3 days prior to admission. Two days before surgery the patient was admitted for a heparin "bridge" infusion (500 U per hour, titrated to a partial thromboplastin time of 60 to 80 seconds). On the morning of surgery, the patient’s international normalized ratio was 1.5, prothrombin time was 17.8 seconds, partial thromboplastin time was 67.2 seconds, and fibrinogen level was 217 mg/dL. The preoperative antithrombin-III (AT-III) activity was normal (91%), but protein C activity (43%) and protein S activity (53%) were decreased. Venodyne leg compression devices were applied throughout the case. Antifibrinolytics were not used. The heparin infusion was continued until 15 minutes before cardiopulmonary bypass (CPB). An upper hemi-sternotomy incision was made. The baseline activated clotting time (ACT) was 140 seconds. Heparin dosing was determined using a heparin level and a heparin dose response curve to achieve our routine target ACT of 350 seconds. The patient was cannulated for CPB using the right atrium and distal aorta. Percutaneous femoral vein cannulation, which is our standard practice in minimally invasive cases, was not used to avoid lower extremity venous compromise. On CPB, the aorta was cross clamped and antegrade cardioplegia was administered. The calcified aortic valve was excised and replaced with a 23-mm Saint Jude mechanical valve (St. Jude Medical, St. Paul, MN). Cross-clamp time was 57 minutes. The patient was easily weaned from CPB. Heparin was neutralized with a protamine dose determined by heparin-protamine titration. No blood products other than two units of autologous cell-saver were required.
After surgery the patient was admitted to the cardiac intensive care unit. Subcutaneous heparin was started on arrival and venodynes were continued on both lower extremities. Postoperatively the AT-III activity was 54% with an INR of 1.8, a prothrombin time of 21.5 seconds, and a partial thromboplastin time of 32.2 seconds.
The patient’s initial postoperative course was complicated by mild anemia (hematocrit 26.2) treated with 1 unit of packed red blood cells. Mediastinal drainage was 240 mL per 24 hours after surgery, decreasing to 50 mL per 24 hours the second day. Warfarin was restarted by postoperative day 2 and the patient was discharged home by postoperative day 6 with an international normalized ratio of 2.3.
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Currently there is no consensus on appropriate perioperative management for patients with hypercoagulable states who are to undergo cardiac surgery [3]. In our patient we proceeded with heparin bridging rather than discontinue anticoagulation preoperatively. This decision was made on the assumption that maintaining anticoagulation with warfarin increased the risk for serious periprocedural bleeding [3, 4]. There is controversy regarding this approach because some studies claim that warfarin does not cause increased bleeding in patients placed on CPB, and may actually decrease blood loss [5].
We avoided epsilon amino caproic acid, tranexamic acid, and aprotinin, because none have been studied in the prothrombin 20210A mutation. Also anti-fibrinolytic use in patients with known hypercoagulable disorders such as factor V Leiden has been linked to fatal thromboses [6].
It is conceivable that a hypercoagulable state may confer protection against blood loss and transfusion after cardiac surgery. In our patient, only one postoperative red blood cell transfusion was required to augment red cell mass.
Donahue and Gailani [7] showed that in cardiac surgery patients, heterozygous for the factor V Leiden polymorphism, blood loss was significantly lower and patients had a decreased risk for transfusion throughout the postoperative period. A follow-up study showed that activated protein C resistance is the most likely mechanism [8]. Although the mechanism of action of hypercoagulability is different for patients with the prothrombin 20210A mutation, the end point in the coagulation cascade is the same (ie, for any given stimulus, more thrombin is generated with greater conversion of fibrinogen to fibrin). Whether patients with prothrombin 20210A mutation are protected from increased blood loss during cardiac surgery as patients with factor V Leiden deserves further study.
Our patient had mild protein C and S deficiencies preoperatively, which was attributed to the residual effect of warfarin. If there were a more dramatic reduction (< 30% activity), our plan was to administer fresh frozen plasma prior to and after CPB to maintain levels less than 50%. If this patient had required saphenous vein grafts to the coronary circulation, we would have been much more aggressive about replenishing the intrinsic anticoagulants. Our patient exhibited an antithrombin III deficiency postoperatively. This was a predicted change related to consumption secondary to high-dose heparin therapy and CPB; however, based on previous studies, the risk for thrombosis was not considered to be elevated [8]. Hence, despite having a therapeutic international normalized ratio when CPB was terminated, heparin therapy was reinstituted shortly after surgery, followed by a transition back to warfarin for appropriate prophylaxis against thromboembolism.
In summary, perioperative management of patients with prothrombin 20210A mutation has yet to be clearly defined. This report constitutes the first description of a patient with prothrombin 20210A mutation undergoing cardiac surgery. As with other hypercoagulable conditions such as factor V Leiden, current data is insufficient to support general preoperative screening or modification of anesthetic management on the basis of a patient’s genotype. Clinical coagulation tests are not optimized for monitoring the effects of the prothrombin 20210A mutation.
Future developments in functional genomics and molecular biology will continue to have a confounding impact on surgical and anesthetic practice. This case serves as an indication that there exists a need for prospective, sufficiently powered gene association studies to clearly identify factors indicative of adverse perioperative thrombotic events. Meaningful genetic screening leading to evidence-based hematologic interventions is the goal, but in the absence of such studies, we are limited to case reports as we seek rational application of genetic data for the care of cardiac surgical patients.
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