Dental extraction for patients on oral anticoagulant therapy Uri Martinowitz, MD,” Avital L. Mazar, DIWD,~Shlomo Taicher, DiUD,b David Varon, MD,O Sanford N. Gitel. PhD.a Bracha Ramot, MD,a and Meir Rakocz, DMD,c Tel Hashomer, Israel THE CHAIM
SHEBA MEDICAL
CENTER
Dental extraction in patients receiving long-term oral anticoagulant therapy is a controversial issue. Continuation of anticoagulation exposes the patient to serious hemorrhage, whereas cessation of therapy increases the risk of thromboembolism. Forty patients treated by coumarin underwent 63 tooth extractions, without a change in the therapeutic protocol of anticoagulation. The biologic adhesive Beriplast was used successfully to achieve local hemostasis at the site of the surgical wound. Apart from one patient who had mild oozing, there were no incidences of postsurgical hemorrhage.
P
atients receiving oral anticoagulant therapy who undergo dental extraction may have prolonged and excessivehemorrhage. I-’ Cessation or decreasein the anticoagulant therapy, however, exposesthe patients, especially those with artificial heart valves, to the risk of thromboembolism.8-14Various protocols have been suggestedfor dental extraction in such patients: continuing the therapy,2-4,6,‘, 15-17decreasing the level of anticoagulation, l* substituting heparin for coumarin,19 and temporarily discontinuing the anticoagulant. ‘35,20,21These approachesare not risk free and usually require close monitoring and hospitalization.21 The aim of this study was to evaluate the local hemostatic effect of a biologic adhesive in patients on anticoagulant therapy who undergo dental extraction without a change in their level of anticoagulation. MATERIAL
AND METHODS
Forty patients underwent 63 tooth extractions without changing their anticoagulant therapy. Only patients with preoperative prothrombin time (PT) values within the therapeutic range (International Normalized Ratio [INR] to 2.5; 4.5)22*23 were included in the study. The patients’ ages ranged between 32 and 75 years (mean 55 years). Indications for anticoagulant therapy are summarized in Table I. BThe Hematology Institute and The National Hemophilia Center. bThe Department of Oral and Maxillofacial Surgery, The Chaim Sheba Medical Center. CDivision of Pediatric and Hospital Dentistry, The Chaim Sheba Medical Center. 7/12/14464 274
Table
I. Indication for anticoagulation Indication Valve replacement Mitral Aortic Both Mitral stenosis Thromboembolism Venous Arterial Myocardial infarction Total
No. of patients
7 6 5 5 7 4 4 40
Local hemostasis was achieved through the application of a biologic adhesive, Beriplast (Behringwerke, Marburg, West Germany), combined with a collagen fleece (Behringwerke). The adhesive contains thrombin, fibrinogen, factor XIII, and aprotinin. Thrombin converts fibrinogen to unstable fibrin clot, factor XIII stabilizes the clot, and aprotinin prevents its degradation (Fig. 1). Teeth were extracted in quadrants and the area was anesthetized either locally or intraligamentarily. The teeth were extracted with minimal trauma to the surrounding tissues. The socket was curetted and thrombin-soaked gauze was inserted for 3 minutes to dry the socket.Subsequently, the biologic adhesive Beriplast was applied along the walls of the socket after which a collagen fleece was inserted. The margins were sutured and adhesive was applied to the sutured area (Figs. 2 to 4). The sutures were removed after 7 days. Preventive antibiotic
Volume70 Number 3
Fig.
Dental extraction for patients on oral anticoagulant
1. Mechanism of action of biologic
therapy
275
adhesive
Beriplast.
Fig. 3. Margins of soft tissue are sutured and more adhesive is applied.
Fig. 2. Biologic adhesive is inserted along sockets’walls, and collagen fleece is inserted.
therapy was administered according to the American Heart Association protocol to patients with mechanical heart valves or valvular pathosis. RESULTS
PT values at the time of extraction ranged from 2.5 to 4.29 INR (average 3.25). Local hemostasis was achieved immediately. The bleeding was of shorter duration than in patients who did not receive anticoagulant therapy. There was no incidence of prolonged or excessive hemorrhage. One patient who had received dipyridamole in addition to coumarin had a delayed mild hemorrhage on the third day. Application of local pressure successfully stopped the hemorrhage. There were no casesof wound infection and the healing processwas normal. None of the patients had thromboembolic phenomena. The initial 15 patients were hospitalized for 1 day, but the rest of the patients underwent dental extraction on an ambulatory basis, inasmuch as hospitalization was found unnecessary. DISCUSSION
Thromboembolism is a serious complication in patients with artificial heart valves.8-‘4Therefore long-
Fig.
4. Sutures are then covered with adhesive.
term anticoagulant therapy has been recommended for these patients.8*12,15-27When tooth extraction in such a patient is planned, the physician is faced with a dilemma: whether to extract the tooth while the PT is within the therapeutic range and risk serious hemorrhage,“’ or to decrease or discontinue the therapy and risk thromboembolism.8-14Various protocols have been suggested: 1. No change in anticoagulation: This approach relies on local measures to control the bleeding.2*5,‘3 l5 In some studies, reporting few or no postoperative cases of bleeding, the ma-
276
Martinowitz
Table
II. Results
No. of patients 40
et al.
ORAL SURCORAL MED ORAL PATHOL September 1990
No. of extracted teeth
Excessive bleeding
63
0
Mild bleeding
1
Infections
0
jority of patients had normal PTs or PTs in the low therapeutic range.28-30Patients with higher PT values may be more likely to have postoperative bleedingq2T 5-7,l5 In somecasesthe bleeding may be intractable295 and vitamin K may be needed to control it.7, I5 2. Change in anticoagulant intensity: Another approach is the reduction or elimination of the anticoagulant dosefor a variable period (from 2 to 6 days) before the extraction.‘, 5,20,31-37This approach increases the risk of thromboembolism, particularly in patients with artificial heart valves.8-14In addition, the theory of rebound hypercoagulability after withdrawal of coumarin”, 38-41was recently supported by a study that shows increased thrombin activity after coumarin withdrawal.42 Whether or not the rebound phenomenon exists, the patient is exposedto thromboembolic risk for a longer period than the reduction or discontinuation of the coumarin, since it takes a few days for the therapeutic level to be reached.43Another disadvantage of this approach is that it requires close monitoring of the PT for several days. 3. Replacement of coumarin by heparin before extractiod9: This approach requires hospital-
ization with close monitoring of the anticoagulant treatment. Postoperatively the patient is at risk of thromboembolism until the therapeutic level of coumarin is once again achieved. This can take several days.43 The rationale behind the present study is to induce clot formation at the site of the surgical wound, with no change in the anticoagulant therapy. Beriplast mimics the final phase of blood clotting. Thrombin causesfibrinogen to coagulate; factor XIII, as an adjuvant, provides for the cross-linkage and stabilization of the fibrin clot; aprotinin, an antiprotease, prevents early disruption of the clot by fibrinolysis. The product posesvirtually no risk of transmission of viral infections due to the pasteurization of the components.44On the basis of the favorable results of the biologic adhesive in patients with congenital coagulopathies45 and taking into consideration the known complications of tooth extractions in patients on anticoagulant therapy, we considered it unethical to study a control group. None of the 40 patients, undergoing 63 tooth extractions, had serious postoper-
ative hemorrhage. Only one patient had a mild hemorrhage, which was stopped by application of local pressure. There was no change in the intensity of the anticoagulation, and all the patients were within the therapeutic range, with PT values above 2.5 INR. Our protocol offers the patients lower postoperative risk of hemorrhage or thromboembolism. Neither hospitalization nor frequent PT testing after the extraction is required. REFERENCES 1. Ziffer AM, Scoop JW, Beck J, Baum J, Berger AR. Profound
2. 3. 4.
5.
bleeding after dental extraction during dicumarol therapy. N Engl J Med 1957;256:351-3. Waldrep Jr AC, McKelvey LE. Oral surgery for patients on anticoagulant therapy. J Oral Surg 1968;26:374-80. JohnsonRL.Bloodlossinoralsurgery. JDentRes 1956;35:1757. Greenberg MS, Miller FM, Lynch MA. Partial thromboplastin time as a predictor of blood loss in oral surgery patients receiving coumarin anticoagulant. J Am Dent Assoc 1972; 84:583-7. Scopp IW, Frederics F. Dental extraction in patients undergoing anticoagulant therapy. ORAL SURG ORAL MED ORAL PATHOL 1958;11:470-4.
6. Sindet-Pedersen S, Ramstrom G, Bernvil S, Blombaeck M. The effect of tranexamic acid mouth wash in anticoagulant treated patients undergoing oral surgery. N Engl J Med 1989;13:840-3. I Beherman SJ, Wright IS. Dental surgery during continuous anticoagulant therapy. JAMA 1961;175:483-8. 8. Robbins RC, Bowman FO, Malm JR. Cardiac valve replacement in children: a twenty-year series. Ann Thorac Surg 1988;45:56-61. 9. Akabrian M, Austen WG, Yurchak PM, Scannell GJ. Thromboembolic complication of prosthetic cardiac valves. Circulation 1968;37:826-31. 10. Lytle BW, Cosgrove DM, Goormastic M, Loop FD. Aortic valve replacement and coronary bypass grafting for patients with aortic stenosisand coronary artery disease:early and late results. Eur Heart J 1988:suppl E:143-7. 11. Marshall J. Rebound phenomenonafter anticoagulant therapy in cerebrovascular disease. Circulation 1963;28:329-32. 12. Gallus AS. Long-term warfarin treatment in artery disease. Blood Rev 1988;2:95-101. 13. Michales L, Beamish RE. Relapse of thromboembolic disease after discontinued anticoagulant therapy. Am J Cardiol 1967;20:670-3. 14. Duvoisin GE, Brandenburg RO, Mcgoon DC. Factors affecting thromboembolism associatedwith prosthetic heart valves. Circulation 1967;35(suppl 1):70-6. 15. Shira RB, Hall RJ, Guernsey LH. Minor oral surgery during prolonged anticoagulant therapy. J Oral Surg 1962;20:93-9. 16. Benoliel R, Leviner E, Katz J, Tzukert A. Dental treatment for the patient on anticoagulant therapy: prothrombin time value-what difference does it make? ORAL SURG ORAL MED ORAL PATHOL 1986;62: 149-S 1.
17. Taylor JJ. Anticoagulant during dental surgery [Letter to the editor]. Lancet 1966;2:231-2. 18. JohnsonWT, Leary JM. Management of dental patients with bleeding disorders: review and update. ORAL SURG ORAL MED ORAL PATHOL 1988;66:297-303.
19. Roser SM, Rosenbloom B. Continued anticoagulant in oral surgery procedures. ORAL SURGORAL MED ORAL PATHOL 1975;40:448-57. 20. Spough JD. Hemostasis in dentistry with special reference to hemocoagulation. ORAL SURG ORAL MED ORAL PATHOL 1964;18:701-12. 21. Mulligan R, Weitzel KG. Pretreatment management of the
Volume 70 Number 3
22. 23. 24. 25. 26. 27.
28. 29. 30.
Dental extraction for patients on oral anticoagulant
patient receiving anticoagulant drugs. J Am Dent Assoc 1988;117:479-83. Poller L, Taberner DA. Dose and control of oral anticoagulant therapy and its control: an international collaborative survey. Br J Haematol 1982;51:479-85. Poller L. Laboratory control of anticoagulant therapy. Semin Thromb Hemost 1986;12:9-13. Prevention of bacterial endocarditis: a committee report of the American Heart Association. Council on Dental Therapeutics. J Am Dent Assoc 1985;110:98-100. Starr A, Boncheck LI, Anderson RP, et al. Late complication of aortic valve replacement with cloth-covered composite-scat prostheses.Ann Thorac Surg 1975;19:289-300. Larsen GL, Alexander JA, Stanford W. Thromboembolic phenomenon in patient with prosthetic aortic valves who did not receive anticoagulants. Ann Thorac Surg 1977;23:323-6. Limet R, Lepage G, Grondin CM. Thromboembolic complications with cloth-covered Starr-Edwards aortic prosthesis in patients not receiving anticoagulants. Ann Thorac Surg 1977;23:529-33. Anavi Y, Sharon A, Gutman D, Laufer D. Dental extraction during anticoagulant therapy. Isr J Dent Med 1981;28:9-12. Tomasi NJ, Wolf JF. Presurgical management of a patient receiving anticoagulant therapy: report of case. J Am Dent Assot 1984;88:1028-9. Rooney TP. General dentistry during continuous anticoagulation therapy. ORAL SURG ORAL MED ORAL PATHOL
1983;56:252-5. 31. Davis FB, Sczupak CA. Outpatient oral anticoagulation:
guidelines for long-term management. Postgrad Med 1979;66:100-9. 32. Rose LF, Godfrey P, Steinberg BJ. Dental correlation. In: RoseLF, Kay D, eds.Internal medicine for dentistry. St Louis: CV Mosby, 1983:577-8. 33. Cohen SG. Anticoagulant therapy. In: Rose LF, Kay D, eds. Internal medicine for dentistry. St Louis: CV Mosby, 1983:42930. 34. Kwapis BW. Anticoagulant therapy and dental practice. J Am Dent Assoc 1963;66:172-5.
therapy
277
35. Little JW, Falace DA. Dental management of the compromised oatient. St Louis: CV Mosbv. 1980:185-6. 36. Kovacs B, Toth K, Kereny G. Post&traction hemostasisduring anticoagulant therapy with a locally applied coagulation active substance. Int J Oral Surg 1976;5:3-7. 37. Sonis S, Fazio RC, Fong L. Principles and practice of oral medicine. Philadelphia: WB Saunders Co, 1984:307. 38. Mulligan R. Responseto anticoagulant drug withdrawal. J Am Dent Assoc 1987;115:435-8. 39. Poller L, Thomson J. Evidence for rebound hypercoagulability after stopping anticoagulants. Lancet 1964;2:62-4. 40. VanCleve R. The rebound phenomenon-fact or fancy? Experience with discontinuation of long-term anticoagulant therapy after myocardial infarction. Circulation 1965;32:87880. 41. Sise HS, Moschos CB, Gauthier J, Becker R. The risk of interrupting long-term anticoagulant treatment: a rebound hypercoagulable state following haemorrhage. Circulation 1961;24:1137-42. 42. Harenberg J, Hass R, Zimmerman R. Plasma hypercoagulability after termination of oral anticoagulants. Thromb Res 1983;29:627-33. 43. Perry MO. Anticoagulation: a surgical perspective. Am J Surg 1988;155:268-76. 44. Hilfenhaus J, Weidman E. Fibrin glue safety: inactivation of potential viral contaminants by pasteurization of the plasma components. Arzneim-Forsh 1985;11:1617-9. 45. Gatti R, Scolari G, Landonio G, Muti G, De Cataldo F, Baudo F. Local hemostasisafter tooth extraction in hemophilia and von Willebrand’s disease.Use of human fibrinogen concentrate [Abstract]. La Ricerca 1986;1:242. Reprint requests to:
Dr. U. Martinowitz Director The National Hemophilia Center The Chaim Sheba Medical Center Tel Hashomer 52621, Israel
SHEBA MEDICAL
CENTER
Dental extraction in patients receiving long-term oral anticoagulant therapy is a controversial issue. Continuation of anticoagulation exposes the patient to serious hemorrhage, whereas cessation of therapy increases the risk of thromboembolism. Forty patients treated by coumarin underwent 63 tooth extractions, without a change in the therapeutic protocol of anticoagulation. The biologic adhesive Beriplast was used successfully to achieve local hemostasis at the site of the surgical wound. Apart from one patient who had mild oozing, there were no incidences of postsurgical hemorrhage.
P
atients receiving oral anticoagulant therapy who undergo dental extraction may have prolonged and excessivehemorrhage. I-’ Cessation or decreasein the anticoagulant therapy, however, exposesthe patients, especially those with artificial heart valves, to the risk of thromboembolism.8-14Various protocols have been suggestedfor dental extraction in such patients: continuing the therapy,2-4,6,‘, 15-17decreasing the level of anticoagulation, l* substituting heparin for coumarin,19 and temporarily discontinuing the anticoagulant. ‘35,20,21These approachesare not risk free and usually require close monitoring and hospitalization.21 The aim of this study was to evaluate the local hemostatic effect of a biologic adhesive in patients on anticoagulant therapy who undergo dental extraction without a change in their level of anticoagulation. MATERIAL
AND METHODS
Forty patients underwent 63 tooth extractions without changing their anticoagulant therapy. Only patients with preoperative prothrombin time (PT) values within the therapeutic range (International Normalized Ratio [INR] to 2.5; 4.5)22*23 were included in the study. The patients’ ages ranged between 32 and 75 years (mean 55 years). Indications for anticoagulant therapy are summarized in Table I. BThe Hematology Institute and The National Hemophilia Center. bThe Department of Oral and Maxillofacial Surgery, The Chaim Sheba Medical Center. CDivision of Pediatric and Hospital Dentistry, The Chaim Sheba Medical Center. 7/12/14464 274
Table
I. Indication for anticoagulation Indication Valve replacement Mitral Aortic Both Mitral stenosis Thromboembolism Venous Arterial Myocardial infarction Total
No. of patients
7 6 5 5 7 4 4 40
Local hemostasis was achieved through the application of a biologic adhesive, Beriplast (Behringwerke, Marburg, West Germany), combined with a collagen fleece (Behringwerke). The adhesive contains thrombin, fibrinogen, factor XIII, and aprotinin. Thrombin converts fibrinogen to unstable fibrin clot, factor XIII stabilizes the clot, and aprotinin prevents its degradation (Fig. 1). Teeth were extracted in quadrants and the area was anesthetized either locally or intraligamentarily. The teeth were extracted with minimal trauma to the surrounding tissues. The socket was curetted and thrombin-soaked gauze was inserted for 3 minutes to dry the socket.Subsequently, the biologic adhesive Beriplast was applied along the walls of the socket after which a collagen fleece was inserted. The margins were sutured and adhesive was applied to the sutured area (Figs. 2 to 4). The sutures were removed after 7 days. Preventive antibiotic
Volume70 Number 3
Fig.
Dental extraction for patients on oral anticoagulant
1. Mechanism of action of biologic
therapy
275
adhesive
Beriplast.
Fig. 3. Margins of soft tissue are sutured and more adhesive is applied.
Fig. 2. Biologic adhesive is inserted along sockets’walls, and collagen fleece is inserted.
therapy was administered according to the American Heart Association protocol to patients with mechanical heart valves or valvular pathosis. RESULTS
PT values at the time of extraction ranged from 2.5 to 4.29 INR (average 3.25). Local hemostasis was achieved immediately. The bleeding was of shorter duration than in patients who did not receive anticoagulant therapy. There was no incidence of prolonged or excessive hemorrhage. One patient who had received dipyridamole in addition to coumarin had a delayed mild hemorrhage on the third day. Application of local pressure successfully stopped the hemorrhage. There were no casesof wound infection and the healing processwas normal. None of the patients had thromboembolic phenomena. The initial 15 patients were hospitalized for 1 day, but the rest of the patients underwent dental extraction on an ambulatory basis, inasmuch as hospitalization was found unnecessary. DISCUSSION
Thromboembolism is a serious complication in patients with artificial heart valves.8-‘4Therefore long-
Fig.
4. Sutures are then covered with adhesive.
term anticoagulant therapy has been recommended for these patients.8*12,15-27When tooth extraction in such a patient is planned, the physician is faced with a dilemma: whether to extract the tooth while the PT is within the therapeutic range and risk serious hemorrhage,“’ or to decrease or discontinue the therapy and risk thromboembolism.8-14Various protocols have been suggested: 1. No change in anticoagulation: This approach relies on local measures to control the bleeding.2*5,‘3 l5 In some studies, reporting few or no postoperative cases of bleeding, the ma-
276
Martinowitz
Table
II. Results
No. of patients 40
et al.
ORAL SURCORAL MED ORAL PATHOL September 1990
No. of extracted teeth
Excessive bleeding
63
0
Mild bleeding
1
Infections
0
jority of patients had normal PTs or PTs in the low therapeutic range.28-30Patients with higher PT values may be more likely to have postoperative bleedingq2T 5-7,l5 In somecasesthe bleeding may be intractable295 and vitamin K may be needed to control it.7, I5 2. Change in anticoagulant intensity: Another approach is the reduction or elimination of the anticoagulant dosefor a variable period (from 2 to 6 days) before the extraction.‘, 5,20,31-37This approach increases the risk of thromboembolism, particularly in patients with artificial heart valves.8-14In addition, the theory of rebound hypercoagulability after withdrawal of coumarin”, 38-41was recently supported by a study that shows increased thrombin activity after coumarin withdrawal.42 Whether or not the rebound phenomenon exists, the patient is exposedto thromboembolic risk for a longer period than the reduction or discontinuation of the coumarin, since it takes a few days for the therapeutic level to be reached.43Another disadvantage of this approach is that it requires close monitoring of the PT for several days. 3. Replacement of coumarin by heparin before extractiod9: This approach requires hospital-
ization with close monitoring of the anticoagulant treatment. Postoperatively the patient is at risk of thromboembolism until the therapeutic level of coumarin is once again achieved. This can take several days.43 The rationale behind the present study is to induce clot formation at the site of the surgical wound, with no change in the anticoagulant therapy. Beriplast mimics the final phase of blood clotting. Thrombin causesfibrinogen to coagulate; factor XIII, as an adjuvant, provides for the cross-linkage and stabilization of the fibrin clot; aprotinin, an antiprotease, prevents early disruption of the clot by fibrinolysis. The product posesvirtually no risk of transmission of viral infections due to the pasteurization of the components.44On the basis of the favorable results of the biologic adhesive in patients with congenital coagulopathies45 and taking into consideration the known complications of tooth extractions in patients on anticoagulant therapy, we considered it unethical to study a control group. None of the 40 patients, undergoing 63 tooth extractions, had serious postoper-
ative hemorrhage. Only one patient had a mild hemorrhage, which was stopped by application of local pressure. There was no change in the intensity of the anticoagulation, and all the patients were within the therapeutic range, with PT values above 2.5 INR. Our protocol offers the patients lower postoperative risk of hemorrhage or thromboembolism. Neither hospitalization nor frequent PT testing after the extraction is required. REFERENCES 1. Ziffer AM, Scoop JW, Beck J, Baum J, Berger AR. Profound
2. 3. 4.
5.
bleeding after dental extraction during dicumarol therapy. N Engl J Med 1957;256:351-3. Waldrep Jr AC, McKelvey LE. Oral surgery for patients on anticoagulant therapy. J Oral Surg 1968;26:374-80. JohnsonRL.Bloodlossinoralsurgery. JDentRes 1956;35:1757. Greenberg MS, Miller FM, Lynch MA. Partial thromboplastin time as a predictor of blood loss in oral surgery patients receiving coumarin anticoagulant. J Am Dent Assoc 1972; 84:583-7. Scopp IW, Frederics F. Dental extraction in patients undergoing anticoagulant therapy. ORAL SURG ORAL MED ORAL PATHOL 1958;11:470-4.
6. Sindet-Pedersen S, Ramstrom G, Bernvil S, Blombaeck M. The effect of tranexamic acid mouth wash in anticoagulant treated patients undergoing oral surgery. N Engl J Med 1989;13:840-3. I Beherman SJ, Wright IS. Dental surgery during continuous anticoagulant therapy. JAMA 1961;175:483-8. 8. Robbins RC, Bowman FO, Malm JR. Cardiac valve replacement in children: a twenty-year series. Ann Thorac Surg 1988;45:56-61. 9. Akabrian M, Austen WG, Yurchak PM, Scannell GJ. Thromboembolic complication of prosthetic cardiac valves. Circulation 1968;37:826-31. 10. Lytle BW, Cosgrove DM, Goormastic M, Loop FD. Aortic valve replacement and coronary bypass grafting for patients with aortic stenosisand coronary artery disease:early and late results. Eur Heart J 1988:suppl E:143-7. 11. Marshall J. Rebound phenomenonafter anticoagulant therapy in cerebrovascular disease. Circulation 1963;28:329-32. 12. Gallus AS. Long-term warfarin treatment in artery disease. Blood Rev 1988;2:95-101. 13. Michales L, Beamish RE. Relapse of thromboembolic disease after discontinued anticoagulant therapy. Am J Cardiol 1967;20:670-3. 14. Duvoisin GE, Brandenburg RO, Mcgoon DC. Factors affecting thromboembolism associatedwith prosthetic heart valves. Circulation 1967;35(suppl 1):70-6. 15. Shira RB, Hall RJ, Guernsey LH. Minor oral surgery during prolonged anticoagulant therapy. J Oral Surg 1962;20:93-9. 16. Benoliel R, Leviner E, Katz J, Tzukert A. Dental treatment for the patient on anticoagulant therapy: prothrombin time value-what difference does it make? ORAL SURG ORAL MED ORAL PATHOL 1986;62: 149-S 1.
17. Taylor JJ. Anticoagulant during dental surgery [Letter to the editor]. Lancet 1966;2:231-2. 18. JohnsonWT, Leary JM. Management of dental patients with bleeding disorders: review and update. ORAL SURG ORAL MED ORAL PATHOL 1988;66:297-303.
19. Roser SM, Rosenbloom B. Continued anticoagulant in oral surgery procedures. ORAL SURGORAL MED ORAL PATHOL 1975;40:448-57. 20. Spough JD. Hemostasis in dentistry with special reference to hemocoagulation. ORAL SURG ORAL MED ORAL PATHOL 1964;18:701-12. 21. Mulligan R, Weitzel KG. Pretreatment management of the
Volume 70 Number 3
22. 23. 24. 25. 26. 27.
28. 29. 30.
Dental extraction for patients on oral anticoagulant
patient receiving anticoagulant drugs. J Am Dent Assoc 1988;117:479-83. Poller L, Taberner DA. Dose and control of oral anticoagulant therapy and its control: an international collaborative survey. Br J Haematol 1982;51:479-85. Poller L. Laboratory control of anticoagulant therapy. Semin Thromb Hemost 1986;12:9-13. Prevention of bacterial endocarditis: a committee report of the American Heart Association. Council on Dental Therapeutics. J Am Dent Assoc 1985;110:98-100. Starr A, Boncheck LI, Anderson RP, et al. Late complication of aortic valve replacement with cloth-covered composite-scat prostheses.Ann Thorac Surg 1975;19:289-300. Larsen GL, Alexander JA, Stanford W. Thromboembolic phenomenon in patient with prosthetic aortic valves who did not receive anticoagulants. Ann Thorac Surg 1977;23:323-6. Limet R, Lepage G, Grondin CM. Thromboembolic complications with cloth-covered Starr-Edwards aortic prosthesis in patients not receiving anticoagulants. Ann Thorac Surg 1977;23:529-33. Anavi Y, Sharon A, Gutman D, Laufer D. Dental extraction during anticoagulant therapy. Isr J Dent Med 1981;28:9-12. Tomasi NJ, Wolf JF. Presurgical management of a patient receiving anticoagulant therapy: report of case. J Am Dent Assot 1984;88:1028-9. Rooney TP. General dentistry during continuous anticoagulation therapy. ORAL SURG ORAL MED ORAL PATHOL
1983;56:252-5. 31. Davis FB, Sczupak CA. Outpatient oral anticoagulation:
guidelines for long-term management. Postgrad Med 1979;66:100-9. 32. Rose LF, Godfrey P, Steinberg BJ. Dental correlation. In: RoseLF, Kay D, eds.Internal medicine for dentistry. St Louis: CV Mosby, 1983:577-8. 33. Cohen SG. Anticoagulant therapy. In: Rose LF, Kay D, eds. Internal medicine for dentistry. St Louis: CV Mosby, 1983:42930. 34. Kwapis BW. Anticoagulant therapy and dental practice. J Am Dent Assoc 1963;66:172-5.
therapy
277
35. Little JW, Falace DA. Dental management of the compromised oatient. St Louis: CV Mosbv. 1980:185-6. 36. Kovacs B, Toth K, Kereny G. Post&traction hemostasisduring anticoagulant therapy with a locally applied coagulation active substance. Int J Oral Surg 1976;5:3-7. 37. Sonis S, Fazio RC, Fong L. Principles and practice of oral medicine. Philadelphia: WB Saunders Co, 1984:307. 38. Mulligan R. Responseto anticoagulant drug withdrawal. J Am Dent Assoc 1987;115:435-8. 39. Poller L, Thomson J. Evidence for rebound hypercoagulability after stopping anticoagulants. Lancet 1964;2:62-4. 40. VanCleve R. The rebound phenomenon-fact or fancy? Experience with discontinuation of long-term anticoagulant therapy after myocardial infarction. Circulation 1965;32:87880. 41. Sise HS, Moschos CB, Gauthier J, Becker R. The risk of interrupting long-term anticoagulant treatment: a rebound hypercoagulable state following haemorrhage. Circulation 1961;24:1137-42. 42. Harenberg J, Hass R, Zimmerman R. Plasma hypercoagulability after termination of oral anticoagulants. Thromb Res 1983;29:627-33. 43. Perry MO. Anticoagulation: a surgical perspective. Am J Surg 1988;155:268-76. 44. Hilfenhaus J, Weidman E. Fibrin glue safety: inactivation of potential viral contaminants by pasteurization of the plasma components. Arzneim-Forsh 1985;11:1617-9. 45. Gatti R, Scolari G, Landonio G, Muti G, De Cataldo F, Baudo F. Local hemostasisafter tooth extraction in hemophilia and von Willebrand’s disease.Use of human fibrinogen concentrate [Abstract]. La Ricerca 1986;1:242. Reprint requests to:
Dr. U. Martinowitz Director The National Hemophilia Center The Chaim Sheba Medical Center Tel Hashomer 52621, Israel
