2. Anticoagulation In Dental Procedures Galila Zaher MRCPath KAU Assistant Professor

3. Function of Homeostasis Function of Normal Homeostasis Prevention of blood loss from intact vessels Arrest of bleeding from damaged vessels

4. BLOOD CLOTTING Plasma protein clotting factors Vascular endoth Platelets Bleeding Thrombosis Clotting factors Natural anticoagulant platelets

5. Normal Hemostasis 1.Vessel wall 1.Local vasoconstriction 2.Platelet release thromboxane A 2 3.Prostacyclin counters effects of Thro-A 2

6. Normal Hemostasis 1.Vessel wall 2.Platelet Adhesion Shape change Aggregation Release Reaction

7. Platelet Activation Adhesion GpIIb/IIIa Aggregation ADP Adrenaline GpIb Collagen Endothelium vWF Collagen Adhesion ADP Adrenaline Thrombin

11. Clotting Factors Names Factors Fibrinogen Prothrombin Thromboplastin Calcium Labile factor Stable factor Antihemophilic factor Antihemophilic factor B Stuart-Power factor Plasma thromboplastin antecedent Hagman factor Fibrin stablizing factors I II III IV V VII VIII IX X XI XII XIII

12. The “Cascade”, “Waterfall” model: APC (PC +PS) AT

15. The “Cascade”, “Waterfall” model: APC (PC +PS) AT

16. TF-Bearing Cell Va TF VIIa Xa X II IIa VIII/vWF VIIIa Normal Hemostasis

17. TF-Bearing Cell Va TF VIIa Xa X II IIa VIII/vWF VIIIa VVa Platelet Normal Hemostasis

18. TF-Bearing Cell Va TF VIIa Xa X II IIa VIII/vWF VIIIa VVa Platelet Activated Platelet Normal Hemostasis

19. TF-Bearing Cell Va TF VIIa Xa X II IIa VIII/vWF VIIIa VVa Platelet TF VIIa IX IXa Activated Platelet Normal Hemostasis

20. TF-Bearing Cell Va TF VIIa Xa X II IIa VIII/vWF VIIIa VVa Platelet TF VIIa IX IXa Activated Platelet VIIIa Va IXa Xa IIa II Normal Hemostasis X

21. Hoffman et al. Blood Coagul Fibrinolysis 1998;9(suppl 1):S61. Activated Platelet Platelet TF VIIIa Va VIIa X II TF-Bearing Cell Va TF VIIa Xa IIa IX VVa II VIII/vWF VIIIa IXa X IXa IIa Xa Normal Hemostasis

22. Platelet Thrombin VIIIa XIa IXa TF VIIa Xa Prothrombin Fibroblast Amplification Activated platelets XIaIXaXa Prothrombin Thrombin Alternative (Cell-based) Model initiation phase

23. Haemostasis: generation of thrombin and clot formation

24. 4. Fibrin threads (scanning electron micrograph) Fibrin forms rapidly in stagnant blood. Thrombin plays a pivotal role in the polymerisation of the fibrin strands. Red blood cells become trapped in the fibrin network as the thrombus grows.

25. Dental extractions Bleeding Thrombosis

26. Bleeding complications Dental extractions OAC 249 :Group 1 INR(1.5–1.99), Group 5 INR >3.5. INR among the groups did not influence incidence of postoperative bleeding. D. Blinderb Dec 2001b

27. Postoperative bleeding 214 patients divided into four groups: Group 1 :no suturing and discontinued Group 2 no suturing & continued warfarin Group 3 suturing and discontinued Group 4 suturing and continued warfarin Dental extractions may be safely performed for patients on OAC provided the INR level < 3.0 Decision to suture should be made on case-by-case basis W. Becker British Dental Journal (2007)

28. Thrombosis & Bleeding Medline,The Cochrane Collaboration database 31 reports Major bleeding rare,Thrombo-embolic events (1.6%) Evid Based Dent. 2005 Descriptive studies (29)1868 patients Thromboembolic rates were for OAC, 0.6% for D/C OAC Major bleeding was rare despite OAC

29. Guidelines on oral anticoagulation (warfarin): third edition – Anticoagulation does not need to be stopped for dental extraction for patients in therapeutic range, i.e. INR <3. 2005 update Evid Based Dent. 2005 DATA SOURCES: Medline & Cochrane database Thrombo-embolic events (1.6%) Major bleeding rare A guideline, based on the evidence available :Certain surgical or invasive procedures can be undertaken with no interruption of OAC Nick Malden Dent Update. 2007 NovNick Malden

31. Fibrin glue Patients OAC without interruption dental extraction Postoperatively, local hemostasis : Group I :166 absorbable gelatin sponge and sutures Group II :154 + fibrin glue Fibrin glue can be safely used to reduce postoperative bleeding TAWFIK, Egypt 2003 Group of 250 outpatient clinic setting OAC (INR 1.8-4) and local haemostatic measures were used. Difference of bleeding complications P= 0.7 ZANON 2003

32. Bridging Therapy Long-term OAC therapy Elective surgical procedure. Retrospective analysis of either IV UH or LMWH The rates of adverse events (thromboembolic event, major and minor bleeding) NSS (p = 0.67). Costs were significantly lower in LMWH ACCP 2004 Large, prospective cohort studies Procedures with a high bleeding risk will necessitate temporary discontinuation of OAC. Bridging therapy with shorter-acting anticoagulants, UFH OR LMWH Curr Hematol Rep. 2005 Alex C

33. RECOMMENDATIONS Anticoagulation does not need to be stopped for patients in therapeutic range, i.e. INR <3. Mechanical pressure Minimize trauma. Fibrin, Gelatin sponge Gauze saturated with tranexamic acid Tranexamic acid mouthwash Silk suture made on case-by-case

34. ThAnk YOu