Anticoagulation In Dental Procedures Galila Zaher MRCPath KAU Assistant Professor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Haemostasis: generation of thrombin and clot formation

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.

Dental extractions Bleeding Thrombosis

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

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)

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

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 < update Evid Based Dent 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 NovNick Malden

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

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 Alex C

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

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