COAGULATION FACTORS AND DENTAL PROCEDURES

ppt on clotting factors and dental procedures

1. COAGULATION FACTORS AND DENTAL PROCEDURES N .Narmadha

2. INTRODUCTION: Coagulants promote coagulation - haemorrhagic states. H aemostasis and blood coagulation - complex interactions between the injured vessel wall , platelets and coagulation factors. COAGULATION DEFINITION: Coagulation or clotting is defined as the process in which blood loses its fluidity and becomes a jelly like mass few minutes after which its is shed out. The process by which blood clots to form solid masses or clots.

3. Bleeding time: Time interval from oozing of blood after a cut or injury till arrest of bleeding. Clotting time: Time interval from oozing of blood after a cut or injury till the formation of clot. Prothrombin time: Time taken by blood to clot after adding tissue thromboplastin to it. Thrombin time: Time between the addition of the thrombin and the clot formation .

4. PROTHROMBIN TIME CLOTTING TIME BLEEDING TIME

5. COAGULATION FACTORS: Coagulation of blood - activation of a group of substances - clotting factors . SYNTHESIS : Liver . v WF - endothelial cells & platelets LOCATION: Plasma (zymogen). Tissue factor - does not circulate in blood. Partial proteolysis - activate the next factor .

6. Factor I - Fibrinogen Factor II - Prothrombin Factor III - Tissue Thromboplastin/Tissue Factor Factor IV - Calcium Ions Factor V - Labile Factor/Pro Accelarin /Accelerator Globulin Factor VII - Stable Factor. Factor VIII- Anti hemophilic Factor/AH Globulin Factor IX - Christmas Factor /Plasma Thromboplastin Component Factor X - Stuart – Prower Factor. Factor XI - Plasma Thromboplastin Antecedent Factor XII – Haegman Factor/Contact Factor. Factor XIII –Fibrin Satabilising Factor( fibrinase ) .

7. FACTOR METABOLISM FUNCTION DISORDERS I FIBRIN Forms mesh around the wound leading to blood clot Afibrinogenemia Hypofibrogenemia Hyperfibrinogenemia II THROMBIN -Convert fibrinogen to fibrin. -Activate factors I,V, VII,VIII,XI &XIII Hemmoraghic diathesis Dysprothrombinemia Hypoprothrombenimia III -Initiates extrinsic pathway. -High affinity receptor for VII. -Acts as cofactor V Acts as cofactor Parahemophilia Myocardial infarction Deep vein thrombosis

8. FACTOR METABOLISM FUNCTION DISORDERS VII Acts as cofactor (IX, X) Epitaxis,Menorrhagia Hematomas,Hemarthrosis Cerebral hemmorhages VIII Cofactor for X Hemophilia A. IX Cofactor for X Hemophilia B X Xa Bleeding diathesis Hemorhages.Epitaxis GI bleeds,hemarthrosis XI Hemophilia c XII XIIa Activates factor XI & prekallikrein . XIII XIIIa Lifelong bleeding diathesis,intercranial bleeding and death.

9. ROLE OF COAGULATION SYSTEM: C onversion of plasma fibrinogen into solid mass of fibrin . I nvolved in both haemostatic process and thrombus formation. Complex interactions between the vascular endothelium , platelets, coagulation factors, natural anticoagulants & fibrinolytic enzymes. Dysfunction - haemorrhage or thrombosis.

10. STAGES OF NORMAL HAEMOSTASIS ( D avidson) STAGE I :Pre injury conditions STAGE II :VASOCONSTRICTION. Early hemostatic response , platelets adhere ,coagulation is activated. STAGE III: Fibrin clot formation,platelets become activated and aggregate. STAGE IV: Limiting clot formation. STAGE V: Fibrinolysis

11. PATHWAYS OF COAGULATION MECHANISM : B lood substances Prothrombin activator. Blood clotting O ccurs through two pathways. 1.Intrinsic pathway 2.Extrinsic pathway.

12. APPLIED PHYSIOLOGY: COAGULATION DISORDERS: Inherited Acquired A ) CONGENITAL 􀂂 Hemophilia A 􀂂 Hemophilia B or Christmas disease (factor IX deficiency) 􀂂 Von Willebrand disease (alteration of factor VIII) 􀂂 Fibrinogen alterations 􀂂 Prothrombin (factor II) deficiency 􀂂 Factor V,VII,X,XI,XII deficiency

13. 􀂂 Combined deficiency of vitamin K-dependent factors (VII, IX,X) 􀂂 Combined deficiency of factors V and VIII 􀂂 Combined deficiency of factors VII and VIII 􀂂 Combined deficiency of factors II, VII, IX and X, and C protein. B) ACQUIRED 􀂂 Liver diseases 􀂂 Vitamin K deficiency: 􀂂 Acquired anticoagulants 􀂂 Disseminated intravascular coagulation (DIC) 􀂂 Primary fibrinogenolysis 􀂂 Anticoagulant drugs .

14. HAEMOPHILIA ( B leeder’s disease, Disease of the hapsburg , The disease of kings): Definition : It is a hereditary blood disorder characterised by a deficiency in the activation of coagulation factor VIII, IX, XI in plasma with normal vWF . Etiology : Sex linked inherited disorder. . Severe hemophilia A, –inversion mutation- on long arm of the X chromosome in bands q28. Hemophilia B-partial or total deletions - on long arm of the X chromosome in bands q27 . Hemophilia C-mutation on chromosome 4 .

15. S.NO TYPES CLOTTING FACTOR DEFICIENCY I HEMOPHILIA A VIII 2 HEMOPHILIA B IX 3 HEMOPHILIA C XI CLASSIFICATION FACTOR ACTIVITY(% ) CAUSES OF HEMORRHAGE Mild > 5 Major trauma or surgery moderate 1-5 Mild to moderate trauma severe <1 Spontaneous hemarthrois,soft tissue bleeding.

16. CLINICAL FEATURES: PREVALANCE- M ales, females are carriers. Persistent bleeding, Haemmorhage into subcutaneous tissues , internal organs, joint –hematomas. Spontaneous cyclic remissions and exacerbations . Petechia usually do not occur . Hemophilia C- absence of bleeding into joints and mucles and occurrence in either genders.

17. ORAL MANIFESTATIONS: Common finding- Hemmorhage . Massive and prolonged gingival hemmorhage . Even physiologic process of tooth eruption and exfoliation occurs with severe prolonged hemmorhage . Mandibular ‘ pseudotumor ’.

18. DIAGNOSIS: Clinical history. Family history - bleeding response to minor traumatism ,or dental manipulations D efinitive diagnosis - quantitation of pro coagulant activity of VIII(REDUCED). DNA analysis - detect carriers and establish prenatal diagnosis. LABORATARY FINDINGS: Coagulation time activated partial thromboplastin time Normal - bleeding time ,prothrombin time, platelet aggregation .

19. MANAGEMENT: Protect from traumatic injuries. M inor operation considered as major one and performed in hospital. Preoperative transfusion of whole blood . A dministration of antihemophilic factor concentrate . Antifibrinolytic agents and desmopressin (DDAVP ). Replacement therapy. Gene therapy.

20. Desmopressin (DDAVP ): synthetic vasopressin analog endothelial cells FVIII and vWF platelet adhesion. Dose - 0.3-0.4 μg /kg iv infusion - 30 minutes / subcutaneous injection. I nhalatory route - 300 μg in adults & 150 μg in children. Antifibrinolytic agents: Routes - oral, intravenous or topical . EACA -300 mg/kg/day in fractions every 4-6 hours; AMCHA 30 mg/kg/day in 2-3 daily doses .

21. DENTAL CONSIDERATIONS: Mild to moderate hemophilia - noninvasive treatments - antifibrinolytic coverage. O ral cleaning procedures , minor surgery - DDAVP . S evere hemophilia - factor VIII .IX,XI replacement .

22. Anesthetic block / IM inj - not carried if (FVIII < 50% ). Preceded by replacement therapy. Infiltrating pericemental and intrabony injections - preferred . PROGNOSIS : N ow able to lead a normal life with few restrictions . Prognosis is variable , many affected persons die during childhood.

23. VON WILLEBRAND’S DIESEASE: ( pseudohemophilia ,vascular hemophilia,vascular purpura) Most common hereditary hemorrhagic disorder in humans and is characterized by a prolonged bleeding time with low FVIII titers ETIOLOGY : vWF deficit or dysfunction . I nherited defect in the quality and quantity of vWF . Mutation, insertion,deletion at the vWF locus on a gene on chromosome 12p .

24. CLASSIFICATION: Type 1:Partial quantitative decrease of normal vWF and factor VIII. Type 2:Qualitative defects of vWF . Autosomal dominant or recessive. Type 3:Marked deficiencies of both vWF & factor VIII in plasma. Common in consanguineous marriage.

25. CLINICAL FEATURE: P ositive family history. Minor trauma -Excessive bleeding, Mucosal membrane bleeding -gingival hemorrhage , epistaxis. Hemarthrosis and musculoskeletal bleeding - more severe forms. Spontaneous nosebleeds & cutaneous ecchymoses . ORAL MANIFESTATIONS: Gingival bleeding either spontaneous or only after brushing of the teeth.

26. LABORATORY FINDINGS: Normal -platelet count, clotting time, serum fibrinogen,prothrombin time. Prolonged –bleeding time(over 300 min,several min,one hour)

27. DIAGNOSIS: C oagulation tests. TREATMENT: DDAVP - autologous secretion of vWF and FVIII . DDAVP - via IV infusion ,subcutaneous or nasal route . Replacement therapy: Antifibrinolytic drugs (EACA and AMCHA) via the iv,oral or topical routes. Estrogens effective for menorrhagia.

28. ACQUIRED DISORDERS LIVER DISEASE: coagulation factors production, exception of FVIII and FvW - endothelial cells. DENTAL CONSIDERATIONS : Pre-operative management: Vitamin k injection-iv 10 mg for 3 days. Fresh frozen plasma – immediately before surgery and at frequent intervals during surgery RD- 10-15 ml/kg

29. Cryoprecipitate- infusion of <100 mg/dl in a dose of one bag of cryoprecipitate per 10 kg of body weight. Intranasal desmopressin -300mcg . Anti fibrinolytics : traneximic acid -10mg/kg loading dose and repeated 3-4 /day for a total of 2-8 days. Recombinant factor VII a-40 mcg/kg

30. Intra operative management: Anesthetic management: Inhalational anesthetic agents:isoflurane,desflurane,sevoflurane and Propofol are prefered Muscle relaxant – atracurium,cisatracurium .

31. VITAMIN K DEFICIENCY : Factors II,VII , IX and X are produced in the liver cells. The most common causes of vitamin K deficiency are: Intestinal malabsorption Inadequate dietary intake liver diseases prolonged antibiotic use ( which eliminates the intestinal flora - a natural source of vitamin K2 ), insufficient ingestion of the vitamin (12 ). Management: Parentral administration of vitamin k rapidly restores vitakin k in liver.

32. DISSEMINATED INTRAVASCULAR COAGULATION (DIC): It is an acquired consumption coagulation disorder resulting from prolonged activation of the coagulation system. Result of underlying pathology. C linical problem of DIC - bleeding due to depletion ( consumption) of the coagulation factors .

33. ANTICOAGULANT DRUGS : Provided with unfractionated or standard heparin , low molecular weight heparin (LMWH) and oral anticoagulants ( coumarins ). DENTAL CONSIDERATIONS: SH countered by administering its antagonist, protamine sulfate , iv 1 mg/100 IU of heparin . Dialyzed patients SH has a half-life( 1-2 hours) ,suffices to carry out dental treatment . LMWH - dental care without changes in medication . postoperative bleeding - controlled by local measures.

34. If heavier bleeding - treatment suspended for a day, with dental treatment taking place the day after. N o need to modify anticoagulant therapy provided the INR is 4 or lower, since bleeding be controlled with local measures.

35. DENTAL PROCEDURES : Hemophilia : S everity of hemophilia - correlates with factor VIII level of the plasma. N ormal plasma contains 1 unit of factor VIII per ml ( 100%). Management: F actor VIII replacement achieved by porcine factor VIII or recombinant factor VIII. 1 unit factor VIII conc./ kg of body weight raises factor VIII by 2 %

36. A verage 70kg individual require infusion of 3500 units to raise the factor level from less than 1% to 100%. Dose to infused (units) = Weight x increment needed(u/dl) /2. Mild hemophiliacs - cover for surgery requires maintanance of normal factor VIII levels ( 1 week),followed by reduced dosage during convalascence . A chieved by repeated bolus injections every 12 hours or by continuos infusion.

37. Adjunct therapy: 50 mg/kg body weight EACA orally as 25% oral rinse every six hours - 7-10 days. Tranexamic acid 10 times more potent than EACA . Pain management: Safer drugs -acetaminophen,codeine,cox-2 inhibitors. Anesthetic management: Regional LA -if VIII (30%) Infiltrations, intraligamentary,intraosseus or intrapulpal injections are still safer. Buccal infiltration used without any factor replacement.

38. Restorative procedures: M etal matrix bands & wooden wedges –risk of bleeding. Cotton rolls wetted before removal. High speed vaccum aspirators and saliva ejectors cause hemotomas - minimized by resting on gauze swab. Endodontics: Avoiding instrumentation through the periapex is of prime importance. Sodium hypochlorite – irrigation followed by calcium hydroxide paste. persistent bleeding –formaldehyde derived substances.

39. Rubber dam isolation : Surgical endodontics: Mild hemophiliacs managed without factor replacement. Desmopressin: Slow iv infusion - 20 min -0.3-0.5 µg/kg 30-60 min prior to surgery – 3 fold increase in VIII activity (9.4 h) Intranasal ly - 1.5 mg/ml. Tranexamic acid: Systemic-1g(30 mg/kg) orally qid , 1hour preoperatively. Infusions-10mg/kg in 20ml normal saline over 20 min. Then 1g tds orally – 5days. Children:20mg/kg.

40. Periodontal treatment: Supragingival scaling Treatment over several visits to prevent excessive blood loss . Chlorhexidine gluconate mouth wash used. S ubgingival scaling can be performed . Prosthodontic treatment: Dentures given. Orthodontic treatment: Can be carried out .

41. Surgical procedures: Rubber band extraction is performed. 1-3 tooth can extracted with factor replacement. Dental extraction: Factor VIII dose in units= weight in kg x 25 given 1h preoperatively . For maxillofacial surgery: Weight in kg x 50 given 1h preoperatively.

42. OPERATION FACTOR VIII LEVEL REQUIRED PREOPERATIVELY GIVEN POATOPERATIVE SHEDULE Dental extraction,dentoalveolar,periodontal surgery Min-50% at operation Factor VIII iv Tranexamic acid 1g iv (or orally 24h pre op) Soft diet ; 10 days –tranexamic acid 1gqid .if bleeding continues,repeat the dose of VIII Maxillofacial surgery 100% at operation. 50% postoperatively Factor VIII( iv) Soft diet. twice daily (iv) – VIII -7-10 days.

43. METHODS OF ACHIEVING HAEMOSTASIS : 1.MECHANICAL METHODS: Pressure Hemostat Sutures and ligation 2.Chemical methods: Adrenaline Thrombin Surgicel Surgicel fibrillar Oxycel Gelatin sponge:gelfoam / surgifoam Microfibrillar collagen( avitene ) Fibrous glue Styptics and astringents Alginic acid. Natural collagen sponge Fibrin sponge Bone wax Ostene -new water soluble hemostatic agent. 3.Thermal agents

44. INVESTIGATIONS :

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