ppt on clotting factors and dental procedures

1. COAGULATION FACTORS
AND
DENTAL PROCEDURES
N.Narmadha

2. INTRODUCTION:
• Coagulants promote coagulation - haemorrhagic states.
• Haemostasis 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. PROTHROMBINTIME
CLOTTINGTIME
BLEEDINGTIME

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

9. 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).

10. 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

11. 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.

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

13. STAGES OF NORMAL HAEMOSTASIS (Davidson)
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

14. PATHWAYS OF COAGULATION MECHANISM :
Blood substances
Prothrombin activator.
Blood clotting
Occurs through two pathways.
1.Intrinsic pathway
2.Extrinsic pathway.

16. 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

17. 􀂂 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.

18. HAEMOPHILIA (Bleeder’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.

19. 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.

20. CLINICAL FEATURES:
• PREVALANCE- Males, 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.

21. 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’.

22. DIAGNOSIS:
• Clinical history.
• Family history - bleeding response to minor traumatism ,or dental
manipulations
• Definitive 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.

23. MANAGEMENT:
• Protect from traumatic injuries.
• Minor operation considered as major one and
performed in hospital.
• Preoperative transfusion of whole blood .
• Administration of antihemophilic factor concentrate .
• Antifibrinolytic agents and desmopressin (DDAVP).
• Replacement therapy.
• Gene therapy.

24. 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.
• Inhalatory 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.

25. DENTAL CONSIDERATIONS:
• Mild to moderate hemophilia- noninvasive treatments -
antifibrinolytic coverage.
• Oral cleaning procedures ,minor surgery - DDAVP.
• Severe hemophilia - factor VIII .IX,XI replacement .

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

27. 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.
• Inherited defect in the quality and quantity of vWF.
• Mutation, insertion,deletion at the vWF locus on a gene on
chromosome 12p .

28. 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.

29. CLINICAL FEATURE:
• Positive 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.

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

31. DIAGNOSIS:
• Coagulation 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.

32. 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

33. • 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

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

35. 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.

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

37. 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.

38. • If heavier bleeding - treatment suspended for a day, with dental
treatment taking place the day after.
• No need to modify anticoagulant therapy provided the INR is 4 or
lower, since bleeding be controlled with local measures.

40. DENTAL PROCEDURES:
Hemophilia:
Severity of hemophilia - correlates with factor VIII level of the plasma.
Normal plasma contains 1 unit of factor VIII per ml (100%).
Management:
Factor 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%

41. • Average 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.
• Achieved by repeated bolus injections every 12 hours or by
continuos infusion.

42. 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.

43. Restorative procedures:
• Metal 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.

44. 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.

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

46. 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.

47. OPERATION FACTOR VIII
LEVEL
REQUIRED
PREOPERATIV
ELY GIVEN
POATOPERATI
VE SHEDULE
Dental
extraction,dentoalv
eolar,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.

48. 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

49. INVESTIGATIONS :

50. Thank you