This document discusses hematology disorders and their management in dental treatment. It begins by explaining the mechanisms of hemostasis and then discusses common causes of bleeding disorders including issues with platelets, thrombocytopenia, and coagulation disorders. It describes how to evaluate patients for bleeding risks through medical history, exam, and screening tests. Based on risk levels, the document outlines dental management strategies such as replacement therapies, antifibrinolytic medications, local hemostatic methods, and considerations for patients on anticoagulants like heparin or coumadin. Specific conditions like thrombocytopenia and hemophilia are also covered.

1. Hematology disorder in dental treatmentHematology disorder in dental treatment
指導老師指導老師 :: 高壽延主任高壽延主任
雷文天醫師雷文天醫師
報告者報告者 :: 林鈞盛林鈞盛
2003/07/182003/07/18

2.  1. Hemostasis mechanism1. Hemostasis mechanism
 2. Etiology of bleeding disorder2. Etiology of bleeding disorder
 3. Evaluation of bleeding disorders3. Evaluation of bleeding disorders
 4. Dental management of bleeding disorders4. Dental management of bleeding disorders
 5. Summary5. Summary

3. Hemostasis :Hemostasis :
 1. Vascular wall integrity1. Vascular wall integrity
 2. Adequate numbers and proper functional platelets2. Adequate numbers and proper functional platelets
 3. Intact coagulation mechanisms3. Intact coagulation mechanisms
 4. Fibrinolytic system4. Fibrinolytic system

4. Hemostasis:Hemostasis:
 1. Vascular phase : vasoconstriction1. Vascular phase : vasoconstriction
 2. Platelet phase : adhesion & aggregation2. Platelet phase : adhesion & aggregation
 3. Coagulation phase : extrinsic & intrinsic pathways3. Coagulation phase : extrinsic & intrinsic pathways

5. Hemostasis:Hemostasis:
 The intrinsic pathway :The intrinsic pathway :
Initiated through surface contact activation of factor XIIInitiated through surface contact activation of factor XII
by exposed subendothelial tissues--collagenby exposed subendothelial tissues--collagen
 The extrinsic pathway :The extrinsic pathway :
Initiated through tissue thromboplastin released byInitiated through tissue thromboplastin released by
injured tissue, which activates factor VIIinjured tissue, which activates factor VII

6. Intrinsic
Surface contact
Factor XII Factor XIIa
Factor XI Factor XIa
Factor IX Factor IXa
Ca++
phospholipid
Extrinsic
Tissue damage
Tissue factor +
Factor VII
Ca++
Factor X Factor Xa
Ca++ phospholipid
Prothrombin (II) Thrombin (IIa)
Fibrinogen
(I)
fibrin
Transformation
catalysis
Common
pathway

7. Etiology of bleeding disorder :Etiology of bleeding disorder :
 1. Nonthrombocytopenia1. Nonthrombocytopenia
 2. Thrombocytopenia purpuras2. Thrombocytopenia purpuras
 3. Disorders of coagulation3. Disorders of coagulation

8. Etiology of bleeding disorder :Etiology of bleeding disorder :
 NonthrombocytopeniaNonthrombocytopenia
1. vascular wall alteration : infection, chemical, allergy1. vascular wall alteration : infection, chemical, allergy
2. Disorder of platelet function :2. Disorder of platelet function :
Genetic defects (bernard-soulier disease)Genetic defects (bernard-soulier disease)
Aspirin, NSAIDs, broad-spectrum antibioticsAspirin, NSAIDs, broad-spectrum antibiotics
Autoimmue diseaseAutoimmue disease

9. Etiology of bleeding disorders :Etiology of bleeding disorders :
 Thrombocytopenia purpurasThrombocytopenia purpuras
1. primary1. primary
2. secondary : Chemicals2. secondary : Chemicals
Physical agent (radiation)Physical agent (radiation)
Systemic disease (leukemiaSystemic disease (leukemia))

10. Etiology of bleeding disorders :Etiology of bleeding disorders :
 Disorders of coagulationDisorders of coagulation
1. Inherited : Hemophilia A1. Inherited : Hemophilia A
Christmas diseaseChristmas disease
2. Acquired : Liver disease2. Acquired : Liver disease
Vitamin K deficiencyVitamin K deficiency
Anticoagulation drugs (heparin, coumarin)Anticoagulation drugs (heparin, coumarin)
AnemiaAnemia

11. Evaluation of bleeding disorders :Evaluation of bleeding disorders :
 1. Take history1. Take history
 2. Physical examination2. Physical examination
 3. Screening clinical laboratory tests3. Screening clinical laboratory tests
 4. Observation of excessive bleeding following a surgical4. Observation of excessive bleeding following a surgical
procedureprocedure

12. History (Symptoms) :History (Symptoms) :
 Bleeding problems in relativesBleeding problems in relatives
 Bleeding problems following operations and toothBleeding problems following operations and tooth
extractions, traumaextractions, trauma
 Use of drugs for prevention of coagulation or painUse of drugs for prevention of coagulation or pain
 Spontaneous bleeding from nose mouth etc..Spontaneous bleeding from nose mouth etc..

13. Physical examination (signs) :Physical examination (signs) :
 Jaundice, pallorJaundice, pallor
 Spider angiomaSpider angioma
 EcchymosisEcchymosis
 Oral ulcerOral ulcer
 Hyperplasia of gingivaHyperplasia of gingiva
 HemarthrosisHemarthrosis

14. EcchymosisEcchymosis

15. Screening laboratory tests :Screening laboratory tests :
 1. Platelet count1. Platelet count
 2. BT (Bleeding Time)2. BT (Bleeding Time)
 3. PT (Prothrombin Time)3. PT (Prothrombin Time)
 4. PTT (Partial Thrombopastin Time)4. PTT (Partial Thrombopastin Time)
 5. TT (Thrombin Time)5. TT (Thrombin Time)

16. Platelet count :Platelet count :
 Test platelet phase: evaluation of platelet functionTest platelet phase: evaluation of platelet function
 Normal (140,000 to 400,000/mm3)Normal (140,000 to 400,000/mm3)
 Clinical bleeding problem <50,000/mm3Clinical bleeding problem <50,000/mm3

17. BT (Ivy method) :BT (Ivy method) :
 Test platelet & vascular phaseTest platelet & vascular phase
 Normal if adequate number of platelets of good qualityNormal if adequate number of platelets of good quality
present intact vascular wallspresent intact vascular walls
 Normal (1 to 6 minutes)Normal (1 to 6 minutes)

18. PT (Prothrombin Time) :PT (Prothrombin Time) :
 Activated by tissue thromboplastinActivated by tissue thromboplastin
 Tests extrinsic (factor VII) and common (I,II,V,X)Tests extrinsic (factor VII) and common (I,II,V,X)
pathwayspathways
 Normal (11-15sec)Normal (11-15sec)
 CoumarinCoumarin therapy- PT at 1.5 to 2.5 timetherapy- PT at 1.5 to 2.5 time

19. Activated PTT :Activated PTT :
 Activated by contact activator (kaolin)Activated by contact activator (kaolin)
 Tests intrinsic and common pathwayTests intrinsic and common pathway
 Normal (25-35 sec)Normal (25-35 sec)
 HeparinHeparin therapy- PTT in 50-65 sec rangetherapy- PTT in 50-65 sec range

20. TT (Thrombin Time) :TT (Thrombin Time) :
 Activated by thrombinActivated by thrombin
 Tests ability to form initial clot from fibrinogenTests ability to form initial clot from fibrinogen
 Normal (9 to 13 seconds)Normal (9 to 13 seconds)

21. 1. No historical bleeding problem
3. Aspirin therapy
4. Coumarin therapy
6. Possible liver disease
7. Chronic leukemia
8. Long term antibiotic therapy
5. Renal dialysis (heparin)
2. History bleeding problem
9. Vascular wall alteration
10 .cancer (fibrinogenolysis)
Following surgical procedure
PT, PTT, TT, BT
BT, PTT
PT
PTT
BT, PT
BT
PT
BT
TT
Dent al management of t he medically compromised pat ient

22. condition
8. thrombocytopenia
2. Coumarin therapy
4. Liver disease
7. Vascular wall
defect
9. hemophilia
1. Aspirin therapy
Platelet count
5. leukemia
6. Long term
antibiotic
3. Heparin therapy
10. fibrinogenolysis
+
-
+
+
+
-
-
++
-
-
BT
+
-
+
+
+
-
+
++
-
-
PTT
+
++
++
++
-
++
-
-
++
+
PT
+
++
-
++
-
++
-
-
-
+
TT
-
-
-
++
-
++
-
-
-
++

23. Patient at low risk :Patient at low risk :
 1. patient with no history of bleeding disorders, normal1. patient with no history of bleeding disorders, normal
examinations, no medications associated with bleedingexaminations, no medications associated with bleeding
disorders and normal bleeding parametersdisorders and normal bleeding parameters
 2. patients with nonspecific history of excessive bleeding2. patients with nonspecific history of excessive bleeding
with normal bleeding parameters (PT, PTT, BT,with normal bleeding parameters (PT, PTT, BT,
platelet count, are within normal time)platelet count, are within normal time)

24. Patient at moderate risk :Patient at moderate risk :
 1. patients in chronic oral anticoagulant therapy1. patients in chronic oral anticoagulant therapy
(coumadin)(coumadin)
 2. patients on chronic aspirin therapy2. patients on chronic aspirin therapy

25. Patient at high risk :Patient at high risk :
 1. patients with known bleeding disorders1. patients with known bleeding disorders
ThrombocytopeiaThrombocytopeia
ThrombocytopathyThrombocytopathy
Clotting factor defectsClotting factor defects
 2. Patient without known bleeding disorders found to2. Patient without known bleeding disorders found to
have abnormal , platelet count, BT, PT, PTThave abnormal , platelet count, BT, PT, PTT

26. Dental management of bleeding disorders :Dental management of bleeding disorders :
 Replacement therapy :Replacement therapy :
1. platelet concentrate : thrombocytopenia1. platelet concentrate : thrombocytopenia
2. Fresh frozen plasma : liver disease, Hemophilia B2. Fresh frozen plasma : liver disease, Hemophilia B
3. Cryoprecipitate : Hemophilia A,3. Cryoprecipitate : Hemophilia A,
4. Factor VIII,IX concentrate4. Factor VIII,IX concentrate
 Antifibrinolytic therapy:Antifibrinolytic therapy:
1. E-aminocaproic acid (EACA, Plaslloid)1. E-aminocaproic acid (EACA, Plaslloid)
2. Tranexamic acid (AMCA, Trasamin)2. Tranexamic acid (AMCA, Trasamin)

27. Local hemostatic methods :Local hemostatic methods :
 splints, pressure packs, sutures; gelfoam with thrombin,splints, pressure packs, sutures; gelfoam with thrombin,
surgicel, oxycel, microfibrillar collagen(avitene), topicalsurgicel, oxycel, microfibrillar collagen(avitene), topical
AHFAHF

28. Heparin (anticoagulant) :Heparin (anticoagulant) :
 Antithrombin-thrombin complex , thrombinAntithrombin-thrombin complex , thrombin
 Complex inhibited (IXa, Xa, XIa, XIIa)Complex inhibited (IXa, Xa, XIa, XIIa)
 Used in deep vein thrombosis , renal dialysisUsed in deep vein thrombosis , renal dialysis
 Rapid onset, Duration 4-6hrs ( given IV)Rapid onset, Duration 4-6hrs ( given IV)
 Monitoring by PTT: 50-65 secMonitoring by PTT: 50-65 sec
 Discontinue 6 hrs before surgery then reinstitutingDiscontinue 6 hrs before surgery then reinstituting
therapy 6-12hrs post –optherapy 6-12hrs post –op
 Protamine sulfate can reverse the effectProtamine sulfate can reverse the effect

29. prothrombin thrombin
activator
Ca
Heparin-antithrombin/
thrombin complex
heparin
Fibrinogen Fibriin
Fibriin clot
Fibrinolytic agent
Plasmin (Fibrinolysin)
Blood clot lysis
Urokinase
streptokinas

30. Heparin- dental management

31. Coumarin (Vit k anatagonist) :Coumarin (Vit k anatagonist) :
 Inhibit Vit K action (Factor II,VII,IX,X)Inhibit Vit K action (Factor II,VII,IX,X)
 Used venous thrombosis, cerebrovascular diseaseUsed venous thrombosis, cerebrovascular disease
 Duration haft-life 40hrsDuration haft-life 40hrs
 Monitored by PT : INR 1.5-2.5Monitored by PT : INR 1.5-2.5
 PT>2.5, reduction coumarin dosage (2-3 days)PT>2.5, reduction coumarin dosage (2-3 days)
 Vit. K can reverse the effectVit. K can reverse the effect

32. Coumadin- dental management

33. Aspirin (antiplatelet) :Aspirin (antiplatelet) :
 Inhibit cycloxygenase, TxA2 formationInhibit cycloxygenase, TxA2 formation
 Analgesic drug impairs platelet functionAnalgesic drug impairs platelet function
 Aterial thrombosis, MIAterial thrombosis, MI
 Tests-BT,PTTTests-BT,PTT
 If tests are abnormal , MD should be consulted beforeIf tests are abnormal , MD should be consulted before
dental surgery is donedental surgery is done
 Stop aspirin for 5 days, substitute alternative drug inStop aspirin for 5 days, substitute alternative drug in
consultation with MDconsultation with MD

34. Blood endothelial cell break
Arachinoid acid
TXA2(Thromboxane)
Aspirin Cycloxygenas
e
(-)
Platelet coagulation
Thrombosis

35. Aspirin- dental management

36. Thrombocytopenia :Thrombocytopenia :
 Disease in number of circulation plateletsDisease in number of circulation platelets
 Idiopathic thrombocytopenia, secondaryIdiopathic thrombocytopenia, secondary
thrombocytopeniathrombocytopenia
 TX : is none indicated unlessTX : is none indicated unless
platelets<20000/mm3, or excessive bleedingplatelets<20000/mm3, or excessive bleeding
 TX : Steroid, platelet transfusionTX : Steroid, platelet transfusion

37. Thrombocytopenia :Thrombocytopenia :
 Gingival oozing : 1.5%H2O2 mouth riseGingival oozing : 1.5%H2O2 mouth rise
 Dental treatment (including extraction) >500,00/mm3Dental treatment (including extraction) >500,00/mm3
 Local packing with microfibrillar collagenLocal packing with microfibrillar collagen
 EACA (E-Aminocaprnic acid) : 100mg/kg orally, thenEACA (E-Aminocaprnic acid) : 100mg/kg orally, then
50mg/kg q6h for 8 days50mg/kg q6h for 8 days

38. Hemophilia :Hemophilia :
 Sex-linked recessive trait, X chromosome, maleSex-linked recessive trait, X chromosome, male
 Prolong PTT, normal BT,PTProlong PTT, normal BT,PT
 Hemophilia A (factor VIII deficiency)Hemophilia A (factor VIII deficiency)
 Hemophilia B or Christmas disease (factor IX deficiency)Hemophilia B or Christmas disease (factor IX deficiency)
 Severity of disorder : severe<1%, moderate 1-5%,Severity of disorder : severe<1%, moderate 1-5%,
mild 6-30%mild 6-30%
 TX : Replacement factors, antifibrinilytic agents, steroidsTX : Replacement factors, antifibrinilytic agents, steroids

39. Hemophilia-dental management :Hemophilia-dental management :
 Preventive dentistryPreventive dentistry
1. tooth brushing, flossing, rubber cup prophylaxis &1. tooth brushing, flossing, rubber cup prophylaxis &
topical fluoride, supragingival scalingtopical fluoride, supragingival scaling
2. without prior replacement therapy2. without prior replacement therapy
 Pain controlPain control
1. block anesthesia: factor level>50%1. block anesthesia: factor level>50%
2. Avoid aspirin, NSAIDs2. Avoid aspirin, NSAIDs

40. Hemophilia-dental management :Hemophilia-dental management :
 Orthodontic treatment :Orthodontic treatment :
1. no contraindication, well-motivated patients1. no contraindication, well-motivated patients
2. care with placement of bands and wires2. care with placement of bands and wires
 Operative dentistryOperative dentistry
1. rubber dam to protect tissue against accidental1. rubber dam to protect tissue against accidental
lacerationlaceration
2. wedges should be place to protect and retract2. wedges should be place to protect and retract
papillapapilla

41. Hemophilia-dental management :Hemophilia-dental management :
 Pulp therapyPulp therapy
1. Preferable to extraction1. Preferable to extraction
2. Avoid overinstrumentation and overfilling2. Avoid overinstrumentation and overfilling
 Periodontal therapyPeriodontal therapy
1. no contraindication of probing and supragingival1. no contraindication of probing and supragingival
scalingscaling
2. deep scaling, curettage, surgery need replacement2. deep scaling, curettage, surgery need replacement
therapytherapy

42. Hemophilia-dental management :Hemophilia-dental management :
 Oral surgery :Oral surgery :
1. Dental extraction: 40%-50% level1. Dental extraction: 40%-50% level
2. Maxillofacial surgery (including surgery2. Maxillofacial surgery (including surgery
extraction of impaction teeth): 80-100%extraction of impaction teeth): 80-100%
3. Antifribrinilytic therapy & local hemastatic3. Antifribrinilytic therapy & local hemastatic
measuremeasure
4. do not open lingual tissue in lower molar regions to4. do not open lingual tissue in lower molar regions to
avoid hemorrhage track down a endanger airwayavoid hemorrhage track down a endanger airway

43. Summary :Summary :
 History, PE, Lab dataHistory, PE, Lab data
 Consultation with physicianConsultation with physician
 Antibiotics to prevent post-op infectionAntibiotics to prevent post-op infection
 Avoid aspirin and NSAIDsAvoid aspirin and NSAIDs
 Local hemostatic measure in very importantLocal hemostatic measure in very important

44. Thanks for your attention !!!Thanks for your attention !!!