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BLEEDING AND
CLOTTING DISORDERS
RESOURCE FACULTY
DR.JYOTSNA RIMAL
Additional professor & HOD
DR.ICHHA KUMAR MAHARJAN
Associate professor
ORAL CONSIDERATION &LABORATORY INVESTIGATIONS OF
PRESENTER:KASHMIRA POKHREL483BDS-2011
Department of oral medicine and radiology
CONTENTS
• PATHOPHYSIOLOGY• BLEEDING DISORDERS• COAGULATION DISORDERS• LABORATORY INVESTGATIONS• ORAL MANIFESTATIONS• DENTAL CONSIDERATION• DENTAL MANAGEMENT• CONCLUSION
PATHOPHYSIOLOGY
• Hemostasis can be divided into 4 phases:
• Vascular phase
• Platelet phase
• Coagulation cascade phase
• Fibrinolytic phase
Principal mechanisms that prevent or diminish the loss of blood following vascular injury
VASCULAR PHASE
Tissue injury
Vasoconstriction of the microvascular bed
Serotonin, histamine,PG’s
PLATELET PHASECirculating platelets exposed to
vascular injury
Normal vWF, endothelial cells, collagen, basement membrane, elastin, microfibrils and other cellular debris
Physical and chemical changes
Aggregation of platelet
Primary platelet plug (adheres to basement membrane)
ADP
Increase in size of plug
PF-3
Activates F-X Conversion of prothrombin to thrombin
Platelet intermixed with other cellular components(RBC,WBC) which further contracts to reduce bleeding and seal vascular bed
COAGULATION CASCADE
FIBRINOLYTIC PHASE
• VESSEL WALL DISORDERS
• PLATELET DISORDERS
• COAGULATION DISORDERS
CLASSIFICATION
• Scurvy
• Cushing’s syndrome
• Ehlers-Danlos syndrome
• Rendu-Osler-weber syndrome
VESSEL WALL DISORDERS
• Thrombocytopenic(quantative platelet deficiency)
1.May-hegglin anomaly
2.Wiskott-aldrich syndrome
3.Neonatal alloimmune thrombocytopenia
• Nonthrombocytopenic(qualitative)
1.Glanzmann’s thromasthenia
2.Platelet type vWD
3.Bernard-soulier syndrome
CONGENITAL
PLATELET DISORDERS
ACQUIRED • Thrombocytopenic(quantitative)
1. Autoimmune or idiopathic thrombocytopenia purpura
2. Thrombotic thrombocytopenia purpura
3. Cytotoxic chemotherapy
4. Drug-induced (eg, quinine, quinidine, gold salts, trimethoprim/ sulfamethoxazole, rifampin)
5. .Leukemia
6.Aplastic anemia
7.Myelodysplasia
8.Systemic lupus erythematosus
9.Associated with infection: HIV, mononucleosis, malaria
10.Disseminated intravascular coagulation
• Nonthrombocytopenic
(qualitative)
1. Drug induced(aspirin,NSAIDS,penicillin,cephalosporin)
2. Uremia
3. Alcohol dependency
4. Liver disease
5. Myeloma
6. Acquired platelet type vWD
• CONGENITAL COAGULOPATHIES1. Hemophilia A&B
2. Factors deficiency
3. von Willebrand’s disease
• ANTICOAGULANT -RELATED COAGULOPATHIES1. Heparin
2. Coumarin
• DISEASE-RELATED COAGULOPATHIES1. Liver disease
2. Vitamin K deficiency
3. Disseminated intravascular coagulation
4. Fibrinolytic disorders
COAGULATION DISORDERS
• History taking
• Physical examination
• Laboratory Investigations
• Observation
IDENTIFICATION OF PATIENT WITH BLEEDING DISORDER
HISTORY TAKINGH/O frequent• epistaxis,
• spontaneous gingival and mucosal bleeding,
• prolonged bleeding from superficial cuts
• Excessive menstrual flow
• Easy bruising
• hematuria
CONTD….• Family history
• Past H/O bleeding after surgical procedures
• Identification of medicine(heparin, aspirin, NSAIDS,coumarin, cytotoxic chemotherapy)
• Active medical conditions (hepatitis,cirrhosis,renal disease, hematological malignancy, thrombocytopenia)
• H/O heavy alcohol intake
Physical examination
• Jaundice
• Petechiae
• Ecchymosis
• Hemarthrosis
Laboratory investigations
• Normal 150,000-450,000/mm3• Spontaneous clinical hemorrhage - <10,000
to 20,000 mm3• Surgical/traumatic hemorrhage-<50,000mm3
• Normal- 1 to 6 minutes• Prolonged - >15 minutes• Test platelet and vascular phase
1. Platelet count
2. Bleeding time
Prothrombin time and INR
• Normal PT-11 to 13 seconds• Evaluates extrinsic coagulation and F-
I,II,V,VII and X• Now reported with it’s INR
INR(international normalised ratio)
• It’s the ratio of PT that adjusts for the sensitivity of the thromboplastin reagants,
• such that normal coagulation profile is reported as an INR of 1.0
aPTT(activated partial thromboplastin time)
• Activator – rare earth • Measures effectiveness of the intrinsic
pathway• Considered normal if the control aPTT
& test aPTT are within 10 secs of each other.
• Control aPTT = 15-35secs.• It is altered in hemophilias A & B. and
with the use of heparin.
• Tests ability to form initial clot from fibrinogen
• Normal - 9 to 13 seconds
• Evaluates the presence of D-dimer of fibrinogens
TT(Thrombin Time)
Fibrin Degradation products
• Normal-60 to 150%
• Torniquet test to assess Rumpel-leede phenomenon
Factor assays
Tests of capillary Fragility
Bleeding Disorder Platelet Count
PT/ INR aPTT BT
Thrombocytopenia Leukemia
F VIII, IX, XI deficiencyHeparin anticoagulation
F II, V, X deficiencyVitamin K deficiencyIntestinal malabsorption
F VII deficiencyCoumarin anticoagulationLiver disease
von Willebrand’s disease
DICSevere liver disease
F XIII deficiency
Vascular wall defect
↓
N
N
N
N, ↓
↓
N
N
N
N
↑
↑
N
↑
N
N
N
↑
↑
N
N, ↑
↑
N
N
↑
N
N
N
↑
↑
N
↑
Principal Agents for Systemic ManagementAgent Description Indications
Platelets 1 unit = 50 mL; may raise count by 6,000 Platelet count
• < 10,000 in non bleeding individuals• < 50,000 presurgical level• < 50,000 in actively bleeding individuals
Fresh frozen plasma
1 unit = 150–250 mLContains factors II, VII, IX, X, XI, XII, XIII and heat-labile V and VII
• Undiagnosed bleeding disorder with active bleeding• Severe liver disease
Cryo-precipitate
1 unit = 10–15 mL • Hemophilia A• von Willebrand’s disease,• when factor concentrates and DDAVP are unavailable• Fibrinogen deficiency
Factor VIII concentrate
1 unit raises factor VIII level 2%
• Hemophilia A with active bleeding• Presurgery
Factor IX concentrate
1 unit raises factor IX level 1–1.5%
Hemophilia B, with active bleeding or presurgery
Desmopressin Synthetic analogue of antidiuretic hormone0.3μg/kg IV or SC
Active bleeding or presurgery for some patients with von Willebrand’s disease,uremic bleeding of liver disease,bleeding esophageal varices
Epsilon-aminocaproic acid
Antifibrinolytic: 25% oral solution (250 mg/mL)Systemic: 75 mg/kg every 6 hours
Adjunct to support clot formation for anybleeding disorder
Tranexamic acid
Antifibrinolytic: 4.8% mouth rinse Systemic: 25mg/kg every 8 hrs
Adjunct to support clot formation for anybleeding disorder
Local hemostatic agents• ABSORBANT GELATIN SPONGE
(GELFOAM)
Dental size - 20x20x7mm3
• OXIDISED CELLULOSE
(SURGICEL)
• TOPICAL THROMBIN• Obtained from bovine plasma• Applied as dry powder or freshly prepared
solution
• TRANXENAMIC ACID• 500mg tablets• 1000mg/10ml injection
• Epsilon Amino caproic Acid• 50mg/kg• Oral rinse 250mg/ml
• Fibrin sealants/Fibrin glue• Cryoprecipitate• 10,000units thrombin powder• 10ml saline• 10ml Calcium Chloride
• Application of local pressure
• suture
Clinical features of bleeding disorders
Feature Vascular or platelet disorders
Coagulation disorders
Bleeding from superficial cuts and scratches
Persistent,often profuse Minimal
Delayed bleeding Rare Common
Spontaneous gingival bleeding
Characteristic Rare
Petechiae Characteristic Rare
Ecchymoses Small and multiple Large and solitary
Epistaxis Common Common
Deep disecting hematomas
Rare Characteristic
Hemarthroses Rare Characteristic
Oral manifestations • Petechiae
• Ecchymoses
• Spontaneous gingival bleeding
Contd….
• Brown colored teeth due to depositsof hemosiderin as a result of continous long term bleeding.
• Hemarthrosis (rarely)
DENTAL MANAGEMENT
• Dental modifications required for the patient depends on
1. type and invasiveness of the dental procedure and
2. Type and severity of bleeding disorder
• For reversible coagulopathies:
Remove the causative agent (eg:coumarin anticoagulants)
Treat the primary illness or defect to allow pt. to return to manageable bleeding risk for the dental treatment period
For irreversible coagulopathies:
Defective element may need to be replaced from exogenous source
Consultation with hematologist
This may involve treatment either in specialized hospital facilities or local general dentist’s office
PLATELET DISORDERS• Platelet level >50,000mm3 required prior to
surgical procedures.
• Avoidance of aspirin therapy recommended 1 week prior to extensive oral surgical procedures
• Aspirin is rarely witheld in case of minor oral surgical procedures such as extraction where local hemostatic agents can be use
• When extensive surgery in emergency is indicated DDAVP can be used
• DDAVP decreases the aspirin induced prolongation of BT and prevents post operative oozing
Considerations in
HEMOPHILIA A and B and vWD
ORAL SURGICAL PROCEDURES
• Surgical treatment, including a simple dental extraction, must be planned to minimize the risk of bleeding, excessive bruising, or hematoma formation.
• Emergency surgical intervention in dentistry is rarely required as pain can often be controlled without resorting to an unplanned treatment.
• All treatment plans must be discussed with the hemophilia unit if they involve the use of prophylactic cover.
PREVENTIVE AND PERIODONTAL THERAPY
• Periodontal probing and supragingival scaling can be done routinely
• Severly inflamed and swollen tissues are best treated initially with chlorhexidine oral rinses and gross debridement with hand instruments to allow gingival shrinkage
• Deep subgingival scaling and root planing should be performed quadrant wise
• Locally applied pressure and post-treatment anti-fibrinolytics oral rinses are successful in controlling protracted oozing.
• Periodontal surgical procedures requires prior elevation of circulating factor levels by 50% and use of post treatment antifibrinolytics.
RESTORATIVE AND PROSTHODONTIC THERAPY
• Rubber dam isolation advised to minimize the risk of lacerating soft
tissue and avoid creating ecchymoses and hematomas
with high speed evacuators or saliva ejectors
• Removable prosthodontic appliances can be fabricated without complications
Denture trauma should be minimized
ENDODONTIC THERAPY• Instrumentation should not extend beyond
apex
• Filling beyond the apical seal also should be avoided
• Application of epinephrine intrapulpally to apical area provides hemostasis
PEDIATRIC DENTAL THERAPY• Administration of factor concentrate before
extraction
• Pulpotomies to be performed without excessive pulpal bleeding
• Topical fluoride application
• Pit and fissure sealant
ORTHODONTIC THERAPY• Care must be taken to avoid mucosal
laceration by orthodontic bands, brackets and wires.
• Fixed orthodontic appliance prefered over removable functional appliance
• Use of extraoral force and
• shorter treatment duration
PAIN CONTROL• Selection of pain control method based on
patient’s pain threshold and invasiveness of the procedure
• Hypnosis, IV diazepam, nitrous oxide/oxygen analgesia can be used
• Anesthetic with vasoconstrictor should be used when possible
• Hemostatic cover(20-30%) required for: inferior alveolar ,posterior superior
alveolar,infraorbital, lingual and long buccal nerve block
As these injections place anesthetic solutions in highly vascularised loose connective tissue with no distinct boundaries where formation of dissecting hematoma is possible
• Hemostatic cover not required for:Intrapulpal, periodontal ligament, gingival
papillary anesthesia
In mild disease-buccal, labial and palatal infiltration for maxillary teeth can be attempted slow injection and local pressure for 3-4 minutes
PATIENTS ON ANTICOAGULANTS
• Higher INR result in high bleeding risk
• Non surgical dental treatment can be successfully accomplished without alteration of anti coagulant regimen
• For surgical procedures, physician consult is advised
• Thromboembolic complication is small and hemorrhagic risk is high coumarin therapy can be discontinued 2 days prior to surgery with prompt reinstitution post operatively.
• Moderate thromboembolic and hemorrhagic risks-coumarin therapy can be maintained within therapeutic range and local measures used to control postoperative oozing
• High thromboembolic and hemorrhagic risk-requires hospitalization
Managed with combination unfractioned heparin-coumarin method
Coumarin is withheld 24 hrs prior to surgeryHeparin therapy instituted on admission is
stopped 6-8 hours preoperativelyCoumarin reinstituted on the night of the
procedure heparin reinstituted 6-8 hrs after surgery
when adequate clot has formed
• Use of aditional hemostatic agents recommended
CONCLUSION• Pre-operative assessment:
– Proper history• Medical history• Family history• Drug intake history
• General physical examination
• Oral examination
• Lab investigations– Full blood count,platelet count– PT and INR– APTT– TT– Serum for blood grouping and cross-matching
• Assess if hemostatic cover is required
• Consult with patient’s physician for drugs like aspirin, warfarin to be discontinued before procedure
• Warn the patient about intra and post operative bleeding
• Consider using antifibrinolytic agents a day before the surgery
• Peri-operative procedure:– The factor that is deficient must be
arranged
– Local hemostatic agents should be used
– Bleeding must be controlled
• post-operative care:
– Prevention of infection
– Management of post-operative bleeding• Tranxenamic acid can be used
– Reinstitution of the oral anticoagulants
MCQ
Which of the following phase does not prevent bleeding?
a) Vascular phase
b) Platelet phase
c) Coagulation phase
d) Fibrinolytic phase
Hemostatic cover is required in patients with bleeding disorder in following
anesthetic techniques:
a)Inferior alveolar nerve block
b)Buccal infiltration
c)Lingual nerve block
d)a and c both
e)All of the above
When extensive surgery is indicated aspirin should be
avoided prior toa) 2 days
b) 24 hours
c) 7 days
d) Not required
Patients on anti-coagulant therapy with high thromboembolic and
hemorrhagic risk is managed bya) coumarin therapy can be discontinued 2
days prior to surgery
b) combination unfractioned heparin-coumarin method
c) Aspirin therapy
d) None
References
• Burket’s Oral Medicine - 1Oth&11th Edition
• Textbook of oral medicine -2nd Edition ByAnil Ghom
• Davidson’s principles and practice of medicine- 20th Edition
• Medical problems in dentistry-6th Edition-crispian scully