BLEEDING &CLOTTING

DISORDERS
Presented by
Dr. R.Sangeetha
I yr pg
CONTENTS
1. Introduction
2. Hemostasis
3. Classification
4. Investigations
5. Dental consideration
6. Conclusion
 INTRODUCTION
• Hemostasis is the process by which bleeding is arrested after injury to blood vessels by
forming a clot
• Functions
– To maintain the blood in the fluid state
– To prevent clots in intact vessels
– To arrest bleeding in the vessels

• Components
– Blood vessels
– Platelets
– Clotting factors
– Fibrinolytic system
NORMAL HEMOSTASIS

• Healthy endothelium prevents the adhesion of

platelets by release of NO, prostacyclin and
ADP phosphatases.
HEMOSTASIS
• Vascular phase
• Platelet phase
• Coagulative phase
• Fibrinolytic phase
Vascular phase-
vasoconstriction

Platelet phase
Platelets adhere to form a
primary hemostatic plug

Coagulative phase
Clotting factors gets activated
and forms the secondary
hemostatic plug. 2 pathways

Fibrinolytic phase – clot

disintegration and vessel wall
repair
COAGULATION
CASCADE
• Coagulation involves a series
of protease reactions
• Conversion of soluble
fibrinogen into insoluble fibrin
• Fibrin and platelets together
forms the secondary
hemostatic plug.
FIBRINOLYTIC CASCADE
• Dissolves fibrin
• Clot dissolution
• Plasminogen is
precursor of plasmin
which breaks fibrin
CLASSIFICATION OF BLEEDING DISORDERS
• Vascular disorders
• Platelet disorders
• Coagulation disorders
• Combination of the above
Clinical
features
 DIFFERENCE BETWEEN BLEEDING AND
CLOTTING DISORDERS
Bleeding disorders Clotting disorders
Platelet and vascular Clotting factors
Bleeding from superficial cuts persistent and profuse Minimal

Spontaneous gingival bleeding Characteristic Rare

Petechiae Characteristic Rare

Ecchymosis Usually small and multiple Usually large and single
Epistaxis Common Common
Hemarthroses Rare Charateristic
Deep dissecting hematoma Rare Characteristic
Torniquet test Positive Negative
Applying pressure May stop bleeding Bleeding reoccurs
LAB INVESTIGATIONS
Platelet function Blood coagulation
• Platelet count • Clotting time
• Bleeding time • Prrothrombin time
• Platelet aggregation test • Activated partial thromboplatin
time
• Platelet adhesion test
• Fibrinogen levels
• Capillary fragile test for vascular
function • Fibrin degradation products
• Coagulation factors assay
BLEEDING TIME
• Time required for a standardised wound to stop bleeding
• Used to check functions of platelets and capillaries
• Normal – 1 to 6 min (modified ivy’s method)
• Increased in
– Thrombocytopenia
– Von willebrand disease
– Vascular abnormalities
– DIC
CLOTTING TIME
• Time required a sample of blood to coagulate invitro
• Normal – 1to 8 minutes
• Increased in haemophilia
PROTHROMBIN TIME & INR
• Normal PT 11 to 13 sec
• INR is introduced by WHO in 1983
• Calculation made to standardise prothrombin time
• Ratio of PT that adjusts for the sensitivity of the thromboplastin reagents, such
that a normal coagulation profile is reported as an INR of 1.0.
• evaluates the extrinsic coagulation system and measures the presence or absence
of clotting Fs I, II, V, VII, and X.
• used to measure the effects of coumarin anticoagulants and reduction of the
vitamin K–dependent Fs II, VII, IX, and X.
INR – PATIENT PT/ *ISI
CONTROL PT

INR ratio
1 Ideal
2 to 3 Therapeutic range of coumadin
Below 2 Associated with minimal
bleeding
3 to 4.5 Associated with severe
bleeding
ACTIVATED PARTIAL THROMBOPLASTIN TIME
• Evaluate the intrinsic pathway and common pathway
• It measures the time (in seconds) needed for the plasma to clot after
the addition of kaolin, cephalin, and Ca2+.
• Normal APTT is 15 to 35 sec
• prolonged only when the factor levels in the intrinsic and common
pathways are less than about 30%.
• It is altered in hemophilias A and B and with the use of the
anticoagulant heparin
THROMBIN TIME
• The TT is used specifically to test the ability to form the initial clot
from fibrinogen and is considered normal in the range of 9 to 13
seconds.
• Additionally, it is used to measure the presence of heparin

FIBRIN DEGRADATION PRODUCT ASSAY

• FDPs are measured using a specific latex agglutination system to
evaluate the presence of the D dimer of fibrinogen and/or fibrin
above normal levels.
• Such presence indicates that intravascular lysis has taken place or is
occurring
VESSEL WALL DISORDERS
SCURVY
• Dietary deficiency of watersoluble vit C below 10mg/dl
• Defect in collagen synthesis
• petechial hemorrhages at the hair follicles and purpura on the back of the lower
extremities that coalesce to form ecchymoses.
• Hemorrhage can occur in the muscles, joints, nail beds, and gingival tissues.
• Gingival involvement may include swelling, friability, bleeding, secondary
infection, and looseningof teeth.
• Implementation of a diet rich in vitamin C and
• administration of 1 g/d of vitamin C supplements provides rapid resolution.
CUSHING’S SYNDROME
• Excessive corticosteroid production or intake
• General protein wasting and atrophy of
surrounding connective tissue
• Skin bleeding and easy bruising

EHLERS – DANLOS SYNDROME

• Inherited disorder of connective tissue matrix
• Fragile skin, easy bruising, hyperelasticity of
skin and hypermobility of joints
RENDU – OSLER – WEBER SYNDROME
• Hereditary hemorrhagic telangiectasia, autosomal dominant disorders
• Abnormal telangiectatic capillaries, frequent episodes of nasal and
gastrointestinal bleeding, and associated brain and pulmonary lesions.
• Common on lips, tongue, palate
• Treatment - cryotherapy, laser ablation, electrocoagulation, or resection.
 PALETLET DISORDERS
THROMBOCYTOPENIA
• Reduced platelet count
– decreased production in the bone marrow
– increased sequestration in the spleen
– accelerated destruction.
CONGENITAL PLATELET DISORDERS
• Hereditary thrombocytopenia
– May-Hegglin anomaly
– Wiskott-Aldrich syndrome
– Neonatal alloimmune thrombocytopenia

• Platelet function defect/ glycoprotein defect

– Glanzmann’s thrombasthenia ( GPIIb & GPIIIa)
– Platelet-type von Willebrand’s disease
– Bernard-Soulier syndrome( GPIb)
ACQUIRED PLATELET DISORDER
• Immune or idiopathic thrombocytopenic purpura
– Autoantibodies against own platelet antigens
– Acute – selflimiting and common in children
– Chronic – indolent and in adults

• Thrombotic thrombocytopenic purpura

– metastatic malignancy, pregnancy, mitomycin C, and high-dose chemotherapy
– Hemolytic uremic syndrome - Microangiopathic hemolytic anemia,
fluctuating neurologic abnormalities, renal dysfunction, and occasional fever.
COAGULATION DISORDERS
• Hemophilia A
– Deficiency of factor VIII(antihemophillic factor)
– X-linked recessive disorder
– Types –mild ( <4% AHF)
moderate (1to 4 % AHF)
moderate to severe (0.0 to 0.9% AHF)
severe (0.0% AHF)
– Signs – easy bruising, hemoarthoses, GI bleeding, hematuria, spontaneous
gingival bleeding
CHRISTMAS DISEASE
• Deficiency of factor IX
• X- linked recessive trait

VON-WILLEBRAND DISEASE
• Defect in von-willebrand factor (F VIII protein complex)
• Autosomal dominant triat
• Menorrhagia, easy bruising, mucosal bleeding, gingival bleeding, epistaxis, GI
bleeding, postpartum bleeding, bleeding after surgery or dental extraction.
DISSEAMINATED INTRAVASCULAR
COAGULATION
• Syndrome in which systemic activation of the coagulation leads to consumption
of coagulation factors and platelets
• Can be dominated by bleeding, vascular occlusion and tissue hypoxemia, or
both
• Common triggers: sepsis, major trauma, certain cancers,obstetric complications
MANAGEMENT
• prevention of hemorrhagic episodes,
• prompt control of bleeding when it occurs
• management of the sequelae of the disease and its therapy.
MANAGEMENT
• Platelet disorders
– Transfusion of platelets below 10,000
– Corticosteroids for ITP and splenectomy
– Bone marrow transplantation

• Hemophilia
– Depends upon the severity of the disease
– Factor replacement
– Commercially prepared Fs VIII and IXcomplex concentrates, desmopressin
acetate, cryoprecipitate and FFP are replacement options
DENTAL CONSIDERATIONS
• Low risk
– No history of bleeding
– Normal laboratory values

• Moderate risk
– Patients under anticoagulants, aspirin drugs
– With INR between 2 to 3

• High risk
– History of bleeding tendency
– Abnormal laboratory values
BLEEDING DISORDERS
Platelet count Dental treatment
1 >75,000 Normal protocol
2 40,000 – 75,000 Platelet transfusion may be considered
preoperatively and post operatively
3 < 40,000 Avoid invasive dental treatment, in
dental emergency supportive measures
should be considered
PAIN MANAGEMENT
• NSAIDs – avoided as it increases bleeding tendency and safest is
paracetamol
• Nerve block anesthesia is contraindicated , increased risk of
hematoma formation
• Anesthetic infiltration and intraligamentary anesthesia
• Anesthetic with a vasoconstrictor should be used when possible
ORAL SURGERY
• High risk of bleeding where safety precautions are necessary
• transfusion of appropriate factors to 50% to 100% of normal levels
is recommended
• Local hemostatic agents and techniques such as pressure, surgical
packs, sutures and surgical stents may be used individually or in
combination.
PERIODONTAL TREATMENT
• Scaling depends on the severity of the probing depths and the
patient’s level of oral hygiene.
• Supragingival scaling with local hemostatic measures (eg,
tranexamic acid) is considered safe
• Ultrasonic scaling results in less tissue trauma

RESTORATIVE & PROSTHETIC TREATMENT

• Can be safely done provided protection of oral mucosa
• Rubberdam placement and suction tips should be used cautiously
PATIENTS ON ANTICOAGULANTS
• Dental procedures are planned based on INR values and level of
thromboembolic risk.
• INR >3.5 to 4 – no surgical treatment with Coumadin dose modification
• INR <3.5 to 4 – minor surgical procedures with expected minimal
bleeding by local measures without modifying Coumadin dose
• INR <3.5 to 4 – multiple extractions with moderate bleeding, local
measures used along with reduction of INR
• INR <2 to 3 – significant bleeding expected , local measures
• INR < 1.5 – extensive flap surgery ,multiple bony extractions
CONCLUSION
• Patients with bleeding disorders should be evaluated carefully
• Patients with mild bleeding disorders can be treated in a primary
care setting after consultation with the hematologist.
• patients with a moderate to severe level of bleeding disorder who
require invasive dental procedures are best treated in a hospital
setting.
THANK YOU