Chapter One Introduction to Oral Medicine

Oral medicine Lecture 4

Introduction to Oral Medicine and Oral Diagnosis

Evaluation of the Dental Patient

Laboratory investigation of bleeding

disorder:
Physiology • Fibrinogen
HEMOSTASIS (Primary vs. Secondary vs. • Platelet Count
Tertiary)
• Bleeding Time
• Primary Hemostasis
• Platelet Plug Formation
Normal Clotting
• Dependent on normal platelet
number & function Response to vessel injury

• Secondary Hemostasis 1. Vasoconstriction to reduce blood flow

• Activation of Clotting Cascade ? 2. Platelet plug formation (von willebrand

Deposition & Stabilization of factor binds damaged vessle and platelets)
Fibrin 3. Activation of clotting cascade with
• Tertiary Hemostasis generation of fibrin clot formation

• Dissolution of Fibrin Clot 4. Fibrinlysis (clot breakdown)

• Dependent on Plasminogen Clotting Cascade

Activation Normally the ingredients, called factors, act like
COAGULATION TESTING a row of dominoes toppling against each other
Basic Testing to create a chain reaction.

• Prothrombin Time If one of the factors is missing this chain

reaction cannot proceed.
• Activated partial thromboplastin time
(aPTT)
• Thrombin Time (Thrombin added to
plasma, & time to clot measured)

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Chapter One
HEMOSTASIS Dependent Upon :
 Vessel Wall Integrity
 Adequate Numbers of Platelets
 Proper Functioning Platelets
 Adequate Levels of Clotting Factors
 Proper Function of Fibrinolytic Pathway
LABORATORY EVALUATION
• PLATELET COUNT
• BLEEDING TIME (BT) provide
assessment of platelet count and function
(2-9 mint)
Introduction to Oral Medicine
• PROTHROMBIN TIME (PT) Measures
effectiveness of the extrinsic pathway
(10-15 SECS)
International normalized ratio (INR):
the ratio of a patient’’ s prothrombin
time to a normal (control) sample
(1) Surgery can be done under INR< 3.0
(2) INR=3.0-3.5, consultation is needed
(3) Delay surgery when INR>3.5
• PARTIAL THROMBOPLASTIN TIME
(PTT) Measures effectiveness of the
intrinsic pathway (25 - 40 SECS)
• THROMBIN TIME (TT) Time for
Thrombin To Convert Fibrinogen to
Fibrin A measure of fibrinolytic pathway
(9-13 SECS)
Therefore, What Causes Bleeding
Disorders?
 VESSEL DEFECTS
 PLATELET DISORDERS
 FACTOR DEFICIENCIES
 OTHER DISORDERS
Evaluation of bleeding disorders
 Take history
 Physical examination
 Screening clinical laboratory tests
 Observation of excessive bleeding
following a surgical procedure
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Chapter One Introduction to Oral Medicine

History - Rickettsial and meningococcal

infections
 Bleeding problems in relatives
- Henoch-Schonlein purpura (immune)
 Bleeding problems following operations
and tooth extractions, trauma Platelet Disorders

 Use of drugs for prevention of  THROMBOCYTOPENIA: Inadequate

coagulation or pain Number Of Platelets

 Spontaneous bleeding from nose mouth  THROMBOCYTOPATHY : Adequate

etc.. number but abnormal function

Physical examination Thrombocytopenia

 Jaundice • Drug induced

• Bone marrow failure
 Petechiae: < 0.2 cm (small pinpoint
hemorrhages • Hypersplenism

 Purpura: 0.2 cm-1 cm • Other causes

OTHER CAUSES
 Eccymoses > 1 cm (larger patches)
 Lymphoma
 Spider angioma
 HIV Virus
 Oral ulcer
 Idiopathic Thrombocytopenia Purpura
 Hyperplasia of gingiva
(ITP)
 Hemarthrosis
Thrombocytopathy
 Uremia
VESSEL DEFECTS
 Inherited disorders
 VITAMIN C DEFICIENCY
 Myeloproliferative disorders
 BACTERIAL & VIRAL INFECTIONS
 Drug induced
 ACQUIRED & HEREDITARY
FACTOR DEFICIENCIES
CONDITIONS
(CONGENITAL)
 Infectious and hypersensitivity
 HEMOPHILIA A
vasculitides eg:
 HEMOPHILIA B

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Chapter One Introduction to Oral Medicine

 von WILLEBRAND’S DISEASE VON WILLEBRAND’S DISEASE

 Deficiency of VWF &
amount of Factor VIII
HEMOPHILIA A (Classic Hemophilia)
 Lab Results – Prolonged(
• 80-85% of all BT, PTT)
Hemophiliacs
Clinical Features of Bleeding Disorders
• Deficiency of Factor VIII
Platelet disorders factor disorders
• Lab Results - Prolonged
(PTT) Petechiae Yes No

HEMOPHILIA B (Christmas Disease) Ecchymoses Small, superficial Large, deep

(“bruises”)
• 10-15% of all
Hemophiliacs Hemarthrosis / Extremely rare Common
muscle bleeding
• Deficiency of Factor IX
Bleeding after cuts & Yes No
scratches
• Lab Test - Prolonged PTT
Immediate Delayed (1-2 days),
Clinical manifestations (hemophilia A & B Bleeding after surgery usually mild often severe
are indistinguishable) or trauma

 Hemarthrosis (most common) Site of bleeding Skin Deep in soft tissues

Mucous
 Fixed joints (epistaxis, gum, membranes
(joints, muscles)
vaginal, GI tract)
 Soft tissue hematomas (e.g., muscle)

 Muscle atrophy
 Shortened tendons
 Other sites of bleeding
 Urinary tract Platelet defect

 CNS, neck (may be life-threatening)

 Prolonged bleeding after surgery or
dental extractions

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Chapter One Introduction to Oral Medicine

Purpura

Petechiae, Purpura

Petechiae Do not blanch with pressure

Not palpable
Ecchymosis

Coagulation defect

Petechiae

Hematoma, Joint bl

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Chapter One Introduction to Oral Medicine

Hemarthrosis

Dental management of bleeding disorders

 Replacement therapy :
1. platelet concentrate: thrombocytopenia (1
unit= 30,000/ uL enough for 1 day)
2. Fresh frozen plasma: liver disease,
Hemophilia B, vWD type III
3. Factor VIII,IX concentrate: Hemophilia A (1
unit /kg can add 2%, so 50 unit /kg add 100% )
4. Factor IX concentrate : Hemophilia B
5. 1-desamino-8-darginine vesopressin
(DDAVP) : Hemophilia A, vWD type I, II

 Antifibrinolytic therapy:
1. E-aminocaproic acid (EACA, Plaslloid)
2. Tranexamic acid (AMCA, Transamin)

 Local hemostatic methods

splints, pressure packs,
sutures, gelfoam with thrombin, surgicel,
oxycel, microfibrillar collagen(avitene)
A 36-year-old male with idiopathic
thrombocytopenia purpura and a platelet count
of 5,000/mm3. Supportive platelet transfusions
and immunoglobulin therapy were used to
control bleeding. A,Labial and tongue
ecchymoses; B,palatal ecchymoses; C,buccal
ecchymoses and fibrinous clot.

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Chapter One Introduction to Oral Medicine

A 46-year-old male with severe liver cirrhosis due

to hepatitis C infection. Shown is purpura of facial
skin 1 week after full mouth extractions

A 68-year-old female with acute myelogenous

leukemia and a platelet count of 9,000/mm3.
Platelet transfusion and ε-aminocaproic acid oral
rinses were used to control bleeding. A,Buccal A 27-year-old male with type III von Willebrand’s
mucosa and palatal ecchymoses. B,Extrinsic stains disease and a 2-week duration of bleeding from the
on teeth from erythrocyte degradation following tongue that reduced his hematocrit to 16%.
continual gingival oozing Hemorrhage control was obtained with
cryoprecipitate.

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Chapter One
A 24-year-old male with severe hemophilia A and
lowtiter inhibitor, 3 days after inferior alveolar
block–induced parapharyngeal hemorrhage. Patient
presented with difficulty swallowing and pending
airway compromise 8 hours after nerve block.
Subsequent treatment with prothrombin complex
concentrates over 3 days controlled the bleeding
and began the resolution of facial swelling.
DENTAL MANAGEMENT
When medical management is unable to restore
platelet counts to above the level of
50,000/mm3 required for surgical hemostasis,
platelet transfusions may be required prior to
dental extractions or other oral surgical
procedures. The therapeutically expected
increment in platelet count from infusion of one
unit of platelets is approximately 10,000 to
12,000/mm3. Six units of platelets are
commonly infused at a time.
Antiplatelet activity of aspirin remains for the
8-to 10-day lifetime of the affected platelets,
avoidance of aspirin is recommended for 1 to 2
weeks prior to extensive oral surgical
procedures. Other NSAIDs have a similar but
Introduction to Oral Medicine
less pronounced antiplatelet effect. Adjunctive
local hemostatic agents are useful in preventing
postoperative oozing when aspirin therapy is in
use at the time of minor oral surgery. When
extensive surgery is emergently indicated,
DDAVP can be used to decrease the
aspirin-induced prolongation of the BT or to
treat aspirin-related postoperative oozing, often
eliminating the need for platelet infusion
NOTE:
Antifibrinolytic drugs such as ε-aminocaproic
acid and tranexamic acid (AMCA;
Cyclokapron;) inhibit fibrinolysis by blocking
the conversion of plasminogen to plasmin,
resulting in clot stabilization.
A regimen of 50 mg/kg of body weight
ε-aminocaproic acid given topically and
systemically as a 25% (250 mg/mL) oral rinse
every 6 hours for 7 to 10 days appears adequate
as an adjunct. Tranexamic acid (4.8%) oral
rinse was found to be 10 times more potent
than was ε-aminocaproic acid in preventing
post extraction bleeding in hemophiliacs
Systemic antifibrinolytic therapy can be given
orally or intravenously as ε-aminocaproic acid
75 mg/kg (up to 4 g) every 6 hours or
tranexamic acid 25 mg/kg every 8 hours until
bleeding stops
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