HEMOSTATIC DISORDERS
DENTAL CONSIDERATIONS
DR AJMAL MOHAMED
HEMOSTASIS
Physiological Process of Stoppage or
Arrest Of Bleeding By Maintaining the
Normal Internal Blood Equilibrium
MECHANISM OF HEMOSTASIS
TOURNIQUET TEST
 Evaluates vascular integrity
 Place B.P. cuff and inflate to 90-100mm Hg over
forearm
 Wait for 5 minutes
 Check for number of Petechiae within a 2.5 cm circle
 Normal-less than 10 Petechiae
 Rumbell Leed phenomenon
BLEEDING TIME
 Time interval taken from oozing of blood to the
arrest of bleeding from a standard cut.
 Normal
 1-6 minutes
 Duke and Ivy methods
 Prick on the finger tip and check for the time taken
for stoppage of blood oozing out

PLATELET COUNT
 Determines increase or decrease of
platelets
 Normal
 1,50,000-4,00,000mm³
 Blood smear examination
 Hemocytometer analyzer
CLOTTING TIME
 Time taken for the blood to clot after collecting
from the body
 Intrinsic clotting factors
 Capillary tube method
 Normal
 5-10 minutes
PROTHROMBIN TIME/I.N.R.
 Indicates total prothrombin present in blood
 Thromboplastin and calcium added to pt serum and is
expressed in ratio(International Normalized Ratio=I.N.R.)
 Normal
 11-13 seconds
 I.N.R.
 1.0-2.0
 Evaluates extrinsic system and F I,II,V,VII,X
ACTIVATED PARTIAL THROMBOPLASTIN TIME
(a.P.T.T.)
 Tests intrinsic and common pathway system
 Activity of VIII,IX,XI,XII
 Kaolin added to patient plasma
 Normal value
 15-35 seconds
THROMBIN TIME
 Test the ability to form initial clot from
fibrinogen
 Thrombin is added to plasma and time taken
to clot is noted
 Normal
 9-13 seconds
CLASSIFICATION OF
HEMOSTATIC DISORDERS
Arises from disorders of
Vessel wall
Coagulation
system
Platelets
VESSEL WALL DISORDERS
HEREDITARY
Hereditary Hemorrhagic
Telangiectasia
Ehlers Danlos
Syndrome
ACQUIRED
scurvy
Henoch schoulein purpura
Senile Purpura
infections
Cushing's syndrome
PLATELET DISORDERS
CONGENITAL
Glanzmanns
Thrombasthenia
Wiskott-aldrich
Syndrome
May Hegglin
Anomaly
Bernaud Soulier
Syndrome
ACQUIRED
Idiopathic
Thrombocytopenic
Purpura
Drug Induced
Thrombocytopenic
Purpura
Thrombotic
Thrombocytopenic
Purpura
COAGULATION DISORDERS
CONGENITAL
HEMOPHILIA A
HEMOPHILIA B
VON WILLEBRAND
DISEASE
OTHER FACTOR
DEFICIENCIES
COAGULATION DISORDERS
ACQUIRED
ANTICOAGULANT
HEPARIN
COUMARIN
DISEASES
LIVER
DISEASE
VIT K
DEFICIENCY
KIDNEY DISEASE
AND UREMIA
D.I.C.
Hereditary Hemorrhagic Telangiectasia
 Rendu Osler Weber Syndrome
 Autosomal Dominant Disorder
 Telangiectasia
 Recurrent Epistaxis
 + ve Family History
 Multiorgan Arteriovenous Malformations
 Hemorrhage
Clinical features
 Spider like telangiectasia
 Skin lesions- face,neck,chest ,legs
 Gastrointestinal bleeding
Oral lesions
 Perioral and intraoral angiomatous nodules
 Telangiectasia- lips,tongue,palate
 Lesions blanch on applied pressure
TREATMENT
 Cryotherapy
 Laser Ablation
 Electrocoagulation
 Resection
 Blood Replacement
 Iron Therapy
Ehlers Danlos Syndrome
 Inherited connective tissue disorder
 Joint Hypermobility
 Cutaneous Fragility
 Hyperextensibility of skin
 11 subtypes –unique biochemical defects and
clinical features
Clinical features
 Type 1-classic form
 Varicose veins and prematurity
 Type VIII
 Early onset periodontal disease
 Type VII
 children
 Microdontia
 Dentinal structural defects in primary dentition
 Bleeding after brushing
Oral Manifestation
 Fragile gingiva and oral mucosa
 Gingival hyperplasia and fibrous nodules
 Hypermobilty of T.M.J.
 Lack of normal scalloping of D.E.J.
 Pulp stones
 Periodontal destruction
 Gorlin sign
SCURVY
 Dietary deficiency of Vit C
 Defect in collagen synthesis
 Petechial hemorrhages at the hair follicles
 Purpura on lower extremities
 Hemorrhage to muscles, joints ,nail beds,
gingival tissues
Oral manifestations
 Gingiva appears ulcerated and boggy
 Foul breath
 Loss of bone
 Loosening of teeth
 Implementation of Vit C
 1 g/d of Vit C-rapid resolution
Cushing's Syndrome
 Corticosteroid intake or production
 Protein wasting and atrophy of connective
tissue
 Skin bleeding and easy bruising
Henoch-Schönlein Purpura
 Immune complex mediated hypersensitivity
 Children with acute infections
 Vasculitis and purpuric lesions
 Joint pain and abdominal pain
 hematuria
Glanzmann Thrombasthenia
 Chronic hereditary hemorrhagic disease
 Autosomal recessive trait
 Deficiency of platelet glycoprotein II b & III a
 Spontaneous bleeding after minor trauma
 Purpuric hemorrhage of skin
 Prolonged bleeding time
 Microfibrillar collagen & C- Aminocaproic Acid
Wiskott-Aldrich Syndrome
 X-linked recessive genetic condition
 Immunoglobulin M Deficiency
 Defect in WAS p
 Thrombocytopenic purpura
 Eczema
 Petechiae and purpuric rashes
 Boils, Otitis Media, Bloody Diarrhea
 Respiratory infection
 High potential for Malignant Lymphoma
Laboratory findings
 Prolonged bleeding time
 Anisocytosis
 Reduced platelet
 Reduced Adenosine Diphosphate Nucleotide
Bernard Soulier Syndrome
 Autosomal dominant disease
 Deficiency of surface membrane
glycoprotein of platelets –binding of Vwf
 Prolonged bleeding time
 Large platelets
 Defective platelet aggregation
May-Hegglin Anomaly
 Thrombocytopenia
 Giant cells
 Inclusion bodies in leucocytes
Thrombocytopenic Purpura
 Bleeding disorder
 Below 1,50,000mm3
 Failure of platelet production
 Disordered platelet distribution
 Increased platelet destruction
I.T.P.
 Werlhofs disease
 Autoimmune Disorder
 High levels of IgG
 Types
 Acute
 chronic
ACUTE
 90% in children
 Below 10 years
 Viral or upper respiratory infections
 Fall and winter seasons
 Onset is sudden and severe
 Recovers within 3-6 months
CHRONIC
 Adults-women
 20-40 years
 Insidious -history of long standing bruises
 S.L.E.,A.I.D.S.,lymphoproliferative disorders
and hemolytic anemia
Clinical features
 Below 40,000 mm³
 Pinpoint Petechial hemorrhages
 Purpura and bruises
 Arms,legs,thighs,chest,neck
 Mucosal bleeding in G.I.T.
 Risk of intracranial hemorrhage-<20,000mm³
Oral manifestations
 Spontaneous bleeding from gingiva
 Blood filled bullae
 Profuse oozing of blood from gingival margin
 Purplish globs of clotted blood on teeth
 Bleeding along occlusal line
 Multifocal Petechial red spots that do not blanch
seen on soft palate
DRUG INDUCED T.P.
 Reversible within 7-10 days of discontinuation
 Aspirin induces functional platelet defect
 Single 100mg-rapid complete inhibition of platelet
cyclooxygenase activity and thrombaxone
production
 Prolonged bleeding time
MOSCHOWITZ DISEASE
 Also called as T.T.P.
 Life threatening multisystem disorder
 Presence of thrombotic microangiopathies
 Micro vascular lesions with platelet
aggregation
Clinical features
 Thrombocytopenia
 Hemolytic anemia
 Transitory neurological dysfunction
 Renal failure
 Young adults-women
 Precipitating factors-
 pregnancy
 Infections
 S.L.E.
DIAGNOSIS
 Widespread microthrombi in arterioles,venules and
capillaries
 Biopsy of gingival tissue confirm diagnosis
 Occlusive subintimal deposits of P.A.S. at arteriolocapillary
junctions
 L.D.H. levels are increased
 Proteinuria
 hematuria
TREATMENT
 Corticosteroids
 Prednisolone 1-2mg/kg
 Antacids for G.I. symptoms
 Plasma exchange therapy combined with corticosteroids-
T.T.P.
 Bone marrow transplantation
 Plasmapheresis-to remove circulating antibodies
 Splenectomy
HEMOPHILIA
 Hemophilia A-factor VIII
 Hemophilia B- factor IX
 Hemophilia C-factor XI
Hemophilia A:
 1 in 10,000
 X-linked recessive bleeding disorder
 Only Males are affected
 1/3rd of patients-no family history
CLINICAL FEATURES
 Hemorrhage to joints, subcutaneous tissues,
internal organs
 Massive hematoma
 30-50%-neonatal bleeding from umbilical cord
 Petechiae is rare
 Cyclic remissions and exacerbations
CLASSIFICATION
Clinical severity depends on extent of
clotting factor deficiency
 <1%-severe with life threatening bleeding
 1-5%-moderate with post traumatic bleeding
 5-20%-mild disease
Oral Manifestations
 Massive and prolonged gingival hemorrhage
 Tooth eruption and exfoliation with bleeding
 Mandibular pseudo tumor
 Subperiosteal bleeding with reactive new bone
formation causing tumor like expansion of bone
 Hematoma formation following nerve block
anesthesia
Investigations
 Prolonged a.P.P.T.(Activated Partial Thromboplastin Time)
 Whole blood coagulation time is prolonged
 Factor VIII is reduced
 Normal bleeding time
 Normal prothrombin time
 Functional assay
Rₓ
 Factor VIII & IX replacement
 30% for mild
 60% for major surgeries
 FRESH FROZEN PLASMA
 Desmopressin
 0.3 µg/kg body weight-I.V. or S.C. before dental procedures
 Increases F VIII,Vwf antigen,ristocetin co factor activity
Von willebrands disease
 Autosomal dominant disorder
 Abnormality of Vwf
 Males and females
 Acquired form
 Wilms tumor
 S.L.E.
TYPES
 Type I
 Partial quantitative decrease of Vwf and F VIII
 Type II
 Qualitative defect of Vwf
 Type III
 Severe form Less than 1%
 Type IV
 Platelet type mimicking platelet disorder
Laboratory Findings
 Prolonged bleeding time
 Normal clotting time
 Normal prothrombin time
 Normal serum fibrinogen
 Increased capillary fragility
 Positive tourniquet test
Treatment
 Type 1-desmopressin
 Factor VIII
 Cryoprecipitate
 Fresh Frozen Plasma
 Local Hemostatic agents
Anticoagulant Coagulopathies
Heparin
 Binds with antithrombin III
 Inhibit activation of F IX,X,XI
 Reduces thrombin generation & fibrin formation
 Duration of action-3-4 hours
 Antidote-Protamine Sulphate
COUMARIN
 Warfarin and dicumarol
 Slow thrombin production and clot formation
 Blocks the action of Vit K
 F II,VI,IX,X reduced
 Anticoagulant effect reversed by F.F.P.
 I.N.R. monitors the anticoagulation levels
 Returns to normal within 2-4 days after discontinuation
 Intramuscular injection cause bleeding and hematoma
 Additive effect when used with aspirin
 Drug potency increased with
 Metronidazole
 Penicillin
 Erythromycin
 Cephalosporin
 Tetracycline
LIVER DISEASES
 Depends on extent of liver damage
 Impaired protein synthesis
 Clotting and fibrinolytic systems reduced
 Acute or chronic disease
 Decreased Vit K dependent factors
 F II,VII,IX,X
 Rx is Vit K therapy for 3 days
 F.F.P.
 Desmopressin
VIT K DEFICIENCY
 Production of poorly functioning Vit K dependant
factors
 Severe hemorrhage in acutely ill patients of 7-10
days
 Rapid fall in F VII elevates I.N.R. resulting
prolongation of a.P.T.T
 Supplementation of Vit K restores the defect
DISSEMINATED INTRAVASCULAR
COAGULATION
 Due to widespread IV activation of clotting cascade
 Initially forms microthrombi and emboli throughout
vasculature
 bleeding tendency due to consumption of clotting factors
 bruising or purpura
 Oozing from venepuncture and surgical wound sites
Causes
 Severe infections
 Hypovolemic shock
 Burns
 Transfusion reaction
 Eclampsia
 Amniotic fluid embolus
 Promyelocytic leukemia
 Widespread mucin secreting metastatic adenocarcinoma
Investigations
 ↑P.P.T. &P.T.
 ↑Fibrin Degradation Products
 ↓serum fibrinogen levels(<1mg/ml)
 ↓ factor V and factor VIII activities
 Thrombocytopenia
Rₓ
 I.V. heparin to prevent thrombi initially
 Fluid resuscitation
 Treat underlying cause
Correct clotting abnormalities with
 Fresh frozen plasma
 Cryoprecipitate
 Platelet transfusion
ORAL FINDINGS & GUIDLINES
 Spontaneous gingival bleeding
 Hemosiderin deposits on tooth surface
 Poor oral hygiene
 Higher caries rate
 Severe periodontal diseases
 Risk of hematoma formation
 Hemarthrosis to T.M.J.
MEDICAL CONSULTATION
 Bleeding
 Alcohol abuse
 Anticoagulation therapy
 Corticosteroid therapy
 Need for additional medications
 Change in dosage or alternative medication
LABORATORY INVESTIGATIONS
 BLEEDING TIME
 PLATELET COUNT
 PROTHROMBIN TIME
 ACTIVATED PARTIAL THROMBOPLASTIN
 I.N.R.
 THROMBIN TIME
 CLOTTING TIME
ORAL SURGICAL PROCEDURES
 Replacement of coagulation factor 50-100%
 Post operative maintenance therapy
 Factor concentrates
 D.D.A.V.P.
 Cryoprecipitate
 F.F.P.
 Packing of extraction socket with Hemostatic
agents
 Gingival bleeding not responding to
antifibrinolytics requires 20-30% F VIII,F IX
 Local Hemostatic methods
 Pressure packs
 Vasoconstrictors
 Suturing
 Surgical stents
 Topical thrombin
ANTIFIBRINOLYTIC AGENTS
 E.A.C.A.
 Tranexamic acid
 Block conversion of plasminogen to plasmin
 Clot stabilization
 50 mg/kg-topically
 250mg/ml-systemically as oral rinse(6hrs,7-10 )
 Fibrin glue
 Forms an adhesive gel & attract platelets
PAIN CONTROL
 Hypnosis
 Intravenous sedation
 Nitrous oxide analgesia
 Intrapulpal anesthesia for pulp extirpation
 Periodontal ligament and gingival papillary
injections
 L.A. with epinephrine
 Aspirin & N.S.A.I.Ds contraindicated
 acetaminophen and codeine
 Intramuscular injections should be avoided
due to risk of hematoma
 Ice packs in area of hematoma during nerve
blocks
PERIODONTAL THERAPIES
 Inflamed and swollen gingiva treated with
chlorhexidine mouth wash
 Use of cavitron or hand instrument prior to deep
scaling
 Deep scaling & root planning performed in
quadrants
 Post treatment Antifibrinolytic oral rinses
 Periodontal surgical procedures-↑50%
RESTORATIVE THERAPY
 Rubber Dam Isolation
 Avoid Trauma with high speed evacuators
 Matrices,wedges,retraction cords use with caution
 Avoid denture related trauma with careful insertion
ENDODONTIC THERAPY
 Root canal treatment is the choice
 Avoid filling beyond apex
 Application of epinephrine to the apical
region provides Hemostasis
PEDIATRIC DENTAL THERAPY
 Extraction of mobile teeth with periodontal space
anesthesia with proper oral hygiene measures
 Bleeding control with gauze pressure
 Crown preparation with minimal removal of
enamel at gingival region
 Topical fluoride therapy
 Pit and fissure sealants
ORTHODONTIC THERAPY
 Avoid mucosal lacerations with brackets,
bands and wires
 Use of extra oral force
 Shorter treatment appointments
PATIENTS ON ANTICOAGULANTS
 I.N.R.- >3.5-4.0
 No treatment without coumarin modification
 I.N.R.- <3.5-4.0
 Minor procedures with local measures without drug modification
 During significant bleeding
 Drug modification
 INR-<2.0-3.0
 Local measures
 Extensive surgeries-I.N.R.-<1.5
EMERGENCIES
 Palliative Treatment
 Infections treated with high dose antibiotics
 Extractions should be avoided till bleeding
controlled
 Aspirin & N.S.A.I.Ds not indicated
 Consultation with physician
To summarize
CONDITIONS TESTS
History of bleeding problem P.T., aP. T.T.,T.T.,B.T.,P.C.
Aspirin therapy B.T., aP.T.T.
Coumarin therapy P.T.
Renal dialysis(heparin) aP.T.T
Liver diseases B.T.,P.T.
Chronic leukemia B.T.
Long term antibiotic therapy P.T.
Vascular wall integration B.T. TOURNIQUET TEST
Cancer(fibrinogenolysis) T.T.
CONCLUSION
 Proper History
 Physical Examination
 Oral Examination
 Laboratory Investigations
 Medical Consultation
 Infection Control
Enjoy The Rain

COAGULATION AND BLEEDING DISORDERS.pptx

  • 1.
  • 2.
    HEMOSTASIS Physiological Process ofStoppage or Arrest Of Bleeding By Maintaining the Normal Internal Blood Equilibrium
  • 3.
  • 5.
    TOURNIQUET TEST  Evaluatesvascular integrity  Place B.P. cuff and inflate to 90-100mm Hg over forearm  Wait for 5 minutes  Check for number of Petechiae within a 2.5 cm circle  Normal-less than 10 Petechiae  Rumbell Leed phenomenon
  • 10.
    BLEEDING TIME  Timeinterval taken from oozing of blood to the arrest of bleeding from a standard cut.  Normal  1-6 minutes  Duke and Ivy methods  Prick on the finger tip and check for the time taken for stoppage of blood oozing out 
  • 11.
    PLATELET COUNT  Determinesincrease or decrease of platelets  Normal  1,50,000-4,00,000mm³  Blood smear examination  Hemocytometer analyzer
  • 12.
    CLOTTING TIME  Timetaken for the blood to clot after collecting from the body  Intrinsic clotting factors  Capillary tube method  Normal  5-10 minutes
  • 13.
    PROTHROMBIN TIME/I.N.R.  Indicatestotal prothrombin present in blood  Thromboplastin and calcium added to pt serum and is expressed in ratio(International Normalized Ratio=I.N.R.)  Normal  11-13 seconds  I.N.R.  1.0-2.0  Evaluates extrinsic system and F I,II,V,VII,X
  • 14.
    ACTIVATED PARTIAL THROMBOPLASTINTIME (a.P.T.T.)  Tests intrinsic and common pathway system  Activity of VIII,IX,XI,XII  Kaolin added to patient plasma  Normal value  15-35 seconds
  • 15.
    THROMBIN TIME  Testthe ability to form initial clot from fibrinogen  Thrombin is added to plasma and time taken to clot is noted  Normal  9-13 seconds
  • 16.
    CLASSIFICATION OF HEMOSTATIC DISORDERS Arisesfrom disorders of Vessel wall Coagulation system Platelets
  • 17.
    VESSEL WALL DISORDERS HEREDITARY HereditaryHemorrhagic Telangiectasia Ehlers Danlos Syndrome ACQUIRED scurvy Henoch schoulein purpura Senile Purpura infections Cushing's syndrome
  • 18.
    PLATELET DISORDERS CONGENITAL Glanzmanns Thrombasthenia Wiskott-aldrich Syndrome May Hegglin Anomaly BernaudSoulier Syndrome ACQUIRED Idiopathic Thrombocytopenic Purpura Drug Induced Thrombocytopenic Purpura Thrombotic Thrombocytopenic Purpura
  • 19.
    COAGULATION DISORDERS CONGENITAL HEMOPHILIA A HEMOPHILIAB VON WILLEBRAND DISEASE OTHER FACTOR DEFICIENCIES
  • 20.
  • 21.
    Hereditary Hemorrhagic Telangiectasia Rendu Osler Weber Syndrome  Autosomal Dominant Disorder  Telangiectasia  Recurrent Epistaxis  + ve Family History  Multiorgan Arteriovenous Malformations  Hemorrhage
  • 22.
    Clinical features  Spiderlike telangiectasia  Skin lesions- face,neck,chest ,legs  Gastrointestinal bleeding Oral lesions  Perioral and intraoral angiomatous nodules  Telangiectasia- lips,tongue,palate  Lesions blanch on applied pressure
  • 27.
    TREATMENT  Cryotherapy  LaserAblation  Electrocoagulation  Resection  Blood Replacement  Iron Therapy
  • 28.
    Ehlers Danlos Syndrome Inherited connective tissue disorder  Joint Hypermobility  Cutaneous Fragility  Hyperextensibility of skin  11 subtypes –unique biochemical defects and clinical features
  • 29.
    Clinical features  Type1-classic form  Varicose veins and prematurity  Type VIII  Early onset periodontal disease  Type VII  children  Microdontia  Dentinal structural defects in primary dentition  Bleeding after brushing
  • 32.
    Oral Manifestation  Fragilegingiva and oral mucosa  Gingival hyperplasia and fibrous nodules  Hypermobilty of T.M.J.  Lack of normal scalloping of D.E.J.  Pulp stones  Periodontal destruction  Gorlin sign
  • 35.
    SCURVY  Dietary deficiencyof Vit C  Defect in collagen synthesis  Petechial hemorrhages at the hair follicles  Purpura on lower extremities  Hemorrhage to muscles, joints ,nail beds, gingival tissues
  • 36.
    Oral manifestations  Gingivaappears ulcerated and boggy  Foul breath  Loss of bone  Loosening of teeth  Implementation of Vit C  1 g/d of Vit C-rapid resolution
  • 38.
    Cushing's Syndrome  Corticosteroidintake or production  Protein wasting and atrophy of connective tissue  Skin bleeding and easy bruising
  • 39.
    Henoch-Schönlein Purpura  Immunecomplex mediated hypersensitivity  Children with acute infections  Vasculitis and purpuric lesions  Joint pain and abdominal pain  hematuria
  • 41.
    Glanzmann Thrombasthenia  Chronichereditary hemorrhagic disease  Autosomal recessive trait  Deficiency of platelet glycoprotein II b & III a  Spontaneous bleeding after minor trauma  Purpuric hemorrhage of skin  Prolonged bleeding time  Microfibrillar collagen & C- Aminocaproic Acid
  • 43.
    Wiskott-Aldrich Syndrome  X-linkedrecessive genetic condition  Immunoglobulin M Deficiency  Defect in WAS p  Thrombocytopenic purpura  Eczema  Petechiae and purpuric rashes  Boils, Otitis Media, Bloody Diarrhea  Respiratory infection
  • 45.
     High potentialfor Malignant Lymphoma Laboratory findings  Prolonged bleeding time  Anisocytosis  Reduced platelet  Reduced Adenosine Diphosphate Nucleotide
  • 46.
    Bernard Soulier Syndrome Autosomal dominant disease  Deficiency of surface membrane glycoprotein of platelets –binding of Vwf  Prolonged bleeding time  Large platelets  Defective platelet aggregation
  • 48.
    May-Hegglin Anomaly  Thrombocytopenia Giant cells  Inclusion bodies in leucocytes
  • 49.
    Thrombocytopenic Purpura  Bleedingdisorder  Below 1,50,000mm3  Failure of platelet production  Disordered platelet distribution  Increased platelet destruction
  • 50.
    I.T.P.  Werlhofs disease Autoimmune Disorder  High levels of IgG  Types  Acute  chronic
  • 51.
    ACUTE  90% inchildren  Below 10 years  Viral or upper respiratory infections  Fall and winter seasons  Onset is sudden and severe  Recovers within 3-6 months
  • 52.
    CHRONIC  Adults-women  20-40years  Insidious -history of long standing bruises  S.L.E.,A.I.D.S.,lymphoproliferative disorders and hemolytic anemia
  • 53.
    Clinical features  Below40,000 mm³  Pinpoint Petechial hemorrhages  Purpura and bruises  Arms,legs,thighs,chest,neck  Mucosal bleeding in G.I.T.  Risk of intracranial hemorrhage-<20,000mm³
  • 55.
    Oral manifestations  Spontaneousbleeding from gingiva  Blood filled bullae  Profuse oozing of blood from gingival margin  Purplish globs of clotted blood on teeth  Bleeding along occlusal line  Multifocal Petechial red spots that do not blanch seen on soft palate
  • 57.
    DRUG INDUCED T.P. Reversible within 7-10 days of discontinuation  Aspirin induces functional platelet defect  Single 100mg-rapid complete inhibition of platelet cyclooxygenase activity and thrombaxone production  Prolonged bleeding time
  • 58.
    MOSCHOWITZ DISEASE  Alsocalled as T.T.P.  Life threatening multisystem disorder  Presence of thrombotic microangiopathies  Micro vascular lesions with platelet aggregation
  • 59.
    Clinical features  Thrombocytopenia Hemolytic anemia  Transitory neurological dysfunction  Renal failure  Young adults-women  Precipitating factors-  pregnancy  Infections  S.L.E.
  • 60.
    DIAGNOSIS  Widespread microthrombiin arterioles,venules and capillaries  Biopsy of gingival tissue confirm diagnosis  Occlusive subintimal deposits of P.A.S. at arteriolocapillary junctions  L.D.H. levels are increased  Proteinuria  hematuria
  • 61.
    TREATMENT  Corticosteroids  Prednisolone1-2mg/kg  Antacids for G.I. symptoms  Plasma exchange therapy combined with corticosteroids- T.T.P.  Bone marrow transplantation  Plasmapheresis-to remove circulating antibodies  Splenectomy
  • 62.
  • 63.
     Hemophilia A-factorVIII  Hemophilia B- factor IX  Hemophilia C-factor XI Hemophilia A:  1 in 10,000  X-linked recessive bleeding disorder  Only Males are affected  1/3rd of patients-no family history
  • 64.
    CLINICAL FEATURES  Hemorrhageto joints, subcutaneous tissues, internal organs  Massive hematoma  30-50%-neonatal bleeding from umbilical cord  Petechiae is rare  Cyclic remissions and exacerbations
  • 67.
    CLASSIFICATION Clinical severity dependson extent of clotting factor deficiency  <1%-severe with life threatening bleeding  1-5%-moderate with post traumatic bleeding  5-20%-mild disease
  • 68.
    Oral Manifestations  Massiveand prolonged gingival hemorrhage  Tooth eruption and exfoliation with bleeding  Mandibular pseudo tumor  Subperiosteal bleeding with reactive new bone formation causing tumor like expansion of bone  Hematoma formation following nerve block anesthesia
  • 70.
    Investigations  Prolonged a.P.P.T.(ActivatedPartial Thromboplastin Time)  Whole blood coagulation time is prolonged  Factor VIII is reduced  Normal bleeding time  Normal prothrombin time  Functional assay
  • 71.
    Rₓ  Factor VIII& IX replacement  30% for mild  60% for major surgeries  FRESH FROZEN PLASMA  Desmopressin  0.3 µg/kg body weight-I.V. or S.C. before dental procedures  Increases F VIII,Vwf antigen,ristocetin co factor activity
  • 74.
    Von willebrands disease Autosomal dominant disorder  Abnormality of Vwf  Males and females  Acquired form  Wilms tumor  S.L.E.
  • 75.
    TYPES  Type I Partial quantitative decrease of Vwf and F VIII  Type II  Qualitative defect of Vwf  Type III  Severe form Less than 1%  Type IV  Platelet type mimicking platelet disorder
  • 77.
    Laboratory Findings  Prolongedbleeding time  Normal clotting time  Normal prothrombin time  Normal serum fibrinogen  Increased capillary fragility  Positive tourniquet test
  • 78.
    Treatment  Type 1-desmopressin Factor VIII  Cryoprecipitate  Fresh Frozen Plasma  Local Hemostatic agents
  • 79.
    Anticoagulant Coagulopathies Heparin  Bindswith antithrombin III  Inhibit activation of F IX,X,XI  Reduces thrombin generation & fibrin formation  Duration of action-3-4 hours  Antidote-Protamine Sulphate
  • 80.
    COUMARIN  Warfarin anddicumarol  Slow thrombin production and clot formation  Blocks the action of Vit K  F II,VI,IX,X reduced  Anticoagulant effect reversed by F.F.P.  I.N.R. monitors the anticoagulation levels  Returns to normal within 2-4 days after discontinuation
  • 81.
     Intramuscular injectioncause bleeding and hematoma  Additive effect when used with aspirin  Drug potency increased with  Metronidazole  Penicillin  Erythromycin  Cephalosporin  Tetracycline
  • 82.
    LIVER DISEASES  Dependson extent of liver damage  Impaired protein synthesis  Clotting and fibrinolytic systems reduced  Acute or chronic disease  Decreased Vit K dependent factors  F II,VII,IX,X  Rx is Vit K therapy for 3 days  F.F.P.  Desmopressin
  • 83.
    VIT K DEFICIENCY Production of poorly functioning Vit K dependant factors  Severe hemorrhage in acutely ill patients of 7-10 days  Rapid fall in F VII elevates I.N.R. resulting prolongation of a.P.T.T  Supplementation of Vit K restores the defect
  • 84.
    DISSEMINATED INTRAVASCULAR COAGULATION  Dueto widespread IV activation of clotting cascade  Initially forms microthrombi and emboli throughout vasculature  bleeding tendency due to consumption of clotting factors  bruising or purpura  Oozing from venepuncture and surgical wound sites
  • 85.
    Causes  Severe infections Hypovolemic shock  Burns  Transfusion reaction  Eclampsia  Amniotic fluid embolus  Promyelocytic leukemia  Widespread mucin secreting metastatic adenocarcinoma
  • 86.
    Investigations  ↑P.P.T. &P.T. ↑Fibrin Degradation Products  ↓serum fibrinogen levels(<1mg/ml)  ↓ factor V and factor VIII activities  Thrombocytopenia
  • 87.
    Rₓ  I.V. heparinto prevent thrombi initially  Fluid resuscitation  Treat underlying cause Correct clotting abnormalities with  Fresh frozen plasma  Cryoprecipitate  Platelet transfusion
  • 88.
    ORAL FINDINGS &GUIDLINES  Spontaneous gingival bleeding  Hemosiderin deposits on tooth surface  Poor oral hygiene  Higher caries rate  Severe periodontal diseases  Risk of hematoma formation  Hemarthrosis to T.M.J.
  • 89.
    MEDICAL CONSULTATION  Bleeding Alcohol abuse  Anticoagulation therapy  Corticosteroid therapy  Need for additional medications  Change in dosage or alternative medication
  • 90.
    LABORATORY INVESTIGATIONS  BLEEDINGTIME  PLATELET COUNT  PROTHROMBIN TIME  ACTIVATED PARTIAL THROMBOPLASTIN  I.N.R.  THROMBIN TIME  CLOTTING TIME
  • 91.
    ORAL SURGICAL PROCEDURES Replacement of coagulation factor 50-100%  Post operative maintenance therapy  Factor concentrates  D.D.A.V.P.  Cryoprecipitate  F.F.P.  Packing of extraction socket with Hemostatic agents
  • 92.
     Gingival bleedingnot responding to antifibrinolytics requires 20-30% F VIII,F IX  Local Hemostatic methods  Pressure packs  Vasoconstrictors  Suturing  Surgical stents  Topical thrombin
  • 94.
    ANTIFIBRINOLYTIC AGENTS  E.A.C.A. Tranexamic acid  Block conversion of plasminogen to plasmin  Clot stabilization  50 mg/kg-topically  250mg/ml-systemically as oral rinse(6hrs,7-10 )  Fibrin glue  Forms an adhesive gel & attract platelets
  • 95.
    PAIN CONTROL  Hypnosis Intravenous sedation  Nitrous oxide analgesia  Intrapulpal anesthesia for pulp extirpation  Periodontal ligament and gingival papillary injections  L.A. with epinephrine
  • 96.
     Aspirin &N.S.A.I.Ds contraindicated  acetaminophen and codeine  Intramuscular injections should be avoided due to risk of hematoma  Ice packs in area of hematoma during nerve blocks
  • 97.
    PERIODONTAL THERAPIES  Inflamedand swollen gingiva treated with chlorhexidine mouth wash  Use of cavitron or hand instrument prior to deep scaling  Deep scaling & root planning performed in quadrants  Post treatment Antifibrinolytic oral rinses  Periodontal surgical procedures-↑50%
  • 98.
    RESTORATIVE THERAPY  RubberDam Isolation  Avoid Trauma with high speed evacuators  Matrices,wedges,retraction cords use with caution  Avoid denture related trauma with careful insertion
  • 99.
    ENDODONTIC THERAPY  Rootcanal treatment is the choice  Avoid filling beyond apex  Application of epinephrine to the apical region provides Hemostasis
  • 100.
    PEDIATRIC DENTAL THERAPY Extraction of mobile teeth with periodontal space anesthesia with proper oral hygiene measures  Bleeding control with gauze pressure  Crown preparation with minimal removal of enamel at gingival region  Topical fluoride therapy  Pit and fissure sealants
  • 101.
    ORTHODONTIC THERAPY  Avoidmucosal lacerations with brackets, bands and wires  Use of extra oral force  Shorter treatment appointments
  • 102.
    PATIENTS ON ANTICOAGULANTS I.N.R.- >3.5-4.0  No treatment without coumarin modification  I.N.R.- <3.5-4.0  Minor procedures with local measures without drug modification  During significant bleeding  Drug modification  INR-<2.0-3.0  Local measures  Extensive surgeries-I.N.R.-<1.5
  • 103.
    EMERGENCIES  Palliative Treatment Infections treated with high dose antibiotics  Extractions should be avoided till bleeding controlled  Aspirin & N.S.A.I.Ds not indicated  Consultation with physician
  • 104.
  • 107.
    CONDITIONS TESTS History ofbleeding problem P.T., aP. T.T.,T.T.,B.T.,P.C. Aspirin therapy B.T., aP.T.T. Coumarin therapy P.T. Renal dialysis(heparin) aP.T.T Liver diseases B.T.,P.T. Chronic leukemia B.T. Long term antibiotic therapy P.T. Vascular wall integration B.T. TOURNIQUET TEST Cancer(fibrinogenolysis) T.T.
  • 108.
    CONCLUSION  Proper History Physical Examination  Oral Examination  Laboratory Investigations  Medical Consultation  Infection Control
  • 109.