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Dental procedures resulting in bleeding can have serious consequences in a pt. having bleeding disorder severe hemorrhage or even death.
VASCULAR PHASE:
After tissue injury immediate vasoconstriction occurs. Serotonin, histamine, PGs etc causes vasoconstriction of the micro vascular bed.
PLATELET PHASE:
Circulating blood platelets are activated Aggregates Primary vascular plug ( es blood loss from small blood vessels & capillaries)
COAGULATION PHASE
Generation of THROMBIN and FIBRIN. INVOLVES VARIOUS PROTEINS:
Fibrinogen,prothrombin,FSINTRINSIC PATHWAY V,VII,IX,X,XI,XII & XIII.--------- Vitamin K EXTRINSIC PATHWAY dependant-FS-II,VII, IX & X. COMMON PATHWAY .
FIBRINpolymerizes to a gel
2 theories::: Prothrombin to thrombin & fibrinogen to fibrin conversion system ( MARKOWITZ----1903) CASCADE / WATERFALL theory(1964)-the coagulation mechanism results in a final explosive change of aliquid to a gel.
COAGULATION FACTORS:
FIBRINOLYTIC PHASE:
Propagation of the clot is limited by fibrinolysis. Tissue plasminogen activator(tPA)released from the endothelial cells converts PLASMINOGEN to PLASMIN. Plasmin degrades fibrinogen & fibrin to fibrin degradation products [FDPs] .
FIBRINOLYTIC SYSTEM:
Factor XII
parakallikren
fibrin
FDPs
CLINICAL FEATURES
Ble edin g from su perf ici al cut s & sc rat che s . Del ayed b leed ing . Spo ntan eo us g ing ival bl eed ing . Pet echi ae . Ecc hymo se s . Epi stax is . Dee p di ss ecti ng hema tom as . Hem arth ro ses .
PLATELET
COUNT:
Normal-150,000 to 450,000/mm3 If < 50,000/mm3 Hemorrhagic stroke Surgical/traumatic hemorrhage etc. may occur. In such cases platelet transfusion may be necessary.
PT & INR
Normal-11 to 30 secs Bcoz of Individual lab.reagant variability & inorder to compare the PT from one lab. To the other its now commonly reported with its INR.
f PT that adjusts for the sensitivity of the thromboplastin reagants,such that nor
USES of PT/INR:
Evaluates extrinsic coagulation system . Measures the presence / absence of Fs - I , II , V , VII & X . Measures the effects of coumarin anti coagulants . Reduction of vit K dependant Fs I , II , VII & X . Measures the metabolic aspects of protein synthesis in liver . Does not measure the reduction of Fs - VIII / IX .
THROMBIN TIME:
Normal-9 to 13 secs. Measure the activity of heparin,FDPs,other para proteins that inhibit conversion of fibrinogen to fibrin.
FACTOR ASSAYS:
IDENTIFY FACTOR DEFICIENCIES.
ANTI COAGULANT RELATED COAGULOPATHIES: Heparin Coumarin. DISEASE RELATED COAGULOPATHIES: Liver disease Vitamin K deficiency DIC Fibrinolytic disorders.
SCURVY( vitamin C
deficiency) When VitC level falls below 10mg/d. VitC is essential for synthesis of collagen. Hemorrhage in muscles , joints , nail beds & gingival tissues. GINGIVA- swelling, friability,
CUSHINGS SYNDROME,EHLERS DANLOS SYNDROME,RENDUOSLER- WEBER SYNDROME(HHT)
CUSHINGS syndrome:
Resulting from excessive corticosteroid Intake / production. Patient shows skin bleeding & easy bruising.
EHLERS-DANLOS syndrome:
Autosomal dominant disorder: Fragile skin vessels & easy bruising.
RENDU-OSLER-WEBER syndrome:
HHT Abnormal telangiectatic capillaries. Frequent episodes of nasal & GI bleeding. Telangiectases common on lips, tongue & palate.
TREATMENT:
Cryotherapy. Laser ablation. Electrocoagulation. Blood replacement & iron therapy.
PLATELET DISORDERS:
ACQUIRED CONGENITAL Thrombocytopaenia-Quantity of - platelets when reduced by * edproduction in the bone marrow * edsequestration in
the spleen.
destruction.
Accelerated
CONGENITAL
THROMBOCYTOPENIC May-hegglin anomaly Wiskott-Aldrich syndrome Neonatal alloimmune thrombocytopenia .
NONTHROMBOCYTOP ENIC Glanzmans thrombasthenia Platelet type vonwillebrands disease Bernard soulier syndrome
ACQUIRED
THROMBOCYTOPE NIC
NONTHROMBOCYTO PENIC
TTP(Thrombotic thrombocytopenic purpura) Cytotoxic chemotherapy Drug induced Leukemia Aplastic anemia Systemic lupus erythematosus DIC Asso with :
Drug induced Uremia Alcohol dependancy Liver disease Myeloma Macroglobulinaemi a Acquired platelet tpe von-
ITP
Caused by accelerated antibody mediated platelet consumption. Oral hematomas & hemorrhagic bullae may occur. Intracerebral hemorrhage is the most common cause of death. Corticosteroids TREATMENT: Splenectomy
Rituximab Anti-D Thrombopoietin like agents.
TTP:
CAUSES:metastaticmalignancy,pregnancy,mit omycin & high dose chemotherapy. SYMPTOMS:
ASPIRIN : USES--- ANTIPLATELET THERAPY FOR THROMBOEMBOLIC PROTECTION. INEXPENSIVE & EFFECTIVE
COAGULATION DISORDERS
HEMOPHILIA A CONGENITAL-- HEMOPHILIA B F XI DEFICIENCY F XII ,, F X ,, F V ,, F XIII & I ,, VON - WILLEBRAND S DISEASE . ACQUIRED- .Secondary to drugs (Heparin , Coumarin) or disease process(Liver disease, Vit K deficiency ,DIC).
HEMOPHILIA
HEMOPHILIA -A
Def of F VIII (Antihaemophilic factor) Inheritted as an X linked trait. 10 times more commonly than hemophilia B. TYPES- Mild(< 4% of AHF) Moderate(1 3 % of AHF) Moderate to severe(0.00.9% of AHF)
CLINICAL FEATURES:
No racial predilection AGE-Bleeding manifestations begin after 6 months of age. SIGNS: Hematomas, Hemarthroses,Hematuria,GI bleeding, Bleeding from laceration , head trauma,spontaneous intra cranial bleeding. Hemorrhage into joints that causes muscle spasm.
ORAL MANIFESTATIONS
Persistant bleeding sites-Frenum of lip & the Tongue. There is prolonged bleeding after tooth extraction. Physiological processes of tooth eruption & exfoliation are associated with severe & prolonged hemorrhage. Gingival hemorrhage occurs due
CT is prolonged BT , platelet count ,PT are all normal. Prothrombin consumbtion time& pTT are prolonged.
HEMATOLOGICAL FINDINGS:
MANAGEMENT:
AIM-Raise the F VIII level. Replacement therapy- Plasma DISADV , Viral transmission Cryoprecipitate . Large volume needed F VIII concentrates.
F VIII CONCENTRATES:
1U= Amount present in 1ml fresh normal plasma. High purity F VIII products mfg. by recombinant & monoclonal antibody purification tech.
VIRAL SAFETY
To reduce complications of above treatments before dental extraction a synthetic analogue of 1-deamino 8-D-arginine vasopressin(DDAVP) in combination with tranexamic acid and Epsilon- aminocaproic acid(EACA) can be given. 0.3g/kg body wt. by IV/SC route. Prior to extractions / surgery.
CHRISTMAS DISEASE:
Heriditary def of F IX. Inheritted as X linked recesive trait. Very rare compared to Hemophilia-A. C/F same as Hemophilia A. TREATMENT:
ANESTHESIA-LA is contra indicated B4 replacement therapy.If to be given-intrapulpal anesthesia,PDL ligament & papillary injection.sedation with dizepam or NO2/O2 analgesia can be given. ENDODONTIC therapy provided care is taken,not to exceed beyond the apex of tooth.
PROSTHODONTIC THERAPY:Maintenance of oral hygiene is necessary.If food entrapped in the clasp------ Gingivitis-------- Hemorrhage.
ORAL SURGICAL PROCEDURE: Local hemostatic agents & techniques are used. Aspirin & other NSAIDs are avoided. Preoperative factor level should be 30 40 % of normal activity. Electro surgery is contra indicated.
F XI DEFICIENCY:
Plasma thromboplastin antecedent deficiency. Mild Autosomal dominant trait. Controlled with infusions of FFP.
FXII DEFICIENCY:
HAGEMAN FACTOR DEFICIENCY. PROLONGED PT & PTT. CLINICAL SYMPTOMS ARE NON EXISTENT HENCE RX IS THEREFOR CONTRA INDICATED.
F V DEFICIENCY:
Proaccelerin def . Rare. Autosomal recessive trait.
plasma.
CLINICAL FEATURES:
Mucosal bleeding. Soft tissue hemorrhage. Menorrhagia in women. Rare hemarthrosis. Both females & males affected.
TYPES:
TYPE I : (85% of vWD)- partial quantitative deficiency. TYPE II : (10-15%)- Qualitative defects. TYPE 2A-Decreased platelet adhesion TYPE 2B Increased affinity for platelet
glycoprotein Ib TYPE 2M- Defective platelet adhesion. TYPE 2N- Decreased affinity for F VIII.
TREATMENT:
Type I- DDAVP, F VIII concentrates,FFP,Cryoprecipita te-for nonresponders to DDAVP. Type II & III- F VIII conc. (Humate P,Koate HS),cryoprecipitate,FFP. DENTAL PROCEDURES: Local hemostatic agents & Antifibrinolytic agents.
COUMARIN
Include Warfarin & dicumarol. USES:Prevent pulmonary thromboembolism, venous thrombosis,stroke, MI,to treat AF & in conjunction with prosthetic valves. ACTION: Slow thrombin production & clot formation by blocking the action of Vit K .VitK dependent factors are
LIVER DISEASE: Impaired protein synthesis-- Fs II,VII,IX & X (Vit K dependant) are reduced. Thrombocytopenia & thrombocytopathy also may result.
VITAMIN K DEF: Fs II, VII, IX,X are reduced & decreased coagulation. TREATMENT: Supplemental Vit K injection restores the clotting mechanism. FFP infusion,DDAVP THERAPY,Antifibrinolytic agents.
RENAL DISEASE:
In uremic patients Dialysis is the primary & therapeutic modality for bleeding control. DDAVP & CRYOPRECIPITATE. Conjugated estrogen preparations & Recombinant Erythropoietin also are beneficial.
DIC (Disseminated Intravascular Coagulation): Here thrombosis results in rapid consumption of both coagulation factors & platelets. Bleeding at skin & mucosal sites. Sometimes massive hemorrhage occurs & can be life threatening.
TREATMENT: IV-unfractionated heparin , LMWH to prevent from thrombin acting on fibrinogen & prevent clot formation. Infusion of activated protein C , Antithrombin III.
FIBRINOLYTIC DISORDERS:
Lead to hemorrhage when clot breakdown mechanism is impaired. Plasminogen activator inhibitor deficiency-- Hemorrhage. TREATED with FFP THERAPY & Antifibrinolytics.
PROGNOSIS
Depends on the APPROPRIATE DIAGNOSIS & the ability to prevent and manage acute bleeding episodes.
IDENTIFICATION OF THE DENTAL PATIENT WITH A BLEEDING DISORDER: Family history of bleeding problems.(inheritted disorders) Past history of bleeding following surgical
Surveying the patient for current medication use. History of heavy alcohol intake. Medical conditions hepatitis/cirrhosis,renal disease,hematologic malignancy&thrombocytopenia predispose patients to bleeding problems.
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