Bleeding disorders /certified fixed orthodontic courses by Indian dental academy


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Bleeding disorders /certified fixed orthodontic courses by Indian dental academy

  1. 1. BLEEDING DISORDERS INDIAN DENTAL ACADEMY Leader in Continuing Dental Education
  4. 4. PLATELETS• INTRODUCTION: Platelets are tiny cells that congregate around ruptures in bloodvessels to provide backbone of clot.the platelets essentially form a temporary plug to stop platelets also stimulate the action of other coagulation proteins.
  6. 6. • Factors controlling thrombopoiesis:1.Interleukins(IL): IL-3,IL-6,IL-11,colony stimulating factors stimulate thrombopoiesis.2.thrombopoietin(TPO): Produced by liver & kidney.It helps the megakaryocyte to produce the platelets rapidly.3.TGFBeta: when excessive thrombopoiesis it is released from platelets and depress the platelet production.
  7. 7. • The life span of platelet is – 7 to 12 days Most of the platelets are destroyed in spleen.• The normal platelet count is 150000 – 400000 / ul of blood
  8. 8. MORPHOLOGY• SHAPE – disc shape ( inactive platelet) spherical (active platelet)• SIZE - 2-4 um in diameter• Platelets exist in red bone marrow,blood &spleen• Platelets have plasma membane , cytosol & no nucleus.• Plamamembrane has 2 layers Outer glycocalyx layer:contains glycoproteins Inner lipoprotein layer:contains phospholipids
  10. 10. • The cytosol consists of 1.Granules: -Alpha granules contain fibronectin, factor V, factor VII, PF4, PDGF. -Dense granules contain ADP, ATP, histamine& Calcium 2.Tubules: -Open tubules: Communicate with extracellular fluid(ECF). During activation,ca++ from ECF enter the inside of platelets via these tubules -Dense tubules: donot communicate with the exterior.They store ca++.
  11. 11. • 3.contractile elements:actin, myosin.• 4.mitochondria & golgiapparatus
  12. 12. Functions of platelets• Primary haemostasis – vascular spasm platelet plug formation• Secondary haemostasis (blood coagulation)
  13. 13. HEMOSTASIS• 1.Vascular spasm• 2.Platelet plug formation• 3.Blood clotting or coagulation
  14. 14. • 1.Vascular spasm:
  15. 15. • 2.Platelet plug formation: a) platelet adhesion. b) plaetelet release reaction. c) platelet aggregation & formation of platelet plug.
  16. 16. * The substances involved in platelet plug formation:• TXA2• ATP• ADP• Ca++• Serotonin• Prostaglandin• Fibrin stabilizing factor• Lysozomes• Platelet derived growth factor (PDGF)
  17. 17. a) Platelet
  18. 18. b)Platelet release
  19. 19. c) platelet aggregation & formation of platelet plug.
  20. 20. * 3.Blood clotting:• Within the vessels blood is in liquid form.when it is drawn from body it thickens and forms a gel.• The gel separates from the liquid.This straw colored liquid is called serum & the gel is called clot.• The process of gel formation – clotting or coagulation.
  21. 21. • Definition : Blood clotting is an complex cascade of enzymatic reactions in which each clotting factor activates many molecules of the next one in a fixed sequence.finally a large quantity of product (clot) is formed.
  22. 22. • THE FACTORS INVOLVED IN CLOTTING:-Clotting factors (CF)-Ca++-Enzymes synthesized by hepatocytes-Molecules associated with platelets
  23. 23. Clotting
  24. 24. * Clotting can be divided into 3 stages.• 1.Formation of prothrombinase by 2 pathways. Extrinsic pathway Intrinsic pathway• 2.Prothrombinase converts prothrombin into thrombin.• 3.Thrombin converts fibrinogen into soluble forms the clot.
  25. 25. Clotting mechanism
  26. 26.
  27. 27. Thrombin has 2 +ve feedback mechanisms
  28. 28. Clot retraction• Clot retraction is the consolidation or tightening of the fibrin clot.As the clot retracts it pulls the edges of the damaged vessel close together.Fibroblasts from ruptured area &new epithelial cells repair the vessel lining.
  29. 29.
  30. 30. • Intra vascular clotting *Clotting in an undamaged bloodvessels – thrombosis. *The clot – thrombus. *A blood clot,bubble of air,fat from broken bones or a piece of debris transported by the blood stream -embolus
  31. 31. Inhibitors of coagulation• Circulatory anti coagulants• The fibrinolytic mechanism• Tissue factor pathway inhibitor (TFPI)• Thrombomodulin
  32. 32. • Role of Vitamin k• Role of VWF• Role of liver• Role of bloodvessels
  33. 33. • Circulatory anticoagulants: Antithrombin Heparin Protein C & protein S
  35. 35. • Fibrinolytic mechanism:
  36. 36. • Thrombomodulin
  37. 37. • TFPI : After the onset of coagulation mechanism, TFPI begins to be formed and inhibits the intrinsic pathway.
  38. 38. • Role of vitamin K : Vitamin K is required for synthesis of factors II,VII,IX&X Source of vitamin K:vegetables Vitamin k is synthesized by intestinal bacterial flora.*Vitamin K deficiency:-Vitamin K free nutrition-Antibiotics like cephalosporins-Newborns-Obstructive jaundice
  39. 39. • Role of blood vessels:-The subendothelium is highly thrombogenic.-The contact of blood with subendothelium triggers the formation of XIIa.-Vascular endothelium synthesize PGI2 (prostacyclin) opposes the action of TXA2 thus prevents the platelet activation.
  40. 40. • Role of liver:-Liver synthesizes prothrombin, fibrinogen, factors V,VII,IX,X & XI.Thus the liver failure causes failure of clot formation.-Liver also synthesizes antithrombin III, heparin, proteinsC & S.Thus liver failure also can cause excessive clotting.
  41. 41. • Role of VWF:- Synthesized by megakaryocytes & vascular endothelium.It acts as a bridge between platelet & denuded endothelium.
  42. 42. * The drugs used for opposing haemostasis:• 1.Anti thromboitics• 2.Anti coagulants• 3.Thrombolytic drugs
  43. 43. * 1.Anti thrombotics• Eg:Aspirin• Aspirin inhibits vasoconstriction & platelet aggregation by blocking synthesis of TXA2.• It reduces the chance of thrombus formation.• Indications : -Transient ischaemic attacks -Myocardial infarction -Angina pectoris -Blockage of peripheral arteries
  44. 44. * 2.Anti coagulants:• In vivo:-Heparin :potentiates the action of anti thrombinIII-Vitamin K antagonists :eg-warfarin Blocks the synthesis of CF II,VII,IX,X.-Indications: Deep venous thrombosis Myocardial infarction Pulmonary embolism
  45. 45. • In vitro: To prevent clotting in donated blood, blood banks and laboratories often add a substance which prevents coagulation by removing the ionized calcium of blood citrate.-Eg : EDTA CPD Oxalates.
  46. 46. • 3.Thrombolytic drugs: These are injected into the body to dissolve clots that have already formed to restore circulation. -The mechanism of action: activate plasminogen. -Eg: Streptokinase Tissue plasminogen activator Urokinase
  47. 47. * The common laboratory tests for diagnosis of bleeding disorders:• 1.Bleeding time(BT)• 2.Clotting time(CT)• 3.Prothrombin time(PT)• 4.Partial thromboplastin time(PTT)• 5.Platelet count
  49. 49. I) BLEEDING DISORDERS CAUSED BY VESSEL WALL ABNORMALITIES• Called non thrombocytopenic purpura.• They induce small haemorrhages such as petchiae and purpura in the skin,mucous membranes,particularly in gingivae.• The platelet count,BT,CT,PTT are normal.
  50. 50. CAUSES:* 1.Infections: Meningococcemia Septicaemia Infective endocarditis. Rickettsia Measles* 2.Drug reactions:The vascular injury is mediated by drug induced Abs and deposition of immune complexes in vessel walls leading to hypersensitivity vasculitis.
  51. 51. • 3.Scurvy & Ehlers - Danlos Syndrome: -Impaired formation of collagens causes microvascular bleeding. -Cushings syndrome-Protein wasting effects of excessive corticosteroid production cause loss of perivascular supporting tissues.
  52. 52. • 4.Amyloid infiltration of blood vessels: Systemic amyloidosis associated with perivascular deposition of amyloid and consequent weakening blood vessel walls.
  53. 53. 5.Henoch-Schonlein purpura: (senile purpura)- Systemic hypersensitivity disease characterizedby a purpuric rash, ployarthralgia,acute glomerulonephritis
  54. 54. * 6.Heriditary haemorrhagic telangiectasia:• is an autosomal dominant disorder characterized by dilated,tortuous blood vessels that have thin walls and hence bleed readily.most commonly occurs under the mucous membranes of the nose,tongue,mouth,eyes,GIT.
  55. 55. • II.BLEEDING DISORDERS DUE TO FAULT OF PLATELETS:A.Related to reduced platelet number (thrombocytopenic purpura)B.Related to defect in platelet function
  56. 56. A.Related to reduced platelet number: (Thrombocytopenic purpura)• Platelet count is < 100000/ul.• post traumatic bleeding is aggravated-when platelet count is 20000-50000/ul.• BT is prolonged.• PT,PTT – normal.• The common sites involved are: -skin -Mucous membrane of GIT & genito urinary tract
  57. 57. CAUSES:1.Decreased production of platelets - Generalized diseases of bonemarrow a) Aplastic anaemia b) Leukaemia - Selective impairment of platelet production a) Drug induced : Alcohol,thiazides,cytotoxicdrugs. b) Infections: measles,HIV. - Infective Megakaryopoiesis a) Megaloblastic anaemia b) Myelodisplastic syndrome c) Paroxysmal nocturnal haemoglobinuria.
  58. 58. 2.Sequestration: - Spleen normally sequesters30-40% of platelets. -In case of hypersplenism orsplenomegaly it sequesters 90% of all platelets. -Treatment: splenectomy3.Dilutional: -Massive transfusions may producethrombocytopenia.Blood stored for longer than24hrs contains virtually no viableplatelets.Thus,plasma volume &RBC arereconstitued by transfusion,but the number ofcirculating platelets is reduced.
  59. 59. 4.Decreased platelet survival:i)Immunologic destuction:a.Auto immune: Idiopathicthrombocytopenic purpura Systemic lupus erythematosis.b.Iso immune: Post transfusion Neonatalc.Drug associated:heparin,quinidine,sulfa compounds.d.Infections: Infectious mononucleosis HIV Cytomegalovirus.
  60. 60. ii)Non immunologic destruction: Disseminated intravascular coagulation(DIC) Thrombotic thrombocytopenic purpura Giant haemangiomas Microangiopathic haemolytic anaemias
  61. 61. i)Immune thrombocytopenic purpura(ITP):• Primary ITP – Acute Chronic (common)• Secondary ITP – Systemic lupus erythomatosis AIDS Viral infections Drug therapy
  62. 62. PRIMARY ITP: CHRONIC:• Most common• Cause:the formation of auto Abs against platelet membrane glycoproteins,most often IIb-IIIa or Ib-IX• Prevalence: F:M=3:1• Age : <40yrs• C/F: -Insidious in onset. -Bleeding into skin,mucousal surface -Petechiae prominent in the dependent areas where the capillary pressure is high.Petechiae become confluent & give rise to ecchymosis. -Long history of easy bruising ,epitaxis,bleeding gums.
  63. 63. • The disease may be manifested first by malena,haematuria and increased menstrual flow.• Subarachnoid haemorrhage & intracerebral haemorrhage very rarely seen.• Diagnosis: -Decreased platelet count -Normal or Megakaryocytes in bone marrow. -Prolonged BT* Treatment:Glucocorticoids & splenectomy
  64. 64. ACUTE ITP:• Occurs in children• M:F=1:1• C/F: -Abrupt in onset -The interval between infection & onset is 2wks -Usually selflimited and resolves spontaneously within 6months. -20% of children may develop chronic ITP.*Treatment:corticosteroid therapy
  65. 65. Secondary ITP:• Drug induced:Heparin Quinidine Sulfa compounds -Heparin induced : occurs in 5% of cases receiving heparin. Two types: TypeI-occurs rapidly after onset of therapy TypeII-5-14 days after onset of therapy.
  66. 66. • HIV associated thrombocytopenia: CD4, the receptor for HIV on T cells demonstrated on megakaryocytes,making it possible for these cells to be infected by HIV.Infected megakaryocytes undergo apoptosis causing impaired platelet production.
  67. 67. • Non immunologic thrombocytopenia -Cause:by mechanical injury. Eg:Thrombotic microangiopathies-thrombotic thrombocytopenic purpura Haemolytic-uremic syndrome
  68. 68. • B.Bleeding disorders related to defective platelet function:1.Congenital2.Acquired
  69. 69. 1.Congenital• On the basis of specific functional abnormalitya)Defect in platelet adhesion to sub endothelial syndrome. Platelet membrane glycoprotein is a receptor for VWF and is essential for platelet adhesion.b)Defect in platelet aggregation Eg:Glanzmann’s thrombasthenia. Platelets fail to aggregate in response to ADP,collagen,thrombin,fail to form glycoprotein complex which forms bridges between platelets.
  70. 70. c)Disorders of platelet secretion:Eg: storage pool disorders. -Characterized by normal initial aggregation withcollagen ADP, but the secretion ofTXA2,prostaglandins, & granule bound ADP areimpaired.
  71. 71. 2.Acquired:a)Ingestion of aspirin & other NSAIDS which increase BT.b)Uremia: Impaired platelet function
  72. 72. • III)BLEEDING DISORDERS RELATED TO ABNORMALITIES IN CLOTTING FACTORS: (FAULT IN SECONDARY HAEMOSTASIS)-The Bleeding is manifested by large post traumatic ecchymosis or haematomas-Prolonged BT-Bleeding into GIT,UT & joints.
  73. 73. • Two types 1.Congenital:deficiency of fac VIII-haemophilia A deficiency of fac IX- haemophilia B 2.Acquired: DIC VitaminK deficiency Liver disorders
  74. 74. • Haemophilia A :-Most common heriditary disorder.-Caused by reduction in amount or activity of fac VIII.-It is inherited as an X-linked recessive trait.-Occurs in males & homozygous females.-30% of pts-no family history.caused by new mutations.
  75. 75. -The severity correlates with the level of fac VIII activity.• <1% of normal activity – severe• 2-5% of normal activity- moderate• 6-50% of normal activity- mild-C/F:Easy bruising & massive haemorrhage after truama or operative procedures.spontaneous haemorrhages occurs in regions of body normallly subject to trauma,particularly in joints(haem arthroses)-Normal BT,platelet count & PT but prolonged PTT.-Treatment:Recombinant fac VIII
  76. 76. • Haemophilia B (Christmas disease):-It is inherited as an X linked recessive trait.-Caused by a wide sprectrum of mutations involving- the fac IX gene.-Clinically indistinguishable from haemophilia A.-14% of pts fac IX is present but non functional.-Prolonged PTT,normal PT& BT. Recombinant fac IX.
  77. 77. • VONWILLEBRAND DISEASE• Caused by an inherited defect in involving platelet adhesion.• C/F:Spontaneous bleeding from mucous membranes,excessive bleeding from wounds,menorrhagia.• Prolonged BT,normal platelet count.• Types:Type1 Type2 Type3
  78. 78. Type 1&3 are associated with a reduced quantity of circulating VWF.• Type1:mild&autosomal dominant.• Type3:severe&autosomal recessive haemarthroses is common Severe deficiency of VWF has a marked effect on stability of fac VIII.• Type 2 is characterized by qualitative defects in VWF. -Because of mutations the VWF is abnormal. C/F:mild to moderate bleeding.
  79. 79. • Patients with Vonwillebrands disease have a compound defect involving platelet function & coagulation pathway.
  80. 80. * Acquired haemophilia• Disseminated intravascular clotting:• It occurs as a secondary complication in a vareity of diseases.• It results from pathologic activation of the extrinsic and/or intrinsic pathways or impairment of clot inhibiting influences.• The mechanisms trigger DIC - release of TF into the circulation - wide spread of injury to endothilial cells.
  81. 81. Release of TF into the circulationCauses Obstetrics complications. - retained dead foetus - septic abortion - amniotic fluid embolism - toximia neoplasms - adenocarcinoma, leukemia infections – gm-ve species, malaria, histoplasmosis aspergillosis
  82. 82. wide spread of injury to endothelial cells Endothelial injury ↓ release TF ↓ promotes platelet aggregation ↓ activates intrinsic pathway
  83. 83. • Consequence of DIC widespread deposition of fibrin ↓ ischemia ↓ microangiopathic haemolytic anaemia.
  84. 84. Haemostatic failure consumption of platelets and CF, ↓ activation of plasminogen ↓ plasmin→ fibrinolysis → inhibition of thrombin ↓ platelet aggregationproteolysis of clotting factors ↓ ↓ bleeding bleeding
  86. 86. PERIODONTAL TREATMENT OF HAEMORRHAGIC DISORDES• Identification of the pt via the health history,clinical examination and lab tests.1.H/O bleeding after previous surgery or trauma.2.Past & present drug history.3.H/O bleeding problems among relatives. www.indiandentalacademy.com4.Illness associated with potential bleeding problems.
  87. 87. • Clinical examination : Ecchymosis Jaundice Spider telangiectasia Haemarthrosis Petechiae Haemorrhage vesicles Spontaneous gingival bleeding Gingival hyperplasia
  88. 88. • LABORATORY TESTS : BT CT PT PTT Complete bloodcell count Torniquet test
  89. 89. * Haemophilia A:• To prevent surgical haemorrhage fac VIII levels of atleast 30% are needed.• Parentral 1-deamino-8-D-arginine vasopressin (DDAVP) can be used to raise fac VIII levels in mild to moderate haemophilia.• In severe case preoperative infusion of fac VIII or cryoprecipitate form is recommended.• Advantage of DDAVP:Avoids the risk of viral disease transmission from fac VIII infusion.
  90. 90. * Haemophilia B:• To prevent surgical haemorrhage fac VIII levels of atleast 30%-50% are needed.• Purified prothrombin complex concentrates or fac IX concentrates can be used to raise fac IX levels .• Mild-DDAVP before periodontal surgery or toothextraction.• Severe-preoperative infusion of fac IX or cryoprecipitate form.
  91. 91. • Probing scaling and prophylaxis – without medical modification.• More invasive treatment such as block local anesthesia,root planning or surgery – prior physician consultation.• Local haemostatic measures:to enhance clot formation. Pressure packs Electro cautery Splints&dressings
  92. 92. • Anti haemostatic agents:may be placed over surgical sites or extraction sockets. -Oxidized cellulose -Gel foam -Surgicel -Avitene -Purified bovine collagen.• Anti fibrinolytic agents: -Epsilon-aminocaproic acid(EACA)-systemically -Amicar systemically -Tranexamic acid-systemically, also available in a mouthrinse. -100mg / kg – preoperatively continued towww.indiandentalacademy.comat a dose 50mg/kg 8-10 days postoperatively qid.
  93. 93. • TREATMENT OF LIVER DISEASES OPPOSING HAEMOSTASIS-physician consultation-Lab tests-Conservative,non surgical periodontal therapy-If surgery is required may require hospitalization-Platelet count should be >80000/mm3-PT <2.5
  94. 94. * TREATMENT IN PTS TAKING ANTI COAGULANT THERAPY• The effectiveness of anticoagulant therapy is monitored by PT.• The recommended INR-2to3.-INR < 3- infiltration anesthesia,scaling & rootplaning.-INR < 2-block anesthesia, minor surgery & simple extractions. <1.5-complex surgeries,multiple extractions.
  95. 95. • Physician consultation to determine the degree of required anticoagulation & dicontinuation of the drug until the desired PT is achieved.May be discontinued for 2-3 days.• The pts taking aspirin <325 mg / day – discontinued for atleast 7-10 days before periodontal therapy in consultation with physician.• NSAIDS like ibuprofen – the effect is transitory,lasting only a short time after the last drug dose.
  96. 96. *Thrombocytopenic purpura• Removal of local irritants to reduce the inflammation & to avoid the aggressive therapy.• Oral hygiene instructions & frequent recall visits.• Platelet count < 60000/mm3-scaling &rootplaning is safe.• Platelet count >80000/mm3-surgical procedures safely can be performed.• Platelet transfusion may be required before surgery.• Atraumatic surgical techniques&local haemostatic measures
  97. 97. * Non thrombocytopenic purpura• Surgical therapy should be avoided unless qualitative & quantitative platelet problems are resolved.• Local haemostatic pressure&atraumatic technique should be applied.
  98. 98. REFERENCES1.Concise medical physiology-Choudhuri2.Principles of anatomy&physiology-Tortora3.Pathologic basis of disease-Robbins4.Clinical periodontology-Carranza5.Management of dental pts with bleeding disorders:Review and Update (Oral surg Oral med Oral pathol 1988;66:297-303.6.Haematology text book-Martin & Peter
  99. 99. THANK