Hemostasis

ppt by k.shivteja

1. HEMOSTASIS PRESENTED BY: K.SHIVA TEJA 1 ST YEAR PG

2. CONTENTS INTRODUCTION STAGES OF HEMOSTASIS FACTORS INVOLVED IN BLOOD CLOTTING CLOTTING MECHANISM BLEEDING DISORDERS APPROACHES TO BLEEDING DISORDERS PERIODONTAL IMPLICATIONS HEMOSTATIC AGENTS MANAGEMENT CONCLUSION REFERENCES

3. INTRODUCTION Hemostasis ( heme -blood, stasis-remain) is the stoppage of bleeding, which is vitally important when blood vessels are damaged. Bleeding is the one of leading causes of death after civil and combat trauma. Adequate hemostasis after trauma and during surgical operation is a big challenge in modern medicine .

4. About 40% traumatic and more than 90% of combat deaths took place in pre-hospital settings. About 50% from these deaths have been reported due to massive blood loss [ Ersoy G 2007 ]. Hemostasis enables an organism to 1) Close off damaged blood vessels 2) Keep the blood in a fluid state 3) Remove blood clots after restoration of vascular integrity.

5. The hemostatic system is a highly conserved machinery, from zebrafish to human, in which blood clotting also referred to as coagulation has a prominent role. Plato already described that the blood forms fibers once it leaves the heat of the body. He was also one of them to coined the term fibrin , where now a days refers to a key blood clotting protein composing those fiber structures.

6. STAGES OF HEMOSTASIS When a blood vessel is injured, the injury initiates a series of reactions resulting in hemostasis. VASOCONSTRICTION

7. FACTORS INVOLVED IN BLOOD CLOTTING

8. SEQUENCE OF CLOTTING MECHANISM In general, blood occurs in three stages: 1. F ormation of Prothrombin activator 2. Conversion of prothrombin into thrombin 3. Conversion of fibrinogen into fibrin Inactive clotting factors are activated and their enzymatic actions produce the successive reactions one after the other. These reactions are explained by enzyme cascade theory .

9. THE COAGULATION CASCADE

10. BLOOD CLOT The entire mass of fibrin meshwork (RBC,WBC AND PLATELETS) and the blood cells entrapped with in this is called as Blood clot. The external blood clot is also called as SCAB. In addition maintenance of clot stability following formation is critical to prevent rebleeding

11. THE NEW MODEL OF HEMOSTASIS Physiol Rev 93: 327–358, 2013

12. BLEEDING DISORDERS A. VASCULAR DISORDERS 1. Hereditary hemorrhagic telangiectasia (Rend-Osler-Weber syndrome ) 2. Acquired vascular purpuras - Purpura from vitamin C deficiency ( scurvy) - Allergic vascular purpuras [ Anaphylactoid purpura ( Schonlein -Henoch syndrome )] B. PLATELET DISORDERS (THROMBOCYTIC PURPURAS) 1. Thrombocytopenia- Idiopathic/Immune Thrombocytopenic Purpura (ITP, Werlhof disease ), Heparin- Induced Thrombocytopenia (HIT), Thrombotic Thrombocytopenic Purpura (TTP), Hemolytic-Uremic Syndrome (HUS ). 2. Thrombocytopathia C. COAGULATION DISORDERS

13. A. VASCULAR DISORDERS (VASCULAR PURPURAS) Rendu -Osler-Weber syndrome

14. Acquired vascular purpuras Purpura from vitamin C deficiency ( scurvy)- microvascular bleeding resulting from impaired formation of collagen and fragile vessel walls . Manifestations: Gingival tumefaction with bleeding gums, perifollicular hemorrhages, disseminated petechiae .

15. Anaphylactoid purpura ( Schonlein -Henoch syndrome) immune vasculitis induced 2-3 weeks after an infection with streptococcus ß-hemolytic in children/young adults . Manifestations: Extra renal manifestations – triad Cutaneous rash, Colicky abdominal pain (due to focal hemorrhages in GI tract) Polyarthralgia (transient arthralgia of large joints) Renal- Acute glomerulonephritis leads to renal failure Idiopathic/Immune Thrombocytopenic Purpura ( ITP/ Werlhof disease) The most common cause of thrombocytopenia due to increased immune destruction of platelets, caused by the formation of autoantibodies (IgG type, in 80% of the cases ) against platelet membrane glycoproteins.

16. Thrombocytopathia characterized by altered platelet function, with normal number of thrombocytes due to: 1. Inherited disorders of: a . Adhesion (Von Willebrand disease and Bernard- Soulier syndrome ) b . Aggregation (Glanzmann thrombasthenia ) 2. Acquired functional defects caused by: a . Drugs (Aspirin and NSAIDs) b . Toxins (Uremia )

17. C. COAGULATION DISORDERS A. Inherited coagulation disorders: a) Hemophilia A – factor VIII deficiency b) Hemophilia B – factor IX deficiency B. Acquired coagulation disorders 1. Decreased synthesis of clotting factors: a) Liver diseases b ) Vitamin K deficiency 2. Increased consumption of clotting factors: a ) Disseminated intravascular coagulation (DIC) Queen Victoria  passed Hemophilia on to many of her descendants Son of the last Tsar of Russia – Aleksy Romanow suffered from Hemophilia A

18. ANTICLOTTING MECHANISM IN THE BODY PHYSICAL FACTORS -Continuous circulation of blood -Smooth endothelial lining of blood vessels CHEMICAL FACTORS (natural anticoagulants) -Heparin - Thrombomodulin

19. PROCOAGULANTS THROMBIN- sprayed upon the bleeding. SNAKE VENOM- v ipers, cobras and rattle snakes contains proteolytic enzymes which activates clotting factors. EXTRACTS OF LUNGS AND THYMUS- extract obtained from them contains thromboplastin. SODIUM OR CALCIUM ALGINATE & OXIDIZED CELLULOSE- activates Hageman factor

20. DRUG INTERACTIONS

21. APPROACH TO BLEEDING disorders CLINICAL ASSESSMENT Is a bleeding tendency present ? Is the condition familial or acquired ? Is the condition one affecting primary hemostasis or one affecting fibrin formation and stability ? Is there any other disorder that could be the cause of or might exacerbate the bleeding tendency ? Is the increased bleeding pharmacologically induced ?

22. Diagnostic clues obtainable by means of proper evaluation of type or site of bleeding Conjunctival ecchymosis Hypertension, thrombocytopenia, anticoagulants Petechiae (skin or mucosa) Thrombocytopenia Papular lesions in legs Cryoglobulinemia , other purpuras Mucosal Rendu -Osler, VWD, platelet disorder Hematomas Single factor congenital deficiency, circulating anticoagulants , traumas Haemartrosis Hemophilia A and B, and less frequently, FII, FVII or FX deficiency Easy bruising Thrombocytopenia, Cushing’s disease

23. LABORATORTY ASSESSMENT BLEEDING TIME- Normal duration 3 to 6 minutes. It is prolonged in purpura . CLOTTING TIME- Normal duration is 3 to 8 minutes. It is prolonged in hemophilia . PROTHROMBIN TIME (PT)- Normal duration is 10 to 12 minutes. It is prolonged in deficiency of prothrombin and factors like I, V, VII and X . Normal in hemophilia. PARTIAL PROTHROMBIN TIME (PPT)/(APPT)- Normal duration is 30 to 45 seconds. It is prolonged in heparin and warfarin therapy, deficiency of factors II, V, VII, IX, X, XI and XII.

24. INTERNATIONAL NORMALIZED RATIO (INR) INR = (patient PT/mean normal PT) ISI INR at 1 normal INR between 2 and 3 in patients taking anticoagulants for AF. INR between 3 and 4 in patients with heart valve disorders. INR > 4 blood clotting is too slow, risk of uncontrolled blood clotting. MANAGING PATIENTS AS RELATED TO THEIR INR VALUES

25. THROMBIN TIME (TT)- Normal duration of thrombin time is 12 to 20 seconds. It is prolonged in heparin and during dysfibrinogenemia. PLATELET COUNT- Normal platelet counts are 250,000 cells/mm 3 Surgically related or traumatic hemorrhage more likely with platelet count < 50,000 to 80,000 cells/mm3. TOURNIQUET TEST- M easures the response to arteriovenule junction to internal stresses. Providing the systolic pressure above 100mm of Hg, a constant 100 mm pressure maintained for 5 minutes. The appearance of multiple petechiae distal to the cuff indicate scurvy and certain purpuras. Normal is up to 5 petechiae .

26. SPECIAL INVESTIGATIONS

27. GUIDELINES FOR THE PREOPERATIVE HEMOSTASIS EVALUATION

28. PERIODONTAL IMPLICATIONS Males lose blood 50 times faster than females during gingival surgery More the time of surgery more is the blood loss. Surgical time < 2hrs- blood loss not more than 125ml Flap surgery in mandible- average blood loss- 151ml in maxilla- average blood loss- 110ml High quantity of blood loss- mandibular right posterior area Least quantity of blood loss- maxillary left posterior area Baab , Amnions, Selipsky Blood Loss During Periodontal Flap Surgery J. Periodontal. November, 1977 Mclvor , J. and Wengraf . A.: Blood loss in periodontal surgery. Dent Pract 16: 448, 1966 Baab , Amnions, Selipsky Blood Loss During Periodontal Flap Surgery J. Periodontal. November, 1977

29. Gingivectomy in posterior mandible: Local infiltration anesthesia- Blood loss: 3-13 ml Regional block anesthesia- B lood loss: 8-31 ml Full mouth gingivectomy - blood loss: 435-624ml Full mouth flap surgery- blood loss: 350ml Blood loss per site(1 or 2 teeth ): Mucoperiosteal flaps: 12-62ml Gingivectomy : 0.7-1.8ml Mclvor , J. and Wengraf . A.: Blood loss in periodontal surgery. Dent Pract 16: 448, 1966 Berdon , J. K.: Blood loss during gingival surgery. J Periodontol 36: 102, 1965.

30. TOPICAL HEMOSTATIC AGENTS Topical hemostatic treatment was applied since ancient time . They used herbs, mixture of wax, grease and barley and also animal hides mixed with hot sand to stop bleeding [ Hardean E. Achneck , 2010 ]. Hardean E. Achneck , 2010 classified all topical hemostatic agents in several groups: Physical agents , Absorbable agents, Biological agents, Synthetic agents and Hemostatic dressings.

31. Absorbable agents are Gelatin Foams, Oxidized Cellulose, and Microfibrillar Collagen is used since 1945 for hemostasis [ Schonauer C , 2004]. Gelatin foams effective control bleeding from small vessels and may be used for bone hemostasis [ Tomizawa Y ., 2005 ]. Biologic agents are most effective to stop bleeding due to its hemostatic nature. This group includes Topical Thrombin, Fibrin Sealants, and Platelet Gel. Thrombin is a naturally derived enzyme that has been characterized by its roles in hemostasis, inflammation, and cell signaling [ Lawson JH , 2005 ].

32. Physical agents are bone wax and ostene achieve hemostasis through occlusion of bleeding channels in bone and subsequent tamponade effect . Synthetic agents include Cyanoacrylates, Polyethylene Glycol Hydrogel, and Glutaraldehyde Cross-Linked Albumin. Cyanoacrylates are liquid monomers that rapidly form polymers in the presence of water and there by quickly glue adjacent surfaces together, were invented in 1942 . They are used as a replacement for sutures [ Toriumi DM , 2002 ].

33. Hemostatic dressings are most applicable for topical hemostasis due to effectiveness and ease of use. Dry Fibrin Dressings has been very successful in animal studies . Chitin and chitosan hemostatic dressings are most promising due to effective blood stop and possible additional properties like antibacterial and stimulatory to regeneration.

34. management General measures Patients taking antiplatelet and anticoagulant drugs Measures to prevent postoperative bleeding Apply firm pressure with gauze for 15 minutes. Local anesthesia with vasoconstrictor may be applied to help control the bleeding, determine the source, and facilitate further investigation . Beware of recurrent hemorrhage after the local effect of the vasoconstrictor dissipates. If the bleeding is from residual granulation tissue (e.g., within an extraction socket or after flap surgery) Consider its removal by curettage . Bony bleeding can be treated with a bone file , hemostat, or rongeur forceps by crushing and burnishing the overlying bone Soft tissue bleeding may be treated by clamping with a hemostat to encourage coagulation. If the bleeding persists after removal of the hemostat, vessel ligation with sutures, laser coagulation, or electrocautery may be necessary.

35. CONCLUSION

36. REFERNCES Textbook of medical physiology 10 th edition by G uyton and Hall. Periodontal medicine by Rose and mealey . Carranza 11 th edition. Essentials of medical physiology 6 th edition by K S embulingam , P rema sembulingam . Textbook of Physiology for Dental Students 3 rd edition by RK Marya , CM Marya . Physiological basis of medical practice 13 th edition by O.P T a ndon , Y. Tripathi . Human physiology 4 th edition by A K Jain. Vander’s human physiology 12 th edition by W idmaier , Raff and S trang . Basic and clinical pharmacology 11 th edition by B etram G. Katzung and Anthony J. T revor.