Bleeding Complications and Prevention

1. Bleeding Complications and Prevention N. Whitney James, DDS Northern Navajo Medical Center Shiprock, New Mexico

2. Bleeding Complications and Prevention • There are many possible complications which can occur during Oral Surgery • Many of these complications are preventable by critical pre-operative patient evaluation and management. • Bleeding complications and be very frustrating and scary.

3. Bleeding Complications and Prevention • Bleeding complications and be very frustrating and scary. • Understanding the stages of coagulation and the coagulation cascade will help the provider understand better how to treat the bleeding patient. • “All bleeding eventually stops”

4. Coagulation • Coagulation is the process that stops bleeding and involves a wide variety of mechanisms • Blood vessel constriction • Platelets • Plasma proteins • Calcium

5. Stages of Coagulation • Stage 1: Immediately after injury vascular constriction occurs at the injury site which limits the flow of blood to the area of injury. At the same time the blood glycoprotein, Von Willebrand Factor, bonds with Calcium ions to form Thromboplastin and aids in platelet adherence to vessel walls.

6. Stages of Coagulation • Thromboplastin converts the protein prothrombin in thrombin. Platelet aggregation to each other and to vessel walls (endothelial cells) forming a primary plug.

7. Stages of Coagulation • Stage 2: Thrombin converts fibrinogen into fibrin. Fibrinogen is primarily responsible for stimulating platelet aggregation. Fibrin, an insoluble protein then forms an intricate network of threadlike structures called fibrils and causes the blood plasma to gel. The blood cells and plasma are enmeshed in the network of fibrils to form the clot.

8. Coagulation Cascade • The coagulation cascade has two branches or pathways • Extrinsic • Activated with injury to tissues • Intrinsic • Activated with injury to blood vessel walls • These two come together in the common pathway and fibrin is formed

9. Coagulation Cascade

10. Coagulation Cascade • Intrinsic • Factors VIII, IX, XI, XII • Measured with PTT • Normal 22 to 36 • Affected by heparin • Extrinsic • Factors II, V, VII, X, Vitamin K • Measured with PT • Normal 11 to 14 • Affected by Coumadin

11. Coagulation Issues • What is a bleeding disorder? • A general term for a wide range of medical problems that lead to poor blood clotting and continuous bleeding • Synonyms • Coagulopathy • Clotting disorders

12. Bleeding Disorders • Complications with bleeding can come from a wide variety of sources • Intrinsic • Born with the problem • Acquired • Pick it up during the course of life

13. Bleeding Disorders • Intrinsic • Hemophilia A • Hemophilia B • von Willebrand Disease • Acquired • Thrombocytopenia • Decreased production • Increased destruction • Medications • Heparin • Coumadin • ASA, NSAIDS • Liver disease • Systemic diseases

14. Hemophilia A • Factor VIII deficiency • X linked • Incidence: 1:5000 to 1:10000 live births • 12,000 Americans • 1/3 result from spontaneous mutations

15. Hemophilia A • Symptom severity related to factor amount • Severe <1% of normal • Moderate 1% to 5% of normal • Mild 6% to 49% of normal • Symptoms • Easy bruising and prolonged bleeding • Blood in urine or stool • Bleeding into joints with pain and swelling

16. Hemophilia B • Factor IX deficiency • AKA “Christmas disease” • X linked • Incidence: 1:34,500 • Seven times less common than Hemophilia A

17. Hemophilia B • Symptom severity also related to factor amount • Symptoms are similar to Hemophilia A

18. Treatment of Hemophilias • Basically treated with the administration of the missing factor • Plasma concentrates are preferential to plasma itself • Less chance of virus transmission • Can be self-administered

19. Dental Considerations • Be cautious • Physician consultation • Avoid intramuscular injections • Therapies • Factor replacement • Desmopressin acetate (DDAVP) • Antifibrinolytic agents

20. Dental Considerations • Avoid drugs that can affect coagulation • Aspirin • NSAIDS

21. von Willebrand Disease • Hereditary deficiency or abnormality of von Willebrand factor • Protein involved with platelet function • Platelets fail to adhere to blood vessel walls • Erik von Willebrand • Finnish physician • Occurs in 1% to 2% of the population • Autosomal transmission

22. von Willebrand Disease • Type I • Mildest form • Most common • Levels of von Willibrand factor are lower

23. von Willebrand Disease • Type II • Factor itself is abnormal • Type IIa • Level of factor decreased and factor is abnormal • Type IIb • Factor is defective but platelet clumping increased • Aggregation vs adhesion

24. von Willebrand Disease • Type III • Severe form • Total absence or very low factor • Factor VIII levels are often < 10% • Pseudo • “Platelet type” • Defect is actually in the platelets

25. Treatment of von Willebrand Dx • Treatment depends upon severity • Many people will never need therapy • Desmopressin (DDAVP, Stimate) • Increases vWF and factor VIII • Factor infusion • Antifibrinolytic agents • Tranexamic acid and Aminocaproic acid

26. Treatment of von Willebrand Dx • Factor Infusion • Fresh frozen plasma • Risk of viral or prion transmission • Viral inactivated factor VIII rich in von Willebrand factor • Much less risk of transmission • Pricey • Humate-P, Alphanate, Koate DVI

27. Treatment of von Willebrand Dx • DDAVP Challenge • Obtain baseline values for bleeding time and vWF levels • Give desmopressin • IV: 0.3mcg/kg • Intranasal: 2-4mcg/kg • Observe response • If poor, will likely need factor (ie Humate-P) • If good, factor may not be needed

28. Dental Considerations • Similar to Hemophilia • Consultation with physician • Avoid situations that cause bleeding • Extraction, other oral or perio surgery • IM injections • Septocaine • Hospitalization may be indicated for factor infusion and/or post-op observation

29. Dental Considerations • Similar to Hemophilia • Good local surgical site measures • Minimize trauma • Hemostatic agents • Surgicel, collagen, Gelfoam • Judicious use of sutures • Ice packs • Strict and repetitive post-op instructions

30. Dental Considerations • Topical Antifibrinolytic agent • Tranexamic acid (Cyklokapron) • 10ml of a 4.8% aqueous solution • Irrigate socket before suturing • Mouthwash • Rx: Tranexamic acid 4.8% solution Swish with 10ml for 2 minutes qid x 1 wk

31. Thrombocytopenia • Platelets migrate to an area after injury and a primary plug is formed • This first phase of hemostatis is measured by the bleeding time • Normal is 2.5 to 9.5 minutes

32. Thrombocytopenia • The bodies bone marrow doesn’t make enough platelets • The bone marrow makes enough platelets, but the body destroys them or uses them up • The spleen hold on to too many platelets • A combination of the above

33. Thrombocytopenia: Bone marrow doesn’t make enough platelets • Conditions and Factors that can damage stem cells: • Cancer • Aplastic Anemia • Toxic Chemicals • Medications • Alcohol • Viruses • Genetic conditions

34. Thrombocytopenia: Cancer • Cancers, such as leukemia or lymphoma can damage the bone marrow and destroy blood stem cells. • Cancer treatments, such as radiation and chemotherapy, also destroy the stem cells.

35. Thrombocytopenia: Aplastic Anemia • Aplastic anemia is a rare, serious blood disorder in which the bone marrow stops making enough new blood cells. This lowers the number of platelets in your blood. • “Fanconi’s anemia” A familial form of Aplastic Anemia. (bone abnormalities, microcephaly, hypogentialism, brown pigmentation of skin)

36. Thrombocytopenia: Toxic Chemicals • Exposure to toxic chemicals-such as pesticides, arsenic and benzene-can slow the production of platelets

37. Thrombocytopenia: Medicines • Some medicines, such as diuretics and chloramphenicol, can slow the production of platelets.

38. Thrombocytopenia: Alcohol • Alcohol also slow the production of platelets, A temporary drop in the platelet count is common among heavy drinkers, especially if they’re eating foods that are low in iron, vitamin B12, or folate.

39. Thrombocytopenia: Viruses • Chickenpox, mumps, rubella, Epstein-Barr virus, or parvovirus can decrease your platelet count for a while. People who have AIDS often develop thrombocytopenia.

40. Thrombocytopenia: Genetic Conditions • Some genetic conditions can cause low number of platelets in the blood. Examples include: • Wiskott-Aldrich syndrome • May-Hegglin syndrome (large non-functional platelets)

41. Thrombocytopenia: Body Destroys Its Own Platelets • A low platelet count can occur even if the bone marrow makes enough platelets. • Autoimmune Diseases • Medicines • Infections • Surgery • Pregnancy • Conditions that cause too much clotting

42. Thrombocytopenia: Autoimmune Disease • ITP Immune thrombocytopenia: Autoimmune disorder the destroys platelets. Etiology – unknown. • Other autoimmune diseases that destroy platelets: Lupus, rheumatoid arthritis

43. Thrombocytopenia: Medicines • A reaction to medicine can confuse the body and cause it to destroy its platelets: • Quinine: found in tonic water and nutritional health products • Antibiotics that contain sulfa: Vancomycin, Rifampin • Some seizure medications: Dilantin

44. Thrombocytopenia: Medicines • Heparin Induced thrombocytopenia (HIT): An immune reaction may trigger the medicine to cause blood clots and thrombocuytopenia. • Usually occurs in hospital settings. • The immune system attacks a substrate formed by heparin and a protein on the surface of platelets activating clot formation leading to DVTs or PE

45. Thrombocytopenia: Infection • A low platelet count can occur after blood poisoning from a widespread bacterial infection. • A virus, such as mononucleosis or cytomegalovirus, also can cause a low platelet count.

46. Thrombocytopenia: Surgery • Platelets can be destroyed when they pass through man made heart valves, blood vessel grafts, or machines and tubing used for blood transfusions or bypass surgery.

47. Thrombocytopenia: Pregancy • About 5 percent of pregnant women develop mild thrombycytopenia when they’re close to delivery. • The exact cause is not known.

48. Thrombocytopenia: Conditions That Cause Excess Blood Clotting • Thrombotic Thrombocytopenic Purpura (TTP): • Causes multiple clot formation in the small blood vessels, including brain, kidneys, heart • This leads to significant drop in platelet counts.

49. Thrombocytopenia: Spleenic Accumulation of Platelets • One third of the bodies platelets are held in the spleen. • If the spleen is enlarged, it will hold on to too many platelets. This means that not enough platelets will circulate in the blood. • Cancer or sever liver disease (Cirrhosis) • Enlarged spleen also might be due to Myelofibrosis (scarring of the bone marrow and unable to produce platelets)

50. Thrombocytopenia: Conditions That Cause Excess Blood Clotting • Disseminated Intravascular Coagulation (DIC): • A complication of pregnancy, sever infections, or tissue trauma leading to tiny blood clots forming suddenly throughout the body. • The multiple clot formation leads to a decrease in platelet counts.