Read Bleeding- Blood disorders -PE II [Read-Only] text version

Normal control of bleeding

Normal control of bleeding

Vascular phase: begins immediately at the site of the wound vasocontriction

Platelet phase: platelets migrate to wound area become "sticky" agglutinate and adhere to endothelial wall of vessel mechanical "plug" of platelets seal up wounded blood vessels occurs soon after injury

Normal control of bleeding

Coagulation phase extravascated blood in surrounding tissue activates extrinsic and common coagulation pathways blood within vessels coagulates by intrinsic and common coagulation pathways coagulation process occurs slowly ( hours)

Coagulation pathway

Extrinisic pathway: starts with tissue thromboplastin Intrinisic pathway: starts with contact activation Common pathway Fibrinolytic system

Detection of the patient with bleeding problems

history clinical examination laboratory tests surgery

Detection of the patient with bleeding problems

history of bleeding problems in past: operations, dental extractions, woundsinjuries, spontaneous history of bleeding problems in relatives medications: ASA, antibiotics, analgesics, anticoagulants illnesses, (viral, liver, hematologic)

Detection of the patient with bleeding problems

history clinical examination laboratory tests surgery

Detection of the patient with bleeding problems

skin color: pallor, jaundice angiomas, petechiae ecchymoses, purpura hemarthroses gingival hyperplasia and bleeding

Detection of the patient with bleeding problems

history clinical examination laboratory tests surgery

Detection of the patient with bleeding problems

Prothrombin time( PT ) or International Normalized Ratio (INR) Partial thromboplastin time (PTT) Thrombin time (TT) Bleeding time (BT) Platelet count

Prothrombin time (PT)

activated by tissue thromboplastin tests extrinsic and common pathways run with a control ( variable with lab : therefore: INR) normal= 11-15 seconds prolonged time = abnormal ( significant > 2.5, 3.0, 3.5...)

Activated partial thromboplastin time (PTT)

Contact activator( kaolin) tests the intrinsic and common pathways run with a control normal= 25-35 seconds prolonged ( 2.5, 3.0, 3.5...)= abnormal

Platelet count

tests numbers of platelets present to form clot normal= 140,000 to 400,000 / cc bleeding problems < 50,000/cc

Bleeding disorders

Nonthrombocytopenic purpuras

vascular platelet

wall alterations function disorder

Thrombocytopenic purpuras

secondary(

Primary ( genetic) acquired: drugs, diseases) acquired

Disorders of coagulation

inherited,

Platelet release disorders

failure to release Factor III usually little problem with bleeding unless another problem is present prolonged BT absence of stabilization of clot ( i.e. second-wave of platelet aggregation)

Thrombocytopenia

platelet count ~ 50,000 ( with or without platelet replacement) < 50,000 = bleeding problem Tx: pack with microfibrillar collagen, EACA 100mg/kg prior to surgery ± EACA 50 mg/kg QID for 5-7 days

von Willebrand's disease

autosomal dominant = most= defect in chromosome #13 = moderate defect in platelet adhesion autosomal recessive= SEVERE von Willebrand factor binds with Factor VIII if not bound, Factor VIII is destroyed

von Willebrand's disease

family history : personal history of bleeding prolonged BT decreased platelet adhesion and aggregation decreased Factor VIII efficacy prolonged PTT

Hemophilia

< 1% Factor VIII = SEVERE >1 % < 10% Factor VIII = MODERATE >10% Factor VIII = MILD 10% of patients develop inhibitors of Factor VIII = SEVERE ( 50% are stable) most dental surgery OK if stable

Hemophilia : treatment

Factor VIII Replacement factors: Cryoprecipitate Fresh frozen plasma purified, heat treated AHF ultrapure AHF:

monoclonal recombinant

Ab or DNA

Anticoagulant therapy

Heparin(standard: half-life >2 hrs.) : hospital only If hemodialysis: Tx day after LMWH : enoxaparin (Lovenox) Others: Normiflo, Fragmin, Fraxiparine, Clivarin, Innohep

No INR : No need to alter Rx for dental treatment

Antiplatelet agents

ASA: best guide= PFA-100( platelet

function analyzer) > 20 min. ! DDAVP ( 1- desamino-8-D- arginine vasopressin) ( Stimate) 20-24 µg nasal spray NSAIDS: COXI- wait 3 half-lives

Antiplatelet agents

Bleeding problems due to Coumadin 10-40 % of hospital admissions for bleeding age-dependent strength and duration of coumadin Rx reduction of bleeding with proper anticoagulant monitoring guideline-based recommendations

Plavix( clopidogrel)or Ticlid( ticlopidine) OK most Sx - if major Sx then d/c 1 wk. Aggrastat( fibrinogen receptor inhinitors ) OK most Sx - if major Sx then d/c 1 wk. COX-2 : (celecoxib, rofecoxib)= OK unless with Coumadin

Coumadin ...dicoumarol...coumarin

Warfarin WARF Wisconsin Alumni Research Foundation

Bleeding problems due to Coumadin Conditions in which Coumadin amy be Rxd: post-CVA, MI, CHF, congenital HD, arrhythmmias, etc. Usual therapeutic range : INR= 2.0-3.0 Some cases: higher INR= 2.0-4.0 Most dental Tx OK if INR < 3.0, including simple oral surgery, use local hemostatic measures

coumarin

Increased Coumadin sensitivity

Vitamin K deficiency: malabsorption, broad spectrum antibiotics displacement of warfarin binding: ASA, indomethacin, ibuprofen, naproxen, phenytoin, oral hypoglycemics, estrogen, sulindac, phenylbutazone, tolmentin, fenprofen, miconazole

Increased Coumadin sensitivity

Synergism with warfarin : Vitamin E, anabolic steroids, Danazol blocking of warfarin metabolism: tricyclic antidepressants, erythromycin, cimetidine, sulfa drugs, chloramphenicol, quinidine, phenothiazine, disulfiram,

Coumadin - therapeutic range

Local hemostatic agents

Oxycel Surgicel Microfibrillar collagen

INR = 2.5- 3.0

Lovenox or Avenox( 40 mg) once! Transexamic acid( Cyklokapron, KabiVitrum) oral rinse, tablets or IV

Local hemostatic agents

BLEEDING DISORDERS dental management

MEDICAL CONSULTATION Usually no special considerations for: Exam, radiographs, anesthesia, endo, ortho, impressions, fluoride Tx, simple prophies, simple operative Usually only surgery or `SIGNIFICANT BLEEDING " (INR > 3.0)

Gelfoam( Upjohn) (± thrombin ) on a stint Instat( J & J) collagen ( ~ Gelfoam ; $ )

Surgicel/Oxycel: cellulose( gelatinous) Avitene/Helistat= microfibrillar collagen hemostat ( MCH) Colla-Cote - bovine collagen( tape or plug)

Thrombostat, Thrombinar, Thrombogen- topical thrombin.......SEVERE BLEEDING

BLEEDING DISORDERS dental management

CONSULTATION with Hematologist Level of factor VIII deficiency and/or replacement Presence of inhibitors Treatment Need for EACA, Tranexamic acid Steroids HOSPITALIZATION

BLEEDING DISORDERS dental management

SPLINTS INFECTIONS Antibiotic prophylaxis LOCAL MEASURES: microfibrillar collagen, gelfoam, thrombin Avoid anticoagulants ( ASA) HBV, HCV, HIV ??(1985)

BLEEDING DISORDERS dental management

Bleeding history-problem with no clue as to cause Screen with PT, PTT, BT, platelet count ASA= BT, PTT COUMARIN= PT(INR) LIVER DISEASE= PT(INR), BT LEUKEMIA= platelets, BT ANTIBIOTICS= PT(INR) Crohns' (etc.) = PT(INR)

BLOOD DYSCRASIAS

potential problems related to dental treatment:

excessive bleeding infections poor wound healing oral lesions mucositis

BLOOD DYSCRASIAS

ANEMIA symptom complex not a disease etiology: low Fe++ intake, lack of intrinsic factor, chronic blood loss, BMT, drugs, erythrocytopenia ( splenomegaly, etc.)

BLOOD DYSCRASIAS

ANEMIA- symptoms weakness, fatigue tingling, numbness, paresthesias dyspnea, syncope palpitations, abdominal pain jaundice bone pain

BLOOD DYSCRASIAS

ANEMIA- physiologic women: menses, pregnancy men: NONE ! LABORATORY TESTS Hb-hemoglobin Hct- hematocrit Sickledex

BLOOD DYSCRASIAS

BLOOD DYSCRASIAS

WHITE BLOOD CELLS granulocytes: neutrophils, eosinophils, basophils lymphocytes: T cells, B cells monocytes Differential WBC

SICKLE CELL ANEMIA- dental management FATAL !! avoid- aggressively treat oral infections AVOID EPINEPHRINE good anesthesia, analgesia, pain control AVOID barbiturates, narcotics, sedation careful with ASA, consider prophylactic antibiotics

BLOOD DYSCRASIAS

LEUKOCYTOSIS- physiologic exercise, pregnancy, emotional stress LEUKOCYTOSIS- pathologic infections, neoplasia, necrosis LEUKOPENIA early phase of leukemia, cyclic neutropenia, drugs, chemicals, radiation

BLOOD DYSCRASIAS

INFECTIOUS MONONUCLEOSIS EBV= Epstein-Barr Virus 10% large reactive T- lymphocytes B- lymphocytes are EBV-infected transmitted easily by intimate contact: most will carry E BV in oropharyngeal region

BLOOD DYSCRASIAS

BLOOD DYSCRASIAS

INFECTIOUS MONONUCLEOSIS medical management bed rest, ASA, irrigation with warm NaCl, possibly corticosteriods, antivirals ?, antibiotics if secondary bacterial infection

INFECTIOUS MONONUCLEOSIS incubation period: 30-50 days: asymptomatic but easily transmitted prodromal period: 3- 5 days: flu-like illness= fever, malaisse, myalgia, headache clinical phase- 1- 3 weeks: fever, lymphadenopathy, pharyngitis, petechiae, skin rash

LEUKEMIA

25,000 - 30,000 cases per year in U.S. ~50 % are acute; 55 % of deaths high morbidity- mortality( without Tx nearly 100% fatal within 1-3 months !!) ALL-Acute lymphocytic leukemia= most common in children CLL- chronic lymphocytic leukemia= most common in adults

LEUKEMIA

etiology: heredity, chromosomal abnormalities, immune system abnormalities, chronic bone marrow dysfunction, ionizing radiation, chemical and drugs, viruses

LEUKEMIA

Acute: sudden onset, fast progression any age immature WBC proliferation severe anemia severe thrombocytopenia WBC decrease then tremendous increase

LEUKEMIA

SYMPTOMS weakness, fatigue, malaisse lymphadenopathy dyspnea, fever, palpitations pharyngitis, myalgia, weight loss recurrent infections, oral lesions spontaneous gingival bleeding

LEUKEMIA

SIGNS pallor, petechiae, ecchymoses lymphadenopathy gingival bleeding, hypertrophy oral lesions, loose teeth, pulpal path

LEUKEMIA

ALL- Acute lymphocytic leukemia= 75 % children ( 3-10 y.o.); 25% teenagersadults kids cure rate with Tx= ~50-70 % adults cure rate with Tx < 20 %; shortterm remission = ~50-70 %

LEUKEMIA

AML- Acute myeloid leukemia = 85 % adults + 15 % children AML: classificationM1- myeloblastic( undifferentiated) M2- myeloblastic( differentiated) M3- Promyelocytic M4- Myelomonocytic M5- Monocytic M6- Erythrocytic M7- Megakyoblastic

LEUKEMIA

AML - all subtypes have similar clinical findings( except slightly different skin, gingival and CNS lesions in M3,M4,M5) Pre-leukemic syndrome occurs in ~25 % of adults: anemia, cytopenia Indicates a poor prognosis

LEUKEMIA

TREATMENT Chemotherapy remission: no signs or symptoms blast cells reduced to billions relapse: re-emergence of signs and symptoms, blast cells increase again

LEUKEMIA

LEUKEMIA

TREATMENT Chemotherapy >>>remission ( shortterm or long term) Cure= no remaining leukemic cells Relapse= return of trillions of cells again; second remission much more difficult, poorer prognosis

Chemotherapy 3 phases of chemo : first hit hard to get remission, consolidation, maintenanceprevent expansion of remaining leukemic

LEUKEMIA

Sanctuaries for leukemic cells = testes, CNS ; special treatment necessary = irradiation and/or methotrexate TREATMENT BONE MARROW TRANSPLANT Children ONLY; must be in remission Induce second remission then BMT

LEUKEMIA

Chronic leukemia(CML) vs. acute leukemia Adults (30-50 y.o.) Slower, insidious onset of symptoms Overall POOR prognosis More functional, mature WBCs (~200,000) Mild anemia, mild thrombocytopenia

LEUKEMIA

Chronic leukemia(CML) If no Tx = death in 2-6 yrs. Mean survival time = 3.5 yrs. 25% asymptomatic at diagnosis 25% transform to blastic stage after Dx 85% DIE in blastic stage

LEUKEMIA

Chronic lymphocytic leukemia (CLL) Mean age = ~ 60 y.o. Rare in children Lower WBC than CML 25% = asymptomatic;Dxed on routine exam Slow onset of symptoms, better prognosis Enlarged lymph nodes and spleen

LEUKEMIA

PROGNOSIS for CLL: Stage A > 10 yrs. Stage B ~ 5 yrs. Stage C < 2 yrs. Treatment has had little effect on survival

LEUKEMIA

SCREENING LABORATORY TESTS WBC with differential Smear Hb, Hct, sickeldex Platelet count monospot

LEUKEMIA

ORAL FINDINGS: Ulcerations Masked or unusual infections Submucosal hemorrhage Spontaneous gingival bleeding paresthesias

LEUKEMIA

Dental management Remission-most routine care = OK prevent infections, bleeding control Poor control or relapse= ANC < 500: emergency care only, prophylactic antibiotics, prevent infections, bleeding control

LYMPHOMA

Hodgkin's ; non-Hodgkin's; Burkitt's Risk= two peaks : early adults and 50's ~7500 cases/yr. In U.S. Mortality varies Tx= radiation and chemotherapy Increased risk for leukemia

Hodgkin's LYMPHOMA

Symptoms: fatigue, weakness, pruritis Fever, lymphadenopathy, night sweats, weight loss Cell of origin unresolved; often localized Extranodal lesions are uncommon Cure rate > 75 %

Non-Hodgkin's LYMPHOMA

Usually multifocal, non-localized ~ 30,000 cases/yr. In U.S. 10% have AIDS B-cell origin= 90 % of cases;10 % = T-cells 66% present with non-painful lymphadenopathy Extranodal lesions < 25 % cure rate !

Burkitt's LYMPHOMA

B-cell proliferation EBV Some AIDS cases African form = jaws American form= lymph nodes, bone marrow

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