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Bleeding disorders thrombocytopenia PowerPoint Presentation

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Bleeding disorders thrombocytopenia سید علی روغنی نیری
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BLEEDING DISORDERS A bleeding tendency is a presentation with bleeding in a patient in whom no anatomical cause for the bleeding (i.e., trauma to a vessel for one of many possible reasons) can be discovered. It is then inferred that the bleeding is due to a functional impairment of the normal hemostatic process.
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What are bleeding disorders and Coagulation disorders?
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Petechiae
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Purpura
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Hemarthrosis
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Ecchymosis
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Hematoma
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Compare between coagulation and platelets disorder
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Hemostasis 1. vascular phase 2. palates phase 3. coagulation phase
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VASCULAR CAUSES OF BLEEDING HERIDITARY Hereditary hemorrhagic telangiectasia Ehlers-Danlos syndrome Marfan's syndrome METABOLIC AND INFLAMMATORY Henoch-Schonlein syndrome Scurvy - Amyloid Steroid purpura senile purpura Rickettsial diseases Polyclonal gammopathies
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Classification Platelets disorders Quantitative Thrombocytopenia Thrombocytosis Qualitative Inherited disorders Acquired disorders
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THROMBOCYTOPENIA Thrombocytopenia is defined as a platelet count less than 150,000 2.5 percent of the normal population will have a platelet count lower than this. Thrombocytopenia results from one or more of three processes: (1) decreased bone marrow production; (2) sequestration, usually in an enlarged spleen; and/or (3) increased platelet destruction.
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Pseudo thrombocytopenia In evaluating a patient with thrombocytopenia, a key step is to review the peripheral blood smear and to first rule out "pseudo thrombocytopenia" It is an in vitro artifact resulting from platelet agglutination via antibodies ,when the calcium content is decreased by blood collection in EDTA tube. If a low platelet count is obtained in EDTA-anticoagulated blood, Repeat platelet count determined in blood collected into sodium citrate (blue top tube) or heparin (green top tube).
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Pseudo thrombocytopenia
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Inherited thrombocytopenia
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INFECTION-INDUCED THROMBOCYTOPENIA Most common non-iatrogenic cause of thrombocytopenia. Can affect both platelet production and platelet survival. Immune mechanisms are proposed to be the cause, as in infectious mononucleosis, HIV and other viral Infections. “A study evaluating the role of bone marrow examination in fever of unknown origin in HIV-infected patients found that for 86% of patients, the same diagnosis was established by less-invasive techniques, notably blood culture." Thus, a bone marrow examination is not routinely recommended in evaluation of thrombocytopenia in infections and it is recommended when the diagnosis is needed urgently or when other, less invasive methods have been unsuccessful.
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Drug-Induced Thrombocytopenia predictable decrease in platelet count occurs after treatment with many chemotherapeutic drugs due to bone marrow suppression. All drugs should be suspect in a patient with thrombocytopenia without an apparent cause and should be stopped, or substituted, if possible. Although not as well studied, herbal and over-the-counter preparations may also result in thrombocytopenia. They are very commonly seen in Quinine and Sulfa drugs. Other examples include Rifampin, Amiodarone, Ampicillin, Digoxin,Diclofenac,lbuprofen,Linezolid,Furosemide.
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Drug-Induced Thrombocytopenia (cont.) Classic drug-dependent antibodies are antibodies that react with specific platelet surface antigens, and result in thrombocytopenia only when the drug is present. The thrombocytopenia typically occurs after a period of initial exposure (median length 21 days), or upon reexposure, and usually resolves in 7-10 days after drug withdrawal. The thrombocytopenia caused by the platelet Gp llb llla inhibitory drugs, such as abciximab, differs in that it may occur within 24 h of initial exposure. This appears to be due to the presence of naturally occurring antibodies that cross-react with the drug bound to the platelet.
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HEPARIN INDUCED THROMBOCYOPENIA Heparin has been used as an anticoagulant medication since the late 1930s and is one of the most prescribed drugs. However, clinicians recognized that some patients developed a syndrome of immune-mediated thrombocytopenia and thrombosis, which came to be called heparin-induced thrombocytopenia (HIT). Drug-induced thrombocytopenia due to heparin differs from that seen with other drugs in two major ways. (1) The thrombocytopenia is not usually severe, with nadir counts rarely <20,000/L. (2) Heparin-induced thrombocytopenia (HIT) is not associated with bleeding and, in fact, markedly increases the risk of thrombosis.
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HEPARIN INDUCED THROMBOCYOPENIA (cont.) HIT occurs when IgG antibodies develop against neoantigens created by multimolecular heparin/platelet factor 4 (PF4) complexes. The antiheparin/PF4 antibody can activate platelets through the FcRIIa receptor and also activate monocytes and endothelial cells. Surgical patients develop the antibodies more often than medical or obstetric patients because surgery results in platelet activation and PF4 release from platelet alpha granules. In general, antibodies can be identified in up to 15% of orthopedic surgical patients and up to 50% of cardiopulmonary bypass patients. Therapeutic heparin doses are not required to stimulate antibody production; even small amounts of heparin can result in antibody formation and clinical HIT.
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HEPARIN INDUCED THROMBOCYOPENIA (cont.) Patients baseline platelet counts should be obtained before initiating heparin therapy. A falling platelet count during therapy raises the suspicion of HIT, and in the usual presentation The platelet count begins to drop after 5 to 10 days of heparin therapy. Patients with recent heparin exposure (within 100 days) may have platelet counts that fall before day 5, often within the first 24 hours. Delayed-onset cases also occur but are uncommon.
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HEPARIN INDUCED THROMBOCYOPENIA (cont.)
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HEPARIN INDUCED THROMBOCYOPENIA (cont.)
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HEPARIN INDUCED THROMBOCYOPENIA (cont.) WHEN TO GO FOR DIAGNOSTIC TESTING? The 4 Ts have been recommended to be used in a diagnostic algorithm for HIT: (Pre test Probability) 1.Thrombocytopenia 2.Timing of platelet count drop 3.Thrombosis and other sequelae such as localized skin reactions 4 .oTher causes of thrombocytopenia not evident Each feature is given a score and patients are classified as high, intermediate, or low probability. Such clinical scoring systems have good Negative predictive value for patients with low scores; patients with moderate or high clinical probability usually require lab testing
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HEPARIN INDUCED THROMBOCYOPENIA (cont.)
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HEPARIN INDUCED THROMBOCYOPENIA (cont.) Steps: Early Recognition, Stop Heparin(Don't switch to LMWH) Go for Imaging Studies( At least lower extremity duplex Doppler) The direct thrombin inhibitors (DTIs) argatroban and lepirudin are to be started If thrombosis present - treat for 3 to 6 months If no evidence - treat for 1 month
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HEPARIN INDUCED THROMBOCYOPENIA (cont.) TREATMENT OF HIT The direct thrombin inhibitors (DT's) ARGATROBAN AND LEPIRUDIN are effective in HITT. The DTI bivalirudin and the antithrombin-binding pentasaccharide fondaparinux are also effective but not yet approved by the U.S. Food and Drug Administration (FDA) for this indication. ARGATROBAN : The dose is 2 mcg/kg/min, adjusted by PTT with a target of 1.5-3 times the baseline. The initial dose should be reduced by 75% in patients with liver dysfunction. LEPIRUDIN : The dose is 0.4 mg/kg via intravenous bolus, which should be followed by an initial maintenance infusion of 0.15 mg/kg/h, adjusted for a target activated partial thromboplastin time (PTT) of 1.5-2.5 times the baseline. It is important to remember that lepirudin is Metabolised by the kidneys and argatroban by the liver.
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HEPARIN INDUCED THROMBOCYOPENIA (cont.) Warfarin therapy in HIT Warfarin should be postponed until substantial platelet recovery. If warfarin has already been started, vitamin K should be given. Introduction of warfarin alone in the setting of HIT or HITT may precipitate thrombosis, particularly venous gangrene, presumably due to clotting activation and severely reduced levels of proteins C and S. HIT patients typically present with an international normalized ratio (INR) greater than 4, which corresponds to severe protein C depletion. Preferably, warfarin should not started before the thrombocyte count is greater than 150 x 10**9/L. Platelet transfusions should be avoided in heparin-induced thrombocytopenia (HIT), as they may increase the thrombogenic effect.
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Immune Thrombocytopenic Purpura (ITP) an acquired disorder in which there is immune-mediated destruction of platelets and possibly inhibition of platelet release from the megakaryocyte. Childhood form (most < 10 yrs old) May follow viral infection, vaccination Peak incidence in fall & winter 50% receive some treatment 75% in remission within 6 mo Adult form No prodrome Chronic, recurrences common Spontaneous remission rate about 5%
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Immune Thrombocytopenic Purpura (cont.) CLINICAL FEATURES ITP is characterized by mucocutaneous bleeding and a low, often very low, platelet count, with an otherwise normal peripheral blood cells and smear. Patients usually present either with ecchymosis and petechiae, or with thrombocytopenia incidentally found on a routine CBC. Mucocutaneous bleeding, such as oral mucosa, gastrointestinal, or heavy menstrual bleeding, may be present. Rarely, life-threatening, including central nervous system, bleeding can occur. Wet purpura (blood blisters in the mouth) and retinal hemorrhages may herald life-threatening bleeding.
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Immune Thrombocytopenic Purpura (cont.) LABORATORY TESTING Laboratory testing for antibodies (serologic testing) is usually not helpful due to the low sensitivity and specificity of the current tests. a Bone marrow examination :can be reserved for older adults (usually >60 years) in patients who do not respond to initial therapy. Peripheral blood smear : May show large platelets Iron deficiency anemia may be present. Testing for HIV infection and hepatitis C (to rule out secondary causes) Serologic testing for SLE, serum protein electrophoresis, and immunoglobulin levels to potentially detect hypogammaglobulinemia. Direct antiglobulin testing (Coombs test) to rule out combined autoimmune hemolytic anemia with ITP (Evans syndrome).
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Immune Thrombocytopenic Purpura (cont.) RhO(D) immune globulin therapy: Only in Rh + Patients at 50-75 mic g/kg The mechanism of action of anti-D is not fully understood however, after administration the anti-D coated red blood cell complexes saturate Fc y receptors sites on macrophages ,resulting in preferential destruction of RBCs, therefore sparing antibody-coated platelets.
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Immune Thrombocytopenic Purpura (cont.)
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Immune Thrombocytopenic Purpura (cont.) STEROIDS: Prednisone to be given at 1 mg/kg. Until platelet counts comes back to normal levels It takes around two to four weeks. Intravenous Immunoglobulin(Iv ig): Intravenous gamma globulin (IVIgG), which is pooled, primarily IgG antibodies, also blocks the Fc receptor system, but appears to work primarily through different mechanism (s). IVIgG is dosed at 2 g/kg total, given in divided doses over 2-5 days.
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Immune Thrombocytopenic Purpura (cont.)
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Thrombotic Thrombocytopenic Purpura a Classic pentad: Microangiopathic hemolytic anemia Thrombocytopenia Renal involvement Neurologic signs Fever Most cases in adults are caused by acquired autoantibodies that inhibit ADAMTS13(a metalloprotease that cleaves vWF within platelet-rich thrombin) Congenital form (Upshaw-Schulman syndrome) is the result of a deficiency of ADAMTS 13.
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Thrombotic Thrombocytopenic Purpura(cont.) DIAGNOSIS TTP is a devastating disease if not diagnosed and treated promptly. Findings to support the TTP diagnosis include: Increased lactate dehydrogenase Increased indirect bilirubin Decreased haptoglobin Increased reticulocyte count Negative direct antiglobulin test. The peripheral smear may show evidence of schistocytes.
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Thrombotic Thrombocytopenic Purpura(cont.) TREATMENT Plasma exchange remains the mainstay of treatment of TTP. Plasma exchange is continued until the platelet count is normal and signs of hemolysis are resolved for at least 2 days. The use of glucocorticoids seems a reasonable approach, but should only be used as an adjunct to plasma exchange. Immunomodulatory therapies have been reported to be successful in refractory or relapsing TTP, including rituximab, vincristine, cyclophosphamide, and splenectomy. A significant relapse rate is noted, 25-45% within 30 days of initial "remission," and 12-40% with late relapses
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