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Thrombocytopenia
- 1. PRESENTED BY:Dr Sachin Giri Moderator:Dr Nikhil Gupta Assistant Professor
- 2. Definitions Stages of platelets Developement Causes Approach to Thrombocytopenic Patient Diagnosis Treatment
- 3. Thrombocytopenia is defined as an count less than 150000/mm₃ Pseudothrombocytopenia –Blood collected in EDTA tube leads to platelets clumping due to the presence of antibodies usually IgG but also IgM IgA
- 5. Decreased Production Hematologic malignancies Aplastic anemia Myelodysplasia Drugs: chemotherapy, alcohol Radiation HIV Hereditary thrombocytopenias Metastatic cancer to bone marrow
- 6. Immune 1. ITP 2. HIT 3. Drug-induced antibodies 4. HIV 5. post transfusion purpura 6. Connective tissue diseases Nonimmune 1. DIC 2. Sepsis 3. TTP-HUS 4. Kasabach Merrit syndrome Sequestrations 1. Hypersplenism
- 7. Histoty usually asymptomatic Presence of petechiae, ecchymoses Mucocutaneous bleeding Purpura Rarely central nervous system bleeding retinal hemorrhages
- 8. History of… Recent Infections Malignancies Pregnancy status in premenopausal woman Recent medications Vaccinations Recent travels Recent transfusions Recent organ transplantation Family history of thrombocytopenia Autoimmune disorders
- 9. presence of petechiae ecchymosis in the skin, wet purpura in mucous membranes Splenomegaly The presence of retinal hemorrhage on ocular fundus examination is a predictor of CNS hemorrhage
- 10. Complete blood counts Peripheral blood smear D-dimer Serum LDH Bone marrow examinations HIV ESR hsCRP
- 12. Due to the presence of naturally occurring antibodies that cross-react with the drug bound to the platelet. The thrombocytopenia occurs after a period of initial exposure of 21 days Resolves in 7–10 days after drug withdrawal. Abciximab exposure causes thrombocytopenia within 24 h of initial exposure.
- 13. Penicillin Phenytoin Piperacillin Abciximab NSAIDs Amiodarone Amlodipine Ampicillin Carbamazepine Ceftriaxone Cephamandole Ciprofloxacin Diazepam Eptifibatide Furosemide Vancomycin
- 14. The thrombocytopenia is not usually severe, rarely <20,000/μL. Heparin-induced thrombocytopenia (HIT) is not associated with bleeding, it increases the risk of thrombosis. Antibodies to complex of platelet factor 4 and heparin HIT after exposure to heparin for 5–14 days.
- 16. HIT (anti-heparin/PF4) antibodies can be detected using two types of assays. The most widely available is an enzyme-linked immunoassay (ELISA). The other assay is a platelet activation assay, most commonly the serotonin release assay,
- 17. Direct thrombin inhibitor (DTI) - Argatroban -Fondaparinux Xa Inhibitor-Danaparoid Warfarin therapy.
- 18. Immune thrombocytopenic purpura (ITP); is an acquired disorder It is immune-mediated destruction of platelets and inhibition of platelet release from the megakaryocyte. In children, it is usually an acute disease. In adults, it is a more chronic disease. Secondary ITP if it is associated with an underlying disorder; autoimmune disorders, particularly systemic lupus erythematosus (SLE), infections, such as HIV and hepatitis C.
- 19. 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 ecchymoses and petechiae. Mucocutaneous bleeding may be present. Rarely, life-threatening, including central nervous system bleeding can occur. retinal hemorrhages
- 20. prednisone at 1 mg/kg, Anti Rh0(D) immune globulin at 50–75 μg/kg, Monitoring patients for 8 h after infusion Intravenous gamma globulin (IVIgG) splenectomy Eltrombopag is FDA approved for use in children over 1 year of age. Romiplostim is not yet FDA approved in children but a randomized trial supports efficacy. Immunosuppressive drugs- mycophenolate mofetil dapsone.
- 21. TTP is related to a deficiency or antibodies to the metalloprotease ADAMTS13, which cleaves VWF. ADAMTS13 activity levels of <10% are more clearly associated with antibody-mediated TTP. Idiopathic TTP appears to be more common in women than in men.
- 23. plasma exchange It decreases mortality from 85–100% to 10– 30%.
- 24. HUS is a syndrome characterized 1) Acute renal failure 2) Microangiopathic hemolytic anemia, 3) Thrombocytopenia. Escherichia coli O157:H7 is the most frequent causative agent Atypical HUS (aHUS) is usually due to genetic defects that result in chronic complement activation or antibodies directed against complement regulatory proteins.
- 25. Indications of platelets tranfusion 10,000/uL - prophylactic transfusion 20,000/uL - in the presence of bleeding, fever, infection, platelet function defect, or coagulopathy 50,000/uL - prior to minor procedures, in actively anticoagulated patients or in the presence of active bleeding 75,000/uL - prior to general surgery 100,000/uL - prior to neurologic or ophthalmologic surgery
- 26. Random donor platelet Single donor platelet
- 27. Thrombocytopenia if platletes <150000/ul then Pseudothrombocytopenia should be ruled out Proper history taking and examination for finding out of different causes Peripheral blood smear to find out causes Indications of platelets transfusion <10000/ul
- 28. Harissons 20th Wintrobes clinical hematology
Editor's Notes
- pseudothrombocytopenia,” particularly in a patient without an apparent cause for the thrombocytopenia. Pseudothrombocytopenia (Fig. 111-1B) is an in vitro artifact resulting from platelet agglutination via antibodies (usually IgG, but also IgM and IgA) when the calcium content is decreased by blood collection in ethylenediamine tetraacetic (EDTA) (the anticoagulant present in tubes collect blood for complete blood counts [CBCs]). If a low platelet count is obtained in EDTA-anticoagulated blood, a blood smear should be evaluated and a platelet count determined in blood collected into sodium citrate (blue top tube) or heparin (green top tube), or a smear of freshly obtained unanticoagulated blood, such as from a finger stick, can be examined
- Mucocutaneous bleeding such as oral mucosa, gastrointestinal, or heavy menstrual bleeding, may be present Wet purpura (blood blisters in the mouth) and retinal hemorrhages may herald life-threatening bleeding. Petechiae size <4 mm Petechiae are pinpoint, nonblanching hemorrhages and are usually a sign of a decreased platelet number and not platelet dysfunction. Echymosis flat blue or purple patch size about >1 cm Purpura small small purple spots size 4-10 mm
- Medical history can provide invaluable information and greatly facilitate diagnosis. Aspects of particular relevance that should be investigated include Congenital thrombocytopenia May-Hegglin anomaly, and Sebastian, Epstein’s, and Fechtner syndromes, all of which have distinct distinguishing features. A common feature of these disorders is large platelets (Fig. 111-1C). Autosomal recessive disorders include congenital amegakaryocytic thrombocytopenia, thrombocytopenia with absent radii, and Bernard-Soulier syndrome. The latter is primarily a functional platelet disorder due to absence of Gp Ib-IX-V, the VWF adhesion receptor. X-linked disorders include Wiskott-Aldrich syndrome recent travels (eg, malaria, rickettsiosis, dengue fever); Recent transfusions; alloimmune Thrombocytopenia
- Splenomegaly exclude any chronic liver ds, leukemia lymphoma other hematological malignancy
- Now I m going to discuss some important cause of thrombocytopenia one by one in brief
- HIT can occur after exposure to low-molecular-weight heparin (LMWH) as well as unfractionated heparin (UFH),it is more common with UFH HIT results from antibody formation to a complex of the platelet-specific protein platelet factor 4 (PF4) and heparin. The anti-heparin/PF4 antibody can activate platelets through the FcγRIIa receptor and also activate monocytes and endothelial cells. It occurs before 5 days in those who were exposed to heparin in the prior few weeks or months (<~100 days)
- Because many patients develop antibodies but do not develop clinical HIT, the test has a low specificity for the diagnosis of HIT. This is especially true in patients who have undergone cardiopulmonary bypass surgery, where ∼50% of patients develop these antibodies postoperatively. IgG-specific ELISAs increase specificity but may decrease sensitivity. which measures the ability of the patient’s serum to activate platelets in the presence of heparin in a concentration-dependent manner. This test has lower sensitivity but higher specificity than the ELISA. However, HIT remains a clinical diagnosis
- Warfarin if started, should be overlapped with a DTI or fondaparinux and started after resolution of the thrombocytopenia and lessening of the prothrombotic state
- (ITP; also termed idiopathic thrombocytopenic purpura) Childs most commonly following an infection, and with a self-limited course although in some adults, spontaneous remission occurs, usually within months of diagnosis Viruses like CMV,Infectious mononucleosis VZV, TUBECULOSIS H pylori
- Mucocutaneous bleeding such as oral mucosa, gastrointestinal, or heavy menstrual bleeding
- Eltrombopag oral s/e hepatotoxicity Romiplostim i/v in week
- TTP is related to a deficiency of, or antibodies to, the metalloprotease ADAMTS13, which cleaves VWF. which are then cleaved by ADAMTS13. The persistence of ultra-large VWF molecules is thought to contribute to pathogenic platelet adhesion and aggregation
- Laboratory testing for DNA variants in complement regulatory genes is available, although assigning pathogenicity to variants remains challenging. Currently there is not a functional assay that is diagnostic of the disease. It is seen preceded by an episode of diarrhea, often hemorrhagic in nature, predominantly in children.
- 1 unit RDP increases plts 5-8 thousands 1 units of SDP increases 30-50 thousands