Hematologic and Coagulation Disorders Associated with Ischemic Stroke

Rami Abdul Naser Abdul Majid AlAbsi


Strokeisanimportantcauseofdeathanddisability. Inabout40%ofallischaemicstrokes,nodefinitecausecanbeidentified,despiteextensiveancillaryinvestigations(Lonneke et al., 2010). Although ischemic stroke occurs mainly in elderly individuals aged 65 years or older,and the incidence of stroke rises exponentially with age, nowadays, it is increasingly found in young individuals, even in children (Visnja et al., 2013). Traditional risk factors for stroke such as hypertension and diabetes are not very frequent in young adults (Ferro et al., 2010), and so there are an other important causes and risk factors associated with stroke in younger patients as hematologic and coagulation disorders. Hypercoagulablestateslikelyexplainthehighpercentageofcasesofcryptogeniccerebralinfarctioninyoungpeople (Naveed et al., 2006). Severalhematologicdisordersandhemostaticdefectsincreaseriskofischemicstroke.Acommonfeatureofthesedisordersisthecreationofaprothromboticstate,nowcommonlyreferredtoas“hypercoagulablestate” .Hematologicabnormalitiesleadtothrombosisinthecerebralvasculature,causingischemiccerebrovascularevents;hematologicabnormalitiesareestimatedtoaccountforabout5%to10%ofallstrokes,beinghigherinyoungpeople.There isaccumulatingevidencethathypercoagulablestatesplayaroleinthedevelopmentofcerebrovasculardiseases(MatijevicandWu, 2006). Managementofcerebrovasculareventsisguidedbythe underlying etiology andiswellstudied forthe establishedcauses.However,inasignificantproportion(particularlyofyoungindividuals)theoriginofstrokeremainsunknown,orcanbeattributedtoso-called“unusual”etiologies.Ofthese,strokesdueto hematologicaldisordersrepresentanon-negligible entity(Buhler and Mattle, 2009). Ischemicstrokeshavebeenattributedtohematological disorders.Some hematologicaldisordershavebeenshowntobecausal,forotherstheassociationwithcerebrovasculareventsislesscertain becauseofthefrequentcoexistenceofothervascular riskfactors(Buhler and Mattle, 2009). The maintenance of hemostasis requires a complex interplay between a large number of checks and balances in the coagulation pathways. Deficiencies of factors inhibiting coagulation (antithrombin III [AT III], protein S, and protein C), increased levels of factors promoting coagulation (factors V and VII), and decreased activity in the fibrinolytic pathway (plasminogen or plasminogen activator deficiencies) have all been implicated in ischemic stroke (Levine et al., 2005). Numerous conditions are known to predispose to vascular thrombosis including cerebral vascular thrombosis, generally accepted or "classically" acquired risk factors include advanced age, prolonged immobilisation, surgery, fractures, use of oral contraceptives and hormone replacement therapy, pregnancy, puerperium, Smoking, Obesity elevated cholesterol levels, Sepsis in disseminated infection, heart failure, autoimmune diseases, Diabetes, Uremia, cancer. In addition to these well-established risk factors, several lines of evidence over the past few decades specify a role of hematologic and coagulation disorders associated with (Ischemic stroke). The most significant breakthrough has been the confirmation of the concept that hypercoagulable conditions are present in a large proportion of patients with ischemic stroke, these include Sickle-cell disease,Thalassemia, Nocturnalparoxysmalhemoglobinuria, Spherocytosis, Polycythemiavera , Anemia, Essential thrombocythemia, Reactive thrombocytosis, Thrombotic thrombocytopenic purpura (TTP), Hemolytic uremic syndrome (HUS), Idiopathic thrombotic thrombocytopenia (ITP), Heparin induced thrombocytopenia (HIT), leukemia, Lymphoma, Myeloma, Waldenstro¨m’s macroglobulinemia, Protein C deficiency, Protein S deficiency, Protein Z deficiency, Antithrombin III deficiency, Heparin cofactor II deficiency, Factor V Leiden mutation (APC), Prothrombin gene mutation (G20210A), Elevated factors V, VII, VIII, VWF, Elevated fibrinogen, Plasminogen deficiency Dysfibrinogenemia, Factor XII (Hageman factor) deficiency, Disseminated intravascular coagulation, Antiphospholipid syndrome, Hyperhomocysteinemia. This broad list of genetic and acquired factors emphasizes that a single cause of venous thrombosis rarely exist alone and that this conditionshould be considered as a complex or multifactorial trait. (Naveed et al., 2006). When ordering tests of coagulation in stroke patients, one should keep in mind whether the results will influence therapy and/or patient outcome. It is generally not advocated to screen all stroke patients for a “hypercoagulable workup” (Levine, 2005). Extensivehematologicalevaluationofunselectedpatientswillyieldlittleusefulinformation.Therefore,moststrokepatientscanbeadequatelyevaluatedwith aroutinehematologicaltesting.Amorethoroughevaluationiswarrantedforpatientswithpreviousunexplainedthromboticepisodes,combinedvenousandarterialthromboticevents,positivefamilyhistoryofrecurrentthromboembolism,orpatientswithpathologicallaboratoryfindings.Inpatientswithhereditaryhematologicaldisorders,studiesshouldbeextendedtoclose relatives(Buhler and Mattle, 2009). Manyofthesepatientsmaybenefitfromurgentanticoagulation,steroids,chemotherapy,phlebotomyorplasmaticexchanges(Ombeline et al., 2011). Combining antiplatelet agents with anticoagulant therapy generally causes more bleeding complications and does not increase benefits to the patient (Allan, 2005). If from clinical history, family history and/or laboratory studies, a patient is felt to have a hypercoagulable state, the decision for long term chronic anticoagulation needs to be individualized (Naveed et al., 2006).

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Other Titles الاضطرابات الدمويةوالتخثريةالمرتبطةبالسكتةالدماغية
Issue Date 2014
URI http://research.asu.edu.eg/handle/12345678/13971

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