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      Watershed Infarct in Beta-Thalassemia Major Patient

      case-report

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          Abstract

          Background. The mechanism of stroke in beta-thalassemia was reported previously as cardioembolic and hypercoagulable state. However, there is no report of watershed infarct in beta-thalassemia anemia. Method. We present an adult β-thalassemia major patient with manifest asymptomatic chronic left carotid occlusion who suffered watershed infarct. Result. In the presence of asymptomatic chronic left internal carotid occlusion, we assumed that severe anemia (hemoglobin = 3) at admission leads to watershed infarct. Conclusion. Watershed infarct seems to be the cause of stroke in cases of β-thalassemia major with severe anemia. Blood transfusion can be applied in the setting of acute brain ischemia in such high risk patients.

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          The pathophysiology of watershed infarction in internal carotid artery disease: review of cerebral perfusion studies.

          Jean-Claude Baron, Isabelle Momjian-Mayor (2005)
          In carotid disease, infarcts can occur in the cortical as well as internal watershed (WS), or both. Better understanding the pathophysiology of WS infarcts would guide treatment. Two distinct hypotheses, namely low-flow and micro-embolism, are equally supported by neuropathological and physiological studies. Here we review the evidence regarding the mechanisms for WS stroke in carotid disease and whether they differ between cortical and internal WS infarcts. After a brief account of the anatomy of the WS and the cerebrovascular physiology in circumstances of low perfusion pressure, the literature concerning the mechanisms of WS infarction in carotid disease is reviewed and discussed with emphasis on imaging and ultrasound studies of the cerebral hemodynamics. The evidence strongly favors a hemodynamic mechanism for internal WS infarction, especially regarding the so-called rosary-like pattern in the centrum semiovale. However, the relationships between cortical WS infarction and hemodynamic compromise appear more complicated. Thus, although severe hemodynamic compromise appears to underlie combined cortical and internal WS infarction, artery-to-artery embolism may play an important role in isolated cortical WS infarcts. Based on the high prevalence of microembolic signals documented by ultrasound in symptomatic carotid disease, a recent hypothesis postulates that embolism and hypoperfusion play a synergetic role, according to which small embolic material prone to lodge in distal field arterioles would be more likely to result in cortical micro-infarcts when chronic hypoperfusion prevails. Future studies combining imaging of brain perfusion, diffusion-weighted imaging, and ultrasound detection of microembolic signals should help resolve these issues.
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            Prevalence of thromboembolic events among 8,860 patients with thalassaemia major and intermedia in the Mediterranean area and Iran.

            Eliezer A Rachmilewitz, Daniela Bignamini, Ghassan Mehio … (2006)
            Beta-thalassaemia is a congenital haemolytic anaemia characterized by partial (intermedia, TI) or complete (major, TM) deficiency in the production of beta-globin chains. The primary aim of this study was to determine the prevalence of thromboembolic events in patients with beta-thalassaemia. To achieve this, a multiple choice questionnaire was sent to 56 tertiary referral centres in eight countries (Lebanon, Italy, Israel, Greece, Egypt, Jordan, Saudi Arabia and Iran), requesting specific information on patients who had experienced a thromboembolic event. The study demonstrated that thromboembolic events occurred in a clinically relevant proportion (1.65%) of 8,860 thalassaemia patients (TI - 24.7% or TM - 75.3%) from the Mediterranean and Iran. Thromboembolism occurred 4.38 times more frequently in TI than TM (p < 0.001), with more venous events occurring in TI and more arterial events occurring in TM. Thrombosis in thalassaemia was also more common in females, splenectomized patients and those with profound anaemia (haemoglobin <9 g/dl). Due to the increased risk of thromboembolic events, the rationale for splenectomy should perhaps be re-assessed and the role of transfusion therapy for the prophylaxis of thrombosis, among other complications, be evaluated prospectively.
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              Sickle cell disease and stroke.

              L Verduzco, R Nathan (2009)
              Twenty-four percent of sickle cell disease (SCD) patients have a stroke by the age of 45 years. Blood transfusions decrease stroke risk in patients deemed high risk by transcranial Doppler. However, transcranial Doppler has poor specificity, and transfusions are limited by alloimmunization and iron overload. Transfusion withdrawal may be associated with an increased rebound stroke risk. Extended blood typing decreases alloimmunization in SCD but is not universally adopted. Transfusions for thalassemia begun in early childhood are associated with lower rates of alloimmunization than are seen in SCD, suggesting immune tolerance. Optimal oxygen transport efficiency occurs at a relatively low hematocrit for SCD patients because of hyperviscosity. Consequently, exchange rather than simple transfusions are more effective in improving oxygen transport efficiency, but the former are technically more demanding and require more blood units. Although viscosity is of importance in the noncerebral manifestations of SCD, inflammation may play a larger role than viscosity in the development of large-vessel stroke. The future of SCD stroke management lies in the avoidance of transfusion. Hydroxyurea and anti-inflammatory measures may reduce the need for transfusion. Recent genome-wide association studies may provide methods for modulating fetal hemoglobin production enough to attenuate stroke risk and other complications of SCD.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Case Rep Neurol Med
                Journal ID (iso-abbrev): Case Rep Neurol Med
                Journal ID (publisher-id): CRINM
                Title: Case Reports in Neurological Medicine
                Publisher: Hindawi
                ISSN (Print): 2090-6668
                ISSN (Electronic): 2090-6676
                Publication date (Print): 2017
                Publication date (Electronic): 27 March 2017
                Volume: 2017
                Electronic Location Identifier: 2736402
                Affiliations
                1Isfahan Neurosciences Research Center, Alzahra Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
                2Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran
                3Department of Neurology, Tehran University of Medical Sciences, Sina Hospital, Tehran, Iran
                Author notes

                Academic Editor: Dennis J. Rivet

                Author information
                http://orcid.org/0000-0003-0368-5888
                http://orcid.org/0000-0001-9425-5132
                Article
                DOI: 10.1155/2017/2736402
                PMC ID: 5385913
                PubMed ID: 28428899
                SO-VID: 3900c989-b98a-4566-a38b-fa1d9e889f46
                Copyright © Copyright © 2017 Behnaz Ansari et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 11 August 2016
                Date revision received : 17 November 2016
                Date accepted : 7 February 2017
                Categories
                Subject: Case Report

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