DOCSLIB.ORG

Ischemic Stroke Complicating Thrombolytic Therapy With

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Ischemic Stroke Complicating Thrombolytic Therapy With Arous et al. Journal of Medical Case Reports (2017) 11:154 DOI 10.1186/s13256-017-1322-3 CASEREPORT Open Access Ischemic stroke complicating thrombolytic therapy with tenecteplase for ST elevation myocardial infarction: two case reports Salim Arous*, Meryem Haboub, Mohamed El Ghali Benouna, Tarik Bentaoune and Rachida Habbal Abstract Background: Hemorrhagic complications are quite common in the rare cases where thrombolysis is performed. Ischemic stroke in the aftermath of thrombolysis for a ST elevation myocardial infarction is a very rare and paradoxical complication. With these observations in mind we report two interesting cases of ischemic stroke which occurred after fibrinolytic therapy with tenecteplase for a ST elevation myocardial infarction. Case presentation: The first case was a 56-year-old African man who presented with an acute infero-basal ST elevation myocardial infarction 6 hours after chest pain onset. Thrombolysis with tenecteplase was performed and few minutes later an ischemic stroke occurred. The second patient was a 65-year-old African man who presented with an acute infero-basal ST elevation myocardial infarction 5 hours after chest pain onset. Thrombolysis was performed and 10 hours later an ischemic stroke occurred. Conclusions: Hemorrhagic stroke is not the only complication of thrombolysis, ischemic stroke can occur even if it is an extremely rare complication. The two cases on which we report shed light on the association between fibrinolytic therapy and ischemic stroke, the pathophysiology of which is not well understood. Keywords: Ischemic stroke, Thrombolysis, Myocardial infarction Background which is well documented in the literature. Ischemic stroke ST elevation myocardial infarction (STEMI) is due to in the aftermath of TT for STEMI worsens the patient’s complete occlusion of the coronary artery. The gold prognosis; it is a paradoxical, very rare complication, the standard therapy for STEMI is recanalization of the pathophysiology of which is not well understood [2]. infarct-related coronary artery as soon as possible by Hence, we report two interesting cases of ischemic stroke pharmacological or mechanical means. The indication after TT for STEMI to shed light on the association be- for this is STEMI presenting within 12 hours of symp- tween TT and ischemic stroke. tom onset. Primary percutaneous coronary intervention (PCI) is superior to thrombolytic therapy (TT), but there are Case presentation many limitations to PCI such as the absence of a nearby Case report 1 angioplasty center. TT is therefore an effective treatment A 56-year-old African man presented to our emergency of choice in STEMI, as it is easy to perform anywhere department 6 hours after severe chest pain onset. He and at any time [1]. was a tobacco smoker, diabetes status unknown, neither The efficacy and safety of various thrombolytic agents hypertensive nor dyslipidemic, and had no history of have been well documented in large clinical trials. The most stroke. He had no personal or family medical history, in- feared complication of TT is intracranial hemorrhage cluding heart disease or heart rhythm disorder, and was not under any treatment prior to diagnosis. He was from a low socio-economic level. An electrocardiogram (EKG) * Correspondence: [email protected] showed a sinus rhythm with ST-segment elevation in in- Department of Cardiology, Ibn Rushd University Hospital, Casablanca, Morocco ferior and posterior leads (Fig. 1). © The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Arous et al. Journal of Medical Case Reports (2017) 11:154 Page 2 of 5 Fig. 1 Electrocardiogram showing ST-segment elevation in inferior leads At admission he was conscious, Glasgow Coma Scale Fig. 2 Cerebral computed tomography showing frontal, temporal, (GCS) of 15/15, without motor deficit or sensory dis- and parietal left ischemic stroke order; his chest pain was constrictive irradiating to his two upper limbs without syncope. Blood pressure (BP) on admission was 140/85 mmHg symmetrical, regular before TT and 5.89 g/l 12 hours after; white blood cells rhythm at 60 beats per minute (bpm), heart sounds count (WBC), 15,000 mm3; and C-reactive protein clearly auscultated with no heart or carotid murmur, (CRP), 72 mg/l. Antithrombotic medication was discon- there was no murmur of mitral insufficiency or ventricu- tinued. His neurological condition worsened progres- lar septal defect, no signs of heart failure including no sively and, after 1 week, he died. crackles, and he was without edema of his lower limbs or turgor of his jugular veins leading to a right ventricu- Case report 2 lar infarction. His peripheral pulses were perceived sym- A 65-year-old African man presented to our emergency metrically. The rest of the examination was strictly department 5 hours after severe chest pain onset. He is normal. Acute inferior and posterior STEMI was diag- a tobacco smoker, diabetes status unknown, neither nosed and intravenously administered TT using tenecte- hypertensive nor dyslipidemic, and had no history of plase (intravenous bolus of 30 mg considering a weight stroke. He had no personal or family medical history, in- of 54 kg) was performed with adjuvant antithrombotic cluding heart disease or heart rhythm disorder, and he medication (aspirin, clopidogrel, and enoxaparin). was not under any treatment prior to diagnosis. He was A few minutes later, he developed motor aphasia and from a low socio-economic level. An EKG showed a right hemiplegia with altered level of consciousness: sinus rhythm with ST-segment elevation in inferior and GCS of 12/15. The first cerebral computed tomography posterior leads (Fig. 3). At admission he was conscious, (CT) performed 1 hour later was normal and the second GCS of 15/15, without motor deficit or sensory disorder; one performed 12 hours later showed a frontal, his chest pain was constrictive irradiating to his two temporal, and parietal left ischemic stroke with a upper limbs without syncope. BP on admission was at hemorrhagic infarct (Fig. 2). On an EKG, the ST- 190/120 mmHg symmetrical, pulse rate at 122 bpm, segment elevation regressed more than 50% at 60 - heart sounds clearly auscultated, no heart or carotid minutes after TT. An echocardiographic examination murmur, there was no murmur of mitral insufficiency or (Vivid 6S) was performed following the therapy. It ventricular septal defect, no signs of heart failure includ- revealed a left ventricle ejection fraction (LVEF) at 50%, ing no crackles, and he was without edema of his lower no mitral insufficiency, pulmonary artery pressure at limbs or turgor of his jugular veins leading to a right 36 mmHg, no thrombus was detected in any cavity, no ventricular infarction. His peripheral pulses were per- ventricular septal defect, and no pericardial effusion. An ceived symmetrically. The rest of the examination was echo-Doppler of the supra-aortic trunks was not per- strictly normal. Acute inferior and posterior STEMI was formed. The laboratory findings were as follows: tropo- diagnosed and intravenously administered TT using nin Ic, 18 ng/ml; normal liver function tests; glomerular tenecteplase (intravenous bolus of 35 mg considering a filtration rate (GFR) by Modification of Diet in Renal weight of 65 kg) was performed after lowering BP at Disease (MDRD) method at 85 ml/1.73 m2 body surface 150/90 mmHg, associated with aspirin 300 mg adminis- area (BSA) per minute; hemoglobin, 13.5 g/dl; platelets tered orally and clopidogrel 300 mg administered orally. count, 500,000/mm3; plasmatic fibrinogen level, 2.49 g/l It is important to note that the first dose of heparin was Arous et al. Journal of Medical Case Reports (2017) 11:154 Page 3 of 5 Fig. 3 Electrocardiogram showing ST-segment elevation in inferior leads and a mirror aspect in V1 to V4 missed. Echocardiographic examination (Vivid 6S) was which was monitored by partial thromboplastin time performed following the therapy. It revealed segmental (PTT), were continued. His neurological condition im- wall motion abnormalities, LVEF at 50%, no mitral valve proved (level of consciousness and motor deficit). He insufficiency, pulmonary artery pressure at 29 mmHg, was discharged after 12 days of hospitalization; physio- and no thrombus or any mechanical complication was therapy and neurological follow-up were planned. One detected. One hour after TT, his chest pain and more month after discharge, PCI using a bare-metal stent than 50% of ST-segment elevation resolved with no (BMS) was performed on a circumflex coronary artery hemorrhagic complications. The laboratory findings lesion. were as follows: troponin Ic, 9 ng/ml; normal liver func- He was followed-up regularly after discharge every tion tests; serum creatinine level, 14.9 mg/l; estimating a 2 months. At 1 year of follow-up, clinically he no longer GFR at 50.5 ml/1.73 m2 BSA per minute using MDRD; presents a deficit, he is without recurrence of chest pain, hemoglobin, 16.3 g/dL; hematocrit, 49.5%; platelets and the ischemic image at a cerebral control scan disap- count, 281,000/mm3; plasmatic fibrinogen level, 7.4 g/l; peared. No hemorrhagic complications were developed WBC, 14,900/mm3; and CRP, 62 mg/l. under dual antiplatelet therapies (DAPT). Clopidogrel Ten hours later, he developed a left hemiparesis with was stopped after 6 months. motor aphasia without sensory disturbance and drowsi- ness: GCS of 14/15. The first cerebral CT performed Discussion 3 hours later was normal and the one performed STEMI, caused by acute occlusion of the infarct-related 24 hours later showed right internal capsule ischemic coronary artery, is an emergency condition.
Load more

Recommended publications
  • Classification and Pathogenesis of Cerebral Hemorrhages After Thrombolysis in Ischemic Stroke
    Classification and Pathogenesis of Cerebral Hemorrhages After Thrombolysis in Ischemic Stroke Paul Trouillas, MD; Ru¨diger von Kummer, MD Background and Purpose—Brain hemorrhage after ischemic stroke is a serious complication of treatment; however, its pathology is poorly understood. A classification based on brain imaging may help to better understand and avoid causal factors. Methods—Review of the results of controlled randomized trials and the available literature. Results—Hemorrhagic infarctions have no impact on clinical outcome and are probably not associated with the thrombolytic itself and the type of reperfusion strategy. They are associated with the extent of ischemic damage and most probably to an ischemic vasculopathy. Parenchymal hematomas are often clinically relevant. Their incidence is affected by the thrombolytic itself, the type, and probably the time point of reperfusion strategy. The loss of hemostatic control seems important in their pathogenesis. Extraischemic hematomas (remote from the infarct), unique or multiple, suggest pre-existing brain pathology, especially cerebral amyloid angiopathy. Conclusions—The radiological description of 3 different types of brain hemorrhage is useful to better understand the specific pathology and the impact on clinical outcome. It may help to avoid clinically relevant brain hemorrhages. (Stroke. 2006;37:556-561.) Key Words: cerebral infarction Ⅲ hemostasis Ⅲ heparin Ⅲ intracranial hemorrhage Ⅲ thrombolysis erebral hemorrhage is the most feared complication of ing an intravenous dose of 100 mg of recombinant tissue Cintra-arterial or intravenous thrombolysis after ischemic plasminogen activator (rt-PA), 9% of patients had a fatal stroke. Such hemorrhages are also a major complication of cerebral hemorrhage on CT. intravenous thrombolysis in myocardial infarction (MI), al- Levy et al3 presented the concept of “symptomatic hemor- though less frequent.
    [Show full text]
  • Stroke and Atrial Fibrillation: Better Detection, Effects on Infarct Evolution and Outcome
    STROKE AND ATRIAL FIBRILLATION: BETTER DETECTION, EFFECTS ON INFARCT EVOLUTION AND OUTCOME Hans T. H. Tu MBBS FRACP Submitted in total fulfilment of the requirements of the degree of Doctor of Philosophy March 2018 Melbourne Brain Centre at the Royal Melbourne Hospital Department of Medicine (Royal Melbourne Hospital) The University of Melbourne Abstract Ischemic stroke is the commonest stroke and a leading cause of disability and death worldwide. Atrial fibrillation (AF) is the most frequent persistent cardiac arrhythmia and a preventable cause of ischemic strokes. The incidence and prevalence of AF have progressively increased over the last few decades and will likely continue to rise, due to the aging population and ongoing growth in other AF risk factors such as obesity, hypertension, diabetes mellitus, heart failure, coronary artery disease and sleep apnea. The social and economic costs associated with the increasing AF burden represent a mounting public health challenge, leading many to consider AF an evolving epidemic in the twenty-first century. Ischemic strokes related to AF usually result from cardioembolism of a large cerebral artery, therefore tend to be larger, more frequently fatal or associated with greater disability than strokes from other causes. However, the pathophysiological mechanisms underlying this association remain unclear. Analysis of serial multimodal magnetic resonance brain imaging in a cohort of acute hemispheric ischemic stroke patients revealed that patients with AF had greater volumes of more severely hypoperfused brain tissue at 3-6 hours following stroke onset, higher infarct growth and larger final infarcts. These findings were best explained by poorer collateral circulation in patients with AF, supporting further investigation of acute stroke therapy that improve cerebral collateral circulation.
    [Show full text]
  • Patterns of Edema in Tumors Vs. Infarcts: Visualization of White Matter Pathways
    251 Patterns of Edema in Tumors vs. Infarcts: Visualization of White Matter Pathways Ahmad Monajati1 The computed tomographic (CT) scans of 339 patients with recent nonhemorrhagic Lucille Heggeness2 cerebral infarct and 155 patients with supratentorial tumors were reviewed to evaluate the appearance of cerebral edema. White matter pathway edema characterized the CT pattern in 106 (68% ) of the 155 tumor cases. In these 106 cases, there were 143 tumors, with edema in the arcuate white matter (73% ), the external capsule (33% ), the internal capsule (12% ), and the corpus callosum (14% ). In contrast, only four of the 339 cases of infarct had edema in the white matter pathways. In addition, 260 (77% ) of the infarct cases had edema in both gray and white matter and 98% had at least gray matter involvement, while only two of the tumor cases had any gray matter edema. White matter pathway involvement with respect to tumor site is useful in differentiating tumor and infarct edema. The computed tomographic (CT) appearance of cerebral edema due to intra­ cranial tumors has been described as an area of low attenuation , usually confined to the topography of the white matter [1 , 2]. In contrast, th e edema associated with cerebral ischemia appears on CT as a typical low density involving both the gray and the adjoining white matter [3-6]. The aim of this study was to analyze th e CT scans of brain tumors and cerebral infarcts to evaluate the specificity of the differential pattern of th e edema in distinguishing neoplastic lesions from acute cerebral ischemia. Special attention was given to the distribution of edema along recognizable white matter pathways.
    [Show full text]
  • The Emergency Diagnosis of Acute Ischemic Bowel
    Yale University EliScholar – A Digital Platform for Scholarly Publishing at Yale Yale Medicine Thesis Digital Library School of Medicine 1989 The mee rgency diagnosis of acute ischemic bowel John A. Thompson Yale University Follow this and additional works at: http://elischolar.library.yale.edu/ymtdl Recommended Citation Thompson, John A., "The mee rgency diagnosis of acute ischemic bowel" (1989). Yale Medicine Thesis Digital Library. 3247. http://elischolar.library.yale.edu/ymtdl/3247 This Open Access Thesis is brought to you for free and open access by the School of Medicine at EliScholar – A Digital Platform for Scholarly Publishing at Yale. It has been accepted for inclusion in Yale Medicine Thesis Digital Library by an authorized administrator of EliScholar – A Digital Platform for Scholarly Publishing at Yale. For more information, please contact [email protected]. YALE MEDICAL LIBRARY Digitized by the Internet Archive in 2017 with funding from The National Endowment for the Humanities and the Arcadia Fund https://archive.org/details/emergencydiagnosOOthom THE EMERGENCY DIAGNOSIS OF ACUTE ISCHEMIC BOWEL BY John A. Thompson B. S. University of Notre Dame A thesis submitted to the Yale University School of Medicine in partial fulfillment of the requirements for the degree of Doctor of Medicine 1989 \ \ T..a, y * \ u o ■ i \zk zfi ns ABSTRACT THE EMERGENCY DIAGNOSIS OF ACUTE ISCHEMIC BOWEL. John A. Thompson, Linda C. Degutis, Christopher C. Baker. Section of General Surgery, Department of Surgery, Yale University, School of Medicine, New Haven, CT. The well-known difficulty of obtaining an early diagnosis of acute ischemic bowel must be overcome to insure prompt life-saving intervention.
    [Show full text]
  • Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions
    Int. J. Mol. Sci. 2013, 14, 1890-1917; doi:10.3390/ijms14011890 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Review Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions Ryan C. Turner 1,2, Brandon Lucke-Wold 1,2, Noelle Lucke-Wold 2,3, Alisa S. Elliott 1,2, Aric F. Logsdon 2,4, Charles L. Rosen 1,2,* and Jason D. Huber 2,4 1 Department of Neurosurgery, One Medical Center Drive, West Virginia University School of Medicine, P.O. Box 9183, Morgantown, WV 26506, USA; E-Mails: [email protected] (R.C.T.); [email protected] (B.L.-W.); [email protected] (A.S.E.) 2 The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA; E-Mails: [email protected] (N.L.-W.); [email protected] (A.F.L.); [email protected] (J.D.H.) 3 Department of Health Restoration, West Virginia University School of Nursing, Morgantown, WV 26506, USA 4 Department of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV 26506, USA * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +1-304-293-5041; Fax: +1-304-293-4819. Received: 9 November 2012; in revised form: 4 January 2013 / Accepted: 10 January 2013 / Published: 17 January 2013 Abstract: The translation of neuroprotective agents for ischemic stroke from bench-to-bedside has largely failed to produce improved treatments since the development of tissue plasminogen activator (tPA). One possible reason for lack of translation is the failure to acknowledge the greatest risk factor for stroke, age, and other common comorbidities such as hypertension, obesity, and diabetes that are associated with stroke.
    [Show full text]
  • Treatment and Outcome of Hemorrhagic
    AHA/ASA Scientific Statement Treatment and Outcome of Hemorrhagic Transformation After Intravenous Alteplase in Acute Ischemic Stroke A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. The American Association of Neurological Surgeons/Congress of Neurological Surgeons Joint Cerebrovascular Section affirms the educational benefit of this document. Shadi Yaghi, MD, Chair; Joshua Z. Willey, MD, MS, FAHA, Vice Chair; Brett Cucchiara, MD, FAHA; Joshua N. Goldstein, MD, PhD, FAHA; Nicole R. Gonzales, MD; Pooja Khatri, MD, MSc, FAHA; Downloaded from Louis J. Kim, MD; Stephan A. Mayer, MD, FAHA; Kevin N. Sheth, MD, FAHA; Lee H. Schwamm, MD, FAHA; on behalf of the American Heart Association Stroke Council; Council 48 on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; and Council on Quality of Care and Outcomes Research 12 http://stroke.ahajournals.org/ Purpose—Symptomatic intracranial hemorrhage (sICH) is the most feared complication of intravenous thrombolytic therapy in acute ischemic stroke. Treatment of sICH is based on expert opinion and small case series, with the efficacy of such treatments not well established. This document aims to provide an overview of sICH with a focus on pathophysiology and treatment. Methods—A literature review was performed for randomized trials, prospective and retrospective studies, opinion papers, case series, and case reports on the definitions, epidemiology, risk factors, pathophysiology, treatment, and outcome of sICH. The document sections were divided among writing group members who performed the literature review, summarized the literature, and provided suggestions on the diagnosis and treatment of patients with sICH caused by systemic thrombolysis with alteplase.
    [Show full text]
  • Status of the Myocardium and Infarct-Related Coronary Artery in 19 Necropsy Patients with Acute Recanalization Using Pharmacolog
    JACC Vol. 9. No. 4 785 April I<J 87:785- 80 I MORPHOLOGIC STUDIES Status of the Myocardium and Infarct-Related Coronary Artery in 19 Necropsy Patients With Acute Recanalization Using Pharmacologic (Streptokinase, r-Tissue Plasminogen Activator), Mechanical (Percutaneous Transluminal Coronary Angioplasty) or Combined Types of Reperfusion Therapy BRUCE F. WALLER, MD, FACC,* DONALD A. ROTHBAUM, MD, FACC,t CASS A. PINKERTON, MD, FACC,t MICHAEL J. COWLEY, MD, FACC,§ THOMAS J. LlNNEMElER, MD, FACC,t CHARLES ORR, MD, FACC,t MICHAEL IRONS, MD,t ROBIN A. HELMUTH , MD,II EDWARD R. WILLS, MD,II CHARLES AUST, MOil Indianapolis. Indiana and Richmond. Virginia In acute myocardial infarction, myocardial salvage is 14 (74%) had hemorrhagic myocardial infarction and dependent on rapid restoration of blood flow. Phar­ they all received pharmacologic or combined forms of macologic (streptokinase, recombinant tissue-type plas­ reperfusion therapy. The remaining five patients (26%) minogen activator), mechanical (percutaneous translu­ had nonhemorrhagic (anemic) infarction and were treated minal coronary angioplasty, guide wire perforation) or with balloon angioplasty therapy alone. Increased lu­ combined forms of reperfusion therap y can accomplish minal cross-sectional area was present in 8 of 9 patients this goal, but their effects on infarcted myocardium and with acute balloon angioplasty but severe coronary ath­ vessel occlusion site have not been compared at necropsy. erosclerotic plaque remained in 9 of 10 patients without The heart of 19 necropsy patients who had received var­ acute balloon angioplasty. Severe hemorrhage sur­ ious forms of acute reperfusion therap y was studied: rounded angioplasty sites in all four patients who also 14 had pharmacologic or combined forms of reperfusion received streptokinase or tissue-type plasminogen acti­ therapy (13 streptokinase and I tissue-type plasminogen vator.
    [Show full text]
  • Neutrophil-To-Lymphocyte Ratio and Symptomatic Hemorrhagic Transformation in Ischemic Stroke Patients Undergoing Revascularization
    brain sciences Article Neutrophil-to-Lymphocyte Ratio and Symptomatic Hemorrhagic Transformation in Ischemic Stroke Patients Undergoing Revascularization Milena Swito´ ´nska 1,* , Natalia Pieku´s-Słomka 2 , Artur Słomka 3 , Paweł Sokal 1 , Ewa Zekanowska˙ 3 and Simona Lattanzi 4 1 Department of Neurosurgery and Neurology, Nicolaus Copernicus University in Toru´n, Ludwik Rydygier Collegium Medicum, 85-168 Bydgoszcz, Poland; [email protected] 2 Department of Inorganic and Analytical Chemistry, Nicolaus Copernicus University in Toru´n, Ludwik Rydygier Collegium Medicum, 85-089 Bydgoszcz, Poland; [email protected] 3 Department of Pathophysiology, Nicolaus Copernicus University in Toru´n,Ludwik Rydygier Collegium Medicum, 85-094 Bydgoszcz, Poland; [email protected] (A.S.); [email protected] (E.Z.)˙ 4 Neurological Clinic, Department of Experimental and Clinical Medicine, Marche Polytechnic University, 60121 Ancona, Italy; alfi[email protected] * Correspondence: [email protected]; Tel.: +48-52-365-5565 Received: 21 September 2020; Accepted: 22 October 2020; Published: 23 October 2020 Abstract: Objectives: Symptomatic hemorrhagic transformation (sHT) is a life-threatening complication of acute ischemic stroke (AIS). The early identification of the patients at increased risk of sHT can have clinically relevant implications. The aim of this study was to explore the validity and accuracy of the neutrophil-to-lymphocyte ratio (NLR) in predicting sHT in patients with AIS undergoing revascularization. Methods: Consecutive patients hospitalized for AIS who underwent intravenous thrombolysis, mechanical thrombectomy or both were identified. The NLR values were estimated at admission. The study endpoint was the occurrence of sHT within 24 h from stroke treatment. Results: Fifty-one patients with AIS were included, with a median age of 67 (interquartile range, 55–78) years.
    [Show full text]
  • Pathology of Cellular Injury and Death. Cellular Adaptations
    What is disease? • A condition in which the presence of an abnormality causes a loss of normal health • Manifests in signs and symptoms subjective: e.g., pain objective: confirmed by diagnostic tests • Duration of disease: short lasting - acute long lasting - chronic • Outcome: varies; can be lethal What is pathology? • The study (logos) of suffering (pathos) • Devoted to the study of - the cause of the disease (etiology) - the mechanism(s) of disease development (pathogenesis) - the structural alterations induced in cells and tissues by the disease (morphologic change) - the functional consequences of the morphologic changes (clinical significance) • The morphologic change can be focal (localized abnormality) or diffuse Teaching program of pathology for medical students General pathology • Basic reactions of cells and tissues to abnormal stimuli, i.e. common features of various disease processes in various cells and tissues Systematic pathology • The descriptions of specific diseases as they affect given organs or organ systems The descriptions and terms used are the basis of medical language Students are expected to attend the lectures, the autopsy and histopathology practicals, and the organ demonstrations. Attendance at the practicals the attendence is always verified. There is no possibility for missed practicals to be repeated later. Students who are absent from more than 25% of the practicals, automatically fail the semester. The grade achieved in the fall-semester examinations will be calculated from the sum of the following: - the first mid-term assessment (maximum 5 points) - the second mid-term assessment (max. 5 points) - the histology examination (max. 5 points) - the autopsy examination (max. 5 points) - the final test (max.
    [Show full text]
  • Hemorrhagic Transformation of Ischemic Stroke – Prediction and Evaluation with Different Computed Tomography Modalities *T
    reE VI W ARTICLES Curierul medical, August 2015, Vol. 58, No 4 Hemorrhagic transformation of ischemic stroke – prediction and evaluation with different computed tomography modalities *T. Plescan1, E. Costru-Tasnic2, M. Gavriliuc2, M. Arion1, I. Dacin1 1Department of Radiology and Neuroimaging, 2Department of Neurology Institute of Neurology and Neurosurgery, Chisinau, the Republic of Moldova *Corresponding author: [email protected]. Manuscript received April 16, 2015; accepted June 08, 2015 Abstract Background: Hemorrhagic transformation (HT) of ischemic stroke is a complex and heterogeneous phenomenon, which involves numerous parameters whose knowledge remains partial. Large HT is often associated with poorer outcome and higher mortality, especially parenchymal hematoma type 2, that’s why the search of strong HT predictors is very important and can improve management of ischemic stroke patients. Our aim was to review the literature regarding computed tomography (CT) imaging predictors of HT and possible input of different computed tomography modalities in diagnosis and evaluation of HT following acute ischemic stroke. The contribution of non-contrast computed tomography, computed tomography angiography (CTA) and dynamic Perfusion CT (PCT) investigation in the prediction of the hemorrhagic transformation risk were studied. Multiple multicentre studies revealed useful information on different CT patterns predictors of symptomatic intracerebral hemorrhage after stroke, which is the most important type of hemorrhagic transformation from a clinician’s point of view. Conclusions: Data from the multiple studies and trials revealed that different CT modalities show high potency in HT prediction and evaluation. Non-contrast CT standard investigation showed high accuracy in HT prediction by assessment of early ischemic signs, quantification of the Alberta Stroke Program Early CT Score (ASPECTS), grading of leukoaraiosis severity.
    [Show full text]