Massive Splenic Infarction with Specific Sonographic Feature: Two
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Atrial Fibrillation and Splenic Infarction Presenting with Unexplained Fever and Persistent Abdominal Pain - a Case Report and Review of the Literature
Case ReportSplenic Infarction Presenting with Unexplained Fever and Persistent Acta Abdominal Cardiol SinPain 2012;28:157-160 Atrial Fibrillation and Splenic Infarction Presenting with Unexplained Fever and Persistent Abdominal Pain - A Case Report and Review of the Literature Cheng-Chun Wei1 and Chiung-Zuan Chiu1,2 Atrial fibrillation is a common clinical problem and may be complicated with events of thromboembolism, especially in patients with valvular heart disease. Splenic infarction is a rare manifestation of the reported cases. The symptoms may vary from asymptomatic to severe peritonitis, though early diagnosis may lessen the probability of severe complications and lead to a good prognosis. We report a 79-year-old man with multiple cardioembolic risk factors who presented with fever and left upper quadrant abdominal pain. To diagnose splenic infarction is challenging for clinicians and requires substantial effort. Early resumption of the anti-coagulation component avoids complications and operation. Key Words: Atrial fibrillation · Splenic infarction · Thromboembolism event · Valvular heart disease INTRODUCTION the patient suffered from severe acute abdominal pain due to splenic infarction. Fortunately, early diagnosis Splenic infarction is a rare cause of an acute abdo- and anticoagulation therapy helped the patient to avoid men. According to a sizeable autopsy series, only 10% emergency surgery and a possible negative outcome. of splenic infarctions had been diagnosed antemortem.1-3 It can occur in a multitude of conditions, with general or local manifestations, and was often a clinical “blind CASE REPORT spot” during the process of diagnosis. However, splenic infarction must be considered in patients with hema- The patient was a 79-year-old man with degenera- tologic diseases or thromboembolic conditions. -
New Jersey Chapter American College of Physicians
NEW JERSEY CHAPTER AMERICAN COLLEGE OF PHYSICIANS ASSOCIATES ABSTRACT COMPETITION 2015 SUBMISSIONS 2015 Resident/Fellow Abstracts 1 1. ID CATEGORY NAME ADDITIONAL PROGRAM ABSTRACT AUTHORS 2. 295 Clinical Abed, Kareem Viren Vankawala MD Atlanticare Intrapulmonary Arteriovenous Malformation causing Recurrent Cerebral Emboli Vignette FACC; Qi Sun MD Regional Medical Ischemic strokes are mainly due to cardioembolic occlusion of small vessels, as well as large vessel thromboemboli. We describe a Center case of intrapulmonary A-V shunt as the etiology of an acute ischemic event. A 63 year old male with a past history of (Dominik supraventricular tachycardia and recurrent deep vein thrombosis; who has been non-compliant on Rivaroxaban, presents with Zampino) pleuritic chest pain and was found to have a right lower lobe pulmonary embolus. The deep vein thrombosis and pulmonary embolus were not significant enough to warrant ultrasound-enhanced thrombolysis by Ekosonic EndoWave Infusion Catheter System, and the patient was subsequently restarted on Rivaroxaban and discharged. The patient presented five days later with left arm tightness and was found to have multiple areas of punctuate infarction of both cerebellar hemispheres, more confluent within the right frontal lobe. Of note he was compliant at this time with Rivaroxaban. The patient was started on unfractionated heparin drip and subsequently admitted. On admission, his vital signs showed a blood pressure of 138/93, heart rate 65 bpm, and respiratory rate 16. Cardiopulmonary examination revealed regular rate and rhythm, without murmurs, rubs or gallops and his lungs were clear to auscultation. Neurologic examination revealed intact cranial nerves, preserved strength in all extremities, mild dysmetria in the left upper extremity and an NIH score of 1. -
Cells, Tissues and Organs of the Immune System
Immune Cells and Organs Bonnie Hylander, Ph.D. Aug 29, 2014 Dept of Immunology [email protected] Immune system Purpose/function? • First line of defense= epithelial integrity= skin, mucosal surfaces • Defense against pathogens – Inside cells= kill the infected cell (Viruses) – Systemic= kill- Bacteria, Fungi, Parasites • Two phases of response – Handle the acute infection, keep it from spreading – Prevent future infections We didn’t know…. • What triggers innate immunity- • What mediates communication between innate and adaptive immunity- Bruce A. Beutler Jules A. Hoffmann Ralph M. Steinman Jules A. Hoffmann Bruce A. Beutler Ralph M. Steinman 1996 (fruit flies) 1998 (mice) 1973 Discovered receptor proteins that can Discovered dendritic recognize bacteria and other microorganisms cells “the conductors of as they enter the body, and activate the first the immune system”. line of defense in the immune system, known DC’s activate T-cells as innate immunity. The Immune System “Although the lymphoid system consists of various separate tissues and organs, it functions as a single entity. This is mainly because its principal cellular constituents, lymphocytes, are intrinsically mobile and continuously recirculate in large number between the blood and the lymph by way of the secondary lymphoid tissues… where antigens and antigen-presenting cells are selectively localized.” -Masayuki, Nat Rev Immuno. May 2004 Not all who wander are lost….. Tolkien Lord of the Rings …..some are searching Overview of the Immune System Immune System • Cells – Innate response- several cell types – Adaptive (specific) response- lymphocytes • Organs – Primary where lymphocytes develop/mature – Secondary where mature lymphocytes and antigen presenting cells interact to initiate a specific immune response • Circulatory system- blood • Lymphatic system- lymph Cells= Leukocytes= white blood cells Plasma- with anticoagulant Granulocytes Serum- after coagulation 1. -
Summary Tabulation 10-05-2021
Summary Tabulation 10-05-2021 Active Substance (High Level) COVID-19 VACCINE ASTRAZENECA (CHADOX1 NCOV-19) Reaction SOC Reaction PT Serious Non Serious Total Blood and lymphatic system disorders Anaemia 2 1 3 Autoimmune haemolytic anaemia 1 0 1 Coagulopathy 40 21 61 Coombs negative haemolytic anaemia 1 0 1 Disseminated intravascular coagulation 1 0 1 Immune thrombocytopenia 1 0 1 Leukocytosis 1 0 1 Leukopenia 1 0 1 Lymphadenopathy 5 2 7 Lymphopenia 1 0 1 Necrotic lymphadenopathy 0 1 1 Neutropenia 3 1 4 Splenic embolism 1 0 1 Splenic infarction 1 0 1 Thrombocytopenia 19 5 24 Cardiac disorders Acute cardiac event 1 0 1 Angina pectoris 2 0 2 Arrhythmia 4 1 5 Bradycardia 1 1 2 Cardiac arrest 2 0 2 Cardiac failure 2 0 2 Cardiovascular disorder 37 6 43 Myocardial depression 1 0 1 Myocardial infarction 2 0 2 Palpitations 30 3 33 Pericarditis 1 0 1 Sinus tachycardia 1 0 1 Tachycardia 25 3 28 Ear and labyrinth disorders Deafness 1 2 3 Deafness unilateral 4 1 5 Ear congestion 0 2 2 Ear discomfort 3 0 3 Ear pain 9 2 11 Hyperacusis 3 0 3 Sudden hearing loss 0 1 1 Tinnitus 4 1 5 Vertigo 21 3 24 Endocrine disorders Adrenocortical insufficiency acute 1 0 1 Goitre 1 0 1 Eye disorders Amaurosis fugax 1 1 2 Asthenopia 2 0 2 Blindness 3 1 4 Blindness unilateral 4 0 4 Conjunctival haemorrhage 1 1 2 Eye haemorrhage 1 2 3 Eye irritation 1 0 1 Eye pain 3 2 5 Eye swelling 2 0 2 Macular oedema 1 0 1 Miosis 1 0 1 Mydriasis 1 0 1 Ocular discomfort 1 0 1 Papilloedema 1 0 1 Photophobia 5 0 5 Photopsia 1 0 1 Retinal artery thrombosis 2 0 2 Retinal ischaemia 1 0 1 Retinal -
Hyperleukocytosis (Re)Visited- Is It Case Series Always Leukaemia: a Report of Two Pathology Section Cases and Review of Literature Short Communication
Review Article Clinician’s corner Original Article Images in Medicine Experimental Research Miscellaneous Letter to Editor DOI: 10.7860/JCDR/2020/40556.13409 Case Report Postgraduate Education Hyperleukocytosis (Re)Visited- Is it Case Series always Leukaemia: A Report of Two Pathology Section Cases and Review of Literature Short Communication ASHUTOSH RATH1, RICHA GUPTA2 ABSTRACT Hyperleukocytosis is defined as total leukocyte count of more than 100×109/L. Commonly seen in leukaemic conditions, non- leukaemic causes are usually not encountered and thought of. We report two such non-malignant cases of hyperleukocytosis. A six-year old girl presented with fever, cough and respiratory distress with a leukocyte count of 125.97×109/L. Another case is of a two-month old female infant, who presented with fever and respiratory distress and a leukocyte count of 112.27×109/L. The present case thrives to highlight various possible causes of hyperleukocytosis with an emphasis on non-malignant causes. Also, important complications and management of hyperleukocytosis are discussed. Keywords: Benign, Leukocytosis, Leukostasis CASE REPORT 1 for methicillin-resistant Staphylococcus aureus and was started A six-year-old girl was admitted with complaints of fever, non- on intravenous Vancomycin along with supportive care. Serial productive cough for one week and severe respiratory distress for monitoring of TLC revealed a gradual reduction and it returned to the the past one day. There was no other significant history. On physical baseline of 15×109/L after eight days. The patient was discharged examination, the patient had mild pallor. Respiratory examination after 10 days of hospital stay. -
Practice Parameter for the Diagnosis and Management of Primary Immunodeficiency
Practice parameter Practice parameter for the diagnosis and management of primary immunodeficiency Francisco A. Bonilla, MD, PhD, David A. Khan, MD, Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD, David I. Bernstein, MD, Joann Blessing-Moore, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Chief Editor: Francisco A. Bonilla, MD, PhD Co-Editor: David A. Khan, MD Members of the Joint Task Force on Practice Parameters: David I. Bernstein, MD, Joann Blessing-Moore, MD, David Khan, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Primary Immunodeficiency Workgroup: Chairman: Francisco A. Bonilla, MD, PhD Members: Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD GlaxoSmithKline, Merck, and Aerocrine; has received payment for lectures from Genentech/ These parameters were developed by the Joint Task Force on Practice Parameters, representing Novartis, GlaxoSmithKline, and Merck; and has received research support from Genentech/ the American Academy of Allergy, Asthma & Immunology; the American College of Novartis and Merck. -
Surgical Management of Atraumatic Splenic Rupture
International Surgery Journal Walker AM et al. Int Surg J. 2016 Nov;3(4):2280-2288 http://www.ijsurgery.com pISSN 2349-3305 | eISSN 2349-2902 DOI: http://dx.doi.org/10.18203/2349-2902.isj20163613 Case Report Surgical management of atraumatic splenic rupture Alyssa M. Walker1*, Eugene F. Foley2 1Mountain Area Health Education Center Obstetrics/Gynecology Specialists, 119 Hendersonville Road, Asheville, NC 28803, United States 2University of Wisconsin Hospital and Clinics, 621 Science Dr., Madison, WI 53711, United States Received: 04 September 2016 Accepted: 04 October 2016 *Correspondence: Dr. Alyssa Walker, E-mail: [email protected] Copyright: © the author(s), publisher and licensee Medip Academy. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT Atraumatic splenic rupture (ASR) is a rare, spontaneous, and potentially life-threatening condition that occurs in the absence of trauma; yet the management of ASR has largely defaulted to the treatment algorithm related to blunt splenic trauma. Our aim is to determine if it is appropriate and safe to use the treatment algorithm for blunt splenic trauma in the management of both pathological and non-pathological ASR. We present a case of non-pathological ASR that was successfully managed without splenectomy. A comprehensive literature review on spontaneous ASR was also performed to include publications from January 1975 to February 2015. 914 total cases of ASR were identified: 70 non-pathological and 844 pathological. Overall, 86.5% of these patients received splenectomy based on the presence or absence of traditional signs of clinical instability or deterioration, as utilized in cases of traumatic splenic rupture. -
Thrombocytosis in Systemic Lupus Erythematosus: a Possible Clue to Autosplenectomy?
Thrombocytosis in Systemic Lupus Erythematosus: A Possible Clue to Autosplenectomy? GABRIELLA CASTELLINO, MARCELLO GOVONI, NAPOLEONE PRANDINI, GESSICA LIMPIDO, SIMONE BERNARDI, DIANA CAMPIONE, FRANCESCO LANZA, and FRANCESCO TROTTA ABSTRACT. Objective. Thrombocytosis can be due to a myeloproliferative disorder or to a reactive or secondary process; among these are connective tissue disorders, in particular systemic lupus erythematosus (SLE). Besides being an expression of active disease, this unusual finding has also been described in SLE com- plicated by autosplenectomy. We evaluated the prevalence of thrombocytosis in a series of SLE patients and its relationship to functional asplenia. Methods. Platelet count was evaluated in 465 consecutive Caucasian patients with SLE (387 women, 78 men, median age 54 yrs). Thrombocytosis was defined as platelet count > 400 × 109/l in at least 3 blood samples. All patients with thrombocytosis underwent peripheral blood smears for erythrocyte abnormalities and instrumental spleen evaluation. Results. Seventeen patients (3.7%) with thrombocytosis were observed. Peripheral blood smear showed Howell-Jolly bodies, spherocytes, and target cells in 3/17 patients (17.6%). In the same 3 patients, ultra- sound and computed tomography failed to evidence the spleen, and liver-spleen scans showed absence of splenic uptake (a finding indicative of functional autosplenectomy). One satisfied criteria for antiphospholipid syndrome (APS), and the other 2 patients had positive IgG antiphospholipid antibod- ies (aPL) at -
Sickle-Cell Disorder
SICKLE-CELL DISORDER RMA ID Reference List for RMA161-2 as at June 2017 Number Addae S, Adzaku F, Mohammed S, Annobil S (1990). Sickle cell disease in 46925 permanent residents of mountain and low altitudes in Saudi Arabia. Tropical and Geographical Medicine, Vol 42 pp 342-348. Al Kahtani MA, AlQahtani M, Alshebaily MM, et al (2012). Morbidity and 79578 pregnancy outcomes associated with sickle cell anemia among Saudi women. Int J Gynecol Obstet, 119(3): 224-6. Alayed N, Kezouh A, Oddy L, et al (2014). Sickle cell disease and 79576 pregnancy outcomes: population-based study on 8.8 million births. J Perinat Med, 42(4): 487-92. Al-Salem AH (2013). Massive splenic infarction in children with sickle cell 79587 anemia and the role of splenectomy. Pediatric Surgery International, 29(3): 281-5. Ashley-Koch A, Yang Q, Olney RS (2000). Sickle hemoglobin (Hb S) allele 46299 and sickle cell disease: a HuGE review. Am J Epidemiol, 151(9):839-45. Babosa SM, Farhat SC, Martins LC, et al (2015). Air pollution and children's 79704 health: sickle cell disease. Cadernos de Saude Publica, 31(2): 265-75. Ballas SK (2007). Current issues in sickle cell pain and its management. 46357 Hematology, 2007:97-105. Barbeau P, Woods KF, Ramsey LT, Litaker MS, et al (2001). Exercise in 46995 sickle cell anemia: effect on inflammatory and vasoactive mediators. Endothelium, 8(2):147-55. Basnyat B, Tabin G (2015). Altitude Illness. Harrison's Principles of Internal 80342 Medicine, 19th Edition, 476e. Baum KF, Dunn DT, Maude GH, Serjeant GR (1987). -
An Unusual Etiology of Cytopenia, Diffuse Lymphadenopathy, and Massive Splenomegaly M
Donald and Barbara Zucker School of Medicine Journal Articles Academic Works 2015 "The Great Mimicker": An Unusual Etiology of Cytopenia, Diffuse Lymphadenopathy, and Massive Splenomegaly M. Zaarour Northwell Health C. Weerasinghe Northwell Health E. Moussaly Northwell Health S. Hussein Northwell Health J. P. Atallah Hofstra Northwell School of Medicine Follow this and additional works at: https://academicworks.medicine.hofstra.edu/articles Part of the Pathology Commons Recommended Citation Zaarour M, Weerasinghe C, Moussaly E, Hussein S, Atallah J. "The Great Mimicker": An Unusual Etiology of Cytopenia, Diffuse Lymphadenopathy, and Massive Splenomegaly. 2015 Jan 01; 2015():Article 683 [ p.]. Available from: https://academicworks.medicine.hofstra.edu/articles/683. Free full text article. This Article is brought to you for free and open access by Donald and Barbara Zucker School of Medicine Academic Works. It has been accepted for inclusion in Journal Articles by an authorized administrator of Donald and Barbara Zucker School of Medicine Academic Works. For more information, please contact [email protected]. Hindawi Publishing Corporation Case Reports in Medicine Volume 2015, Article ID 637965, 6 pages http://dx.doi.org/10.1155/2015/637965 Case Report (The Great Mimicker): An Unusual Etiology of Cytopenia, Diffuse Lymphadenopathy, and Massive Splenomegaly Mazen Zaarour,1 Chanudi Weerasinghe,1 Elias Moussaly,1 Shafinaz Hussein,2 and Jean-Paul Atallah3 1 Department of Medicine, Staten Island University Hospital, North Shore-LIJ Health System, Staten Island, New York, NY 10305, USA 2Department of Pathology, Staten Island University Hospital, North Shore-LIJ Health System, Staten Island, New York, NY 10305, USA 3Division of Hematology and Oncology, Department of Medicine, Staten Island University Hospital, North Shore-LIJ Health System, StatenIsland,NewYork,NY10305,USA Correspondence should be addressed to Mazen Zaarour; [email protected] Received 11 August 2015; Accepted 4 October 2015 Academic Editor: Masahiro Kohzuki Copyright © 2015 Mazen Zaarour et al. -
Original Article Anemia, Leukocytosis and Eosinophilia in a Resource-Poor
Original Article Anemia, leukocytosis and eosinophilia in a resource-poor population with helmintho-ectoparasitic coinfection Daniel Pilger1, Jörg Heukelbach2, Alexander Diederichs1, Beate Schlosser1, Cinthya Pereira Leite Costa Araújo3, Anne Keysersa1, Oliver Liesenfeld1, Hermann Feldmeier1 1Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Institute of Microbiology and Hygiene, D-12203 Berlin, Germany 2Department of Community Health, School of Medicine, Federal University of Ceará, Fortaleza, CE 60430-140, Brazil 3Department of Hematology, Estate University of Health Science of Alagoas, Alagoas, CEP 57010-300, Brazil Abstract Introduction: Eosinophilia and anemia are very common hematological alterations in the tropics but population-based studies scrutinizing their value for diagnosing parasitic infections are rare. Methodology: A cross-sectional study was conducted in a rural district in northeast Brazil where parasitic infections are common. Stool and blood samples were collected and individuals were clinically examined for the presence of ectoparasites. Results: In total, 874 individuals were examined. Infection with intestinal helminths occurred in 70% (95% CI 67 – 75), infestation with ectoparasites in 45% (95% CI 42 - 49) and co-infection with both helminths and ectoparasites was found in 33% (95% CI 29% - 36%) of all inhabitants. Eosinophil counts ranged from 40/µl to 13.800/µl (median: 900/µl). Haemoglobin levels ranged from 4.8 g/dl to 16.8 g/dl (median: 12.5 g/dl), and anemia was present in 24% of the participants. Leukocytosis was found in 13%, eosinophilia in 74%, and hypereosinophilia in 44% of the participants. Eosinophilia was more pronounced in individuals co-infected with intestinal helminths and ectoparasites (p < 0.001) and correctly predicted parasitic infection in 87% (95% CI 84%-90.7%) of all cases. -
Leukocytosis & Lymphocytosis
Leukocytosis Leukocytosis >11 (Repeated) Blood Smear AND History & EMERGENT REFERRAL Refer to Blasts on Smear Physical Exam Lymphocytes >4 Page Hematologist On-Call Lymphocytosis Algorithm Include nodes and spleen Myeloid Cells Basophils Monocytes Neutrophils Eosinophils CONCERNING FEATURES CONCERNING FEATURES CONCERNING FEATURES » Count >2 or increasing, or persistent » Count >50 » Count >2 or increasing or persistent » Not explained by infection » Promyelocytes and myelocytes » Dysplasia YES » Dysplasia » Dysplasia YES » Anemia » Immature forms » Basophilia » New organ damage » Anemia/thrombo-cytopenia » Splenomegaly » NOT explained by infection, allergies » Splenomegaly » NOT associated with acute infection or collagen vascular disease NO NO NO Consider Consider » Cancer Reactive Causes » drugs NO » Collagen VD YES e.g. Infection / inflammation, NO NO » Infections YES » Chronic infection autoimmune, drugs esp. steroids » Allergies » Marrow recovery » Collagen Vascular Disease Refer to Hematology Treat and Observe for recovery Refer to Hematology Treat and Observe for recovery © Blood Disorder Day Pathways are subject to clinical judgement and actual practice patterns may not always follow the proposed steps in this pathway. Lymphocytosis Lymphocytosis >4 (Repeated) Concerning Features “Reactive” Lymphocytes Asymptomatic » Lymphocytes >30 Patient symptoms of infection or acute illness » Hgb <100 » Night sweats/ weight loss » Splenomegaly Flow Cytometry AND Flow Cytometry IF PERSISTENT Work-up for secondary causes »Immunization »Viral