Mycoplasma Pneumoniae Bronchiolitis Mimicking Asthma in an Adult
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Section 8 Pulmonary Medicine
SECTION 8 PULMONARY MEDICINE 336425_ST08_286-311.indd6425_ST08_286-311.indd 228686 111/7/121/7/12 111:411:41 AAMM CHAPTER 66 EVALUATION OF CHRONIC COUGH 1. EPIDEMIOLOGY • Nearly all adult cases of chronic cough in nonsmokers who are not taking an ACEI can be attributed to the “Pathologic Triad of Chronic Cough” (asthma, GERD, upper airway cough syndrome [UACS; previously known as postnasal drip syndrome]). • ACEI cough is idiosyncratic, occurrence is higher in female than males 2. PATHOPHYSIOLOGY • Afferent (sensory) limb: chemical or mechanical stimulation of receptors on pharynx, larynx, airways, external auditory meatus, esophagus stimulates vagus and superior laryngeal nerves • Receptors upregulated in chronic cough • CNS: cough center in nucleus tractus solitarius • Efferent (motor) limb: expiratory and bronchial muscle contraction against adducted vocal cords increases positive intrathoracic pressure 3. DEFINITION • Subacute cough lasts between 3 and 8 weeks • Chronic cough duration is at least 8 weeks 4. DIFFERENTIAL DIAGNOSIS • Respiratory tract infection (viral or bacterial) • Asthma • Upper airway cough syndrome (postnasal drip syndrome) • CHF • Pertussis • COPD • GERD • Bronchiectasis • Eosinophilic bronchitis • Pulmonary tuberculosis • Interstitial lung disease • Bronchogenic carcinoma • Medication-induced cough 5. EVALUATION AND TREATMENT OF THE COMMON CAUSES OF CHRONIC COUGH • Upper airway cough syndrome: rhinitis, sinusitis, or postnasal drip syndrome • Presentation: symptoms of rhinitis, frequent throat clearing, itchy -
Understanding Asthma
Understanding Asthma The Mount Sinai − National Jewish Health Respiratory Institute was formed by the nation’s leading respiratory hospital National Jewish Health, based in Denver, and top ranked academic medical center the Icahn School of Medicine at Mount Sinai in New York City. Combining the strengths of both organizations into an integrated Respiratory Institute brings together leading expertise in diagnosing and treating all forms of respiratory illness and lung disease, including asthma, chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD) and bronchiectasis. The Respiratory Institute is based in New York City on the campus of Mount Sinai. njhealth.org Understanding Asthma An educational health series from National Jewish Health IN THIS ISSUE What Is Asthma? 2 How Does Asthma Develop? 4 How Is Asthma Diagnosed? 5 What Are the Goals of Treatment? 7 How Is Asthma Managed? 7 What Things Make Asthma Worse and How Can You Control Them? 8 Nocturnal Asthma 18 Occupational Asthma 19 Medication Therapy 20 Monitoring Your Asthma 29 Using an Action Plan 33 Living with Asthma 34 Note: This information is provided to you as an educational service of National Jewish Health. It is not meant as a substitute for your own doctor. © Copyright 1998, revised 2014, 2018 National Jewish Health What Is Asthma? This booklet, prepared by National Jewish Health in Denver, is intended to provide information to people with asthma. Asthma is a chronic respiratory disease — sometimes worrisome and inconvenient — but a manageable condition. With proper understanding, good medical care and monitoring, you can keep asthma well controlled. That’s our treatment goal at National Jewish Health: to teach patients and families how to manage asthma, so that they can lead full and productive lives. -
Exercise-Induced Dyspnea in College-Aged Athletes
A Peer Reviewed Publication of the College of Health Care Sciences at Nova Southeastern University Dedicated to allied health professional practice and education http://ijahsp.nova.edu Vol. 11 No. 3 ISSN 1540-580X Exercise-Induced Dyspnea in College-Aged Athletes Katherine R. Newsham, PhD, ATC 1 Ethel M. Frese, PT, DPT, CCS2 Richard A. McGuire, PhD, CCC-SLP 3 Dennis P. Fuller, PhD, CCC-SLP 4 Blakeslee E. Noyes, MD 5 1. Assistant Professor, Department of Physical Therapy and Athletic Training, Saint Louis University, St. Louis, MO 2. Associate Professor, Department of Physical Therapy and Athletic Training, Saint Louis University, St. Louis, MO 3. Professor, Department of Communication Sciences & Disorders, Saint Louis University, St. Louis, MO 4. Associate Professor, Department of Communication Sciences & Disorders, Saint Louis University, St. Louis, MO 5. Professor, Saint Louis University School of Medicine, St. Louis, MO, Director of Pulmonary Medicine, Cardinal Glennon Children’s Medical Center, St. Louis, MO United States CITATION: Newsham K, Frese E, McGuire R, Fuller D, Noyes B. Exercise-Induced Dyspnea in College-Aged Athletes. The Internet Journal of Allied Health Sciences and Practice. July 2013. Volume 11 Number 3. ABSTRACT Purpose: Shortness of breath or difficulty breathing during exercise is referred to as exercise-induced dyspnea (EID), and is a common complaint from athletes. The purpose of this study was to assess the prevalence of EID among college aged athletes and to explore the medical encounters, including diagnostic testing, arising from this complaint. Method: We surveyed intercollegiate (n=122) and club sport (n=103) athletes regarding their experience with EID, including medical diagnoses, diagnostic procedures, environmental factors, and treatment effectiveness. -
Asthma Exacerbation Management
CLINICAL PATHWAY ASTHMA EXACERBATION MANAGEMENT TABLE OF CONTENTS Figure 1. Algorithm for Asthma Exacerbation Management – Outpatient Clinic Figure 2. Algorithm for Asthma Management – Emergency Department Figure 3. Algorithm for Asthma Management – Inpatient Figure 4. Progression through the Bronchodilator Weaning Protocol Table 1. Pediatric Asthma Severity (PAS) Score Table 2. Bronchodilator Weaning Protocol Target Population Clinical Management Clinical Assessment Treatment Clinical Care Guidelines for Treatment of Asthma Exacerbations Children’s Hospital Colorado High Risk Asthma Program Table 3. Dosage of Daily Controller Medication for Asthma Control Table 4. Dosage of Medications for Asthma Exacerbations Table 5. Dexamethasone Dosing Guide for Asthma Figure 5. Algorithm for Dexamethasone Dosing – Inpatient Asthma Patient | Caregiver Education Materials Appendix A. Asthma Management – Outpatient Appendix B. Asthma Stepwise Approach (aka STEPs) Appendix C. Asthma Education Handout References Clinical Improvement Team Page 1 of 24 CLINICAL PATHWAY FIGURE 1. ALGORITHM FOR ASTHMA EXACERBATION MANAGEMENT – OUTPATIENT CLINIC Triage RN/MA: • Check HR, RR, temp, pulse ox. Triage level as appropriate • Notify attending physician if patient in severe distress (RR greater than 35, oxygen saturation less than 90%, speaks in single words/trouble breathing at rest) Primary RN: • Give oxygen to keep pulse oximetry greater than 90% Treatment Inclusion Criteria 1. Give nebulized or MDI3 albuterol up to 3 doses. Albuterol dosing is 0.15 to 0.3mg/kg per 2007 • 2 years or older NHLBI guidelines. • Treated for asthma or asthma • Less than 20 kg: 2.5 mg neb x 3 or 2 to 4 puffs MDI albuterol x 3 exacerbation • 20 kg or greater: 5 mg neb x 3 or 4 to 8 puffs MDI albuterol x 3 • First time wheeze with history consistent Note: For moderate (dyspnea interferes with activities)/severe (dyspnea at rest) exacerbations you with asthma can add atrovent to nebulized albuterol at 0.5mg/neb x 3. -
08-0205: N.M. and DEPARTMENT of the NAVY, PUGET S
United States Department of Labor Employees’ Compensation Appeals Board __________________________________________ ) N.M., Appellant ) ) and ) Docket No. 08-205 ) Issued: September 2, 2008 DEPARTMENT OF THE NAVY, PUGET ) SOUND NAVAL SHIPYARD, Bremerton, WA, ) Employer ) __________________________________________ ) Appearances: Oral Argument July 16, 2008 John Eiler Goodwin, Esq., for the appellant No appearance, for the Director DECISION AND ORDER Before: DAVID S. GERSON, Judge COLLEEN DUFFY KIKO, Judge JAMES A. HAYNES, Alternate Judge JURISDICTION On October 30, 2007 appellant filed a timely appeal from a November 17, 2006 decision of the Office of Workers’ Compensation Programs denying his occupational disease claim. Pursuant to 20 C.F.R. §§ 501.2(c) and 501.3, the Board has jurisdiction over the merits of the claim. ISSUE The issue is whether appellant has established that he sustained occupational asthma in the performance of duty due to accepted workplace exposures. On appeal, he, through his attorney, asserts that the Office did not provide Dr. William C. Stewart, the impartial medical examiner, with a complete, accurate statement of accepted facts. FACTUAL HISTORY On December 8, 2004 appellant, then a 57-year-old insulator, filed an occupational disease claim (Form CA-2) asserting that he sustained occupational asthma and increasing shortness of breath due to workplace exposures to fiberglass, silicates, welding smoke, polychlorobenzenes, rubber, dusts, gases, fumes and smoke from “burning out” submarines from 1991 through January -
Clinical Perspectives on the Association Between Respiratory Syncytial Virus and Reactive Airway Disease Nele Sigurs
Respiratory Research Vol 3 Suppl 1 Sigurs Clinical perspectives on the association between respiratory syncytial virus and reactive airway disease Nele Sigurs Department of Pediatrics, Borås Central Hospital, Borås, Sweden Corresponding author: Nele Sigurs (e-mail: [email protected]) Received: 24 May 2002 Accepted: 30 May 2002 Published: 24 June 2002 Respir Res 2002, 3 (suppl 1):S8-S14 © 2002 BioMed Central Ltd (Print ISSN 1465-9921; Online ISSN 1465-993X) Abstract Asthma is a leading cause of morbidity and mortality among children worldwide, as is respiratory syncytial virus (RSV). This report reviews controlled retrospective and prospective studies conducted to investigate whether there is an association between RSV bronchiolitis in infancy and subsequent development of reactive airway disease or allergic sensitization. Findings indicate that such a link to bronchial obstructive symptoms does exist and is strongest for children who experienced severe RSV illness that requires hospitalization. However, it is not yet clear what roles genetic predisposition and environmental or other risk factors may play in the interaction between RSV bronchiolitis and reactive airway disease or allergic sensitization. Randomized, prospective studies utilizing an intervention against RSV, such as a passive immunoprophylactic agent, may determine whether preventing RSV bronchiolitis reduces the incidence of asthma. Keywords: allergy, asthma, bronchiolitis, reactive airway disease, respiratory syncytial virus Introduction nesses are at even greater risk for serious infection and Childhood asthma is a serious global public health hospitalization from RSV [3]. problem. According to the World Health Organization [1], asthma is the most common chronic disease in children. In RSV bronchiolitis is characterized by expiratory wheezing some areas of the world the incidence in children is over and respiratory distress [4]. -
Management of Acute Exacerbation of Asthma and Chronic Obstructive Pulmonary Disease in the Emergency Department
Management of Acute Exacerbation of Asthma and Chronic Obstructive Pulmonary Disease in the Emergency Department Salvador J. Suau, MD*, Peter M.C. DeBlieux, MD KEYWORDS Asthma Asthmatic crisis COPD AECOPD KEY POINTS Management of severe asthma and chronic obstructive pulmonary disease (COPD) exac- erbations require similar medical interventions in the acute care setting. Capnography, electrocardiography, chest x-ray, and ultrasonography are important diag- nostic tools in patients with undifferentiated shortness of breath. Bronchodilators and corticosteroids are first-line therapies for both asthma and COPD exacerbations. Noninvasive ventilation, magnesium, and ketamine should be considered in patients with severe symptoms and in those not responding to first-line therapy. A detailed plan reviewed with the patient before discharge can decrease the number of future exacerbations. INTRODUCTION Acute asthma and chronic obstructive pulmonary disease (COPD) exacerbations are the most common respiratory diseases requiring emergent medical evaluation and treatment. Asthma accounts for more than 2 million visits to emergency departments (EDs), and approximately 4000 annual deaths in the United States.1 In a similar fashion, COPD is a major cause of morbidity and mortality. It affects more than 14.2 million Americans (Æ9.8 million who may be undiagnosed).2 COPD accounts for more than 1.5 million yearly ED visits and is the fourth leading cause of death Disclosures: None. Louisiana State University, University Medical Center of New Orleans, 2000 Canal Street, D&T 2nd Floor - Suite 2720, New Orleans, LA 70112, USA * Corresponding author. E-mail address: [email protected] Emerg Med Clin N Am 34 (2016) 15–37 http://dx.doi.org/10.1016/j.emc.2015.08.002 emed.theclinics.com 0733-8627/16/$ – see front matter Ó 2016 Elsevier Inc. -
Comparative Radiographic Features of Community Acquired Legionnaires' Disease, Pneumococcal Pneumonia, Mycoplasma Pneumonia, and Psittacosis
Thorax: first published as 10.1136/thx.39.1.28 on 1 January 1984. Downloaded from Thorax 1984;39:28-33 Comparative radiographic features of community acquired legionnaires' disease, pneumococcal pneumonia, mycoplasma pneumonia, and psittacosis JT MACFARLANE, AC MILLER, WH RODERICK SMITH, AH MORRIS, DH ROSE From the Departments of Thoracic Medicine and Radiology, City Hospital, Nottingham ABSTRACT The features of the chest radiographs of 49 adults with legionnaires' disease were compared with those of 91 adults with pneumococcal pneumonia (31 of whom had bacteraemia or antigenaemia), 46 with mycoplasma pneumonia, and 10 with psittacosis pneumonia. No distinctive pattern was seen for any group. Homogeneous shadowing was more frequent in legionnaires' disease (40/49 cases) (p < 0.005), bacteraemic pneumococcal pneumonia (25/31) (p < 0.01) and non-bacteraemic pneumococcal pneumonia (42/60) (p < 0.05) than in myco- plasma pneumonia (23/46). Multilobe disease at presentation was commoner in bacteraemic pneumococcal pneumonia (20/31) than in non-bacteraemic pneumococcal pneumonia (15/60) (p < 0.001) or legionnaires' disease (19/49) (p < 0.025). In bacteraemic pneumococcal pneumonia multilobe disease at presentation was associated with increased mortality. Pleural effusions and some degree of lung collapse were seen in all groups, although effusions were commoner in bacteraemic pneumococcal pneumonia. Cavitation was unusual. Lymphadenopathy occurred only in mycoplasma pneumonia (10/46). Radiographic deterioration was particularly a feature of legionnaires' disease (30/46) and bacteraemic pneumococcal pneumonia (14/27), and these groups also showed slow radiographic resolution in survivors. Radiographic resolution was fastest with mycoplasma pneumonia; psittacosis and non-bacteraemic pneumococcal pneumonia http://thorax.bmj.com/ cleared at an intermediate rate. -
Global Strategy for Asthma Management and Prevention, 2019. Available From
DISTRIBUTE OR COPY NOT DO MATERIAL- COPYRIGHTED ASTHMA MANAGEMENT AND PREVENTION GLOBAL STRATEGY FOR Updated 2019 9 Global Strategy for Asthma Management and Prevention (2019 update) DISTRIBUTE OR COPY NOT DO The reader acknowledges that this reportMATERIAL- is intended as an evidence-based asthma management strategy, for the use of health professionals and policy-makers. It is based, to the best of our knowledge, on current best evidence and medical knowledge and practice at the date of publication. When assessing and treating patients, health professionals are strongly advised to use their own professional judgment, and to take into account local or national regulations and guidelines. GINA cannot be held liable or responsible for inappropriate healthcare associated with the use of this document, including any use which is not in accordance with applicable local or national regulations or COPYRIGHTEDguidelines. This document should be cited as: Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2019. Available from: www.ginasthma.org 1 Table of contents Tables and figures ............................................................................................................................................................... 5 Preface ................................................................................................................................................................................. 7 Members of GINA committees (2018) ................................................................................................................................ -
Cryptogenic Organizing Pneumonia
462 Cryptogenic Organizing Pneumonia Vincent Cottin, M.D., Ph.D. 1 Jean-François Cordier, M.D. 1 1 Hospices Civils de Lyon, Louis Pradel Hospital, National Reference Address for correspondence and reprint requests Vincent Cottin, Centre for Rare Pulmonary Diseases, Competence Centre for M.D., Ph.D., Hôpital Louis Pradel, 28 avenue Doyen Lépine, F-69677 Pulmonary Hypertension, Department of Respiratory Medicine, Lyon Cedex, France (e-mail: [email protected]). University Claude Bernard Lyon I, University of Lyon, Lyon, France Semin Respir Crit Care Med 2012;33:462–475. Abstract Organizing pneumonia (OP) is a pathological pattern defined by the characteristic presence of buds of granulation tissue within the lumen of distal pulmonary airspaces consisting of fibroblasts and myofibroblasts intermixed with loose connective matrix. This pattern is the hallmark of a clinical pathological entity, namely cryptogenic organizing pneumonia (COP) when no cause or etiologic context is found. The process of intraalveolar organization results from a sequence of alveolar injury, alveolar deposition of fibrin, and colonization of fibrin with proliferating fibroblasts. A tremen- dous challenge for research is represented by the analysis of features that differentiate the reversible process of OP from that of fibroblastic foci driving irreversible fibrosis in usual interstitial pneumonia because they may determine the different outcomes of COP and idiopathic pulmonary fibrosis (IPF), respectively. Three main imaging patterns of COP have been described: (1) multiple patchy alveolar opacities (typical pattern), (2) solitary focal nodule or mass (focal pattern), and (3) diffuse infiltrative opacities, although several other uncommon patterns have been reported, especially the reversed halo sign (atoll sign). -
Legionnaires• Disease: Clinical Differentiation from Typical And
Legionnaires’ Disease: Clinical Differentiation from Typical and Other Atypical Pneumonias a,b, Burke A. Cunha, MD, MACP * KEYWORDS Clinical syndromic diagnosis Relative bradycardia Ferritin levels Hypophosphatemia HISTORY An outbreak of a severe respiratory illness occurred in Washington, DC, in 1965 and another in Pontiac, Michigan, in 1968. Despite extensive investigations following these outbreaks, no explanation or causative organism was found. In July 1976 in Philadel- phia, Pennsylvania, an outbreak of a severe respiratory illness occurred at an Amer- ican Legion convention. The US Centers for Disease Control and Prevention (CDC) conducted an extensive epidemiologic and microbiologic investigation to determine the cause of the outbreak. Dr Ernest Campbell of Bloomsburg, Pennsylvania, was the first to recognize the relationship between the American Legion convention in 3 of his patients who attended the convention and who had a similar febrile respiratory infection. Six months after the onset of the outbreak, a gram-negative organism was isolated from autopsied lung tissue. Dr McDade, using culture media used for rickettsial organisms, isolated the gram-negative organism later called Legionella. The isolate was believed to be the causative agent of the respiratory infection because antibodies to Legionella were detected in infected survivors. Subsequently, CDC investigators realized the antecedent outbreaks of febrile illness in Philadelphia and in Pontiac were caused by the same organism. They later demonstrated increased Legionella titers in survivors’ stored sera. The same organism was responsible for the pneumonias that occurred after the American Legionnaires’ Convention in Philadelphia in 1976. a Infectious Disease Division, Winthrop-University Hospital, 259 First Street, Mineola, Long Island, NY 11501, USA b State University of New York School of Medicine, Stony Brook, NY, USA * Infectious Disease Division, Winthrop-University Hospital, 259 First Street, Mineola, Long Island, NY 11501. -
Mycoplasma Pneumonia with Fulminant Evolution Into Diffuse Interstitial Fibrosis
Thorax: first published as 10.1136/thx.35.2.140 on 1 February 1980. Downloaded from Thorax, 1980, 35, 140-144 Mycoplasma pneumonia with fulminant evolution into diffuse interstitial fibrosis J M KAUFMAN, C A CUVELIER, AND M VAN DER STRAETEN From the Departments of Medicine and Pathology, State University Hospital, Gent, Belgium ABSTRACT A fatal case of interstitial pneumonia caused by Mycoplasma pneumoniae with fulminant evolution into diffuse interstitial fibrosis is reported. Treatment with tetracycline and corticosteroids failed to arrest the progress of the disease. Fatal Mycoplasma pneumoniae infections have been reported previously and some degree of pulmonary fibrosis has been described in a few cases but as far as could be ascertained there are no other well-documented cases of diffuse interstitial fibrosis with proved Mycoplasma pneumoniae infection. Mycoplasma pneumoniae is a well-documented became more pronounced during the morning. and recognised cause of pneumonia, although in She also complained of vertigo and anorexia, and most cases infection remains subclinical or limited vomited once. The next morning she became to upper respiratory tract involvement.'-4 Clinical severely dyspnoeic and was admitted to a localcopyright. and radiographic features are inconstant and do hospital. Arterial blood gas analysis revealed a not allow for differentiation from pneumonias carbon dioxide tension (Pco2) of 35 mmHg and an caused by other micro-organisms.5 6 Mycoplasma oxygen tension (Po2) of 75 mmHg while breathing pneumoniae usually has a rather benign, self- 4 litres of oxygen per minute. The chest radio- limiting course. However, besides important extra- graph showed patchy lobular shadows involving pulmonary complications such as haemolytic both lower zones (fig 1).