DOCSLIB.ORG

Asthma and Chlamydial Infection: a Case Series David L

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Asthma and Chlamydial Infection: A Case Series David L. Hahn, MD, and Rjurik Golubjatnikov, PhD, MPH Madison, Wisconsin Background. Adult-onset asthma is frequently associ­ asthma for the first time during the study period. ated with antecedent respiratory symptoms that could Thirty' (22.9%) patients were classified with acute asth­ represent either previously undiagnosed asthma or pre­ matic bronchitis, and 89 (67.9%) had nonwheezing ill­ vious lung infections that result in subsequent asthma. ness. Two of the newly diagnosed asthmatics met sero­ To further investigate a reported association of Chla­ logic criteria for acute C pneumoniae infection, and one mydia pneumonias infection and adult reactive airway had serologic evidence for acute M pneumoniae infec­ disease, we looked for evidence o f atypical infections in tion. Compared with patients with nonwheezing respi­ patients with acute wheezing and nonwheezing respira­ ratory' illnesses, C pneumoniae seroreactivity was signifi­ tory illnesses. cantly (P < .001) associated with both chronic asthma and with acute asthmatic bronchitis. Methods. Pharyngeal cultures and acute and convales­ cent serology for C pneumoniae and Mycoplasma pneu­ Conclusions. Acute wheezing illness was encountered moniae were obtained from 131 primary care outpa­ frequendy in this primary care setting. Although most tients (mean age, 36 years) with acute wheezing or acute wheezing respiratory' illness resolved without ob­ nonwheezing respiratory illnesses. Peak flow measure­ vious chronic sequelae, some patients had persistent ments were obtained in patients with cough or wheeze. symptoms and were diagnosed with chronic asthma. C Spirometry before and after bronchodilator use was pneumoniae seroreactivity was associated with both obtained to substantiate the diagnosis of chronic acute and chronic wheezing, suggesting that pulmo­ asthma in patients who had persistent wheezing and nary' infection with this intracellular pathogen plays a dyspnea after enrollment. role in the natural history of reactive airway disease. Results. Twelve (9.2%) of 131 patients were classified Key words. Asthma; bronchitis; Chlamydia pneumoniae; as having chronic asthma, 5/12 developed chronic Mycoplasma pneumoniae. (/ Fam Pract 1994; 38:589-595) The cause of asthma, a common chronic inflammatory bacteria (Mycoplasma pneumoniae and Chlamydia pneumo­ airway condition, is not well understood. It was once niae) may play a role in these reported associations.5-9 thought that infection played an important causative role Given these preliminary' results and our limited under­ in asthma,1"3 but there are no convincing scientific stud­ standing of asthma etiology, it is worthwhile to investi­ ies documenting “bacterial allergy” as a cause.4 More gate further the possibility that atypical infections arc- recent epidemiologic studies and clinical reports have involved in the initiation and exacerbation o f asthma, or documented that respiratory diagnoses including bron­ even the promotion of asthma in persistently infected, chiolitis,5 acute bronchitis,6 chronic bronchitis7 and susceptible individuals. pneumonia8 are associated with the development of sub­ Mycoplasma pneumoniae infection is a recognized sequent asthma in both adults and children. Some re­ cause of acute respiratory illnesses, including atypical ports have presented preliminary evidence that atypical pneumonia and tracheobronchitis, and may also cause asymptomatic infection in about 20% of cases.10 M pneu­ moniae infection is more common in children than in Submitted, revised, December 30, 1993. adults,11 and has been associated with varying propor­ From the Arcand Park Clinic, Division o f Dean Medical Center (D.L.H.), and tions of acute infectious exacerbations of asthma, usually Wisconsin State Laboratory o f Hygiene (R.G.), Madison, Wisconsin. Requests for reprints should be addressed to David L. Hahn, MD, Arcand Park Clinic, 3434 East in children12-14 but also sometimes in adults.15 A pro­ Washington Ave, Madison, W I 53704. longed carrier state beyond several months postinfection ® 1994 Appleton & Lange ISSN 0094-3509 The Journal of Family Practice, Vol. 38, No. 6(Jun), 1994 5 8 9 Asthma and Chlamydial Infection H ahn and Golubjatnikov in immunocompetent patients has not been document­ study are greater, therefore, than comparable figures ed,16 making it unlikely that persistent M pneumoniae (13% and 3%, respectively) from our previous study infection frequently promotes chronic asthma.5 which enrolled all patients systematically.9 Another atypical respiratory pathogen, Chlamydia Our definition of “asthmatic bronchitis” differs from pneumoniae, has emerged as an important cause of acute that used in some standard references of pulmonary med­ respiratory illness, including bronchitis and pneumo­ icine. Thus, asthmatic bronchitis has been used to de­ nia.17 Like M pneumoniae, most primary infections occur scribe patients in whom the diagnoses of chronic bron­ in younger age groups. Unlike M pneumoniae, however, chitis and asthma coexist, or are difficult to distinguish.^ the majority of patients with Cpneumoniae infections are The term “wheezy bronchitis,” as used in another refer­ asymptomatic or only mildly symptomatic,18 and repeat ence,27 denotes episodes of wheezing during acute bron­ infections are common and occur throughout adult­ chitis, occuring mainly in children. Acute asthmatic hood.19 Chronic intracellular infection is typical for chla- bronchitis, as used in this paper, refers to the latter type mydiae.20 Persistent infection has been documented for of wheezing during acute bronchitis but is not limited to C pneumoniae21 and has been implicated in some chronic children, since there is mounting evidence that a signif­ cardiopulmonary diseases including sarcoidosis,22 coro­ icant proportion (15% to 30%) of episodes of acute nary artery disease,23-25 and adult-onset asthma.9 bronchitis in adult outpatients from primary care settings In a previous prospective study designed to assess may involve bronchospasm or wheezing.6'9-28'29 the role o f acute C pneumoniae infection in bronchitis and atypical pneumonia, we found post hoc associations of C Pulmonary Function Measurement and pneumoniae scroreactivity with wheezing, asthmatic Diagnosis of Asthma bronchitis, and adult-onset asthma.9 We now report re­ sults of culture and serology for M pneumoniae and C Patients with acute asthmatic bronchitis had peak expi­ pneumoniae in a series of patients with asthma confirmed ratory flow measurements documented (best of three by pulmonary function testing, studied during a M pneu­ values) using a Wright peak flow meter (Armstrong moniae epidemic. Asthma patients arc compared with Industries, Inc, Northbrook, 111). Standardized normal patients who had acute asthmatic bronchitis or acute values for age, sex, and height were also recorded. Pa­ nonwheezing respiratory illnesses. tients with persistent wheezing and dyspnea in whom a diagnosis of asthma was suspected had spirometric test­ ing performed using a spirometer (System 21, Gould Methods Medical Products Inc, Dayton, OH). This study em­ ployed American Thoracic Society (ATS) guidelines for Study Setting the diagnosis of asthma and chronic obstructive pulmo­ One hundred thirty-one patients who visited a primary nary disease (COPD).30-31 care office with complaints o f respiratory illness between Clinical diagnoses of acute asthmatic bronchitis and October 1989 and January 1991 (16 months) were en­ asthma and serologic results o f patients (n = 50) enrolled rolled in the study. The study site was a community- between October and December 1989 were included in based, four-physician family practice office affiliated with our first report associating C pneumoniae infection with a large multispecialty, multisite group practice located in reactive airway disease.9 The resuits of pulmonary func­ a metropolitan area of south central Wisconsin (Dane tion testing for this group have not been published County), with a predominantly white, middle-class pop­ previously. When these original patients were compared ulation. with the 81 patients enrolled after December 1989, there were no significant differences in mean age, sex, history Enrollment Criteria of smoking, Cpneumoniae seroreactivity, titer category' ot acute antibody, or diagnoses of acute asthmatic bronchi­ Enrollment was offered to all patients who were encoun­ tis, asthma, or COPD. tered by the clinician-investigator during the course of usual practice and who had laryngitis, biphasic illness (pharyngitis and/or laryngitis, followed by bronchitis or Bacteriologic and Serologic Data pneumonia), wheezing, or atypical pneumonia. Patient Acute sera for microimmunofluorescence (MIF) testing refusal was not documented but is believed to be mini­ for C pneumoniae and complement fixation (CF) testing mal. Enrollment of patients with other respiratory ill­ for At pneumoniae and oropharyngeal culture for C pneu­ nesses was less systematic. The proportions of acute moniae and M pneumoniae were obtained at the time of asthmatic bronchitis (23%) and asthma (9%) in this study enrollment for all patients. Because 17 patients 5 9 0 The Journal of Family Practice, Vol. 38, No. 6(Jun), 1994 \sthma and Chlamydial Infection Hahn and Golubjamikov failed to return for follow-up testing, convalescent sera Respirator)^ diagnoses at enrollment and for the were available from only 114 patients (87%). Serologic 6 -month period before and after enrollment were tabu­ criteria for acute
Recommended publications
  • Section 8 Pulmonary Medicine

    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

    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

    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.
  • A Case of Cryptogenic Organizing Pneumonia in a Seventh-Decade Woman

    A Case of Cryptogenic Organizing Pneumonia in a Seventh-Decade Woman

    Saudi Journal of Medicine ISSN 2518-3389 (Print) Scholars Middle East Publishers ISSN 2518-3397 (Online) Dubai, United Arab Emirates Website: http://scholarsmepub.com/ A case of Cryptogenic Organizing Pneumonia in a seventh-decade woman. "Yahya Al-FIFI’s Diagnostic Criteria for Cryptogenic Organizing Pneumonia (COP) Without Lung Tissues Biopsies for Histopathology". Is This the Truth of the Reality Or The Reality of the Truth? Yahya Salim Yahya AL-FIFI Consultant, Internal Medicine &Infectious Diseases, Department of Medicine, Infection Diseases Division, Prince Mohammad Bin Nasser Hospital, Jizan, Jazan, Saudi Arabia. Email: [email protected] Abstract: We describe the first and rare case report of a cryptogenic organizing *Corresponding author pneumonia (COP) in a seventh decade diabetic and hypertensive woman from low Yahya Salim Yahya highlands, Jazan, Saudi Arabia. The evidence of the clinical scenario, laboratories testing, radiological images findings followed by a significant improvement due to Article History steroid treatment are quite enough to diagnose COP, irrespective of the lung tissues Received: 19.11.2017 biopsies procedures and processing accessibility for histopathology, in a timely manner Accepted: 24.11.2017 as reveals in “Yahya Al-FIFI’s diagnostic criteria for cryptogenic organizing pneumonia Published: 30.11.2017 (COP) without lung tissues biopsies for histopathology”. We started a methylprednisolone forty milligrams intravenously every eight hourly for seven days DOI: which is showing a dramatic clinical improvement within initial twenty-four hours of 10.21276/sjm.2017.2.7.4 the first seven days and complete recovery clinically and radiologically, at the end of the following fourteen days of tapering prednisolone doses without a relapse for seven months.
  • Asthma Exacerbation Management

    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.
  • Lansdell Vs. Georgia-Pacific Corporation Awcc# F007360

    Lansdell Vs. Georgia-Pacific Corporation Awcc# F007360

    BEFORE THE ARKANSAS WORKERS’ COMPENSATION COMMISSION CLAIM NO. F007360 ALVIN LANSDELL, EMPLOYEE CLAIMANT GEORGIA-PACIFIC CORPORATION, SELF-INSURED EMPLOYER RESPONDENT OPINION FILED SEPTEMBER 3, 2003 Upon review before the FULL COMMISSION in Little Rock, Pulaski County, Arkansas. Claimant represented by HONORABLE GREGORY R. GILES, Attorney at Law, Texarkana, Arkansas. Respondent represented by HONORABLE MARK A. PEOPLES, Attorney at Law, Little Rock, Arkansas. Decision of the Administrative Law Judge: Affirmed as modified. OPINION AND ORDER The claimant appeals an Administrative Law Judge’s opinion filed August 21, 2002. The Administrative Law Judge found that Act 1281 of 2001 made substantive law changes to the burden of proof for occupational disease and was to be applied prospectively. The Administrative Law Judge therefore found, “Claimant has failed to prove by clear and convincing evidence that he sustained an occupational disease which arose out of and in the course of his employment.” After reviewing the entire record de novo, the Lansdell - F007360 2 Full Commission finds that our recent decision in a companion case, Sikes v. Georgia-Pacific Corporation, Workers’ Compensation Commission F000657 (July 7, 2003), is controlling in this matter as to the appropriate burden of proof. We therefore find that the Legislature meant to apply Act 1281 retroactively, so that the “preponderance of the evidence” standard of Ark. Code Ann. § 11-9-601 (e)(1)(B) applies to the instant matter. The Full Commission further finds that the claimant failed to prove by a preponderance of the evidence that he sustained a compensable occupational disease. We therefore affirm, as modified, the opinion of the Administrative Law Judge.
  • Pediatric Ambulatory Community Acquired Pneumonia (CAP)

    Pediatric Ambulatory Community Acquired Pneumonia (CAP)

    ANMC Pediatric (≥3mo) Ambulatory Community Acquired Pneumonia (CAP) Treatment Guideline Criteria for Respiratory Distress Criteria For Outpatient Management Testing/Imaging for Outpatient Management Tachypnea, in breaths/min: Mild CAP: no signs of respiratory distress Vital Signs: Standard VS and Pulse Oximetry Age 0-2mo: >60 Able to tolerate PO Labs: No routine labs indicated Age 2-12mo: >50 No concerns for pathogen with increased virulence Influenza PCR during influenza season Age 1-5yo: >40 (ex. CA-MRSA) Blood cultures if not fully immunized OR fails to Age >5yo: >20 Family able to carefully observe child at home, comply improve/worsens after initiation of antibiotics Dyspnea with therapy plan, and attend follow up appointments Urinary antigen detection testing is not Retractions recommended in children; false-positive tests are common. Grunting If patient does not meet outpatient management criteria Radiography: No routine CXR indicated Nasal flaring refer to inpatient pneumonia guideline for initial workup Apnea and testing. AP and lateral CXR if fails initial antibiotic therapy Altered mental status AP and lateral CXR 4-6 weeks after diagnosis if Pulse oximetry <90% on room air recurrent pneumonia involving the same lobe Treatment Selection Suspected Viral Pneumonia Most Common Pathogens: Influenza A & B, Adenovirus, Respiratory Syncytial Virus, Parainfluenza No antimicrobial therapy is necessary. Most common in <5yo If influenza positive, see influenza guidelines for treatment algorithm. Suspected Bacterial
  • Secondary Pulmonary Alveolar Proteinosis in Hematologic

    Secondary Pulmonary Alveolar Proteinosis in Hematologic

    review Secondary pulmonary alveolar proteinosis in hematologic malignancies Chakra P Chaulagain a,*, Monika Pilichowska b, Laurence Brinckerhoff c, Maher Tabba d, John K Erban e a Taussig Cancer Institute of Cleveland Clinic, Department of Hematology/Oncology, Cleveland Clinic in Weston, FL, USA, b Department of Pathology, Tufts Medical Center Cancer Center & Tufts University School of Medicine, Boston, MA, USA, c Department of Surgery, Tufts Medical Center Cancer Center & Tufts University School of Medicine, Boston, MA, USA, d Division of Critical Care, Pulmonary and Sleep Medicine, Tufts Medical Center Cancer Center & Tufts University School of Medicine, Boston, MA, USA, e Division of Hematology/Oncology, Tufts Medical Center Cancer Center & Tufts University School of Medicine, Boston, MA, USA * Corresponding author at: Cleveland Clinic Florida, 2950 Cleveland Clinic Blvd., Weston, FL 33331, USA. Tel.: +1 954 659 5840; fax: +1 954 659 5810. Æ [email protected] Æ Received for publication 29 January 2014 Æ Accepted for publication 1 September 2014 Hematol Oncol Stem Cell Ther 2014; 7(4): 127–135 ª 2014 King Faisal Specialist Hospital & Research Centre. Published by Elsevier Ltd. All rights reserved. DOI: http://dx.doi.org/10.1016/j.hemonc.2014.09.003 Abstract Pulmonary alveolar proteinosis (PAP), characterized by deposition of intra-alveolar PAS positive protein and lipid rich material, is a rare cause of progressive respiratory failure first described by Rosen et al. in 1958. The intra-alveolar lipoproteinaceous material was subsequently proven to have been derived from pulmonary surfactant in 1980 by Singh et al. Levinson et al. also reported in 1958 the case of 19- year-old female with panmyelosis afflicted with a diffuse pulmonary disease characterized by filling of the alveoli with amorphous material described as ‘‘intra-alveolar coagulum’’.
  • 08-0205: N.M. and DEPARTMENT of the NAVY, PUGET S

    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

    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

    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.
  • Global Strategy for Asthma Management and Prevention, 2019. Available From

    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) ................................................................................................................................