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Reactive airway disease after chlorine gas exposure. S L Demeter and E W Cordasco Chest 1992;102;984b-984 DOI 10.1378/chest.102.3.984b The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/102/3/984b.citation Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1992by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692 Downloaded from chestjournal.chestpubs.org by guest on October 22, 2010 1992 American College of Chest Physicians wald E, ed. Heart disease, 3rd ed. Philadelphia: WB Saunders Co. 1988; 180-227 3 Schamroth L. An introduction to electrocardiography, Oxford, England: Blackwell Scientific Publications, 6th ed. 1982; 140 4 Dunn PM, Levinson WL. The lack of effect of clinical information on electrocardiographic diagnosis of acute myocardial infarction, Arch Intern Med 1990; 150:1917-19 Reactive Airway Disease after Chlorine Gas Exposure To the Editor: We read with great interest in the September 1991 issue of Chest the case report by Moore and Sherman.' Chlorine gas exposure has multiple toxic effects ate airflow obstruction, on the respiratory system, including immedi- ARDS, and death. The long-term effects can include abnormalities in gas transfer, restriction, and airflow obstruction. These generally resolve with time to a variable degree. Additionally, the severity and resolution of these effects appear to be related to the degree of exposure, premorbid pulmonary status, and the degree of hypoxemia on initial presentation. In 1990, we reported two cases of reactive airway dysfunction syndrome (RADS) following chlorine exposure to chlorine gas.5 Both patients had an asthmatic diathesis extending over time. One individual has had persistent asthmatic symptoms for the past six years; the symptoms have ameliorated with time, although she continues to be symptomatic. She is receiving minimal medication at the present time, compared with her immediate postexposure needs. Before exposure, she was neither a smoker nor an asthmatic. The other individual was also exposed to chlorine fumes. There was no history of preexposure asthma, and he had discontinued smoking several years prior to his exposure. Not only did this individual have asthmatic symptoms, which responded to bronchodilators, but he also had persistent hypoxemia, which has resolved over the years. His exercise stress test initially accentuated and his primary symptoms were those of dyspnea his hypoxemia, on exertion. His condition has ameliorated with time. Thus, chlorine exposure can present with asthmatic and BADS, as described by Brooks et al.' Our experience symptoms has been that the amount of asthma (diagnosed either by symptoms or by the medication needs) ameliorates with time. Hypoxemia with poor cardiopulmonary reserve was observed in one individual, and this also resolved with time. Northeastern Stephen L. Demeter, M.D., EC.C.P, Ohio Universities College of Medicine, Akrrns, Ohio; and Edward W Cordasco, Cleveland M.D., Clinic, Cleveland REFERENCES 1 Moore BB, Sherman M. Chronic reactive airway disease following acute chlorine gas exposure in an asymptomatic atopic patient. Chest 1991; 100:855-56 2 Demeter SL, Cordasco EM. Reactive airways dysfunction syn- drome: a subset of occupational asthma. J Disability 1990; 1:23- 39 3 Brooks SM, Weiss MA, Bernstein IL. Reactive airways dysfunc- tion syndrome (RADS): persistent asthma syndrome after high level irritant exposures. Chest 1985; 88:376-84 To the Editor: We welcome the comments agree that our patient probably of Drs Demeter and Cordasco. We does have BADS, although he does 984 not fulfill all of the criteria set forth by Brooks et al.' Clearly the cases reported by Demeter and Cordasco represent persistent hyperactive airways disease after chlorine gas exposure.2 Our patient differs from theirs in that his symptoms and level of disability have not ameliorated with time. On the contrary, six years after the exposure this patient still requires home oxygen therapy, oral corticosteroids at high doses, frequent use of beta-agonist inhalers, and frequent injections of subcutaneous epinephrine. In a recent telephone conversation, he informed us that his symptoms have actually worsened since our report was submitted. He is barely able to perform normal activities of daily living and reported that his physicians referred him to a transplant center for possible heart- lung transplantation. Division of Allergy, Brad B.Moo,-e,M.D., and Michael Sherman, M.D., F.C.C.P, Pulmonary, and Critical Care Medicine, Hahenann University Hospital, Philadelphia REFERENCES 1 Brooks SM, Weiss MA, Bernsteiis IL. Reactive airways dysfunc- tion syndrome (RADS): persistent asthma syndrome after high level irritant exposures. Chest 1985; 88:376-84 2 Demeter SL, Cordasco EM. Reactive airways dysfunction syn- drome: a subset of occupational asthma. J Disability 1990; 1:23- 39 Pulmonary Lymphangioleiomyomatosis To the Editor: I read the very interesting case report by HumI et al,' which appeared in the December 1991 issue of Chest. I was curious to know whether the patient described so well by the authors had sarcoidosis or a localized sarcoidal reaction. It would be helpful in making this distinction if the authors were to state whether noncaseating granulomata were observed outside the thorax in the organs examined at autopsy. It would also be of interest to know something of the patient's ethnic background. Jerome M. Reich, M.D., Division of Pulmonary Disease, Bess Kaiser Medical Center, Portland, Oregon REFERENCE 1 HumI JP, Borkgren MW, Henley LB, Fahey PJ. Pulmonary Iymphangioleioniyomatosis associated with pulmonary parenchy- mal, hilar, and mediastinal noncaseating granulomas. Chest 1991; 100:1726-28 To the Editor: In our case report, the absence of multiorgan involvement with noncaseating granulomas speaks against systemic sarcoidosis. No evidence of noncaseating granulomas was found outside the thorax. This raises the very interesting possibility that an immunologic mechanism may play a role in the etiology or that the presence of noncaseating granulomas may represent a localized insmunologic reaction to lymphangioleiomyomatosis. Further study and clinical correlation are necessary to prove this hypothesis. Jeffrey P Hum!, M.D., F.C.C.P, Marilyn W Borkgren, RN., MS., and PatnickJ. Fahey, M.D., F.C.C.P, Elk Grove Village, Illinois Communications to the Editor Downloaded from chestjournal.chestpubs.org by guest on October 22, 2010 1992 American College of Chest Physicians Reactive airway disease after chlorine gas exposure. S L Demeter and E W Cordasco Chest 1992;102; 984b-984 DOI 10.1378/chest.102.3.984b This information is current as of October 22, 2010 Updated Information & Services Updated Information and services can be found at: http://chestjournal.chestpubs.org/content/102/3/984b.citation Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.chestpubs.org/site/misc/reprints.xhtml Reprints Information about ordering reprints can be found online: http://www.chestpubs.org/site/misc/reprints.xhtml Citation Alerts Receive free e-mail alerts when new articles cite this article. To sign up, select the "Services" link to the right of the online article. Images in PowerPoint format Figures that appear in CHEST articles can be downloaded for teaching purposes in PowerPoint slide format. See any online figure for directions. Downloaded from chestjournal.chestpubs.org by guest on October 22, 2010 1992 American College of Chest Physicians