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Chronic reactive airway disease following acute chlorine gas exposure in an asymptomatic atopic patient. B B Moore and M Sherman Chest 1991;100;855-856 DOI 10.1378/chest.100.3.855 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/100/3/855 Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1991by 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 1991 American College of Chest Physicians directly resulting from perforated Thorac Surg 1967; 4:160-65 bronchogenic carcinoma. Ann 6 Heimlich HJ, Rubin M. Spontaneous pneumothorax as a pre- senting feature of primary carcinoma of the lung. Dis Chest 1955; 27:457-64 7 Mahajan V, Kupferer CF. Van Ordstrand HS. Pneumothorax: a rare manifestation of primary lung cancer. Chest 1975; 68:730- 32 8 Matarese SL, Matthews JI. Zinc chloride (smoke bomb) inha- lational lung injury. Chest 1986; 89:308-09 9 Berkmen YM . The many facets of alveolar.cell carcinoma of the lung. Radiology 1969; 92:793-98 10 Ohba 5, Takashima T, Hamada 5, Kitagawa M. Multiple cystic cavitary alveolar-cell carcinoma. Radiology 1972; 104:65-6 Chronic Reactive Airway Disease following Acute Chlorine Gas Exposure in an Asymptomatic Atopic Patient* Brad B. Moore, M.D.; and Michael Sherman, M.D., EC.C.P While chlorine gas inhalation has previously been reported to cause temporary mucous membrane irritation, acute pneumonitis, pulmonary edema, and transient broncho- spasm, there is controversy about the existence of long- term pulmonary sequelae. We report the case of a 25-year- old man in whom chronic, after exposure to a chlorine His course since the exposure exacerbations necessitating and multiple hospitalizations. sistence of symptoms years the literature. recurrent asthma developed gas leak in an enclosed space. has been notable for frequent chronic corticosteroid therapy To our knowledge, the per- after the exposure is unique in (Chest 1991; 100:855-56) C hiorine is widely used in water purification and in the manufacture ofplastics, bleaches, and alkalis. Although its pungent odor is detected in concentrations as low as 0.5 ppm, it causes respiratory damage only at levels above 20 ppm. Discovery ofthe highly toxic effects ofchlorine gas on the human respiratory tract resulted in its deployment as the first chemical weapon at Ypres, France, in 1915. Despite extensive study since that time, controversy still exists about long-term pulmonary sequelae after acute chlorine-induced lung injury. We report a unique case of severe, chronic asthma following acute exposure to chlorine gas. CASE REPORT A 25-year-old man came to the Hahnemann University Hospital Emergency Room with severe dyspnea. He had a history of mild childhood asthma, which had resolved at the age of 5 years. Four years prior to admission, the patient was exposed to a chlorine gas leak while working for a regional sewerage authority. The patient had worked for 2 h in a chlorine-filled enclosed environment without a protective respirator mask. Immediately following this exposure, the patient experienced a transient episode of hemoptysis followed by acute shortness of breath and wheezing. A regimen of amino- phylline and inhaled beta-agonists was started in a local emergency *Fmm the Department of Medicine, Hahnemann pital, Philadelphia. Reprint requests: Di Sherman, Pulmonary Division, Hahnemann University, Philadelphia 19102 University HosMail Stop 107, room, which resulted in some improvement in his symptoms. His course over the next 4 years was notable for frequent hospitalizations for asthma and increasing use of oral and inhaled corticosteroids. He was admitted to Hahnemann University Hospital for manage- ment ofan acute exacerbation ofhis illness and a diagnostic workup. Physical examination revealed an afebrile, cushingoid patient in moderate respiratory distress. Auscultation of the chest revealed diffuse expiratory wheezes in all lung fields with prolonged expira- tion. An arterial blood gas evaluation on room air revealed a pH of 7.45, a Pco5 of32.2, and a Po, of73.6. The eosinophil count was 8 cu mm; the immunoglobulin G activity was markedly elevated at 431 U/ml(normal, <122 U/mI). A chest roentgenogram was normal except for minimal penbronchial thickening. An esophagram dem- onstrated minimal gastroesophageal reflux without aspiration. An Asper gillus skin test was negative. A flow volume loop and otorhi- nolaryngologic obstruction. (52 percent evaluation showed no evidence Pulmonary function testing revealed of the predicted value [1W]), an of upper airway an FVC of 2.71 FEV of 1.42 (35 percent of PV), an FEV1/FVC of 52 percent, an FRC of 5.09 (154 percent of PV), and a TIC of 7.43 (107 percent of PV)-values consistent with severe obstruction (normal values from Crapo et all). Administration ofaerosolized albuterol improvement in FEV1 and a 26 percent produced a 54 percent improvement in FVC, which was reproduced in multiple studies. The single breath diffusion capacity for carbon monoxide was 31.95 (89 percent). Intravenous methylprednisolone, intravenous aminophylline, and aerosolized terbutahne were given with significant improvement in the patient's symptoms and flow rates, although moderate obstruc- tion remained. After several days, the patient was discharged on a regimen of high-dose oral corticosteroids with persistent airflow obstruction. DiscussIoN Although today most reported cases of chlorine exposure occur in industrial sethngs, at water treatment facilities, or as a result of transportation accidents,5e several cases of toxic chlorine inhala- tion have occurred in more unusual circumstances. An increasingly common source of exposure to chlorine gas is fumes liberated from chlorine products used in residential pools and spas. Cases of exposure resulting from chlorine gas released during mixing of a variety ofhousehold cleaning agent? have prompted the placement of consumer warnings on many such products. One episode of voluntary exposure has also been reported.b0 The long-term pulmonary sequelae ofchlorine gas inhalation are controversial. Studies ofsoldiers gassed during the First World War showed evidence of obstructive airway disease and permanent disability." It is difficult to ascribe abnormalities found in these patients solely to chlorine inhalation for two reasons: chlorine was used only for a short time in chemical warfare, and most subjects studied were exposed to multiple war gases.'2 More recent series describe an initial obstructive defect, often with partial reversibil- ity"'4; restrictive defects with accompanying diffusion abnormali- ties have also been reported.' These initial changes reverted to normal within a few months in almost all patients studied. In fact, in a study involving 820 patients, Jones'5 found no radiologic or clinical evidence ofpermanent pulmonary damage following indus- trial chloride exposure. Lawson" also found no long-term residual changes in laboratory parameters, chest roentgenographic findings, or pulmonary function test results in over 457 cases of acute industrial chlorine gas exposure. In contrast, Kaufman and Burkons" found persistent obstructive lung disease up to 14 months following chronic chlorine exposure, and KOWitZ et al' fuund persistent residual restrictive disease and low diffusing capacities up to 3 years following acute chlorine exposure. In another study, Jones et al fuund that long-term sequelae after acute chlorine gas exposure were affected more by cigarette smoking than by the CHEST I 100 I 3 / SEPTEMBER, 1991 855 Downloaded from chestjournal.chestpubs.org by guest on October 22, 2010 1991 American College of Chest Physicians chlorine gas exposure. Other authors' have suggested that preex- isting lung conditions do not affect the occurrence of pulmonary sequelae following chlorine gas exposure. Our patient was exposed to chlorine gas in an industrial setting. Although the patient had a history of cigarette smoking and childhood asthma, he had had no symptoms of reactive airways disease for 20 years prior to this event. Following the chlorine exposure, the patient's symptoms rapidly became severely debili- tating, necessitating daily therapy with high-dose corticosteroids, frequent use of home oxygen, and self-administered subcutaneous epinephrine. To our knowledge, this case is unique in the literature. Charan et al showed reversible acute airway obstruction shortly after exposure, and Hasan et al's reported the cases of two asthmatic patients in whom chlorine gas may have exacerbated a state of underlying hyperactivity. No one, however, has reported new onset of severe reversible airway obstruction that persisted several years after chlorine gas exposure. Thus, we believe that our patient represents a unique case of persistently debilitating asthma follow- ing acute chlorine gas exposure. ACKNOWLEDGMENT: Editorial services were provided by Bette R. Haitsch. The authors would like to thank Angela K. Dorman for her assistance in manuscript preparation. REFERENCES 1 Crapo RO, Morris AH, Gardner RM. Reference spirometric values using techniques and equipment that meets ATh recom- mendations. Am Rev Respir Dis 1981; 123:659 2 Beach FXM, Jones ES, Scarrow GD. Respiratory effects of chlorine gas. Br J md Med 1969; 26:231-36 3 Charan NB, Lakshminarayan 5, Myers GC, Smith DD. Effects of accidental chlorine inhalation on pulmonary function. West J Med 1985; 143:333-36 4 FletaJ, Calvo C, ZunigaJ, Castellano M, Bueno M. Intoxication of76 children by chlorine gas. Hum Toxicol 1986; 5:99-100 5 Kowitz TA, Beba RC, Parker Ri', et al. Effects of chlorine gas upon respiratory function. Arch Environ Health 1967; 14:545- 58 6 Jones RN, Hughes JM, Glindmeyer H, Weill H. Lung function after acute chlorine exposure. Am Rev Respir Dis 1986; 134: 1190-95 7 Ploysongsang Y, Beach BC, DiLisio RE. Pulmonary function changes after acute inhalation ofchlonne gas. South Med J 1982; 75:23-26 8 Mustchin CP, Pickering CAC. "Coughing water": bronchial hyperactivity induced by swimming in a chlorinated pool. Thorax 1979; 34:682-83 9 Murphy DMF, Fairman RP, Lapp NL, Morgan KC. Severe airway disease due to inhalation of fumes from cleansing agents. Chest 1976; 69:372-76 10 Rafferty P Voluntary chlorine inhalation: a new form of self- abuse? Br Med J 1980; 281:1178-79 11 Sandall TE. The later effects of gas poisoning. Lancet 1922; 2:857. 12 Kaufman J, Burkons D. Clinical, roentgenologic and physiologic effects of acute chlorine exposure. Arch Environ Health 1971; 23:29-34 13 Hasan FM, Gehshan A, Fuleihan FJD. ResolLition of pulmonary dysfunction following acute chlorine exposure. Arch Environ Health 1983; 35:70-80 14 Colardyn F, Van Der Straten M, Tasron J, Van Egmond J. Acute chlorine gas intoxication. Acta Clin BeIg 1976; 31:70-77 15 Jones AT Noxious gas and fumes. Proc R Soc Med 1952; 45:609 16 Lawson JJ. Chlorine exposure: a challenge to the physician.Am Fam Physician 1981; 23:135-38 17 Barret L, Faure J. Chlorine poisoning, letter. Lancet 1984; 1:581-62 856 Successful Management of CMV Pneumonia in a Mechanically Ventilated Patient* Steven E. Sommet; M.D.; David Emanuel, Jeffrey S. Gmeger, M.D., bC.C.P; and Graziano C. Car/on, M.D., F.C.C.P M.D.; We report a case of severe respiratory failure due to cytomegalovirus pneumonitis in a patient who underwent an allogeneic bone marrow transplant, who was successfully treated with the combination of ganciclovir and high-dose intravenous immune globulin. We also reviewed the ration- ale for the use of combination therapy with an antiviral agent and immunotherapy. Because of the bone marrow toxicity of ganciclovir, an aggressive diagnostic approach, including bronchoalveolar lavage and open lung biopsy, may be necessary to establish a definitive diagnosis prior to institution of therapy. (Chest 1991; 100:856-58) =CMV cytomegalovirus; ABMT allogeneic bone transplant; IVIG intravenous immune globulin; posttransplant day; CVII graft-versus-host marrow PTD espiratory failure secondary to cytomegalovirus pneu- monitis is a serious complication in allogeneic bone marrow transplant patients. Even though encouraging re- suits have been reported in patients treated with a combi- nation of ganciclovir and intravenous immune g1obulin,', none of them was intubated or mechanically ventilated. We report a case of severe respiratory failure secondary to documented CMV pneumonitis requiring mechanical intu- bation and mechanical ventilation in an ABMT patient who was successfully treated with a combination of ganciciovir and high dose IVIG. CASE REPORT A 33-yeam'.oldwhite woman was diagnosed with acute myeloblastic leukemia in December 1988. She underwent induction chemother- apy with daunorubicin, cytosine arabinoside, and thioguanine at that time and consolidation chemotherapy with the same agents in January 1989. She subsequently received a non-T-cell depleted ABMT on April 12, 1989. The posttransplant course was compli- cated by pulmonary hemorrhage and respiratory failure on post- transplant day 14, requiring ICU admission, intubation, and me- chanical ventilation. The patient was treated with broad spectrum antibiotics and amphotericin B for persistent fevers, despite negative bacterial cultures and was extubated on PTD 20. On PTD 43, she developed a nonproductive cough; pulmonary function tests re- vealed a Dco of4l percent and a PaO of55 mm Hg while breathing room air. Intravenous pentamidine was added at this time for possible Pneumocystis carinii pneumonia. Bronchoscopy with hi- opsy of the right middle lobe and bronchoalveolar lavage were negative for bacterial cultures, PCP stains, Legionella DFA, AFB smear, CMV monoclonal antibiotics, and mycology stains. A gallium scan demonstrated mild increased uptake in the right lower lobe. Over the next several days, there was a progression of the RLL infiltrate associated with persistent nonproductive cough and fever. On PTD 49, the patient underwent a right thoracotomy for open lung biopsy; histologic findings and monoclonal AB were positive *Fmm the Department of Anesthesiology and cine, and the Bone Marrow Transplantation Sloan-Kettering Cancer Center and Cornell College, New York. Critical Care Mcdi- Service, Memorial University Medical Successful Management of CMV Pneumonia (Sommereta!) Downloaded from chestjournal.chestpubs.org by guest on October 22, 2010 1991 American College of Chest Physicians Chronic reactive airway disease following acute chlorine gas exposure in an asymptomatic atopic patient. B B Moore and M Sherman Chest 1991;100; 855-856 DOI 10.1378/chest.100.3.855 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/100/3/855 Cited Bys This article has been cited by 1 HighWire-hosted articles: http://chestjournal.chestpubs.org/content/100/3/855#related-urls 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. 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