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Trauma Cases from Harborview Medical Center

Airway Injury After Acute Chlorine Exposure

¹ Department of Radiology, Harborview Medical Center, University of Washington School of Medicine, 325 Ninth Ave., Box 359728, Seattle, WA 98104-2499.
² Department of Medicine, Harborview Medical Center, University of Washington School of Medicine, Seattle, WA 98104-2499.

Received February 6, 2005; accepted after revision February 16, 2005.

Address correspondence to F. A. Mann.

Keywords: chest • emergency radiology • lung

A23-year-old man presented with hypoxia, progressive dyspnea, and cough after exposure to chlorine gas at an indoor pool after a leak from the maintenance room. An initial chest radiograph was normal. Thirty-six hours after exposure, his chest radiograph and thin-section CT showed diffuse nodular opacities consistent with acute small airways injury (Figs. 1A and 1B). The patient was discharged home on corticosteroids and an albuterol inhaler.

View larger version (119K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A —23-year-old man with acute toxic bronchiolitis from acute chlorine gas exposure. Posteroanterior chest radiograph shows diffuse nodular opacity in both lungs.

View larger version (73K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B —23-year-old man with acute toxic bronchiolitis from acute chlorine gas exposure. Unenhanced thin-section CT shows diffuse nodular opacities in peribronchiolar distribution.

Discussion

After exposure to chlorine gas, patients can present with cough, dyspnea, hemoptysis, and chest tightness. Physical examination may reveal wheezing, crackles, and tachypnea. The majority have complete resolution of symptoms and respiratory deficits. Residual effects from acute chlorine exposure are inconsistently observed. These residual effects include decreased pulmonary function, diffusing capacity deficits, asthma, dyspnea, and cough [1-3].

Chest radiographs can be normal, or they can sometimes show diffuse nodular opacities, patchy consolidation, pulmonary edema, and signs of vascular congestion. Radiographic abnormalities may appear late as lung injury develops and progresses. Persistent hyperreactivity and airflow obstruction may manifest radiographically as air trapping [1, 4]. The role of CT in evaluating lung injury is not established. CT paired inspiratory and expiratory thin-section techniques may be used to evaluate patients with chronic pulmonary dysfunction after chlorine exposure.

Current understanding of the toxicity of chlorine inhalation in humans primarily comes from experience during and immediately after World War I as well as from industrial accidents. Exposure from household chemicals and at swimming pools is also well known [2]. Depending on the concentration and duration of chlorine exposure, toxicity can range from irritation of the upper aerodigestive tract epithelium to diffuse lung injury and hemorrhagic necrosis leading to death.

The mechanism by which chlorine gas injures the respiratory tract epithelium is related to its ability to form hydrochloric and hypochlorous acids in the respiratory tree. Because of its relatively low solubility in water, chlorine can reach the periphery of the lungs and cause extensive damage, unlike highly soluble gasses, such as ammonia, that are removed from the proximal airway by mucociliary clearance.

Injury begins with edema of the upper airway and lung parenchyma, followed by development of a cellular exudate in the alveoli. As injury progresses, severe edema, hemorrhage, and destruction of the bronchiolar mucosa can develop [2]. Treatment is primarily supportive, including oxygen and bronchodilators. The efficacy of corticosteroids is not fully established, although patients may be treated empirically with a short course.

Other common toxic inhalants (e.g., hydrochloric acid, nitric oxide, phosgene, and sulfur dioxide) can also damage the distal airways. Depending on the severity of exposure, these patients may present a similar clinical picture, and their imaging may show interstitial and small airways abnormalities. While most exposures occur at industrial sites, both firefighters and victims of fires may present with inhalation injury when these fumes are generated from combustion of various natural and synthetic products [4].

References

1. Das R, Blanc PC. Chlorine gas exposure and the lung: a review. Toxicol Ind Health 1993;9 : 439-455[Medline]
2. Winder C. The toxicology of chlorine. Environ Res 2001; 85:105 -114[Medline]
3. Schwartz D, Smith D, Lakshminarayan S. The pulmonary sequelae associated with accidental inhalation of chlorine gas. Chest 1990; 97:820 -825[Abstract/Free Full Text]
4. Weiss SM, Lakshminarayan S. Acute inhalation injury. Clin Chest Med 1994;15 : 103-116[Medline]

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This Article Figures Only Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Kanne, J. P. Articles by Stern, E. J. Search for Related Content PubMed PubMed Citation Articles by Kanne, J. P. Articles by Stern, E. J. Social Bookmarking                      What's this?