Case Report

Pneumomediastinum from acute inhalation of Chlorine gas in 2 young patients

Abstract

TrichloroisocyanUric acid is a high-efficiency and-low toxicity fungicide and bleach. It is commonly used as disinfectant for industrial Circulating water, swimming pools, restaurants, and other public places in China. When trichloroisocyanuric acid is put into water, chlorine gas is produced. Chlorine gas is a potent pulmonary irritant that causes acute damage in both the upper and lower respiratory tracts (J Toxicol Clin Toxicol. 1998;36(1-2):87-93). Pneu- momediastinum is a rare complication in patients with acute chlorine gas poisoning. A small amount of gas can be asymptomatic, but a large amount of gas entering the mediastinum suddenly will lead to respiratory and circula- tory disorder, mediastinal swing, or even cardiopulmonary arrest. Severe chlorine gas poisoning patients usually need mechanical ventilation; if the pneumomediastinum is not found on time, threat to life would be greatly increased. It requires a high index of suspicion for diagnosis and rapid treatment. The proper use of ventilator, timely and effective treatment of original disease, and multiple system organ support had significant impact on the prognosis. The pneumomediastinum case secondary to inhalation of chlo- rine gas that we report here should remind all emergency department physicians to maintain a high index of suspicion for this disease and seek immediate and proper intervention when treating patients with acute chlorine gas poisoning, once diagnosed, especially in younger patients.

A large amount of trichloroisocyanuric acid powder was dropped onto a side of a community pool by accident in August 2009. Then a staff member, without knowledge of what happened, washed them into the swimming pool when people were swimming in Nanjing city of China, which produced a large amount of chlorine gas in a very short time, causing many people being exposed to chlorine. A total of 27 patients were admitted to the Department of Emergency Medicine, Nanjing General Hospital, of Nanjing

Military Command (Nanjing Jinling Hospital), Jiangsu, China. A total of 11 cases were diagnosed as Severe poisoning, in which 2 young patients had the complication of pneumomediastinum. Pneumomediastinum is a rare complication in patients with acute chlorine gas poisoning. A small amount of gas can be asymptomatic; but a large amount of gas entering into the mediastinum suddenly will lead to respiratory and circulatory disorder, mediastinal swing, or even cardiopulmonary arrest. Severe chlorine gas poisoning patients usually need mechanical ventilation; if the pneumomediastinum is not found on time, the threat to life would be greatly increased. It requires a high index of suspicion for diagnosis and rapid treatment. We report two cases of pneumomediastinum secondary to inhalation of chlorine gas that should remind all emergency department (ED) physicians to maintain a high index of suspicion for this disease and seek immediate and proper intervention once diagnosed when treating patients with acute chlorine gas poisoning, especially in younger patients.

Case 1: A nonsmoking, previously healthy 13-year-old girl presented to the ED together with 26 other people 10 minutes after inhaling the chlorine gas. The patient was exposed to chlorine gas for about 2 minutes. She got Throat pain, tears, shortness of breath, and dyspnea immediately after inhaling the chlorine gas. Dry and moist rale could be heard in both lungs. Chest radiograph showed a diffuse alveolar pulmonary edema. She denied a history of respiratory diseases, cardiovascular diseases, or any systemic illness. The initial electrocardiograph showed sinus tachy- cardia. She had a blood pressure of 115/68 mm Hg, a heart rate of 140 beats/min, respiratory rate of 25 breaths/min, and a body temperature of 36.9?C. The laboratory results were as follows: white blood count of 15 400/uL with 87.5% segmented neutrophils and C-reactive protein level of 30.80 mg/L. The arterial blood gas analysis results on 51% oxygen inhaled through nasal catheter were PaO2 62 mm Hg and PaCO2 48 mm Hg. The other results were unremarkable. The patient was admitted to the EICU for further evaluation and treatment. After 2 hours, the patient appeared irritable and experienced dysphagia and shortness of breath, and peripheral O₂ saturation declined. Over the next few hours,

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the patient’s cough became productive of scant blood- tinged sputum. Artery blood analysis showed respiratory failure (type I). But the bedside chest radiograph obtained at that time showed that the diffuse alveolar pulmonary edema was worse than before. Endotracheal intubation and ventilator-assisted breathing were obtained. Vocal cord and Laryngeal edema was seen through the laryngoscope. The mode of ventilator was SIMV + PSV, pressure support was 12 cm H₂O, PEEP was 8 cm H₂O, and frequency was 18 times per minute. The hypoxemia gradually improved. In the afternoon 2 days after admission, soft tissue emphyse- ma was found in the patient’s chest and neck, and pneumothorax and pneumomediastinum were confirmed by chest computed tomography scan. We made a skin incision 1 cm under the sternal notch; when squeezed the nearly skin a large number of bubbles pouring out from the incision. A continuous drainage tube was placed. 3 days after incision, and the pneumothorax and pneumomedias- tinum disappeared, as seen from a review of chest CT. On the fifth hospital day, the tracheal tube was pulled out; her oxyhemoglobin saturation (measured via pulse oximetry) was 99% while inhaling 33% oxygen inhaled through a nasal catheter. The patient’s symptoms gradually improved, and she was discharged from the hospital with oxygen therapy, respiratory support, glucocorticoid, anti-infection, and nutrition support treatment for 18 days.

Case 2: This case involved a 15-year-old boy. He also denied a history of hypertension, diabetes, cardiovascular diseases, or any systemic illness. The chest radiograph 3 hours after admission suggested diffuse nodular opacities in both lungs. The Radiological diagnosis was interstitial pulmonary edema. The arterial blood gases on 51% oxygen inhaled by nasal catheter showed hypoxemia, PaO2 74 mm Hg, and PaCO2 53 mm Hg. The patient was admitted to the hospital for further evaluation and treatment. The day after chlorine gas exposure, a chest radiograph prompted that the

interstitial lung edema was worse than before. The hypoxemia did not show significant improvement. Chest CT revealed pneumomediastinum (Fig. 1). There was no special treatment, but peripheral O₂ saturation and arterial blood were closely inspected. Pneumomediastinum disap- peared 3 days later. He completely recovered and was discharged from the hospital after 15 days (Fig. 2).

Pneumomediastinum can be caused by variety of reasons [1]. The inhalation of chlorine is a rare cause. Akdur and colleagues reported [2] 1 case of a 26-year-old female patient caused by inhalation of gas produced by a mixture of household cleaning products in 2009. Tanyalak et al [3] reported a patient with diffuse bronchiolitis and reviewed a series of chlorine gas exposures at swimming pools. To our knowledge, this is the first reported case of pneumome- diastinum resulting from chlorine gas exposure at a swimming pool. That improper use of ventilator may increase the risk of pneumomediastinum in patients with lung disease was a consensus. It is noted that these adult patients diagnosed as having severe poisoning admitted to the hospital at the same time did not get pneumothorax or pneumomediastinum in the application of a higher level of PEEP. Perhaps, the fact that the young patients’ respiratory system grows incompletely compared with that of adults can account for this. Macklin and Macklin [4] described the pathophysiological mechanism of the spontaneous pneumo- mediastinum in 1944, and their description is still valid today. Trigger factors have been described as all those non- iatrogenic factors contributing to an increase in the pressure gradient between the alveoli and the interstitium. Thus, rupture of marginal alveoli because of increased intra- alveolar pressure and dissection of the air along the pulmonic vascular sheaths into the mediastinum is seen [5]. Absorbing large quantities of chlorine gas in a short time can damage the respiratory mucosa and lead to respiratory mucosa and alveolar epithelium congestion,

Fig. 1 Computed tomogram shows pneumomediastinum.

Fig. 2 Computed tomogram obtained 15 days after the exposure of chlorine gas shows normal results.

degeneration, and necrosis. Alveolar rupture and gas diffusion may occur in some patients, and then pneumo- mediastinum is formed. The early clinical manifestations are usually shown as decreased blood oxygen pressure, Chest tightness, and soft tissue emphysema. Chest imaging can help to diagnose it, and CT can improve the sensitivity for the diagnosis of pneumomediastinum by avoiding the duplication of tissue compared with radiography. Two patients reported in this article were diagnosed by chest CT examination. Radiography in a patient with less severe poisoning did not show pneumomediastinum. Gardikis et al

[6] pointed out that 30% cases of pneumomediastinum would be missed when simply relying on chest radiography. A small amount of mediastinal gas causes less damage to the body, but large Mediastinal emphysema can raise the mediastinal pressure, constrain the vena cava, obstruct the venous return, and even lead to heart failure. Lung function was significantly affected for alveolar edema and both lungs and pulmonary pressed by pneumomediastinum [7]. In such situation, premediastinal incision and drainage or local skin incision to exhaust gas should be applied as soon as possible. Hypoxemia, infection, and pulmonary edema were big threats to severe poisoning patients; therefore, we did not stop using the ventilator in patients with pneumome- diastinum. Early oxygen therapy and a certain level of PEEP played a very important role in improving hypoxemia and reducing pulmonary edema. Many studies [8,9] showed that positive pressure ventilation was required in severely affected subjects. We believe that giving 3 to 5 cm H₂O of PEEP for severe chlorine gas poisoning in young patients with pneumomediastinum is effective and safe. But when the face, neck, or chest has subcutaneous emphysema, skin incision should be promptly carried out to exhaust. If a patient was diagnosed as having tension pneumomediasti- num, premediastinal incision and drainage will be neces- sary. Computed tomography scan of the thorax showed a

complete resolution of the pneumomediastinum. The 2 patients were discharged and recovered completely. Five months after the accident, imaging examination and pulmonary function test showed normal results. Frank et al [10] conducted a 5-year retrospective poison control center review of chlorine exposure in 598 patients and concluded that exposure to chlorine tablets and liquid rarely requires hospital referral, with almost all symptoms resolving within 24 hours. In this accident, all exposed individuals had survived without sequelae. But most patients had a long hospitalization length.

For patients with acute chlorine gas poisoning, especially for young patients, pneumomediastinum is a potential dangerous complication that all ED physicians should pay more attention to. The sensitivity of CT is higher than that of radiography in diagnosing it. We should give the appropriate treatment according to the extent and type of pneumome- diastinum and the patient’s status. Rational use of ventilators, timely and proper treatment for emphysema, and multiorgan support have important impact on the prognosis.

Baiqiang Li

Ling Jia Danbing Shao Hongmei Liu Shinan Nie MD Wenjie Tang Baohua Xu Zongfeng Hu Haichen Sun MD

Department of Emergency Medicine Nanjing Jinling Hospital and

Nanjing University College of Medicine

Jiangsu, China E-mail addresses: [email protected]

[email protected]

doi:10.1016/j.ajem.2010.04.007

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