Clinical Toxicology (2009) 47, 595597 Copyright Informa UK, Ltd.

. ISSN: 1556-3650 print / 1556-9519 online DOI: 10.1080/15563650903012333

BRIEF COMMUNICATION
LCLT

Bilateral pneumothorax following acute inhalation injury

MUSTAFA SERINKEN1, OZGUR KARCIOGLU2, FATMA EVYAPAN3, and HLYA SUNGURTEKIN4
Pneumothorax following acute inhalation injury

Department of Emergency Medicine, Pamukkale University Medical School, Denizli, Turkey Department of Emergency Medicine, School of Medicine, Acibadem University, Istanbul, Turkey 3 Department of Chest Diseases, School of Medicine, Pamukkale University, Denizli, Turkey 4 Department of Anesthesiology and Reanimation, School of Medicine, Pamukkale University, Denizli, Turkey
2

Introduction. Inhalation injury can be thermal and/or chemical. We report bilateral pneumothorax following acute inhalation injury. Case report. A male worker in an upholstery factory was confined in the tanning machine for 15 min. The device was used to contain sodium sulfate, sulfur dioxide, and sulfuric acid. On admission, he was confused with Glasgow coma scale score as 9. His vital signs were as follows: blood pressure, 80/58 mmHg; pulse rate, 114 bpm; respiratory rate, 30 bpm; temperature, 37.1C; and oxygen saturation, 48%. He was intubated. Physical examination disclosed extensive subcutaneous emphysema on the neck and pinkish foamy discharge from the mouth. Chest X-ray showed bilateral pneumothoraces and pneumomediastinum that warranted bilateral tube thoracostomy. Bronchoscopy demonstrated web-shaped hyperemic areas on the upper airway mucosa with aphtous lesions in the base. Extensive hemorrhage and edema were evident around epiglottis. The patient was admitted to the intensive care unit and mechanically ventilated. He was discharged without any sequelae on day 8. Conclusion. Exposure to irritant gases such as sulfuric acid and sulfur dioxide can cause severe pulmonary injury leading to pneumothorax and pneumomediastinum. Keywords Acute inhalation injury; Pneumothorax; Pneumomediastinum; Acute lung injury

Introduction
Inhalation injury can result from thermal and/or chemical insults. Inhalation of high concentration of irritant gas or aerosols may cause severe respiratory injury and death.1 The level of the respiratory tract affected depends mostly on physicochemical properties of the inhaled material. The deposition of gas is principally determined by its water solubility. Duration of exposure and the minute ventilation of the affected person are also important factors for effects on the respiratory tract. Early effects of exposure may vary from upper airway irritation to lung edema depending on the concentration of inhaled gas. Chemical pneumonitis and bronchiolitis obliterans may ensue in these cases.2 Acute inhalational exposure can even lead to rapidly progressive acute respiratory distress syndrome (ARDS).3 Pneumothorax as a complication of acute inhalation injury is probably underreported in the literature. There are reports of unilateral pneumothorax after thermal injury and burn.4 This report is the first one to describe bilateral pneumothorax following acute inhalation injury.

Case report
A male worker in an upholstery factory was confined in the closed tanning machine for 15 min. The room was 4 4 5 m and designed to boil the raw pieces of leather. He was found unconscious and immediately brought to the hospital emergency department (ED). His coworkers reported that he had been working in the factory for 6 months, had no diseases, and had not used any medications. The worker had entered the machine to repair it, as he had been informed it was out of order. He did not use any personal protective equipment. The machine was cold at that moment but used to contain sodium sulfate, sulfur dioxide, and sulfuric acid. On admission, he was confused with a Glasgow coma scale score as 9 (E3M4V2). Blood pressure was 80/58 mmHg; pulse rate, 114 bpm; respiratory rate, 30 bpm; temperature, 37.1C, and oxygen saturation, 48%. Physical examination disclosed extensive subcutaneous emphysema on the neck and pinkish foamy discharge from the mouth. Breath sounds were diminished bilaterally. The patient received intravenous fluids via line and supplemental oxygen. His arterial oxygen saturation level raised up to 69%. His ECG revealed sinus tachycardia, and arterial blood gases obtained before intubation were pH = 7.48, PaO2 = 46 mmHg, PaCO2 = 27.8 mmHg, HCO3 = 21.1 mEq/L, and SatO2 = 72.3. Blood count showed that the white blood cell count was 16 103/mm3. Other laboratory analyses were within normal limits. The patient was intubated within a few minutes of admission to

Received 13 March 2009; accepted 30 April 2009. Address correspondence to Mustafa Serinken, Department of Emergency Medicine, Pamukkale University Medical School, Denizli, Turkey. E-mail: mserinken@hotmail.com

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596 the ED using rapid sequence intubation protocol for agitation, altered mental status, and resistant hypoxia. The epiglottis was noted to be edematous with bleeding foci. Chest X-ray showed bilateral pneumothoraces and pneumomediastinum (Fig. 1) that warranted bilateral thoracostomy and drainage. Bilateral patchy consolidation, especially in the middle and lower zones, of the left lung was also noted on X-ray. Arterial blood gases recovered to pH = 7.36, PaO2 = 58 mmHg, PaCO2 = 37.1 mmHg, HCO3 = 21.0 mEq/L, and SatO2 = 92.3. Bronchoscopy demonstrated web-shaped hyperemic areas on the upper airway mucosa with aphtous lesions in the base. Extensive hemorrhage and edema were evident around the epiglottis. The lower airway could not be visualized by fiberoptic bronchoscopy because of mucosal fragility and epiglottic edema. Thoracic CT also showed bilateral pneumothoraces, mediastinal and subcutaneous emphysema, airspace consolidation with air

M. Serinken et al. bronchograms, and bilateral apical ground glass opacities especially in the left upper zone (Fig. 2). The patient was admitted to the intensive care unit and mechanically ventilated with continuous intermittent mandatory ventilation mode. Steroid therapy was also instituted. Within 3 days of therapy in the intensive care unit, chest X-ray showed that the lungs were expanded and bilateral infiltrations had regressed. Arterial blood gases analyzed when the patient was on ambient air read as pH = 7.39, PaO2 = 106 mmHg, PaCO2 = 27.1 mmHg, and SatO2 = 98. The patient was extubated, weaned and the chest tubes were removed on day 7. He was discharged without any sequelae on day 8. There was no residual bronchial hyperreactivity in the pulmonary function tests including bronchial provocation test performed twice- one and 4 months later.

Discussion
Pulmonary parenchymal injury caused by irritants may ensue clinically as chemical pneumonitis, pulmonary edema, and ARDS.2,3 Pneumomediastinum and pneumothorax are very rare conditions reported following chemical inhalational injury. Nash et al.4 cited a young patient diagnosed with unilateral pneumothorax following inhalation of caustic soda fumes. Literature search yielded two case reports in patients suffering from thermal inhalation injury associated with pneumomediastinum and spontaneous pneumothorax.5,6 This article describes an unusual case of bilateral pneumothorax following chemical inhalation injury. It can be postulated that increased intrabronchial pressure because of the cough triggered by the airway injury and mucosal irritation may have caused transmission of air to the peribronchial area resulting in pneumothoraces and pneumomediastinum. Acute irritant inhalation may also cause a Valsalva maneuver leading to the rupture of distal alveoli or an injury as a direct result of inhalation injury. We consider the first mechanism as

Fig. 1. Bilateral pneumothoraces detected in the chest X-ray.

Fig. 2. Extensive subcutaneous emphysema, pneumomediastinum, and bilateral pneumothoraces can be seen in the thoracic CT. Bilateral airspace consolidation areas including air bronchograms, apical ground glass opacities especially in the left upper zone are remarkable.

Clinical Toxicology vol. 47 no. 6 2009

Pneumothorax following acute inhalation injury the likely rationale of mediastinal emphysema and pneumothorax in this patient. Dixit et al.5 hypothesized that spontaneous pneumomediastinum following thermal inhalation injury is caused by an air leak associated with a rise in intrathoracic pressure because of bouts of coughing. In the present case, the exact cause for the injury is still uncertain. Of the potential agents, sulfuric acid and sulfur dioxide are known to cause a wide range of lung injuries. Mixtures of toxic substances can act synergistically on tissues. Our case emphasizes the need for care in industrial environments and the need for appropriate protection when maintaining industrial plant.

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