INTRODUCTION: In 1991, Nierenberg and colleagues published a case report of a patient presenting with respiratory failure and cardiac arrest after intense exposure to mineral spirits (1). Mineral spirits are a heterogeneous mixture of hydrocarbons found in various commercial products including wood stains and cleaning solutions. We present a case of a patient with similar exposure history.
CASE PRESENTATION: The patient is a 54-year-old obese white male who was in good health. He had been applying a floor staining product, Minwax ™ in his basement when he became acutely dyspneic. He was found by emergency services in his backyard, unresponsive, with pink frothy sputum, but with adequate pulse and BP. In the ED, he required an emergency tracheostomy and ventilatory support. His past medical history was notable for a myocardial infarction two years ago. He was a non-smoker, did not use illicit drugs or have HIV risk factors. He worked as a printer where he is exposed to paper dusts but has not had any prior respiratory symptoms. He had no family history of respiratory disease. On examination his vital signs were stable. He sustained laceration and abrasion injuries to his forehead and nose. He had a normal chest wall configuration and scattered rales were heard on lung exam. The rest of his exam was unremarkable. His initial chest radiograph demonstrated diffuse alveolar infiltrates. A trauma CT series revealed no significant injuries but showed patchy bilateral alveolar infiltrates. His initial EKG showed a normal sinus rhythm and a left bundle branch block, age unknown. Initial laboratory data were unremarkable including normal cardiac enzymes and BNP. He was oxygenating and ventilating well on a tidal volume of 700 and a fiO2 of 60%. Because of his history of CAD, he was admitted to the coronary care unit to rule out MI. His cardiac work-up including cardiac enzymes and a 2Decho were unremarkable. The following day bronchoscopy was performed. BAL was not suggestive of acute eosinophilic pneumonia or hypersensitivity pneumonitis. His follow up CXR showed dramatic clearing of the infiltrates. He was liberated from the ventilator to trach collar within 4 days and quickly decannulated. He was discharged without any functional limitation.
DISCUSSIONS: An exposure history is very important when evaluating respiratory failure. We feel our patient suffered from acute lung injury (ALI) secondary to exposure to a product containing mineral spirits (Minwax ™). Mineral spirits are commonly found in commercial and industrial products like varnishes and sealants. They are petroleum distillate mixtures of hydrocarbons. There are reports of noncardiogenic pulmonary edema following inhalation of other common commercial compounds like phosgene and sulfuric acid(2). The pathogenic mechanism is likely that of ALI. Radiographically, ALI can appear as normal appearing lungs to diffuse alveolar filling. Clinically, it can progress to ARDS. Residual lung function can vary from normal to permanent respiratory dysfunction. Our patient presented with acute respiratory failure and pulmonary edema. He was ruled out for an MI. Given his inhalation history plus the negative cardiac work-up, ALI from mineral spirits was considered. Other less common but important pulmonary etiologies were ruled out like acute eosinophlic pneumonia and hypersensitivity pneumonitis. Our patient dramitically improved and was discharged with no functional limitations.
CONCLUSION: Exposure history is of the utmost importance. This case illustrates the development of acute lung injury secondary to mineral spirits, a common component of many commercial and industrial compounds.
DISCLOSURE: Francis Castiller, None.