The Case Files

FigureFigureFigureFigureA 59-year-old man with a history of frequent crack cocaine use presented with difficulty breathing for four hours. He had no prior medical problems or known allergies. He admitted to smoking crack cocaine four days before his symptoms began. He reported a one-day history of productive cough but denied chest pain, sore throat, and fever. He was a well-developed man in mild distress. His temperature was 36.5°C, pulse 90 bpm, blood pressure 188/108 mm Hg, and respiratory rate 20 bpm. His oxygen saturation was 100% on four liters by nasal cannula. Inspiratory stridor was noted with supraclavicular retractions and accessory muscle use. His lungs were otherwise clear to auscultation. His oral cavity and oropharynx were normal in appearance. The remainder of his physical exam was unremarkable. A chest x-ray was obtained. What should be the next steps in this patient's evaluation and treatment? The patient was diagnosed with crack cocaine-induced subglottic edema. The chest x-ray revealed a “steeple sign” (arrow) indicative of subglottic stenosis, similar to that seen in children with croup. This finding was later confirmed on CT of his chest. Initial treatment with inhaled nebulized albuterol was followed by nebulized racemic epinephrine and 10 mg IV dexamethasone. Flexible fiberoptic laryngoscopy was performed at the bedside by the otolaryngology service, which revealed only bilateral nonobstructive arytenoid edema with an otherwise normal hypopharynx, true vocal cords, epiglottis, and other supraglottic structures. Cocaine is one of the most common illicit drugs of abuse leading to emergency department visits. The cocaine epidemic that began in the mid-1980s in the United States was fueled by the introduction of crack, a free-base form of the drug not destroyed by heat that can be inhaled. Crack cocaine use can achieve concentrations in the blood comparable with that of intravenous cocaine at a much cheaper price. Reported pulmonary complications of crack cocaine use include acute exacerbations of asthma, barotrauma, noncardiogenic pulmonary edema, diffuse alveolar hemorrhage, interstitial pneumonitis, and pulmonary infiltrates with distinct histologic features referred to as crack lung. (Curr Opin Pulm Med 2001;7[2]:43.) Thermal injury to the laryngeal and supraglottic structures of the upper airway from crack cocaine use has also been described. (Am J Emerg Med 2017;35[2]:381e5.) The mechanism of injury is similar to inhalation of hot vapors or particulate matter in a room containing fire. Cocaine free-base melts at 98°C and vaporizes at higher temperatures. (N Engl J Med 1986;315[23]:1495.) It is typically smoked through a short pipe, with a fine mesh screen or Brillo pad placed at the bottom of the pipe bowl to protect the user from aspirating foreign material. This metal screen becomes hot and may partially disintegrate, resulting in aspiration of burning metal debris or smoldering crack particles. The combination of efficient heat dissipation in the upper airway, low heat capacity of air, and reflex closure of the larynx usually results in superheated air causing injury only to supraglottic structures, which includes the aryepiglottic folds, epiglottis, false vocal cords, and arytenoid mucosa. (Scand J Trauma Resusc Emerg Med 2013;21:31.) Thermal injury to the airway may not become evident for more than 48 hours after the initial insult. (Laryngoscope 1997;107[5]:620.)FigurePresenting symptoms of these injuries after smoking crack cocaine include throat pain, dysphagia, odynophagia, cough, foreign body sensation in the throat, shortness of breath, and voice change. Stridor may also be present. (Laryngoscope 1997;107[5]:620.) Symptoms, signs, and radiologic and laryngoscopic findings may mimic infectious epiglottitis. (J Emerg Med 1997;15[4]:483.) Further confusing this issue is the fact that a significant percentage of these patients may not initially report their crack cocaine use. (Laryngoscope 1997;107[5]:620.) Management of upper airway injury secondary to inhalation of crack cocaine lacks universal guidelines, though some research has yielded recommendations for treatment. (Ear Nose Throat J 2003;82[1]:53; Laryngoscope 1997;107[5]:620.) Most patients can be managed expectantly in an intensive care setting, with intubation used as a final resort to stabilize the airway. The decision to intubate these patients should be guided by their overall clinical status. The upper aerodigestive tract should be examined by laryngoscopy for mucosal injury and the presence of foreign bodies. While controversial, corticosteroids may have a role in decreasing airway edema and should be administered. Nebulized racemic epinephrine may also be used for this purpose. Antibiotics may be given until an infectious source of the airway injury can be definitively excluded. This patient was admitted to the intensive care unit and treated with 10 mg IV dexamethasone every eight hours and nebulized racemic epinephrine as needed. The patient's symptoms resolved within 24 hours, and he was discharged after an unremarkable of his hospital stay.