CASE PRESENTATION: A 44 year old man with active crack cocaine abuse presented with worsening dyspnea. 3-months prior, stridor had been noted during an admission for small bowel obstruction. Head and neck computed tomography (CT) revealed bilateral, right greater than left, thickening of the aryepiglottic folds (image 1). Further work up was not completed as the patient failed to attend outpatient Otolaryngology appointments. On presentation, he was in significant respiratory distress and unable to provide further history. Examination was remarkable for an ill appearing man with audible inspiratory and expiratory stridor. Respiratory rate was 34/minute and arterial blood gas showed acute respiratory acidosis (pH 7.34, pCO2 49mmHg). He was intubated with fiberoptic assistance. The aryepiglottic folds were diffusely edematous and multiple attempts were required to pass the endotracheal tube beyond the vocal cords. Repeat neck CT confirmed diffuse glottic edema with effacement of the piriform sinuses but without definitive abscess (image 1). He was afebrile and systemic markers of inflammation were within normal limits. Steroids were administered for airway edema, and on hospital day 3, he was taken to the operating room for monitored extubation. During operative evaluation, pus was expressed from the aryepiglottic folds and a subglottal eschar complicated by a small tracheoesophageal fistula was seen. Cultures grew Streptococcus anginosus. A 3-week course of ampicillin-sulbactam was started and naso-gastric tube placed for feeding to bypass the fistula. Following 48 hours of antibiotics, flexible laryngoscopy revealed resolving epiglottic edema without purulence, and after 2-weeks, stridor had resolved and pharyngoesophagram demonstrated closure of the fistula.