Abstract

A 42-yr-old man was admitted to hospital for emergent coronary angioplasty. The patient’s trachea was intubated prior to catheterization and a trial tracheal extubation was attempted four days into his admission; however, the patient was promptly reintubated with a subglottic secretion drainage endotracheal tube after developing severe epistaxis. He had no documented stridor at that time. Nine days into his admission, the patient’s trachea was extubated successfully, and he was transferred to the ward where he experienced a progressive voice change. On day 12, he developed sudden onset stridor and required heliox to maintain oxygenation. He was started on corticosteroids and empiric antibiotics and was admitted to the intensive care unit. The otolaryngologist was consulted to perform fibreoptic laryngoscopy, the results of which revealed normal vocal cords. The patient was sent for computed tomography (CT) (Fig. 1), and those results showed a casting of debris within the upper trachea (a craniocaudal dimension of 27 mm) that narrowed the tracheal airway to 5 mm in diameter. The patient then underwent rigid bronchoscopy. He was sedated initially with sevoflurane for laryngoscopy and then sedated further with fentanyl and ketamine and paralyzed with succinylcholine. A rigid bronchoscope was introduced just above the obstructing lesion. At this point, jet ventilation was inadequate to maintain oxygenation; therefore, the bronchoscope was

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