Recurrent postoperative stridor requiring tracheostomy in a patient with spasmodic dysphonia.

The patient was a 67-yr-old woman with a horseshoe kidney and bilateral uteropelvic junction obstruction who presented for bilateral pyeloplasty. Medical history included long-standing SD for which she had undergone left recurrent laryngeal nerve (RLN) sectioning and Teflon injections (DuPont, Wilmington, DE) of the left VC. She had also been receiving botulinum toxin (Botox; Allergan Pharmaceuticals, Irvine, CA) injections into the thyroaretynoid muscles every 3–4 months for many years. After a diagnostic laryngoscopy several years earlier, she developed postoperative stridor that required tracheal intubation. She had also undergone surgical dilatation of an esophageal stricture. Additional medical history included hypertension, hypercholestrolemia, and peptic ulcer disease. Her medications were simvastatin, indapamide, nifedipine, famotidine, and aspirin. On the day of surgery, she had no shortness of breath or stridor. After placement of routine monitors and sedation with midazolam, an unsuccessful attempt was made to place a thoracic epidural catheter. General anesthesia was induced with thiopental, and mask ventilation was established with ease. Succinylcholine 1.5 mg/kg was given, and the trachea was intubated atraumatically with a 6.5 cuffed endotracheal tube (ETT). There was no resistance to placement of the ETT, and the cuff was inflated with the minimum volume of air required to eliminate the leak. Anesthesia was maintained using air/oxygen mixture, isoflurane, fentanyl, and pancuronium. At the end of the procedure, after complete reversal of neuromuscular blockade with neostigmine and glycopyrrolate, the trachea was extubated. Ventilation was unobstructed, and the patient was transferred to the postanesthesia care unit with supplemental oxygen. Twenty minutes after extubation, soon after arrival in the postanesthesia care unit, the patient developed progressive stridor. She was manually ventilated with 100% oxygen using bag and mask and was treated with nebulized racemic epinephrine with little improvement. After the administration of a hypnotic and succinylcholine, the trachea was reintubated with a 6.0-mm ETT. She was mechanically ventilated, sedated with propofol and fentanyl, and received dexamethasone 4 mg intravenously every 6 h. On the morning of postoperative day 1, the trachea was extubated over a fiberoptic bronchoscope. Examination of the airway as the ETT was being removed revealed limited abduction of the right VC, a thickened immobile left VC, and 50% narrowing of the glottic opening caused by scar formation at the posterior commissure. In addition, there was subglottic stenosis and mild edema of the true and false VC. The ETT was advanced back into the trachea. Because there was a leak around the ETT upon deflation of the cuff, it was judged that an extubation attempt would be appropriate. A tube exchanger was positioned into the trachea, and the ETT was removed. The tube exchanger was left in the trachea to permit rapid reintubation if required. The patient received nebulized racemic epinephrine and inhaled corticosteroids. The patient continued to have mild stridor and hoarseness but maintained adequate gas exchange and arterial oxygen saturation with a respiratory rate of 16–20 breaths/min. The tube exchanger was removed 3 h after extubation. Thirty-six hours after the conclusion of surgery, she was transferred from the postanesthesia care unit to a step-down subacute care unit for vigilant monitoring. On postoperative day 2, the patient again developed severe inspiratory stridor resulting in arterial oxygen desaturation that required immediate reintubation of the trachea. In view of her inability to maintain a patent airway, a flap tracheostomy was * Staff Anesthesiologist, Division of Anesthesiology and Critical Care Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio.