Chlorothiazide relieves asthmatic wheezing.

We wish to thank Dr. Wilson for suggesting that the bilateral vocal cord paralysis we reported in a patient with Guillain Barre syndrome may have resulted from trauma secondary to intubation with a cuffinflated endotracheal tube. Although this explanation could have contributed to the paralysis, we believe it was primarily the result of the Guillain Barr6 syndrome because: 1. Prior to intubation the patient's cough reflex was absent and he could speak in only a whisper, suggesting the paralysis had already begun. 2. Laryngoscopy during intubation revealed partially abducted cords with minimal movement. 3. The cuff of the endotracheal tube (size 9 foam cuffed Bivona) was not manually inflated and the cuff's port was left open to the atmosphere. 4. The intubation was easy and atraumatic. 5. Two otolaryngologists examined the patient and dismissed trauma as a cause for the paralysis. 6. The paralysis persisted for more than two years which is markedly different from the four-eight weeks required to regain normal function in the group of patients studied by Cox and Welborn.' In summary, the pre-intubation onset of paralysis, the apparent lack of trauma to the cords or trachea, and the duration of the paralysis suggests that our patient's vocal cord paralysis was a result of the Guillain Barre syndrome and not from damage to the recurrent laryngeal nerve. The patient mentioned by Dr. Wilson is interesting because the duration of her bilateral vocal cord paralysis is uncommon in cases of recurrent laryngeal nerve damage. Our experience is that edematous and poor moving (partially paralyzed) vocal cords are sometimes seen in anesthetized patients intubated with an air-filled endotracheal tube. We find this type of vocal cord malfunction always resolves within eight weeks, as also reported by Cox and Welborn.