Residual paralysis: a real problem or did we invent a new disease?

Over the past three decades, many studies have shown a high proportion of patients in the recovery room with residual neuromuscular blockade after anesthesia. The purpose of this Continuing Professional Development module is to present the physiological consequences of residual paralysis, estimate the extent of the problem, and suggest solutions to prevent its occurrence.

Residual paralysis is defined as a train-of-four ratio (TOFR) < 0.9 at the adductor pollicis. While tidal volume and, to a lesser extent, vital capacity are well preserved as the intensity of blockade increases, the probability of airway obstruction, impaired swallowing, and pulmonary aspiration increases markedly as TOFR decreases. In recent studies, incidences of residual paralysis from 4-57% have been reported, but surveys indicate that anesthesiologists estimate the incidence of the problem at 1% or less. The decision to administer neostigmine or sugammadex should be based on the degree of spontaneous recovery at the adductor pollicis muscle (thumb), not on recovery at the corrugator supercilii (eyebrow). The most important drawback of neostigmine is its inability to reverse profound blockade, which is a consequence of its ceiling effect. When spontaneous recovery reaches the point where TOFR > 0.4 or four equal twitch responses are seen, reduced doses of neostigmine may be given. The dose of sugammadex required in a given situation depends on the intensity of blockade.

Careful monitoring and delaying the administration of neostigmine until four twitches are observed at the adductor pollicis can decrease the incidence of residual paralysis. The clinical and pharmacoeconomic effects of unrestricted sugammadex use are unknown at this time.