Residual paralysis caused by the use of muscle relaxants during surgery, or incomplete neuromuscular reversal, is associated with postoperative complications such as hypoxemia and upper airway obstruction [
21‐
23]. It also has a strong association with pulmonary complications and morbidity in postoperative patients [
24,
25]. Neuromuscular recovery to TOFR ≥0.9 is important because below this level of recovery pharyngeal dysfunction remains, increasing the risk of pulmonary aspiration when TOFR values are 0.7–0.8 measured at the adductor pollicis muscle [
26,
27]. Therefore, current recommendations include confirmation of sufficient neuromuscular recovery to TOFR ≥0.9 by electromyography, and acceleromyographic recovery of TOFR ≥1.0 [
28‐
30]. The incidence of residual paralysis is reported to be 20–60% of patients upon arrival in the post anesthesia care unit (PACU) when non-depolarizing muscle relaxants were used during the surgery [
30‐
33]. Brueckmann et al. reported that all patients receiving sugammadex for neuromuscular blockade reversal had TOFR ≥0.9 at PACU admission, while 43% of patients treated with neostigmine / glycopyrrolate had a TOFR <0.9 at PACU arrival [
34]. However, Unterbuchner [
35] and Todd [
36] have reported that high incidence of residual paralysis after antagonism with neostigmine was likely due to inappropriate intraoperative neuromuscular monitoring in this study. Kotake et al. reported that the use of sugammadex did not eliminate the risk of residual paralysis (up to 9.4% of the patients showed TOFR <0.9 after tracheal extubation) when the decision to extubate the trachea was not based on objective neuromuscular monitoring [
3]. It is uncontroversial that neuromuscular reversal with sugammadex decreases the incidence of residual paralysis compared to acetylcholinesterase inhibitors [
2,
32]. Moreover, unrestricted use of sugammadex might decrease postoperative pulmonary complications [
37,
38]. However, it is imperative that a sufficient number of molecules of sugammadex be administered to bind all of the free rocuronium molecules that diffuse from the neuromuscular junction back into the plasma. The only way to estimate the quantity of these remaining unbound rocuronium molecules is to monitor neuromuscular function and determine more precisely the most appropriate dose of sugammadex necessary for complete antagonism. Therefore, quantitative intraoperative neuromuscular monitoring is strongly recommended to prevent postoperative residual paralysis [
3,
39‐
41]. Without such objective monitoring, even the unrestricted use of sugammadex cannot completely eliminate the risk of residual paralysis [
42]. Consequently, the purpose of neuromuscular monitoring is dual: on the one hand, the most effective dose should be administered in order to exclude residual paralysis. On the other hand, the lowest effective dose should be administered to ensure that excessive sugammadex does not later interfere with the potential need to re-establish neuromuscular blockade emergently. This topic will be discussed in the next section.