Laryngospasm is a rare but potentially life-threatening complication of general anesthesia, which may lead to cardiac arrest, aspiration, and negative pressure pulmonary edema.13 The mechanism of laryngospasm was the related afferent limb of the reflex arc will still take effects without appropriate anesthesia depth after the muscle return to normal,10and lead to a physiological exaggeration of the glottis closure reflex.14 Laryngospasm often simulated by laryngoscopes, blood or secretion, anesthetic agents,15 and always presented several obvious clinical signs: paradoxical breathing, stridor, and ineffective chest wall movement.2,16
However, our case presented atypically: no instrument (laryngoscopes) involved, not an insufficient anesthesia, no certain stimuli (aspirating food, foreign bodies, blood or secretion), total intravenous anesthesia without any inhalational agents. Moreover, sugammadex was observed with no superiorities than neostigmine in reducing risk of any individual pulmonary complication, 17,18 and the previous reports19 had confirmed the sugammadex related larygonspasm. Nobuyasu Komasawa20 suggested that sugammadex administration after recovery of consciousness can decrease the incidence of laryngospasm. Compare our case to a previous reported case about sugammadex induced laryngospasm,14 there were several similarities: an elder man with a long smoking history, combined with lung disease, and laryngospasm happened just after the injection of sugammadex with a sharply increased PIP. Therefore, we highly suspected the atypical laryngospasm was induced by sugammadex and did a comparation among the previous reports and ours. Table.1
During the enmergency, the airway spasm followed close behind the provide of sugammadex, we experienced an atypical laryngospasm, but we were not sure if there was a bronchospasm for the previous reports.21,22 The mechanism of the obstruction could be the sugammadex induced hypersensitivity and anaphylaxis,23–25 and the associated allergic actions were concealed under a deep neuromuscular blockade until muscle tone reversed by sugammadex to normal, the efferent never impulses cross the neuromuscular junctions increased relatively and finally caused an adduction of the vocal cords.26 Moreover, the positive IDT and the significant hemodynamics fluctuation (HR increased by 30%) also can state the anaphylaxis to some extent.
Fortunately, the ventilation came into effect just seconds after the rocuronium provided, and sugammadex revealed a high capacity in binding non-depolarizing neuromuscular blockade(NMB) and a fast reversion of rocuronium induced muscular relaxation usually take effect within 1–2 minutes,27,28 then excreted in urine in prototype.29 It may be the rapid, effective, reliable and predictable feature on NMBDs reversion 30–32 that makes rocuronium as a key to relieve the sugammadex induced Laryngospasm.
Although it is well known that the sugammadex could cause hypersensitivity and anaphylaxis, the following adverse events, especially the atypical laryngospasm after the muscular relaxation reversion should be highly regarded among all the anesthetic members. And simultaneously, it may not be optimal rescue with rocuronium for such an enmergency, which at least is an option,