As we know, this is the first clindamycin’s unusual long lasting effect report on the neuromuscular blocking effect. Fewer studies have reported the antibiotics’effect on no depolarizing neuromuscular blocking especially the rapacuronium bromide[1–4]. But all these reported cases occurred about 20 years ago. There is no such report in recent years.
Rapacuronium bromide is a no depolarizing neuromuscular blocking drug with a rapid onset and short duration of action. So cisatracurium besylate was applied in the anesthesia maintenance stage. The clinical duration of a rapacuronium block may be prolonged a few minutes with the use of volatile anesthetics, antibiotics and magnesium .
Volatile anesthetics affect the potency of NDMRs, possibly by enhancing antagonist affinity at the receptor site, contributing to the clinically observable enhancement of neuromuscular blockade by volatile anesthetics . Sevoflurane and isoflurane inhibit exocytosis evoked by sodium-dependent depolarization and might act on sodium channels , which is the mechanism of the effecting of volatile anesthetics prolonging the neuromuscular blocking. This factor was not taken into account since volatile anesthetics were not used in this case.
Antibiotics were divided into β-lactams, aminoglycosides, macrolides, quinolones antibiotics, tetracyclines, chloramphenicols, lincomycin antibiotics according to its effect sites. Previous studies have reported that aminoglycosides, colistin and clindamycin. At clinically relevant doses, the penicillins, cephalosporins, tetracyclines are apparently no effects at the neuromuscular junction. Clindamycin, a macrolide antibiotic resembling erythromycin in antimicrobial activity, prolongs no depolarizing muscle relaxants such as pancuronium, vecuronium, and it has also been found to produce profound neuromuscular blockade at large dose. Previous studies reported that a profound neuromuscular block with 2400 mg of clindamycin that was given to a patient who had fully recovered (TOF of 1.0) from succinylcholine  and 15 mg/kg that prolonged rapacuronium block by approximately 65 minutes . However, the dose in this patient was relatively low (300mg,twice a day) which can significantly prolong the neuromuscular block time is extremely rare especially when we used it at the beginning of surgery.
Till to now, the mechanism of antibiotics -induced neuromuscular block is not fully understood. Its mechanism maybe in the following aspects which are illustrated in the normal neuromuscular transmission: Calcium ion promotes the fusion of the vesicle membrane in the axon and the rupture of the anterior membrane of the joint; The acetylcholine in the vesicle is released into the neuromuscular junction space; Acetylcholine binds to a receptor on the membrane behind the joint, triggering an endplate potential. For clindamycin, it appears to cause muscle relaxation predominantly by a direct action on muscle contractility and cholinergic receptors, rather than by inhibition of neuromuscular transmission.
Interestingly, this patient is a vegetarian. When general anesthesia is given for vegetarians, it is imperative that control of the electrolyte balance smoothly. Although the preoperative results of laboratory tests were almost normal, there is still lack of some exams such as examination of osteoporosis and respiratory muscle tone .