Rocuronium for Tracheal Intubation

Laura S. Willets, Pharm.D.


Pediatr Pharm. 2000;6(10) 

In This Article


Rocuronium is structurally related to vecuronium, and has a similar pharmacokinetic profile with the exception of a more rapid onset of action. On average, maximal neuromuscular block following an intravenous dose occurs within one minute. Following intramuscular (IM) administration into the deltoid, plasma concentrations peak at 13 minutes. Approximately 80% of the drug is absorbed systemically after an IM dose.[12]

Clinical duration of action for rocuronium ranges from 30 minutes to 1 hour. Mean duration in children aged 3 months to 1 year is reported to be 41 minutes, significantly longer than the mean of 27 minutes found in children aged 1 to 12 years.[3,5]

Rocuronium is a polar molecule and distributes into extracellular fluid; protein binding has minimal effect.[13,14] In a pharmacokinetic study by Vuksanaji and Fisher of children ages 4 to 11 years, the clearance (Cl) of rocuronium varied inversely with body weight. Volume at steady state (Vss) did not vary, resulting in an increase in half-life with age and weight.[15] The impact of these changes is relatively small. The average half-life for an infant between 3 and 12 months of age is 1.3±0.5 hrs, compared to 0.8±0.3 hrs for a child between 3 and 8 years of age.

Several studies have found that newborn infants demonstrate an increased Vss, a slower Cl, and an increased mean recovery time for rocuronium compared to older infants and children.[14] Several factors may be responsible for these differences. The neuromuscular junction changes during the first two months of life. The immature receptor remains open for a longer period of time, allowing for easier depolarization, but may have a decreased affinity for nondepolarizing agents. Infants have a smaller muscle mass to fat ratio resulting in a decreased number of cholinergic receptors that need to be inhibited to allow for muscle relaxation.[1,13] In addition, the infant diaphragm has fewer type I fibers (slow-twitch) which are more sensitive to neuromuscular blockade than type II fibers (fast-twitch). As a result, the diaphragm may remain more active than peripheral muscles.[1] While these sometimes opposing physiologic factors are not yet fully understood, they may explain the variation in response observed in newborns given neuromuscular blockers.

Rocuronium is primarily eliminated via hepatic reuptake and biliary excretion. After a 0.6 mg/kg dose, 12 to 22% is excreted unchanged in the urine. Rocuronium has one metabolite, 17-desacetylrocuronium, which is unlikely to contribute to its neuromuscular blocking action. While there is no documented evidence that renal dysfunction adversely affects the clearance of rocuronium, recovery parameters tend to be longer and more variable in the elderly and those with some degree of renal impairment. Patients with hepatic dysfunction, particularly cirrhosis, demonstrate increased volume of distribution, decreased clearance, and increased half-life.[5,14]


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