Blog with interesting cases and/or problems related to anesthesia with discussion based on best evidence in the literature.

December 7, 2010

follow up on weakness after succinylcholine

In this month's Anesthesiology, Herbstreit F et al. published an article demonstrating that neostigmine/glycopyrrolate given after full recovery from NDMB paralysis resulted in a sudden increase in weakness. The weakness predominated in the upper airway dilator muscles, in particular, they measured the strength of the genioglossus muscle. Their findings suggest that in patients who may have recovered from neuromuscular block and are given reversal "to be safe" without measuring the train of four, the reversal could actually put the patient at risk. This is relevant to the most recent post in this blog. In that case report, the patient emerged from anesthesia, but never fully gained consciousness. The patient also appear slightly weak. The patient had been given rocuronioum earlier in the case, but sufficient time had passed in order that it was expected that the neuromuscular block had worn off. Nevertheless, given the patients clinical condition, 1 mg of neostigmine was administered in an attempt to improve the upper airway obstruction that continued to hinder the patient's full recovery. The patient did not improve, and in fact, may have deteriorated slightly. Therefore, it was necessary to intubate, and succinylcholine was adminstered that resulted in a prolonged period of mechanical ventilation.

This month's journal article underscores the importance in border line cases, in particular in patients at high risk of upper airway obstruction, of monitoring carefully the dose of neuromuscular blockers in addition to train of four monitoring. Upper airway dilator musculature seems to be more susceptible to both neostigmine caused weakness as well as to the block caused by neuromuscular blockers. Eikerman M et al. in the BJA 2008 (101) comment that this may result from the different frequencies of neuronal firing (15 to 25 Hz in genioglossus motor units vs. 8 to 13 Hz in the diaphragmatic firing rate).

The mechanism by which neostigmine causes weakness is thought to be one of 3 (or more likely) a combination of the three things: 1) desensitization of nActR, 2) depolarization block and 3) open channel block.

This should be considered anytime the clinician is faced with a patient who is at risk for post operative upper airway obstruction and has received NDMBs.

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