We would like to comment on the recent case report on the use of succinylcholine in a patient with postpoliomyelitis syndrome (PPS).1Poliomyelitis results from infection by a picornavirus. The polio virus can cause destruction of anterior horn motor neurons with resultant limb paralysis. Motor axon terminal sprouting reinnervates previously denervated muscle fibers creating a giant motor unit. This is associated with clinical improvement in motor strength weeks and months after an acute attack of polio. After decades, a postpoliomyelitis syndrome can develop, with muscle atrophy potentially progressing to complete paralysis. This syndrome is thought to occur secondary to increased functional demands, or overuse, of the giant motor unit, which results in the death of its sprouts.2,3 

There have been a few reports over the years using succinylcholine in patients with pathology similar to that seen in PPS. For example, succinylcholine-induced hyperkalemia and circulatory collapse were reported in a patient with acute idiopathic anterior horn cell disease4; the serum potassium during this cardiac arrest was 7.9 mEq/l. Another study of denervated baboons found an increase in intravascular potassium up to 5.5 mEq/l.5PPS is similar in pathophysiology to the baboon denervation study, and one could assume that hyperkalemia could also be seen in PPS patients. There have been numerous reports of hyperkalemia in patients with neuromuscular disease.4–8It would have been informative to have had the prepotassium and postpotassium measurements from the patient in the report of Wernet et al.  1to determine the magnitude and time frame of the increase of serum potassium.

The avoidance of neuraxial anesthesia was also discussed by Wernet et al.  Successful neuraxial anesthesia in patients with PPS has been reported without adverse complications.9,10Many clinicians provide regional anesthesia for labor and delivery in patients with a history of PPS.11 

If general anesthesia needs to be induced, the potential hazard of using succinylcholine in patients with PPS has been acknowledged.12If the need for rapid sequence induction exists in a PPS patient, we believe one should choose a short-acting nondepolarizing muscle relaxant in lieu of succinylcholine; the only caveat would be to consider using a decreased dose because of the increase risk of muscular weakness.13 

The mere fact that succinylcholine was used in the current case does not preclude the possible occurrence of severe, acute hyperkalemia in subsequent cases in patients with PPS. We do not believe that one can conclude from this single case that succinylcholine should be used in patients with PPS.

*Tufts University School of Medicine, Baystate Medical Center, Springfield, Massachusetts. neil.roy.connelly@bhs.org

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