Succinylcholine and the hemiplegic patient

(This is a follow-up post to a previous blog regarding Suxamethonium and neurological disorders).

The hemiplegic patient does indeed present a risk. There are a number of case reports of stroke patients arresting on the end of a syringe of sux^1,2,3.

Brown and Charlton⁴ studied 12 hemiplegic patients and observed larger muscle action potentials and smaller fade ratios when compared with the normal side. Interestingly dennervation causes a more pronounced response than immobilisation⁵. Age or severity of the stroke did not seem to correlate with muscle activity.

There is now evidence that a pathological isoform of the acetylcholine receptor (AChR), neuronal (nicotinic) 7AChR, not usually found in normal adult muscle, is expressed and up-regulated in muscle during denervation⁶. This up-regulation of AChRs, when depolarized with succinylcholine, leads to an efflux of intracellular potassium into the plasma causing acute hyperkalaemia.

The period on vulnerability to hyperkalaemia for hemiplegic patients is not well defined but case reports have suggested the period to be as early as one week⁵ and as late as six months¹.

Others:

Some of the other conditions reported to cause hyperkalaemia with succinylcholine have included: gastrointestinal mucositis⁸, necrotizing pancreatitis⁹, catatonic schizophenia¹⁰, meningitis¹¹, and purpura fulminans¹².

Thoughts:

I guess this adds more weight to the argument to use Roc in many more time-critical intubation situations.

References:

1. Smith, R. B. and Grenvik, A. 1970. “Cardiac arrest following succinylcholine in patients with central nervous system injuries.” Anesthesiology 33(5): 558.

2. Gronert, G.A., Theye, R.A. 1975. Pathophysiology of hyperkalemia induced by succinylcholine. Anesthesiology; 43:89–99.

3. Martyn, J.A.J., White, D.A., Gronert, G.A., Jaffe, R.S., Ward, J.M. 1992. Up-and-down regulation of skeletal muscle acetylcholine receptors: Effects on neuromuscular blockers. Anesthesiology; 76:822–43.

4. Brown, J., Charlton, J. et al. 1975. “A regional technique for the study of sensitivity to curare in human muscle.” Journal of Neurology, Neurosurgery & Psychiatry 38(1): 18-26.

5. Martyn, J. A. J. and M. Richtsfeld 2006. “Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms.” Anesthesiology 104(1): 158.

6. Fischer, U., Reinhardt, S., Albuquerque, E.X., Maelicke, A. 1999. Expression of functional alpha7 nicotinic acetylcholine receptor during mammalian muscle development and denervation. Eur J Neurosci; 11:2856–64.

7. Thomas, E. T. 1969. “Circulatory collapse following succinylcholine.” Anesthesia & Analgesia 48(3): 333-337.

8. Al-Khafaji, A.H., Dewhirst, W.E., Cornell, C.J., Quill, T.J. 2001. Succinylcholine- induced hyperkalemia in a patient with mucositis secondary to chemotherapy. Crit Care Med 2001; 29:1274–76.

9. Matthews, J.M. 2000. Succinylcholine-induced hyperkalemia and rhabdomyolysis in a patient with necrotizing pancreatitis. Anesth Analg 2000; 91:1552–4.

10. Cooper, R.C., Baumann, P.L., McDonald, W.M. 1999. An unexpected hyperkalemic response to succinylcholine during electroconvulsive therapy for catatonic schizophrenia. Anesthesiology; 91:574–5.

11. Hansen, D. 1998. Suxamethonium-induced cardiac arrest and death following 5 days of immobilization. Eur J Anaesthesiol; 15:240–1.

12. Kovarik, W.D., Morray, J.P. 1995. Hyperkalemic cardiac arrest after succinylcholine administration in a child with purpura fulminans. Anesthesiology; 83:211–3.

‘Qui rogat, non errat’