C. Badetti et Jc. Manelli, NEUROMUSCULAR BLOCKING-AGENTS IN BURNED P ATIENTS, Annales francaises d'anesthesie et de reanimation, 13(5), 1994, pp. 705-712
Bums of more than 15 % of the body surface area result in major physio
logical changes with an alteration of cardiovascular, pulmonary, hepat
ic and renal functions, as well as modifications in the pharmacokineti
cs and the pharmacodynamics of many drugs. Among these, a major change
in the activity of muscle relaxants occurs which can be specific to t
his pathology. Succinylcholine is contraindicated during recovery from
a burn trauma because of a possible hyperkaliemic response, directly
related to the dose, the post-burn delay and the area of burned body s
urface. The kaliemic response and the related cardiac complications re
main unpredictable. The height of twich depression with small doses of
succinylcholine such as 0,1 to 0,2 mg.kg(-1), demonstrates the hypers
ensitivity to this agent and does cause neither metabolic disturbances
nor cardiac arrest. Nevertheless, the administration of succinylcholi
ne is contra-indicated for from the 5(th) day on at least two years af
ter the burn injury. Conversely, the action of non-depolarizing muscle
relaxants is characterized by a resistance, which is correlated to bo
th the posttraumatic delay and the extent of the burned area. It start
s an about the seventh day, reaches peak intensity between day 15 and
day 40 and can persist up two years after the thermal injury. In the c
ourse of a burn, the so-called ''immature'' acetylcholine receptors, c
haracterized by the substitution of the sub-unit epsilon by a protein
gamma, increase at the level of the end plate areas and the extrasynap
tic muscle membrane. These receptors explain both the hyperkaliemic re
sponse and the hypersensitivity to succinlycholine. The reduction in t
he activity of non-depolarizing muscle relaxants can be explained, in
part, by the increase of nicotinic receptors. However some other facto
rs have a part in this resistance. Elements such as increased protein
binding, alteration of renal excretion and an ''anti-curare'', plasmat
ic substance all participate in this phenomenon.