Succinylmonocholine

Abstract

CONGENITAL OBSTRUCTION OF INTESTINE hBnrr 767 MmWICAI Jouiu-x. strongly advocated (Rickham, 1952). Most paediatricians will agree that certain congenital abnormalities such as oesophageal atresias and genito-urinary malformations require the specialized surgical techniques available only at regional contres. Abdominal malformations of the alimentary tract, particularly obstructions of the small intestine, are probably the most urgent of the remedial congenital malformations. Early diagnosis and immediate pre-operative treatment are required. Available statistics suggest that after 96 hours the operative mortality even in the most capable hands is practically 100%. The delay and disturbance necessarily involved in transferring such cases from outlying hospitals to regional centres is unjustified. Rickham (1952) points out that a surgeon working in one hospital group is unlikely to see more than one or two such cases a year, and therefore unlikely to gather enough experience to deal correctly with the complicated surgical problems. On the other hand, the general surgeon, owing to the development of other surgical specialties, is a specialist in abdominal surgery, and neonata,l abdominal surgery should rightly remain within his province.

Cholinesterase Its significance in anaesthetic practice

“…On the other hand, the function of plasma cholinesterase is still the cause of some debate and, although there are several hypotheses, none has been universally accepted. In 1953, Lehman & Silk [6] suggested that plasma cholinesterase prevented inhibition of acetylcholinesterase by removal of choline esters formed during metabolism thus indicating that plasma cholinesterase acts as a protector. Bergman & Wurzel [7] postulated a rôle in the transmission of slow nerve impulses.…”

Degradation and elimination of succinylcholine and succinylmonocholine and definition of their respective detection windows in blood and urine for forensic purposes

“…In this context, however, it has to be acknowledged that not only the soluble butyrylesterases but also true cholinesterases (e.g., the membrane bound acetylcholinesterases of erythrocytes or lymphocytes) may influence SMC degradation. While the BChE undoubtedly does act faster on SUX than on SMC, true cholinesterases hydrolyze even low concentrations of SMC but do not degrade SUX [11]. Such effects are impossible to grasp using cell free sample matrices (e.g., serum or plasma), and their relevance for the pharmacology of SMC have thus never before been detected or investigated.…”

“…However, in absence of respiratory assistance, a therapeutic dose of SUX may cause a potentially lethal respiratory paralysis [1][2][3]. The drug is degraded within minutes [4][5][6][7][8][9][10] by unspecific cholinesterases (butyrylesterase; EC 3.1.1.8), yielding succinylmonocholine (SMC) as the first, and succinate and choline as subsequent degradation products [11][12][13]. Its fast degradation to eventually endogenous compounds as well as the fact that both SUX and SMC are analytically challenging compounds led to SUX having the reputation of an undetectable poison.…”

Pharmacokinetic Properties of Succinylmonocholine in Surgical Patients

“…Possible candidates for such polymorphism do not primarily include the BChE (large differences in this enzyme's performance would become manifest in prolonged apnea and therefore be easily discernible), but rather less investigated enzymes with no or more subtle effects on SUX anesthesia [e.g., membrane-bound acetylcholinesterases of (red) blood cells] (25). The present work undoubtedly establishes interindividual differences in the pharmacokinetics of SMC and can therefore be seen to basically support Foldes and Norton's position (21).…”