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IV SUXAMETHONIUM TEST
Br. J. Anaesth. (1982), 54,475
CORRESPONDENCE PREOPERATTVE BUPRENORPHINE DOES NOT PREVENT MYOCLON1A SEEN AFTER ETOMIDATE
NIELS-OLE KLAUSBN SOPHUSH JOHANSEN FINN JANSTRUP JORN GREEN HANSEN
Herlev, Denmark REFERENCES
Holdcroft, A , Morgan, M., Whirwam, J G , and Lumley, J (1976). Effect of dose and premedication on induction complications with etomidate. Br J. Anaath., 48, 199. Kay, B , and Roily, H (1977) Total intravenous anaesthesia with etomidate. Acta Anaesthiswl. Belg., 3,157. Lees, N. W., Glasser, J., McGroarty, F J , and Miller, B M (1981). Etomidate and fentanyl for maintenance of anaesthesia. Br. J. Anaesth , 53, 959.
J. PLOTZ W. SCHREIBER
Bamberg, Germany
REFERENCES I V SUXAMETHONIUM TEST
Sir,—Our use of suxamethonium 5 mg as described by Baraka (1978) in conscious subjects led to unexpected observations during occlusion the fingers could be moved freely (no neuromuscular blockade), several seconds after release of the tourniquet they became immovable and generalized neuromuscular blockade required artificial ventilation for 6 min; immobility of the fingers persisted for several minutes after the return of full muscle activity elsewhere in the body (Schreiber and Plotz, 1980).
Baraka, A. (1978). Suxamethonium-induced muscle contxacture following traumatic denervanon m man Br. J. Anaesth., 50, 195. La Cour, D , Juul-Jensen, P., and Reske-Nielsen, E (1973) Central and peripheral mechanism! in malignant hyperthermia; in International Symposium on Malignant Hyperthermia, p 380 Springfield/U.S.A.: Charles C. Thomas. Lehmann, H , and Liddell, J. (1969) Human chounesterase (pseudochohnesterase): genetic variants and their recognition Br.J. Anaesth., 41, 233.
TABLE I. Ptasmachohnesterase activity and genotype (E\° Ef) after unexpected hypersensttwity to suxamethonium (invtstigatums earned out by Drs Viby-Mogensen (Copenhagen) and Doenicke (Munich). *Rcpeated studies
Observed value Normal range
Chohnesterase activity (u. litre"1)
Dibucaine number*
Fluoride number
Chloride number
Scohne number
Urea number
653 677-1560
66-71 78-86
46 55-65
21 1-22
72 89-95
58 41-52
Downloaded from http://bja.oxfordjournals.org/ at UQ Library on June 18, 2015
Sir,—Diving the development of a total i.v anaesthesia technique based on a combined infusion of etomidate and subanaesthetic doses of ketamine, we found that one disadvantage of this combination is the myoclonia associated with etomidate (Kay and Roily, 1977). Benzodiazepincs and fentanyl reduce the frequency and seventy (Holdcroft et al., 1976, Lees et al ,1981) We tested buprenorphine 0.2 mg sublingually as a premedicant before etomidate-ketamine in a parallel study of 14 patients undergoing surgery for inguinal hernia or varicose veins m an outpatient surgical unit. We found that this dose of buprenorphine did not prevent myoclonia and we did not consider a larger dose justifiable in outpatients because of postoperative sedation. However, we found that preoperanve sublingual buprenorphine gave good preoperanve sedation, and reduced the requirements for analgesic drugs in the period immediately after operation.
In an attempt to explain this, suxamethonium 1.5-5 mg diluted in volumes ranging from 2.5 to 40 ml was administered to anaesthetized patients while neuromuscular transmission was recorded simultaneously (adductor pollicis twitch method) (Plotz, Schreiber and Braun, 1981). During ischaemia, a twitch depression of varying degree (in some cases missing) was observed; about 30 s after release of the tourniquet a significant increase in twitch depression began. In three of eight simultaneous control studies of the other hand twitch depression commenced at the same time, although the effects were less extensive than on the test side. From these findings it was deduced that the number of suxamethonium molecules required for maximal depression reached the specific receptors not during occlusion but only systemically when the tourniquet was released. The extent of regional and systemic effects may be determined by individual sensitivity to suxamethonium. Torda and Klonymus (1967) observed a temporary increase in the neuromuscular blockade lasting 30-60 s immediately after tourniquet release in some patients, but was unable to explain the phenomenon. Baraka (1978) observed a mild ptosis, apnoea commenced in the cited case and m another patient (La Cour, Juul-Jensen and Reske-Nielsen, 1973). Plasmacholinesterase studies (table I) revealed a hereditary heterozygote status which might be responsible for the sensitivity This genotype occurs in one in 480 individuals (Lehmann and Liddell, 1969) or even more frequently (Viby-Mogensen and Hanel, 1978) and responds unexpectedly to suxamethonium. The occurrence of unforeseeable neuromuscular effects including apnoea, constitutes a contraindication to the use of the i.v. regional suxamethonium test m conscious patients
CORRESPONDENCE PREOPERATTVE BUPRENORPHINE DOES NOT PREVENT MYOCLON1A SEEN AFTER ETOMIDATE
NIELS-OLE KLAUSBN SOPHUSH JOHANSEN FINN JANSTRUP JORN GREEN HANSEN
Herlev, Denmark REFERENCES
Holdcroft, A , Morgan, M., Whirwam, J G , and Lumley, J (1976). Effect of dose and premedication on induction complications with etomidate. Br J. Anaath., 48, 199. Kay, B , and Roily, H (1977) Total intravenous anaesthesia with etomidate. Acta Anaesthiswl. Belg., 3,157. Lees, N. W., Glasser, J., McGroarty, F J , and Miller, B M (1981). Etomidate and fentanyl for maintenance of anaesthesia. Br. J. Anaesth , 53, 959.
J. PLOTZ W. SCHREIBER
Bamberg, Germany
REFERENCES I V SUXAMETHONIUM TEST
Sir,—Our use of suxamethonium 5 mg as described by Baraka (1978) in conscious subjects led to unexpected observations during occlusion the fingers could be moved freely (no neuromuscular blockade), several seconds after release of the tourniquet they became immovable and generalized neuromuscular blockade required artificial ventilation for 6 min; immobility of the fingers persisted for several minutes after the return of full muscle activity elsewhere in the body (Schreiber and Plotz, 1980).
Baraka, A. (1978). Suxamethonium-induced muscle contxacture following traumatic denervanon m man Br. J. Anaesth., 50, 195. La Cour, D , Juul-Jensen, P., and Reske-Nielsen, E (1973) Central and peripheral mechanism! in malignant hyperthermia; in International Symposium on Malignant Hyperthermia, p 380 Springfield/U.S.A.: Charles C. Thomas. Lehmann, H , and Liddell, J. (1969) Human chounesterase (pseudochohnesterase): genetic variants and their recognition Br.J. Anaesth., 41, 233.
TABLE I. Ptasmachohnesterase activity and genotype (E\° Ef) after unexpected hypersensttwity to suxamethonium (invtstigatums earned out by Drs Viby-Mogensen (Copenhagen) and Doenicke (Munich). *Rcpeated studies
Observed value Normal range
Chohnesterase activity (u. litre"1)
Dibucaine number*
Fluoride number
Chloride number
Scohne number
Urea number
653 677-1560
66-71 78-86
46 55-65
21 1-22
72 89-95
58 41-52
Downloaded from http://bja.oxfordjournals.org/ at UQ Library on June 18, 2015
Sir,—Diving the development of a total i.v anaesthesia technique based on a combined infusion of etomidate and subanaesthetic doses of ketamine, we found that one disadvantage of this combination is the myoclonia associated with etomidate (Kay and Roily, 1977). Benzodiazepincs and fentanyl reduce the frequency and seventy (Holdcroft et al., 1976, Lees et al ,1981) We tested buprenorphine 0.2 mg sublingually as a premedicant before etomidate-ketamine in a parallel study of 14 patients undergoing surgery for inguinal hernia or varicose veins m an outpatient surgical unit. We found that this dose of buprenorphine did not prevent myoclonia and we did not consider a larger dose justifiable in outpatients because of postoperative sedation. However, we found that preoperanve sublingual buprenorphine gave good preoperanve sedation, and reduced the requirements for analgesic drugs in the period immediately after operation.
In an attempt to explain this, suxamethonium 1.5-5 mg diluted in volumes ranging from 2.5 to 40 ml was administered to anaesthetized patients while neuromuscular transmission was recorded simultaneously (adductor pollicis twitch method) (Plotz, Schreiber and Braun, 1981). During ischaemia, a twitch depression of varying degree (in some cases missing) was observed; about 30 s after release of the tourniquet a significant increase in twitch depression began. In three of eight simultaneous control studies of the other hand twitch depression commenced at the same time, although the effects were less extensive than on the test side. From these findings it was deduced that the number of suxamethonium molecules required for maximal depression reached the specific receptors not during occlusion but only systemically when the tourniquet was released. The extent of regional and systemic effects may be determined by individual sensitivity to suxamethonium. Torda and Klonymus (1967) observed a temporary increase in the neuromuscular blockade lasting 30-60 s immediately after tourniquet release in some patients, but was unable to explain the phenomenon. Baraka (1978) observed a mild ptosis, apnoea commenced in the cited case and m another patient (La Cour, Juul-Jensen and Reske-Nielsen, 1973). Plasmacholinesterase studies (table I) revealed a hereditary heterozygote status which might be responsible for the sensitivity This genotype occurs in one in 480 individuals (Lehmann and Liddell, 1969) or even more frequently (Viby-Mogensen and Hanel, 1978) and responds unexpectedly to suxamethonium. The occurrence of unforeseeable neuromuscular effects including apnoea, constitutes a contraindication to the use of the i.v. regional suxamethonium test m conscious patients