Death following Injection of Neostigmine

Macintosh, R. R.

doi:10.1136/bmj.1.4610.852-a

Cited by 44 publications

(19 citation statements)

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“…Arrhythmias have not been reported in dogs during the antagonism of neuromuscular block. In contrast, neostigmine and edrophonium have caused cardiac arrest in man (Bain and Broadbent 1949;Clutton-Brock 1949;Hill 1949;MacIntosh 1949;Lawson 1956;Youngberg 1979) a n d arrhythmias a p p e a r to be relatively common. Atropine a n d neostigmine combinations have caused atrioventricular dissociation, junctional rhythm, increased P-R interval, premature atrial contractions, ectopic beats, inverted P waves, wandering pacemaker a n d premature ventricular depolarisations (Ovassapian 1969;Mirakhur, Dundee and Clarke 1977;Ostheimer 1977).…”

Section: Discussionmentioning

confidence: 99%

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Edrophonium-induced asystole following neuromuscular blockade antagonism in a dog: a case report

Clutton

Petersen‐Jones

1991

Journal of Veterinary Anaesthesia

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Section: Discussionmentioning

confidence: 99%

“…Fatal cardiac arrest is a relatively rare complication of neuromuscular blockade antagonism in man, but has been reported (Clutton-Brock 1949;Hill 1949;Bain and Broadbent 1949;MacIntosh 1949). However, heart rate changes and arrhythmias are not infrequent at this time (Atlee 1985).…”

Section: Introductionmentioning

confidence: 99%

Edrophonium-induced asystole following neuromuscular blockade antagonism in a dog: a case report

Clutton

Petersen‐Jones

1991

Journal of Veterinary Anaesthesia

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“…The doses selected were within recommended ranges: atropine (20 to 100 pg/kg); glycopyrrolate ( 5 to 20 jig/kg); neostigmine (7 to 100 pg/kg). [14][15][16][17][18][19][20][21][22][23][24][25][26][27]28 The comparison of atropine at 40 pg/kg with glycopyrrolate at 10 jiglkg was based arbitrarily on doses used in this clinic to treat bradyarrhythmias. Although unpredictable heart rate changes follow antimuscarinic and anticholinesterase drug administration, the accepted reason for autonomic changes during neuromuscular blockade antagonism is the unsynchronized or unbalanced effects of the simultaneously injected comp o n e n t~.~…”

Section: Discussionmentioning

confidence: 99%

Autonomic and Cardiovascular Effects of Neuromuscular Blockade Antagonism in the Dog

Clutton¹,

Boyd

Flora

et al. 1992

Veterinary Surgery

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Autonomic and cardiovascular changes were studied when neuromuscular blockade was antagonized in 96 dogs with one of eight anticholinesterase-antimuscarinic drug combinations. Neostigmine (50 or 100 micrograms/kg) was administered before or after atropine (40 micrograms/kg) or glycopyrrolate (10 micrograms/kg). The high dose of neostigmine (100 micrograms/kg) caused bradyarrhythmias, salivation, and signs of bronchosecretion when used with either antimuscarinic agent and irrespective of the administration sequence. The heart rate increased, but not significantly, when atropine was injected before either dose of neostigmine. This did not occur when this administration sequence was reversed. Arrhythmias and cardiovascular and autonomic changes did not occur when glycopyrrolate was injected before or after neostigmine at 50 micrograms/kg.

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“…Besides, the cholinesterase inhibitors had many adverse effects. In 1949, Macintosh [3] had already described a patient dying immediately after the administration of atropine and neostigmine for reversal of tubocurarine. Studies with 4‐aminopyridine, which stimulates the release of acetylcholine, were giving disappointing results [4].…”

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confidence: 99%

Cyclodextrins and the emergence of sugammadex

Booij

2009

Anaesthesia

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Residual paralysis, with its subsequent postoperative pulmonary sequelae, is one of the major complications of anaesthesia, and was recognised shortly after the introduction of neuromuscular blocking drugs into routine clinical practice. Although its incidence decreased with the introduction of intermediate duration drugs, and further diminished with routine neuromuscular monitoring and reversal with cholinesterase inhibitors, residual paralysis still remained a problem. In the search for alternatives to stop the effect of neuromuscular blocking drugs and to match their duration of action to clinical need, chelation of the non-depolarising neuromuscular blocking drugs was considered. It was recognised that cyclodextrins could encapsulate steroidal molecules and thereby inactivate the aminosteroidal neuromuscular blocking drugs. In order to improve the binding of rocuronium to the cyclodextrin and to increase the compound's water solubility, the molecule was modified. This led to the development of sugammadex (Org 25969), a modified gamma-cyclodextrin. The modification of the molecule and the initial in vitro studies that led to in vivo and later human studies of this conceptually new drug for anaesthesia are described.

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Death following Injection of Neostigmine

Cited by 44 publications

References 0 publications

Edrophonium-induced asystole following neuromuscular blockade antagonism in a dog: a case report

Edrophonium-induced asystole following neuromuscular blockade antagonism in a dog: a case report

Autonomic and Cardiovascular Effects of Neuromuscular Blockade Antagonism in the Dog

Cyclodextrins and the emergence of sugammadex

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