Antibiotic-Induced Paralysis

Pittinger, Charles B.; Eryasa, Yilmaz; Adamson, Richard

doi:10.1213/00000539-197005000-00033

Cited by 91 publications

(33 citation statements)

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“…Importantly, present observations also provide a mechanistic explanation for cardiac irregularities occasionally detected in patients treated with aminoglycoside antibiotics (4,(21)(22)(23).…”

Section: Resultsmentioning

confidence: 52%

Gentamicin blockade of slow Ca++ channels in atrial myocardium of guinea pigs.

Adams¹,

Durrett²

1978

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 52%

Gentamicin blockade of slow Ca++ channels in atrial myocardium of guinea pigs.

Adams¹,

Durrett²

1978

J. Clin. Invest.

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“…16 When clindamycin was added to the guinea pig lumbrical muscle-nerve preparation, it produced neuromuscular blockade in concentrations of 180-240 ~tg. ml-J, 17 which is similar to the concentrations anticipated to have occurred in the present case if it is assumed that the volume of distribution is approximately 0.66 L. kg-l. 7 This case demonstrates that when clindamycn is given in doses of 40 mg. kg-I it may be followed by profound and prolonged neuromuscular block even when it is given in the absence of clinical neuromuscular blockade. The block cannot be reversed with calcium or anticholinesterases.…”

Section: Discussionmentioning

confidence: 84%

Clindamycin-induced neuromuscular blockade

Ahdal¹,

Bevan²

1995

Can J Anaesth

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The purpose of this article is to report the case of a patient who developed prolonged neuromuscular block after a large dose of clindamycin (2400 rag). A 58-yr-old, 65 kg woman with severe rheumatoid arthritis was admitted for wrist arthrodesis. After d-tubocurarine (3 rag) and fentanyl (1.5 ~tg'kg-l), anaesthesia was indaced with thiopentone (4 rag. kg -~) followed by succinycholine (1.5 mg" kg -~) Clindamycin is a semi-synthetic, propylhygrinic acid derivative whose antimicrobial activity is mediated by its action on 50 s subunit of bacterial ribosome leading to suppression of protein synthesis. There are several reports of its local anaesthetic I and neuromuscular blocking actions. 2-5 In doses of 600-1200 mg it has been shown to prolong the neuromuscular blocking actions of pancuronium, 2 vecuronium 3 but recovery from pipecuronium was not affected by a dose of 300 mg. 4 There is uncertainty whether the block is reversible with calcium or with anticholinesterases although both have been recommended. 5The purpose of this report is to record a very prolonged neuromuscular block which occurred when an unintentional overdose of clindamycin was given to a patient CAN J ANAESTH 1995 / 42:7 / pp 614-7

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“…Neuromuscular block produced by a number of antibiotics has been widely documented in both man and experimental animals (Hokkanen, 1964;Pittinger, Eryasa & Adamson, 1970;Pittinger & Adamson, 1972;Chinyanga & Stoyka, 1974). Polymyxin B is amongst the most potent of the antibiotics in producing neuromuscular block and has been shown to depress the twitch responses of the indirectly stimulated mouse diaphragm in the same dose range as (+ )tubocurarine (Singh, Harvey & Marshall, 1978).…”

Section: Introductionmentioning

confidence: 99%

The Action of Polymyxin B at the Frog Neuromuscular Junction

Durant

Lambert

1981

British J Pharmacology

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I The effects of polymyxin B at the neuromuscular junction of the frog were studied by conventional electrophysiological and voltage clamp techniques.2 At a concentration of 2.5 jig/ml polymyxin B produced neuromuscular blockade in 10 to 15 min and endplate potentials (e.p.ps) could be recorded. Resting membrane potential was unaffected. The neuromuscular block was characterized by a depressed e.p.p. quantal content (28 ± 7), which was similar to that determined from endplates exposed to 13 mm magnesium (23 + 3), and a low e.p.p. quantal size, which was similar to that determined from endplates exposed to 3 /M (+ -tubocurarine. 3 Polymyxin B (0.25 to 0.75 jg/ml) decreased mean miniature e.p.p. amplitude with little effect on frequency. 4 At a concentration of 5 tg/ml polymyxin B markedly shortened the duration of endplate currents (e.p.cs) and abolished the relationship between holding potential and the time to half-decay at negative potentials greater than -60 mV. This action is consistent with block of open acetylcholine activated ionic channels. 5 4-Aminopyridine (20 jiM) antagonized the depressed e.p.p. quantal content produced by polymyxin B but did not alter the shortened e.p.c. duration. 6 It is concluded that polymyxin B decreases quantal release and produces some degree of postjunctional receptor blockade and a marked and persistent blockade of acetylcholine activated channels. The latter action may explain the difficulty of reversal of polymyxin B-induced neuromuscular blockade and its non-competitive nature.

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Antibiotic-Induced Paralysis

Cited by 91 publications

References 0 publications

Gentamicin blockade of slow Ca++ channels in atrial myocardium of guinea pigs.

Gentamicin blockade of slow Ca++ channels in atrial myocardium of guinea pigs.

Clindamycin-induced neuromuscular blockade

The Action of Polymyxin B at the Frog Neuromuscular Junction

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