Misuse of neostigmine for reversal of neuromuscular block.
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Biomedical subjects
Publications and source records attributed to A Baraka.
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The rationale of "crash induction" in patients with full stomach is reviewed. The technique does not precipitate regurgitation in normal patients having competent cardia, provided respiratory obstruction and IPPV are avoided during induction. On the other hand, in patients with incompetent cardia such as intestinal obstruction or hiatus hernia, excessive material may accumulate in the lower oesophagus. The accumulation will be suddenly released with the cricopharyngeal relaxation subsequent to "crash induction". The stomach and oesophagus should be adequately decompressed pre-operatively, and precautionary measures such as backward cricoid pressure must be taken during induction.
In 20 adult patients undergoing inguinal herniorrhaphy neuromuscular block was induced with tubocurarine 10 mg. In 10 patients, neostigmine 1--2 mg antagonized the block and restored the twitch response to its baseline value. Physostigmine, up to 4 mg, did not produce significant antagonism of the neuromuscular block.
The effects of the systemic and of the i.v. regional administration of suxamethonium were investigated in 23 patients with traumatic nerve injury. Following the systemic administration of suxamethonium 100 mg, normally innervated muscles showed muscle fasciculations initially, followed by muscular relaxation. On the other hand, denervated muscles did not fasciculate and, in 21 patients, manifested suxamethonium-induced contractures. In the other two patients no response was observed. In 10 of the patients, the i.v. regional administration of suxamethonium 5 mg was followed by a contracture of the denervated muscle which was maintained until the tourniquet was deflated. No systemic reaction to suxamethonium, other than mild ptosis, followed the release of the tourniquet.
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Ten volunteers were given 2 mg scopolamine intravenously (IV) to produce substantial drowsiness and sleepiness. Galanthamine, 0.5 mg/kg IV, effectively reversed the central anticholinergic syndrome produced by scopolamine. Electroencephalographic monitoring of two subjects matched the observed changes of consciousness: scopolamine replaced the dominant awake alpha rhythm with a disorganized, slow, 4- to 6-Hz activity. Galanthamine promptly returned to EEG pattern to the control, awake state. Galanthamine produces effective, safe, and long-lasting reversal of the central anticholinergic syndrome in man.
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The effect of neostigmine 0.05 mg/kg on the neuromuscular block produced by suxamethonium was investigated in 10 normal patients and in five patients with atypical plasma cholinesterase activity, by recording the twitch response to ulnar nerve stimulation. In the normal patients, neostigmine potentiated the block produced by suxamethonium whether it was of the depolarizing or desensitizing type. On the other hand, in patients with atypical plasma cholinesterase activity, neostigmine potentiated the depolarizing phase of suxamethonium block, while antagonizing the desensitizing phase. The degree of antagonism was not related to the magnitude of neuromuscular block, but was proportional to the degree of desensitization at the time of antagonism.
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Depolarization and desensitization neuromuscular blockade was induced with suxamethonium. Rate of recovery of neuromuscular transmission did not vary with the nature of the blockade.