Control de nausea y vómito postoperatorio: estudio comparativo entre difenidol, droperidol, metoclopramida versus placebo / Comparative study between difenydol, droperidol, metoclopramide versus placebo for the control of post-operative nausea and vomiting

Se estudiaron 60 pacientes, programados para cirugía de cabeza y cuello bajo anestesia general balanceada, con estado físico 1 y 2 (ASA). A quienes se les administró 30 minutos antes de finalizar él acto anestésico, droperidol a dosis de 15 a 20 mg/Kg IV, difenisol a dosis de 150 mg/Kg IV, metoclopramida a dosis de 150 mg/kgIV, solución salina 3 mg IV. Se evaluó la náusea y vómito de acuerdo a la escala de Bellville, cada 15 minutos por espacio de una hora y 4 hrs posteriores de haber abandonado la sala de recuperación. La incidencia de náusea fue de 6.6 porciento y vómito de 6.6 porciento en el grupo droperidol comparandolo con el grupo control en el cual la incidencia de náucea fue de 26.6 porciento y de vómito 20 porciento encontrandose diferencia estadisticamente significativa de p<0.05. En el grupo difenisol la incidencia observada de náusea fue de 20 porciento y de vómito de 6.6 porciento. En el grupo metoclopramida la incidencia de náusea fue de 26.6 porciento y de vómito de 6.6 porciento. En base a estos resultados concluimos, que droperidol es efectivo en la prevención y tratamiento de náusea y vómito posterior a anestesia general balanceada, no así metoclopramida o difenidol quienes fueron inefectivos para tal fin.

Anticonvulsant actions of anticholinergic drugs in soman poisoning.

The acute effects of the organophosphorus cholinesterase inhibitor soman include hypersecretions, convulsions, and death. The purpose of this study was to evaluate the anticholinergic compounds aprophen, atropine sulfate, azaprophen, benactyzine, benztropine, biperiden, scopolamine HBr, and trihexyphenidyl for their efficacy in preventing soman-induced hypersecretions and convulsions. Male rats were injected with the oxime HI-6 (125 mg/kg, i.p.), to increase survival time, along with various intramuscular doses of the anticholinergics 30 min prior to a dose of soman (180 micrograms/kg, s.c.; equivalent to 1.6 x the median lethal dose) that produced 100% convulsions. Signs of intoxication as well as the time-to-onset of convulsions were observed. The calculated anticonvulsant median effective dose values were 0.18, 0.33, 0.36, 0.55, 2.17, 2.30, 2.45, and 31.09 mumol/kg for scopolamine HBr, biperiden, trihexyphenidyl, benactyzine, benztropine, azaprophen, aprophen, and atropine sulfate, respectively. The same rank order of potency for inhibition of hypersecretions among these compounds was observed. Parallel studies with quaternary analogs of atropine sulfate and scopolamine HBr demonstrated, however, that these charged compounds afford no protection against soman-induced hypersecretions and convulsions. The results indicate that tertiary anticholinergic compounds afford protection against soman-induced convulsions and hypersecretions and that the beneficial anticonvulsant effects are mediated through the central cholinergic system. Excitatory amino acid neurotransmitter systems may be involved in the effectiveness of these compounds.