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Intraocular tension may be acutely changed by many drugs and by various physiologic events. AN acute rise in intracoular tension may be catastrophic if it occurs when the globenis open and leads to expulsion of contents. Most general anesthetics cause a decrease in intraocular pressure, although a few causes increased intraocular pressure. Midazolam is a 1,4-benzodiazepin derivative synthesized by Walser and Freyer in 1975. Earlier studies with midazolam have demonstrated it efficacy for induction of anesthesia and premedication. It is also desirable to know if all anesthetic agents which produce general anesthesia and which are pharmacologically different affect intraocular pressure in a similar manner. Therefore investigation of the influence of midazolam on intraocular pressure in 25 patients was undertaken at the Department of Anesthesiology, Hanyan University. All patients had no known eye abnormalities. The patients were not premedicated. In all patients the intraocular pressure was measured before induction of anesthesia, after instilling a 0.5% tetracaine into the conjunctival sac. A second reading was taken after induction of midazolam (0.2mg/kg of body weight) and a third after injection of succinylcholine(1mg/kg of body weight) and a fourth after endotracheal intubation. A Schiotz tonometer with a 5.5gm and a 7.5gm weight was used. In addition to the tonometric determination, the blood pressure, pulse rate and respiratory rate were recorded before and after induction of midazolam. An attempt was tried to keep the intraocular pressure changed as many and to minimize the other factors affecting intraocular pressure. To achieve this, supine position and constant gas flow was maintained. Special care was taken to avoid pressure on the patients eye and to maintain a fully patent airway to prevent respiratory disturbances leading to straining and increased venou pressure. Endotracheal intubation was performed with the aid of succinylcholine to avoid cough or laryngospasm. The results of the observation with the above mentioned method were tested by student t-test statistically. Each patient acted as his own control. There was a fall in intraocular pressure in 17 patients among 25 patients(average 1.8mmHg), but no significant change followed by the use of midazoam. The blood pressure variations were between 10 and 40 mmHg, during the course of anesthesia and could not be related to intraocular pressure changes. Intraocular pressure changes had no relation to pulse and respiratory rate variations. This finding indicated that benzodiazepine as a class of drugs have well described muscle relaxant properties that are primarily central(supraspinal)rather than peripheral(myoneural) in action. There was a rise in intraocular pressure in 19 patients among 25 patients, followed by the use of succinylcholine and 23 patients among 25 patients, after endotracheal intubation. According to Feldman and Crawley, diazepam potentiated the myoneural blocking effects of gallamine and antagonizes the effects of succinylcholine. Nevertheless Dretchen demonstrated that the clinical doses of diazepam did not potentiated the muscle relants. Our finding showing no apparent succinylcholine interaction with midazolam are consistent with the finding of Dretche.
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