[Anesthesia and intraocular pressure]

General anesthesia has been in use for ophthalmic surgery since 1847. The subsequent predominance of local anesthetic techniques made ophthalmic anesthesia the "Cinderella of anesthesia services" until its clinical and scientific rehabilitation in the second half of this century. Precise control of intraocular tension is an accepted advantage of general anesthesia. The exercise of such control requires understanding of intraocular physiology and the effects exerted by anesthetic techniques. Hence, the impact of anesthetic drugs on intraocular pressure (IOP) must be considered when ophthalmic surgery is to be carried out under general anesthesia. Intravenous anesthetics and volatile agents reduce IOP, with the possible exception of ketamine. Underlying mechanisms include a direct effect on cerebral IOP control centers and indirect effects mediated through the balance between production and drainage of aqueous humor, general circulation and ocular muscle tone. IOP is likely to be elevated during induction and recovery. Currently suggested measures to prevent the increase in IOP associated with laryngoscopic tracheal intubation facilitated by succinylcholine include oral premedication with clonidine, intravenous administration of lidocaine 3 min prior to laryngoscopy, and anesthetic induction with propofol or narcotics. Non depolarizing neuromuscular blocking drugs either do not affect IOP or produce a slight decrease; depolarizing muscle relaxants increase IOP. It remains controversial whether this effect, which is pronounced with succinylcholine, may be reliably abolished by any concomitant medication. The new competitive relaxants atracurium and vecuronium provide stable conditions with respect to IOP and systemic circulation, combined with a rapid onset and intermediate duration of action.