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EFFECT OF ANESTHETIC DRUGS ON INTRAOCULAR PRESSURE
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Most anesthetic drugs either reduce intraocular pressure or have no effect (Table 27–1). Intraocular pressure decreases with inhalational anesthetics in proportion to anesthetic depth. There are multiple causes for this. Decreased blood pressure reduces choroidal volume, relaxation of the extraocular muscles lowers wall tension, and pupillary constriction facilitates aqueous outflow. Intravenous anesthetics also decrease intraocular pressure, with the exception of ketamine, which usually raises arterial blood pressure and does not relax extraocular muscles.
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Succinylcholine increases intraocular pressure by 5–10 mm Hg for 5–10 min after administration, principally through prolonged contracture of the extraocular muscles. However, in studies of hundreds of patients with open eye injuries, no patient experienced extrusion of ocular contents after administration of succinylcholine. Thus, succinylcholine is not contraindicated in cases of open eye injuries.
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THE OCULOCARDIAC REFLEX
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Traction on extraocular muscles, pressure on the eyeball, administration of a retrobulbar block, and trauma to the eye can elicit a wide variety of cardiac arrhythmias ranging from bradycardia and ventricular ectopy to sinus arrest or ventricular fibrillation. This oculocardiac reflex consists of a trigeminal (V1) afferent and a vagal efferent pathway and is most commonly encountered in children undergoing strabismus surgery, though it can be evoked in all age groups and during a variety of ocular procedures. In awake patients, the oculocardiac reflex may be accompanied by nausea.
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Routine prophylaxis for the oculocardiac reflex is controversial, especially in adults. Anticholinergic medication may prevent the oculocardiac reflex. Intravenous atropine or glycopyrrolate given immediately before traction on extraocular muscles is more effective than intramuscular premedication administered preoperatively. However, anticholinergic medication should be administered with caution to any patient who has or may have coronary artery disease because of the potential for an increase in heart rate sufficient to induce myocardial ischemia. Retrobulbar blockade or deep inhalational anesthesia may also preempt the oculocardiac reflex, though administration of a retrobulbar block may itself initiate the oculocardiac reflex.
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Management of the oculocardiac reflex includes (1) immediate notification of the surgeon and cessation of surgical stimulation until heart rate recovers; (2) confirmation of adequate ventilation, oxygenation, and depth of anesthesia; (3) administration of intravenous atropine (10 μg/kg) if bradycardia persists; and (4) in ...