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INTRODUCTION

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Ophthalmic surgery presents unique challenges to the anesthesia provider. Though these surgeries are commonly performed as ambulatory procedures, many of the patients who present for such surgery represent the extremes of age. Elderly patients, in particular, may present with multiple comorbidities. Ophthalmic surgery can induce the oculocardiac reflex which is discussed below. Ocular dynamics may be altered by anesthetic agents and maneuvers. Further, attention must be paid to the systemic effects associated with topical eye medications used to dilate the operative eye prior to surgery. Anesthetic technique varies from straight local, to minimum alveolar concentration (MAC) with local, to MAC with regional block, to general anesthesia.

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Intraocular Pressure

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Intraocular pressure (IOP) is the tissue pressure of intraocular contents. While there is diurnal variation, normal IOP ranges between 10 and 20 mmHg. IOP is maintained at equilibrium when there is a balance between aqueous humor production and drainage of this fluid through the episcleral veins. When venous drainage of the eye is slowed or blocked IOP rises. Prolonged elevations in IOP can lead to retinal ischemia or hemorrhage which in turn may result in permanent vision loss. External forces such as extraocular muscle contraction or hardening of the eye’s sclera and lens (which normally occurs with aging) can increase IOP. Coughing, straining, and bucking on induction all increase venous pressure and, in doing so, can increase IOP by as much as 40 mmHg. This is a major concern in the context of an open globe injury as a rapid increase in IOP may cause expulsion of the intraocular contents and lead to permanent damage. Hypoventilation (hypercarbia) and hypoxemia increase IOP, while hyperventilation (hypocarbia) and hypothermia decrease IOP.

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Most intravenous (IV) and inhaled anesthetic agents have been shown to either decrease or have no effect on IOP. Mechanisms for this reduction in IOP include central nervous system (CNS) depression, increased aqueous humor drainage, decreased aqueous humor production, and relaxation of the extraocular muscles. Ketamine is an exception as it may can cause nystagmus and blepharospasm, so would be a poor choice for ophthalmic procedures.

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Nondepolarizing muscle relaxants decrease IOP through relaxation of extraocular muscles. Succinylcholine causes a transient elevation in IOP of 5–10 mmHg for 5–10 minutes after administration. Unlike skeletal muscle, extraocular muscles have multiple neuromuscular junctions and constant depolarization from succinylcholine can cause prolonged contraction of the muscle. In the context of a penetrating eye injury, such elevation of IOP can cause extrusion of intraocular contents. Commonly, the increase in IOP caused by succinylcholine subsides after approximately 10 minutes, and IOP pressure returns to baseline. Pretreatment with a β-blocker, lidocaine, or a small dose of nondepolarizing muscle relaxant or acetazolamide may minimize these effects, but this is not often practiced clinically.

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SYSTEMIC EFFECTS OF OPHTHALMIC DRUGS

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It is important to remember that many of topical eye medications cause systemic effects as these ...

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