Intraocular Pressure

Management of anesthesia for ophthalmic surgery requires control of IOP before, during, and after the procedure. Because control of IOP is often important to success of the procedure, the anesthesiologist must understand the physiologic effects of IOP and the implications of anesthetic drugs and maneuvers on IOP. Cunningham and Barry,^[47] Murphy,^[48] and Patil and Dowd^[21] have thoroughly reviewed the physiologic determinants of IOP and its relationship to management of anesthesia.

Physiologic Determinants of Intraocular Pressure

Normal IOP is approximately 12 to 20 mm Hg, with a diurnal variation of 2 to 3 mm Hg and positional changes of 1 to 6 mm Hg. The most important influences on IOP are aqueous humor dynamics, changes in choroidal blood volume (CBV), central venous pressure, and extraocular muscle tone. Events such as coughing, straining, the Valsalva maneuver, or vomiting can cause transient, but significant increases in IOP.

Aqueous humor dynamics, the main physiologic determinant of IOP, is a balance between the production of aqueous humor and its eventual elimination through Fontana's spaces and Schlemm's canal at the iridocorneal angle into the episcleral venous system. The volume of

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Changes in CBV also affect IOP significantly. The choroid is a vascular meshwork of arterial anastomoses located in the posterior chamber. Choroidal blood flow is usually autoregulated over a range of perfusion pressures to keep IOP stable. Sudden increases in systolic arterial blood pressure cause a transient swelling of CBV; subsequent temporary outflow adjusts IOP toward normal. Hypotension (systolic arterial blood pressure below 90 mm Hg) may reduce IOP as CBV decreases. Sudden increases in CBV can force vitreous gel forward into the anterior chamber during open eye surgery or can increase IOP in the intact eye. Coughing, bucking, emesis, and the Valsalva maneuver will increase central venous pressure, thereby increasing both CBV and IOP. IOP will also tend to increase in response to respiratory acidosis and hypercapnia. The choroidal circulation may dilate in response to hypoxia and cause mild increases in IOP.

When the eye is open during surgery, IOP may be somewhat lower than normal. Transluminal pressure on the choroidal vessels is greater, and a sudden increase in choroidal pressure caused by hypertension, increased venous pressure, or hypercapnia is likely to result in spontaneous bleeding of the choroidal vessels.

The CNS exerts some degree of control over IOP. Experiments on the cat diencephalon have indicated areas that affect IOP. Some responses seem to be mediated neurovascularly, whereas others relate to increased extraocular muscle tone. These centers are usually depressed by sedatives, barbiturates, and volatile inhaled anesthetics.

Murphy^[48] and Macri^[50] reviewed factors affecting intraocular blood volume and concluded that because of autoregulation, arterial blood pressure exerts only a minimal effect on IOP within a normal physiologic range of blood pressure. A more definite, direct relationship exists between central venous pressure and IOP. A slight head-up tilt during intraocular surgery helps counteract the effects of central venous pressure.

Intraocular vascular tone is predominantly affected by carbon dioxide and control areas in the diencephalon. A linear relationship exists between IOP and increasing carbon dioxide partial pressure. Hypocapnia decreases IOP through vasoconstriction of the choroidal blood vessels and decreases the formation of aqueous humor through reduced carbonic anhydrase activity. The increased IOP associated with hypoventilation and hypercapnia occurs as a result of vasodilation of CBV and increases in central venous pressure.

Sudden external pressure on the eyeball will initially increase IOP and may induce an oculocardiac vagal reflex. The increased IOP promotes outflow of aqueous humor, thus returning IOP toward normal. The effects of direct external compression of the eyeball on vitreous gel and CBV have not been documented.

Injecting a large volume (8 to 10 mL) of fluid into the orbit (e.g., a peribulbar block) may significantly increase IOP.^[24] If IOP reaches the level of retina arterial pressure, retinal ischemia can result.

Anesthesia and Intraocular Pressure

In general, narcotics, tranquilizers, and anesthetics reduce IOP. They relax extraocular muscle tone, depress the CNS (i.e., the diencephalon), improve the outflow of aqueous humor, reduce aqueous production, and lower venous and arterial blood pressure. Only succinylcholine and ketamine may increase IOP. IOP will also increase in response to the stimulus of laryngoscopy and endotracheal intubation. ^[51] Insertion of a laryngeal mask airway after propofol induction has been shown to have minimal effect on IOP.^[52]

Antisialagogues such as atropine, scopolamine, and glycopyrrolate, given intramuscularly for premedication, have no significant effect on IOP. However, anticholinergic drugs applied topically to the eye may cause mydriasis and increase IOP. The use of neostigmine and atropine in combination to reverse the effects of nondepolarizing muscle relaxants does not seem to increase IOP. Major tranquilizers, including intravenous doses of midazolam (0.03 mg/kg), lower IOP. Even in patients with glaucoma, narcotic premedication causes no change or only a slight decrease in IOP.

CNS depressants generally lower IOP. Sleep doses of barbiturates such as thiopental significantly decrease IOP by their central depressive effect on the diencephalic control of IOP and by improving the outflow of aqueous humor. Two other anesthetic induction drugs, Althesin (the combination of alfadolone and alfaxalone) and etomidate, also lower IOP. The effect of propofol on IOP during induction of general anesthesia is similar to that of thiopental.^[53] During controlled ventilation and normocapnia, volatile inhaled anesthetics reduce IOP in proportion to the depth of anesthesia. Reductions of 14% to 50% have been noted. Neuroleptanalgesia produced by mixtures of fentanyl and droperidol decrease IOP 12% in normocapnic patients.

The effect of ketamine on IOP varies. Early studies reported an increase in IOP after the intramuscular or intravenous administration of ketamine. Ketamine given after premedication with diazepam and meperidine does not affect IOP, and intramuscularly administered ketamine may even lower IOP in children.^[47]

The nondepolarizing muscle relaxants lower IOP. By contrast, succinylcholine causes a transient (4- to 6-minute), but significant increase in IOP of 10 to 20 mm Hg. Although the mechanism is unclear, the increase is not attributable simply to induced muscle fasciculations. Studies of the effects of succinylcholine on IOP have been reviewed concisely and thoroughly by Cunningham and Barry.^[47]

The increase in IOP after the administration of succinylcholine may depend on the timing and dose, on the

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None of the many attempts at preventing an increase in IOP after succinylcholine has been consistently successful. On the other hand, there are no clinical case reports of further eye damage, loss of vitreous, or other complications in open eye surgery associated with succinylcholine administered by these methods. ^[54]

The effectiveness of giving a small pretreatment dose of d-tubocurarine, a benzodiazepine, a β-adrenergic receptor blocking drug, acetazolamide, or even succinylcholine to attenuate the increase in IOP after succinylcholine administration has produced contradictory results. These studies have used different timing schedules, doses, anesthetics, and measurement techniques. Preventing fasciculations with a pretreatment of d-tubocurarine (0.05 mg/kg IV) does not necessarily prevent the increase in IOP after succinylcholine (also see Chapter 13 ).

Laryngoscopy and endotracheal intubation are the anesthesia-related practices most likely to increase IOP significantly (i.e., at least 10 to 20 mm Hg). ^{[2] [46] [47]} The mechanism is not clear but is probably related to sympathetic cardiovascular responses to tracheal intubation.

Several pretreatment regimens have been advocated to control the sympathetic response to tracheal intubation; some have been successful in attenuating the IOP response to tracheal intubation.^{[2] [11] [48]} Such pretreatments include the intravenous administration of lidocaine (1.5 mg/kg), sufentanil^[55] (0.05 to 0.15 µg/kg), or remifentanil (0.5 to 1.0 µg/kg) 3 to 5 minutes before induction. Oral administration of the centrally acting antihypertensive drug clonidine (5 µg/kg) 2 hours before induction of anesthesia will blunt the IOP response to intubation.^[56] Intranasal administration of nitroglycerin^[57] or a β-adrenergic receptor blocking drug has also been suggested in this regard.

If the clinical situation permits, control of IOP during induction of general anesthesia is best accomplished after narcotic (e.g., remifentanil) pretreatment, a full dose of induction anesthetic (e.g., propofol), and smooth placement of a laryngeal mask airway. If necessary, a rapid-onset, short-acting, nondepolarizing muscle relaxant may be administered.