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INTRAOCULAR PRESSURE DYNAMICS
The eye can be considered a hollow sphere with a rigid wall. If the contents of the sphere increase, the intraocular pressure (normal: 12–20 mm Hg) must rise. For example, glaucoma is caused by an obstruction to aqueous humor outflow. Similarly, intraocular pressure will rise if the volume of blood within the globe is increased. A rise in venous pres-sure will increase intraocular pressure by decreasing aqueous drainage and increasing choroidal blood volume. Extreme changes in arterial blood pressure and ventilation can also affect intraocular pressure (Table 36–1). Any event that alters these parameters (eg, laryngoscopy, intubation, airway obstruction, coughing, Trendelenburg position) can affect intra-ocular pressure.
Alternatively, decreasing the size of the globe without a proportional change in the volume of its contents will increase intraocular pressure. Pressure on the eye from a tightly fitted mask, improper prone positioning, or retrobulbar hemorrhage can lead to a marked increase in intraocular pressure.
Intraocular pressure helps to maintain the shape, and therefore the optical properties, of the eye. Temporary variations in pressure are usually well tolerated in normal eyes. For example, blinking raises intraocular pressure by 5 mm Hg, and squint-ing (forced contraction of the orbicularis oculi muscles) may increase intraocular pressure greater than 50 mm Hg. However, even transient episodes of increased intraocular pressure in patients with underlying low ophthalmic artery pressure (eg,
deliberate hypotension, arteriosclerotic involvement of the retinal artery) may jeopardize retinal perfu-sion and cause retinal ischemia.
When the globe is open by surgical incision (Table 36–2) or traumatic perforation, intraocularpressure approaches atmospheric pressure. Any factor that increases intraocular pressure in the
setting of an open globe may cause drainage of aque-ous or extrusion of vitreous through the wound. The
latter is a serious complication that can permanently worsen vision.
Most anesthetic drugs either lower intraocular pres-sure or have no ef fect (Table 36–3). Inhalational anesthetics decrease intraocular pressure in propor-tion to the depth of anesthesia. The decrease has multiple causes: a drop in blood pressure reduces choroidal volume, relaxation of the extraocular mus-cles lowers wall tension, and pupillary constriction facilitates aqueous outflow. Intravenous anesthetics also decrease intraocular pressure, with the excep-tion of ketamine, which usually raises arterial blood pressure and does not relax extraocular muscles.
Topically administered anticholinergic drugs result in pupillary dilation (mydriasis), which may precipitate or worsen angle-closure glaucoma. Systemically administered atropine or glycopyrrolate for premedication are not associated with intraocu-lar hypertension, even in patients with glaucoma.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. Unlike other skeletal muscle, extraocular muscles contain myo-cytes with multiple neuromuscular junctions, and repeated depolarization of these cells by succinyl-choline causes the prolonged contracture. The result-ing increase in intraocular pressure may have several effects. It will cause spurious measurements of intra-ocular pressure during examinations under anes-thesia in glaucoma patients, potentially leading to unnecessary surgery. Lastly, prolonged contracture of the extraocular muscles may result in an abnor-mal forced duction test, a maneuver utilized in stra-bismus surgery to evaluate the cause of extraocular muscle imbalance and determine the type of surgical correction. Nondepolarizing neuromuscular block-ers (NMBs) do not increase intraocular pressure.
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