Eye Emergencies

Published on 10/02/2015 by admin

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Last modified 10/02/2015

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26 Eye Emergencies

Eye Trauma? Red Eye?

Physiology

Light passes through the cornea and then through an opening in the iris, the pupil. The iris is responsible for controlling the amount of light that enters the eye by dilating and constricting the pupil. This light then reaches the lens, which refracts the light rays onto the retina. The anterior chamber is located between the lens and the cornea and contains aqueous humor, which is produced by the ciliary body. This fluid maintains pressure and provides nutrients to the lens and cornea. It is reabsorbed from the anterior chamber into the venous system through the canal of Schlemm. The vitreous chamber, located between the retina and the lens, contains a gelatinous fluid called vitreous humor. Light rays pass through the vitreous humor before reaching the retina. The retina lines the back of the eye and contains photoreceptor cells called rods and cones. Rods help vision in dim light, whereas cones aid light and color vision. The cones are located in the center of the retina in an area called the macula. The fovea is a small depression in the center of the macula that contains the highest concentration of cones. The optic nerve is located behind the retina and is responsible for transmitting signals from the photoreceptor cells to the brain (Fig. 26.1).

The extraocular muscles (Fig. 26.2) help in stabilization of the eye. Six extraocular muscles assist in horizontal, vertical, and rotational movement. These muscles are controlled by impulses from cranial nerves III, IV, and VI, which tell the muscles to relax or contract.

image

Fig. 26.2 Extraocular muscles.

(Courtesy Ted Montgomery, OD. Available at www.tedmontgomery.com/the_eye/.)

Glaucoma

Epidemiology

More than 3 million Americans suffer from glaucoma, the leading cause of preventable blindness in the United States.3 The term glaucoma refers to a group of disorders that damage the optic nerve and thereby lead to loss of vision. The two main classifications of glaucoma are open angle and angle closure. Acute angle-closure glaucoma is more common in white persons and women. Its peak incidence occurs between the ages of 55 and 70.4 African Americans, patients older than 65 years, and people with diabetes and ocular trauma are at increased risk for open-angle glaucoma. Differentiation between the two types of glaucoma lies in the mechanism of obstruction of outflow, as described later. Intraocular pressure (IOP) is determined by the rate of aqueous humor production relative to its outflow and removal. Normal IOP is between 10 and 20 mm Hg. This discussion focuses mainly on acute angle-closure glaucoma.

When the angle of the anterior chamber is reduced, outflow of aqueous humor is blocked, which results in elevated IOP and ultimately visual compromise. Patients with a shallow anterior chamber, hyperopic (farsighted) eyes, and eyes with lens abnormalities such as cataracts are more prone to acute angle-closure glaucoma. Pupillary dilation, caused by events such as presence in a dark room, is the most significant event that can cause an acute attack of glaucoma because the flaccid iris can be pushed against the trabecular meshwork and result in obstruction.

Treatment

Acute angle-closure glaucoma is an ophthalmologic emergency. Because outcome depends on the duration of elevated IOP, treatment should be initiated promptly. Therapy is geared toward decreasing aqueous production, increasing aqueous outflow, and reducing vitreous volume to lower IOP.

Initial treatment includes a topical, nonselective beta-blocker such as 0.5% timolol to reduce aqueous production. Topical beta-blockers are absorbed and can cause systemic effects. Intravenous administration of a carbonic anhydrase inhibitor such as acetazolamide, 500 mg, will also rapidly reduce aqueous humor production. Intravenous mannitol will create an osmotic gradient between the vitreous and blood and thereby cause a reduction in vitreous volume, so it may be useful for severe cases. Tonometry can be performed frequently, even every 15 minutes, to assess progress.

Topical 2% pilocarpine is used to help reopen the angle. Miotics such as the direct-acting parasympathomimetic agent pilocarpine might be less effective at very high IOP because the iris is relatively ischemic and therefore less responsive. Sometimes pilocarpine is used after IOP has been reduced to less than 40 mm Hg. Pilocarpine will therefore be more effective as the initially high pressures are reduced with the initial beta-blocker drops and acetazolamide. Topical 1% prednisolone acetate may sometimes be added to reduce inflammation. For ongoing treatment, topical 2% pilocarpine and prednisolone acetate may be administered every 6 hours and oral acetazolamide two times per day. Sedatives and antiemetics may be administered as needed. When the inflammation has been reduced sufficiently, the patient will be taken for iridotomy by the ophthalmologist.

Central Retinal Artery Occlusion

Epidemiology

Retinal artery occlusion affects less than 1 per 100,000 persons annually.5,6 It is most commonly caused by an embolus from the carotid artery that lodges in a distal branch of the ophthalmic artery. Central retinal artery occlusion most commonly affects elderly patients and men. Although most emboli are formed from cholesterol, they may also be calcific, fat, or bacterial from cardiac valve vegetations.

Treatment

Treatment must be initiated immediately because the visual loss is generally irreversible after 2 hours of ischemia. Regardless, the outcome is generally poor. Several approaches may be used. Intermittent globe massage can be performed in an effort to dislodge the clot and propel it distally: moderate pressure is applied for 5 second and then released for 5 seconds, and the cycle is repeated. The use of anterior chamber paracentesis for visual loss is based on the principle that decreased IOP allows better perfusion of the retinal artery and may propel the clot distally. Acetazolamide can be administered intravenously for the same purpose. Inhaled carbogen (mixture of 95% oxygen and 5% carbon dioxide) can be used to dilate the vasculature and thereby increase retinal PO2.

Other treatment options are intraarterial thrombolysis and hyperbaric oxygen; however, studies have shown limited improvement in visual outcome with early administration of both these treatment modalities.710 One retrospective study found that even with thrombolysis, vision did not improve to better than 20/300 in the affected eye.7 Another study investigated the outcomes of 32 patients with central retinal artery occlusion, 17 of whom underwent fibrinolysis.6 This study found that all but six of the treated patients reported improvement in their visual compromise but that only five of the untreated patients had any improvement. In this study, patients with a duration of symptoms of up to 24 hours were treated.

Patients with sudden visual loss are admitted to the hospital so that the underlying cause can be sought.

Central Retinal Vein Occlusion

Treatment

No effective therapeutic regimen exists for central retinal vein occlusion. The emergency physician (EP) should arrange for immediate ophthalmologic consultation. A search for a cause should be performed to protect the contralateral eye from the same problem. The prognosis largely depends on the type of retinal venous occlusion. Nonischemic vein occlusion, unless the macular involvement is extensive, offers a better outcome than the ischemic type does. Spontaneous resolution may occur in some cases.

Although no specific treatment is available, a number of interventions have been proposed and practiced.11,12 However, these interventions have not been based on evidence of efficacy. Laser photocoagulation, for example, cauterizes leaking vessels with the aim of halting further visual loss. This procedure can be especially helpful for branch retinal vein occlusion. With nonischemic vein occlusion, attempts to reduce macular edema can be helpful. The reduction is accomplished with the administration of topical corticosteroids. Studies have been conducted to determine the benefit of steroids in treating both forms of retinal vein occlusion. Jonas et al.11 conducted a prospective, comparative, nonrandomized clinical interventional study to evaluate the visual outcomes in 32 patients with central retinal vein occlusion after intravitreal administration of triamcinolone acetate. The study included patients with both the ischemic and nonischemic forms of retinal vein occlusion. These researchers found that the medication resulted in temporary (up to 3 months) improvement in visual outcome but also raised IOP. Anticoagulants are not recommended because they may propagate hemorrhage.

Optic Neuritis

Treatment and Disposition

Ophthalmologic and neurologic consultation should be obtained if optic neuritis is suspected. Approximately 31% of patients with optic neuritis have a recurrence within 10 years of the initial episode.13 The goals of treatment are to restore visual acuity and prevent propagation of the underlying disease process. The Optic Neuritis Treatment Trial was a randomized, 15-center clinical trial involving 457 patients that was performed to evaluate both the benefit of corticosteroid treatment of optic neuritis and the relationship of this entity to multiple sclerosis. Use of intravenous steroids in conjunction with oral steroids reduced the short-term risk for the development of multiple sclerosis as determined by MRI evaluation. No long-term immunity from or benefit for multiple sclerosis was reported, however. The study concluded that although intravenous steroids have only minimal, if any effect on the patient’s ultimate visual acuity, they do expedite recovery from optic neuritis. Use of oral steroids alone is associated with a higher recurrence rate of optic neuritis. The dosage regimen recommended on the basis of the study results was methylprednisolone, 250 mg intravenously every 6 hours for 3 days, followed by prednisone, 1 mg/kg/day orally for 11 days.14

Retinal Detachment

Retinal detachment is a true ophthalmologic emergency. Unfortunately, it is also relatively common and affects 1 in 300 people. Before the introduction of and improvement in a number of treatment modalities, this entity was uniformly blinding. Early diagnosis and treatment are imperative for preservation of vision. Retinal detachment may be associated with vascular disorders, congenital malformations, metabolic disarray, trauma, shrinking of the vitreous, myopia, degeneration, and less commonly, diabetic retinopathy and uveitis. It is generally more common in older patients. Three different types of retinal detachment are recognized, each associated with different conditions.

Treatment

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