Ординатура / Офтальмология / Английские материалы / Primary Care Ophthalmology_Palay, Krachmer_2005

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FIGURE 11–2 A, Normal cup-to-disc (C/D) ratio of 0.1. B, Likely normal C/D ratio of 0.5. C, C/D ratio of 0.8 vertically with inferior notching (1) of the nerve (glaucomatous change). D, C/D ratio of 0.90 vertically (glaucomatous change). C, cup; D, disc.

•Glaucoma is more prevalent, develops at an earlier age, and is more severe in African Americans than in white persons.

•A family history of open-angle glaucoma is associated with a fivefold to sixfold increase in the risk of glaucoma development.

•The prevalence of ocular hypertension in patients with diabetes mellitus is two to three times higher than in the general population. The possibility of an increased risk of ocular hypertension in patients with systemic hypertension has not been determined definitively.

•Note: Corneal thickness in patients with ocular hypertension plays an important role in the risk of developing glaucoma. Patients with thinner-than-average corneas are at higher risk, whereas those with thicker-than-average corneas are at lower risk.

Workup

•Measurement of IOP (see Chapter 1): The “gold standard” is Goldmann applanation tonometry. IOP is determined by measurement of the force required to flatten the central cornea. Fluorescein dye and a topical anesthetic are required, as is skill

192 CHAPTER 11 • Glaucoma

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in interpretation of the fluorescent semicircles to determine the IOP directly, using a scale associated with this device.

•A relatively new device, the Tono-Pen, can be used more easily to measure IOP. Multiple applanation measurements are averaged by this instrument, which displays the IOP as a digital readout. Greater cost is one drawback to the Tono-Pen.

•Pupillary examination: A relative afferent pupillary defect may be present in asymmetrical cases of glaucoma.

•Ophthalmoscopy: Evaluation with a direct ophthalmoscope provides important diagnostic clues. Because the IOP may be in the normal range in a patient with glaucoma, the clinician who measures IOP and also examines the optic nerve is more likely to diagnose glaucoma correctly. A cup-to-disc ratio (see Fig. 11–2C and D) of 0.6 or greater is one sign of glaucoma. Asymmetry of 0.2 or greater in the cup- to-disc ratio and focal asymmetry in the neuroretinal rim also are highly suggestive.

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FIGURE 11–4 A, Pupillary block prevents flow of aqueous into the anterior chamber. The iris is pressed firmly against the lens (1), blocking aqueous flow (2) into the anterior chamber (3). The iris is pushed against the trabecular meshwork

(4). The peripheral anterior chamber angle is thus closed (5), blocking aqueous outflow and raising the intraocular pressure. B, A small hole in the peripheral iris (1) is made with a laser (laser iridectomy), allowing aqueous to enter the anterior chamber of the eye. This opens the anterior chamber angle (2), so that aqueous can drain normally through the trabecular meshwork (3).

Dilation of the pupil with tropicamide 1% and phenylephrine 2.5% ophthalmic solutions greatly facilitates optic nerve evaluation.

•Eyes with a narrow chamber angle should not be dilated. (A simple penlight test for this condition is shown in Figure 11–5.)

Treatment

•Any patient with abnormal findings on optic nerve examination, an afferent pupillary deficit, or an elevated IOP measurement should be referred to an ophthalmologist for evaluation and possible treatment.

194 CHAPTER 11 • Glaucoma

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FIGURE 11–5 Use of the penlight to demonstrate a shallow anterior chamber. A, A penlight aimed obliquely to the eye will illuminate nearly the entire iris with a deep anterior chamber. B, With a shallow anterior chamber, only a portion of the iris is illuminated, with shadowing over the remainder.

•Treatment usually begins with medication:

Medications work by one of two methods to lower IOP: decreasing the production of aqueous or increasing the outflow of aqueous. Medications that decrease aqueous production include topical beta blockers (levobunolol [Betagan], betaxolol [Betoptic], carteolol [Ocupress], metipranolol [OptiPranolol], and timolol [Betimol, Timoptic]), oral carbonic anhydrase inhibitors (acetazolamide [Diamox] and methazolamide [Neptazane]), topical carbonic anhydrase inhibitors (dorzolamide [Trusopt] and brinzolamide [Azopt]), and alpha-2 agonists (apraclonidine [lopidine] and brimonidine tartrate [Alphagan P]). Medications that improve aqueous outflow include prostaglandin analogs (latanoprost [Xalatan], travoprost [Travatan], bimatoprost [Lumigan], and unoprostone isopropyl [Rescula]), topical miotic agents (pilocarpine [Pilocar] and echothiophate [Phospholine Iodide]), and epinephrine preparations (Epifrin and Propine).

Eyedrops gain access to the systemic circulation by way of the nasal mucosa of the nasolacrimal system, and systemic side effects can be noted with these medications (see Chapter 17).

•Surgical options include the following:

Open-angle glaucoma not responsive to medical therapy can be treated with laser and incisional surgery.

Laser trabeculoplasty involves placement of multiple, low-energy burns to the trabecular meshwork, decreasing the IOP significantly in approximately 80% of cases.

FIGURE 11–6 The whitish, elevated area on the superior portion of the eye is a filtering bleb in a patient with openangle glaucoma.

Trabeculectomy bypasses the normal outflow pathway by the creation of a surgical fistula. An elevation of the conjunctiva known as a filtering bleb is a sign of a successful trabeculectomy (Fig. 11–6).

Conjunctivitis associated with a filtering bleb should prompt immediate referral to an ophthalmologist because of the risk of infection spreading inside the eye (endophthalmitis).

Acute Angle-Closure Glaucoma

Symptoms

•Vision is blurred, usually in one eye.

•Halos are seen around lighting fixtures (this symptom is almost always monocular).

•Intense ocular pain and photophobia are important symptoms.

•Vasovagal symptoms such as diaphoresis, nausea, and vomiting are possible.

Signs

•A mid-dilated pupil is seen (Fig. 11–7A).

•Conjunctival injection and lid edema are present.

•Corneal edema with blurring of the light reflex develops.

Associated Factors and Diseases

•Women are affected three to four times more commonly than men.

•The peak age range for occurrence of angle-closure glaucoma is between the ages of 55 and 70 years.

•The disorder occurs in shorter, smaller, far-sighted eyes with narrow chamber angles (see Fig. 11–7B).

196 CHAPTER 11 • Glaucoma

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FIGURE 11–7 Acute angle-closure glaucoma. A, Acutely elevated pressure produces an inflamed eye with corneal edema (note fragmented light reflex) and a mid-dilated pupil. B, Slit lamp examination shows a very shallow central anterior chamber (space between cornea and iris) (1) and no peripheral chamber (2).

•Stress, a darkened room, and drugs that can dilate the pupil may precipitate an acute angle-closure attack. Many systemic medications with anticholinergic or sympathomimetic action carry a warning against use in persons with glaucoma. This caveat applies to patients with a narrow chamber angle only, not to patients with openangle glaucoma. Because most glaucoma cases are of the open-angle type, these medications are rarely contraindicated in clinical practice. Consultation with the patient’s ophthalmologist is recommended for the primary care physician if a question arises over a possible medication contraindication.

Treatment

•Acute angle-closure glaucoma represents an ophthalmic emergency and requires immediate referral to an ophthalmologist.

•Initial medical treatment to lower the IOP involves a topical beta blocker (e.g., Timoptic 0.5%, 1 drop), a topical alpha agonist (e.g., Alphagan P, 1 drop), a carbonic anhydrase inhibitor (e.g., Diamox 500 mg intravenously or two 250-mg tablets orally), and osmotic agents (e.g., oral 50% glycerin 2 to 3 mL/kg or intravenous mannitol, 1 to 2 g/kg given over 45 minutes; 500 mL of mannitol 20% contains 100 g of mannitol).

•In most cases, laser iridectomy (creating a full-thickness opening in the peripheral iris) reopens at least a portion of the angle, with subsequent marked lowering of the IOP (see Fig. 11–4A and B).

Follow-up

•After an acute angle-closure event, a portion of the angle may remain closed because of scarring of peripheral iris tissue to the cornea, causing chronic angle-closure glaucoma. Chronic angle-closure glaucoma also may occur without any symptoms, just like open-angle glaucoma. Treatment involves medications and incisional surgery such as trabeculectomy.

•Laser trabeculoplasty is not effective. Laser iridectomy may be recommended for persons with very narrow angles who are at significant risk for the development of either acute or chronic angle-closure glaucoma.

200 CHAPTER 12 • Neuro-ophthalmology

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FIGURE 12–1 The visual system, with visual field defects resulting from lesions at various points in the visual pathway. Here, an optic nerve lesion affects the visual field of only one eye (1). Bilateral optic nerve lesions, however, are not uncommon. Lesions of the body of the chiasm tend to produce bilateral temporal visual field defects (2) (see also Fig. 12–9). Optic tract lesions (and all lesions posterior to the chiasm) produce defects that are homonymous (on the same side in both eyes) (3). Lesions at the junction of the optic nerve and the chiasm severely affect vision in the ipsilateral eye but produce an often asymptomatic temporal peripheral visual field defect in the contralateral eye (4). Complete homonymous hemianopic visual field defects are nonlocalizing; that is, they can occur anywhere from the optic tract to the occipital lobe (5 and 8). A unilateral homonymous hemianopia does not decrease visual acuity. Lesions in the temporal lobe produce superior homonymous defects (6). Parietal lesions cause inferior homonymous defects (7). Occipital lobe lesions are highly congruous (9 to 11). Be aware that bilateral occipital infarctions can profoundly affect visual acuity and visual fields bilaterally, with normal-appearing fundi and normal pupillary responses (not shown). A lesion deep in the visual cortex can produce a visual field defect in the temporal visual field of one eye only (12).

Visual Field Loss Patterns in Lesions of the Chiasm and

Posterior Visual Pathways

Axons from retinal ganglion cells that represent right visual space are routed through the chiasm to form the left optic tract, synapsing in the left lateral geniculate body (and vice versa for left visual space) (Fig. 12–1). Anatomically, this means that axons originating in the nasal half of the retina (which map the temporal visual field) cross in the chiasm to the opposite side. Therefore, mass lesions compressing the chiasm disrupt these crossing fibers, causing temporal visual field defects in both eyes. Lesions posterior to the chiasm (optic tract and posterior visual pathways) produce homonymous (on the same side in both eyes) visual field defects that respect the vertical meridian. From the chiasm posteriorly, corresponding axons from the right and left eyes that represent the same point in visual space move closer together as they converge on a common point in the occipital cortex. Thus, the more posterior a lesion is, the more congruous the resultant visual field defects become: the homonymous visual defects in each eye look more alike in shape and depth.

Optic Nerve Disorders

The optic disc is the proximal end of the optic nerve and can be observed with the ophthalmoscope. Optic nerve lesions may produce visible disc edema (swelling), infiltration, pallor, or pathologic cupping (from glaucoma). Lesions of the nerve more distant from the disc may not cause any observable optic disc abnormality acutely (such as with retrobulbar optic neuritis), but with time the normally pink neural rim turns pale.

Nonarteritic Anterior Ischemic Optic Neuropathy (NAION)

Symptoms

• A sudden, painless loss of vision occurs, frequently noted on arising in the morning.

Signs

•Patients usually are older than 40 years of age.

•The unilateral optic disc swelling often is segmental, and flame-shaped hemorrhages may be observed. Disc pallor is seen as the edema resolves over 4 to 6 weeks (Fig. 12–2A and B).

•An altitudinal (affecting upper or lower quadrants) visual field defect is common (Fig. 12–2C).

•A relative afferent pupillary defect is present if the fellow eye is unaffected.