Ординатура / Офтальмология / Английские материалы / Ophthalmology A Short Textbook_Lang_2000

10.2 Examination Methods 243

Measuring the twenty-four-hour pressure curve (Fig. 10.6): This examination is performed to analyze fluctuations of the pressure level over a 24-hour period in patients with suspected glaucoma.

A single measurement may not be representative. Only a 24-hour curve provides reliable information about the pressure level.

Intraocular pressure fluctuates in a rhythmic pattern. The highest values frequently occur at night or in the early morning hours. In normal patients, these fluctuations in intraocular pressure rarely exceed 4–6 mm Hg.

Pressure is measured on the ward at 6:00 a.m., noon, 6:00 p.m., 9:00 p.m., and midnight. Outpatient 24-hour pressure curves without nighttime and early morning measurements are less reliable.

In glaucoma patients maintained on eyedrops, special attention should be given to the time of application. Pressure is measured immediately prior to applying the eyedrops. In this manner, measurements are obtained when the effect of the eyedrops is weakest.

Tonometric self-examination: Recent developments have made it possible for patients to measure intraocular pressure themselves at home in a manner similar to self-monitoring of blood pressure and blood glucose (Fig. 10.7). The patient tonometer makes it possible to obtain a 24-hour pressure curve from

Twenty-four-hour pressure curve.

Fig. 10.6 The colored dots represent the times of the measurements. The time of the initial application of anti-glaucoma eyedrops is marked (arrow). The time, frequency, and eye of eyedrop application are also identified.

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Tonometric self-examination.

Fig. 10.7 The patient places the tonometer on his or her forehead and uses the fixation light to align it in the proper position. The head of the tonometer then automatically presses against the cornea, measures intraocular pressure, and retracts. Pressure is indicated in a digital display.

any number of measurements obtained under normal everyday conditions. A patient tonometer may be prescribed in applicable cases (such as increased risk of acute glaucoma). However, using the device requires a certain degree of skill on the part of the patient. Patients who have problems applying eyedrops are best advised not to attempt to use a patient tonometer. Younger and well motivated patients are the best candidates for tonometric self-examina- tion.

10.2.5Optic Disk Ophthalmoscopy

The optic disk has a physiologic indentation known as the optic cup. In the presence of persistently elevated intraocular pressure, the optic cup becomes enlarged and can be evaluated by ophthalmoscopy.

Stereoscopic examination of the optic disk through a slit-lamp biomicroscope fitted with a contact lens provides a three-dimensional image. The optic cup may be examined stereoscopically with the pupil dilated.

The optic nerve is the eye’s “glaucoma memory.” Evaluating this structure will tell the examiner whether damage from glaucoma is present and how far advanced it is.

10.2 Examination Methods 245

Normal optic cup (Fig. 10.8): The normal anatomy can vary widely. Large normal optic cups are nearly always round and differ from the vertical elongation of the optic cup seen in eyes with glaucoma.

Documenting the optic disk: Recording findings in sketches is suitable for routine documentation and follow-up examination of the optic disk. Photographing the optic disk with a fundus camera permits longer-term followup. Stereoscopic photography also provides a three-dimensional image. Optic disk measurement and tomography can provide precise measurements of the optic nerve.

Optic disk measurement. The area of the optic disk, optic cup, and neuroretinal rim (vital optic disk tissue) can be measured by planimetry on two-dimen- sional photographs of the optic nerve.

Normal optic disk.

Fig. 10.8 The optic disk is sharply demarcated. It is level with the retina, and its color indicates vital tissue. The small central optic cup (arrow) is discernible as brighter area.

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Optic disk tomography. Modern laser scanning ophthalmoscopes permit three-dimensional documentation of the optic nerve (Fig. 10.9).

Glaucomatous changes in the optic nerve: Glaucoma produces typical changes in the shape of the optic cup. Progressive destruction of nerve fibers, fibrous and vascular tissue, and glial tissue will be observable. This tissue atrophy leads to an increase in the size of the optic cup and to pale discoloration of the optic disk (Fig. 10.10).

Progressive glaucomatous changes in the optic disk are closely associated with increasing visual field defects (Figs. 10.11a – d).

10.2.6Visual Field Testing

Detecting glaucoma as early as possible requires documenting glaucomatous visual field defects at the earliest possible stage. We know that glaucomatous visual field defects initially manifest themselves in the superior paracentral nasal visual field or, less frequently, in the inferior field, as relative scotomas that later progress to absolute scotomas (Fig. 10.11a – d).

Optic disk tomography.

Fig. 10.9 A laser beam scans the optic disk (a1 and a2) to produce a vertical map (b) and horizontal map (c) of the height and depth of the optic disk. The computer then calculates crucial data for the optic disk and presents a stereometric analysis (d).

10.2 Examination Methods 247

Glaucomatous lesions in the optic nerve.

Fig. 10.10 The optic disk is sharply demarcated and pale (a sign of tissue atrophy). The optic cup is enlarged and almost completely covers the disk. The blood vessels abruptly plunge into the deep cup, indicated by their typical bayonetshaped kinks in the image (arrow).

Computerized static perimetry (measurement of the sensitivity to differences in light) is superior to any kinetic method in detecting these early glaucomatous visual field defects. Computer-controlled semiautomatic grid perimetry devices such as the Octopus or Humphrey field analyzer are used to examine the central 30 degree field of vision (modern campimetry; Fig. 10.12).

Reproducible visual field findings are important in follow-up to exclude any enlargement of the defects.

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Overview of glaucomatous visual field defects.

Peripheral optic cup in a temporal and inferior location (with damage to the optic nerve fibers in this area).

Increase in the size of the optic cup with thinning of the vital rim. The lamina cribrosa is visible.

Advanced generalized thinning of the neuroretinal rim with an increasingly visible lamina cribrosa and nasal displacement of the blood vessels.

Total glaucomatous atrophy of the optic nerve: Complete atrophy of the neuroretinal rim, kettleshaped optic cup, bayonet kinks in the blood vessels on the margin of the optic disk, some of which disappear. The lamina cribrosa is diffusely visible. Only remnants of the atrophic tissue of the optic disk remain. The optic disk is surrounded by a ring of chorioretinal atrophy (glaucomatous halo) due to pressure atrophy of the choroid and lysis of the retinal pigmented epithelium.

Fig. 10.11

10.2 Examination Methods 249

An enlarged blind spot and a superior paracentral nasal scotoma. The paracentral scotomas precede the enlargement of the blind spot.

Narrowing of the peripheral superior paracentral visual field. The insular paracentral scotomas converge and extend to the blind spot.

Further loss of superior nasal visual field. Circumscribed horizontal penetration of the Bjerrum's scotoma into the nasal half of the field of vision. A new inferior nasal scotoma is a sign of a superior temporal nerve fiber lesion.

A small central and peripheral residual field of vision remains. The arc-shaped scotoma has expanded into a ring-shaped scotoma surrounding the focal point. As the focal point degenerates, the center of vision disappears and only a peripheral residual field of vision remains.

250 10 Glaucoma

Thirty degree visual field test for glaucoma screening.

Fig. 10.12 The central field of vision is examined for scotomas with an automatic perimeter as studies of early glaucoma have shown that the initial defects occur in this area (see Fig. 10.11a – d). The figure shows the visual field defect in the early stages of glaucoma. The blind spot is slightly enlarged (arrow), and an arc-shaped paracentral Bjerrum’s scotoma is present (arrowhead). The standardized examination conditions in automatic perimetry not only permit early detection of glaucoma; the reproducible results also aid in the prompt diagnosis of worsening findings.

10.2.7Examination of the Retinal Nerve Fiber Layer

The retinal nerve fibers have a characteristic arrangement, which explains the typical visual field defects that occur in primary open angle glaucoma. In addition to the early progressive optic nerve and visual field defects, arcshaped defects also occur in the nerve fiber layer. These defects may be observed in light with red components (Fig. 10.13).

10.3 Primary Glaucoma 251

Examination of the retinal nerve fiber layer.

Fig. 10.13 The arcshaped nerve fiber defect (between the arrows) is a sign of an early glaucomatous optic nerve lesion.

10.3Primary Glaucoma

10.3.1Primary Open Angle Glaucoma

Definition

Primary open angle glaucoma begins in middle-aged and elderly patients with minimal symptoms that progressively worsen. The angle of the anterior chamber characteristically remains open throughout the clinical course of the disorder.

Epidemiology: Primary open angle glaucoma is by far the most common form of glaucoma and accounts for over 90% of adult glaucomas. The incidence of the disorder significantly increases beyond the age of 40, reaching a peak between the ages of 60 and 70. Its prevalence among 40-year-olds is 0.9% as compared to 4.7% among patients over the age of 50.

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There appears to be a genetic predisposition for primary open angle glaucoma. Over onethird of glaucoma patients have relatives with the same disorder.

Patients with a positive family history are at greater risk of developing the disorder.

Etiology (See also physiology and pathophysiology of aqueous humor circulation): The cause of primary open angle glaucoma is not known, although it is known that drainage of the aqueous humor is impeded. The primary lesion occurs in the neuroretinal tissue of the optic nerve as compression neuropathy of the optic nerve.

Symptoms: The majority of patients with primary open angle glaucoma do not experience any subjective symptoms for years. However, a small number of patients experience occasional unspecific symptoms such as headache, a burning sensation in the eyes, or blurred or decreased vision that the patient may attribute to lack of eyeglasses or insufficient correction. The patient may also perceive rings of color around light sources at night, which has traditionally been regarded as a symptom of angle closure glaucoma.

Primary open angle glaucoma often does not exhibit typical symptoms for years. Regular examination by an ophthalmologist is crucial for early diagnosis.

Primary open angle glaucoma can be far advanced before the patient notices an extensive visual field defect in one or both eyes.

It is crucial to diagnose the disorder as early as possible because the prognosis for glaucoma detected in its early stages is far better than for advanced glaucoma. Where increased intraocular pressure remains undiagnosed or untreated for years, glaucomatous optic nerve damage and the associated visual field defect will increase to the point of blindness.

Diagnostic considerations: Measurement of intraocular pressure. Elevated intraocular pressure in a routine ophthalmic examination is an alarming sign.

Twenty-four-hour pressure curve. Fluctuations in intraocular pressure of over 5–6 mm Hg may occur over a 24-hour period.

Gonioscopy. The angle of the anterior chamber is open and appears as normal as the angle in patients without glaucoma.

Ophthalmoscopy. Examination of the optic nerve reveals whether glaucomatous cupping has already occurred and how far advanced the glaucoma is. Where the optic disk and visual field are normal, ophthalmoscopic examination of the posterior pole under green light may reveal fascicular nerve fiber defects as early abnormal findings.