Ординатура / Офтальмология / Английские материалы / Ophthalmology A Short Textbook_Lang_2000
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10 Glaucoma
Gerhard K. Lang
10.1Basic Knowledge
Definition
Glaucoma is a disorder in which increased intraocular pressure damages the optic nerve. This eventually leads to blindness in the affected eye.
Primary glaucoma refers to glaucoma that is not caused by other ocular disorders.
Secondary glaucoma may occur as the result of another ocular disorder or an undesired side effect of medication or other therapy.
Epidemiology: Glaucoma is the second most frequent cause of blindness in developing countries after diabetes mellitus. Fifteen to twenty per cent of all blind persons lost their eyesight as a result of glaucoma. In Germany, approximately 10% of the population over 40 has increased intraocular pressure. Approximately 10% of patients seen by ophthalmologists suffer from glaucoma. Of the German population, 8 million persons are at risk of developing glaucoma, 800 000 have already developed the disease (i.e., they have glaucoma that has been diagnosed by an ophthalmologist), and 80 000 face the risk of going blind if the glaucoma is not diagnosed and treated in time.
Early detection of glaucoma is one of the highest priorities for the public health system.
Physiology and pathophysiology of aqueous humor circulation (Fig. 10.1): The average normal intraocular pressure of 15 mm Hg in adults is significantly higher than the average tissue pressure in almost every other organ in the body. Such a high pressure is important for the optical imaging and helps to ensure several things:
Uniformly smooth curvature of the surface of the cornea.
Constant distance between the cornea, lens, and retina.
Uniform alignment of the photoreceptors of the retina and the pigmented epithelium on Bruch’s membrane, which is normally taut and smooth.
The aqueous humor is formed by the ciliary processes and secreted into the posterior chamber of the eye (Fig. 10.1 [A]). At a rate of about 2–6 µl per
234 10 Glaucoma
Physiology of aqueous humor circulation.
Canal of Schlemm |
Cornea |
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Collecting channel |
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Episcleral venous plexus |
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Conjunctiva |
Trabecular meshwork |
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C |
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D |
Iris |
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E |
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B |
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A
Lens
Ciliary body
Fig. 10.1 As it flows from the nonpigmented cells of the ciliary epithelia A to beneath the conjunctiva D , the aqueous humor overcomes physiologic resistance from two sources: the resistance of the pupil B and the resistance of the trabecular meshwork C .
minute and a total anterior and posterior chamber volume of about 0.2–0.4 ml, about 1–2% of the aqueous humor is replaced each minute.
The aqueous humor passes through the pupil into the anterior chamber. As the iris lies flat along the anterior surface of the lens, the aqueous humor cannot overcome this pupillary resistance (first physiologic resistance; Fig. 10.1 [B]) until sufficient pressure has built up to lift the iris off the surface of the lens. Therefore, the flow of the aqueous humor from the posterior chamber into the anterior chamber is not continuous but pulsatile.
Any increase in the resistance to pupillary outflow (pupillary block) leads to an increase in the pressure in the posterior chamber; the iris inflates anteriorly on its root like a sail and presses against the trabecular meshwork (Table 10.2). This is the pathogenesis of angle closure glaucoma.
Various factors can increase the resistance to pupillary outflow (Table 10.1). The aqueous humor flows out of the angle of the anterior chamber through two channels:
The trabecular meshwork (Fig. 10.1 [C]) receives about 85% of the outflow, which then drains into the canal of Schlemm. From here it is con-
10.1 Basic Knowledge 235
Table 10.1 Factors that increase resistance to pupillary outflow and predispose to angle closure glaucoma
Increased contact between the margin of the pupil and lens with:
Increased viscosity of the aqueous humor with:
Small eyes
Large lens (increased lens volume) due to:
–Age (lens volume increases with age by a factor of six)
–Diabetes mellitus (osmotic swelling of the lens)
Miosis
–Age (atrophy of the sphincter and dilator muscles)
–Medications (miotic agents in glaucoma therapy)
–Iritis (reactive miosis)
–Diabetic iridopathy (thickening of the iris)
Posterior synechiae (adhesions between lens and iris)
Inflammation (protein, cells, or fibrin in the aqueous humor)
Bleeding (erythrocytes in the aqueous humor)
ducted by 20–30 radial collecting channels into the episcleral venous plexus (D).
A uveoscleral vascular system receives about 15% of the outflow, which joins the venous blood (E).
The trabecular meshwork (C) is the second source of physiologic resistance. The trabecular meshwork is a body of loose sponge-like avascular tissue between the scleral spur and Schwalbe’s line. Increased resistance in present in open angle glaucoma.
Classification: Glaucoma can be classified according to the specific pathophysiology (Table 10.2).
The many various types of glaucoma are nearly all attributable to increased resistance to outflow and not to heightened secretion of aqueous humor.
236 |
10 Glaucoma |
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Table 10.2 Classification of glaucoma |
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Form of |
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Incidence |
glaucoma |
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Open angle |
Primary |
Over 90% of all |
glaucoma |
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glaucomas |
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Secondary |
2 – 4% of all |
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glaucomas |
Angle closure |
Primary |
About 5% of all |
glaucoma |
(pupillary |
glaucomas |
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block |
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glaucoma) |
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Secondary |
2 – 4% of all |
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glaucomas |
Juvenile |
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1% of all |
glaucoma |
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glaucomas |
Absolute |
This is not a separate form of glaucoma, rather it describes an |
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glaucoma |
often painful eye blinded by glaucoma |
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10.1 Basic Knowledge 237
Angle |
Angle |
Outflow impediment |
(anatomic) |
(gonioscopy) |
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Open |
Completely open. Structures |
In the trabecular meshwork |
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appear normal. |
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Open |
Completely open. Trabecular |
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meshworks and secondary occlud- |
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ing cells visible. |
Erythrocytes, pigment, and inflammatory cells occlude the trabecular meshwork.
Blocked |
Occluded. No angle structures |
Iris tissue occludes the |
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visible |
trabecular meshwork. |
Blocked |
Occluded. No angle structures |
Displacement of the |
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visible. Occluding structures |
trabecular meshwork pro- |
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visible. |
duces anterior synechiae, |
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scarring, and neovasculari- |
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zation (rubeosis iridis) |
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Undifferentiated |
Open. Occluding embryonic tissue |
In the trabecular meshwork |
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and lack of differentiation visible. |
(which is not fully differen- |
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tiated and/or is occluded by |
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embryonic tissue) |
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238 10 Glaucoma
10.2Examination Methods
10.2.1Oblique Illumination of the Anterior Chamber
The anterior chamber is illuminated by a beam of light tangential to the plane of the iris. In eyes with an anterior chamber of normal depth, the iris is uniformly illuminated. This is a sign of a deep anterior chamber with an open angle (see Fig. 1.12).
In eyes with a shallow anterior chamber and an angle that is partially or completely closed, the iris protrudes anteriorly and is not uniformly illuminated (see Fig. 1.12).
10.2.2Slit-Lamp Examination
The central and peripheral depth of the anterior chamber should be evaluated on the basis of the thickness of the cornea. An anterior chamber that is less than three times as deep as the thickness of the cornea in the center with a peripheral depth less than the thickness of the cornea suggests a narrow angle (Fig. 10.2). Gonioscopy is essential for further evaluation.
To evaluate the depth of the anterior chamber with a slit-lamp biomicroscope, select a narrow setting for the light beam. The beam should strike the eye at a slight angle to the examiner’s line of sight.
10.2.3Gonioscopy
The angle of the anterior chamber is evaluated with a gonioscope placed directly on the cornea (Fig. 10.3a and b).
Slit-lamp examination to evaluate the depth of the anterior chamber.
Fig. 10.2 The depth of the anterior chamber is less than the thickness of the cornea on its periphery. The corneal reflex and iris reflection touch each other (arrow), indicating a shallow anterior chamber. Gonioscopy is indicated.
10.2 Examination Methods 239
Gonioscopy and morphology of the angle structures.
Line of sight into the an of the anterior c
from the slit lam
Mirror
Fig. 10.3
a Schematic diagram of gonioscopy. The angle of the anterior chamber can be visualized with a gonioscope placed on the cornea.
b Gonioscopic image of the angle.
a
b
240 10 Glaucoma
Gonioscopy can differentiate the following conditions:
Open angle: open angle glaucoma.
Occluded angle: angle closure glaucoma.
Angle access is narrowed: configuration with imminent risk angle of an acute closure glaucoma.
Angle is occluded: secondary angle closure glaucoma, for example due to neovascularization in rubeosis iridis.
Angle open but with inflammatory cellular deposits, erythrocytes, or pigment in the trabecular meshwork: secondary open angle glaucoma.
Gonioscopy is the examination of choice for identifying the respective presenting form of glaucoma.
10.2.4Measuring Intraocular Pressure
Palpation (Fig. 1.15, p. 15): Comparative palpation of both eyeballs is a preliminary examination that can detect increased intraocular pressure.
If the examiner can indent the eyeball, which fluctuates under palpation, pressure is less than 20 mm Hg.
An eyeball that is not resilient but rock hard is a sign of about 60–70 mm Hg of pressure (acute angle closure glaucoma).
Schiøtz indentation tonometry (Figs. 10.4a and b): This examination measures the degree to which the cornea can be indented in the supine patient. The lower the intraocular pressure, the deeper the tonometer pin sinks and the greater distance the needle moves.
Indentation tonometry often provides inexact results. For example the rigidity of the sclera is reduced in myopic eyes, which will cause the tonometer pin to sink more deeply for that reason alone. Because of this, indentation tonometry has been largely supplanted by applanation tonometry.
Applanation tonometry: This method is the most common method of measuring intraocular pressure. It permits the examiner to obtain a measurement on a sitting patient within a few seconds (Goldmann’s method, see Fig. 10.5 a–c) or on a supine patient (Draeger’s method). A flat tonometer tip has a diameter of 3.06 mm for applanation of the cornea over a corresponding area (7.35 mm2). This method eliminates the rigidity of the sclera as a source of error (see also tonometric self-examination).
Intraocular pressure of 22 mm Hg is regarded as suspicious. Caution: Infection is possible in the presence of conjunctivitis.
Pneumatic non-contact tonometry: The electronic tonometer directs a 3 ms blast of air against the cornea. The tonometer records the deflection of the cornea and calculates the intraocular pressure on the basis of this deformation.
10.2 Examination Methods 241
Schiøtz indentation tonometry.
Base plate of the
tonometer Tonometer pin
Fig. 10.4 a The tonometer is placed on the anesthetized cornea. The examiner retracts both eyelids and the patient focuses on his or her thumb with the other eye.
b Detail view of the tonometer pin indenting the cornea. The harder the eyeball, the shallower the indentation and the smaller the movement of the indicator needle.
Advantages:
Does not require the use of a topical anesthetic.
Non-contact measurement eliminates risk of infection (may be used to measure intraocular pressure in the presence of conjunctivitis).
Disadvantages:
Calibration is difficult.
Precise measurements are possible only within low to middle range pressures.
Cannot be used in the presence of corneal scarring.
Examination is unpleasant for the patient.
Air flow is loud.
The instrument is more expensive to purchase than an applanation tonometer.
242 10 Glaucoma
Goldmann applanation tonometry.
Fig. 10.5
a Slit-lamp measurement of intraocular pressure: After application of anesthetizing eyedrops containing fluorescein, the tonometer tip is placed on the cornea.
b The cornea is applanated (flattened) over an area measuring precisely
7.35 mm2. The external pressure required is directly proportional to intraocular pressure.
c View through a slit lamp: The pressure reading is taken when the two inner menisci of the fluorescein arcs touch (arrow).
