Ординатура / Офтальмология / Английские материалы / Shields Textbook of Glaucoma, 6th edition_Allingham, Damji, Freedman_2010

Figure 3.7 Schematic representation of penetration of acoustic sound waves by different ultrasound frequencies. (Modified with permission from Cynthia Kendall.)

High-resolution ultrasound biomicroscopy allows for a noninvasive means of visualizing anterior ocular structures at high resolution. In the management of patients with glaucoma, high-resolution ultrasound biomicroscopy is helpful to define the anterior chamber angle anatomy, when it cannot be seen gonioscopically, as well as structure and relationships among the iris, ciliary body, crystalline lens, intraocular lens, and anterior vitreous. (The use of high-resolution ultrasound biomicroscopy in managing the various forms of glaucoma is considered in Section II.)

OPTICAL COHERENCE TOMOGRAPHY OF THE ANTERIOR SEGMENT

Introduced in 2006, anterior-segment optical coherence topography, or AS-OCT, provides a noncontact, noninvasive means to image the anterior chamber angle anatomy (11, 12). The AS-OCT uses a 1310-nm wavelength, compared with the 820-nm wavelength for posterior-segment imaging. The AS-OCT has higher resolution, compared with high-resolution ultrasound biomicroscopy, for imaging structures in the iris and the angle anatomy. The AS-OCT is limited to imaging the cornea, anterior chamber, angle anatomy, and central portion of the lens through the pupil (Fig. 3.8). This instrument is unable to adequately image the anatomy of the ciliary body or tissue masses behind the iris.

AQUEOUS HUMOR DYNAMICS

There are several techniques used to measure and calculate the determinants of IOP, which include aqueous humor flow, facility of aqueous outflow, uveoscleral outflow, and episcleral

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venous pressure (13). These techniques include (a) fluorophotometry, a noninvasive and noncontact technique to measure the rate of fluorescein disappearance from the anterior segment and to calculate

aqueous humor flow; (b) tonography, a noninvasive but contact technique to estimate the facility of aqueous outflow; and (c) the episcleral venometer, a noninvasive but contact technique to estimate episcleral venous pressure.

Figure 3.8 Montage of anterior-segment OCT images showing normal anterior segment (A), iris cyst (B), and subluxated lens with shallow anterior chamber and narrow angle (C).

Mathematical Models for IOP

The mathematical relationship of the determinants of IOP is based on Poiseuille law that relates the velocity of flow (F) of fluid in a rigid tube to the following: the radius of the tube (r), the pressure drop per length of tube [(P1 — P 2)/1], and the coefficient of viscosity (?) of the fluid

(http://hyperphysics.phy-astr.gsu.eu/hbase/ppois.html):

In 1949, Goldmann applied Poiseuille law to aqueous outflow (14). Goldmann proposed that the rate of aqueous flow through the trabecular meshwork (F) is directly proportional to the IOP (P0) minus the

episcleral venous pressure (Pv) and inversely proportional to the resistance to outflow (R):

Building on earlier observations by Pagenstecher (in 1878) and Schiotz (in 1905) that eye massage and repeated tonometry reduced IOP, Polak-van Gelder in 1911 described a technique of repeated tonometer applications for 1 to 2 minutes to differentiate healthy from glaucomatous eyes. Schoenberg modified this technique by using a continuous application of the tonometer while reading the pressure fall on the scale of the instrument. Later in 1950, Grant introduced tonography using electronic continuous IOP measurement and proposed an alternative factor to collectively express “outflow resistance” as the coefficient of outflow facility (C), which is reported in microliters per minute per millimeter of mercury in the following equation (15):

F= C(P0 — P v) The C value is an expression of the degree to which a change in the IOP will cause a

change in the rate of aqueous outflow, which is an indirect expression of the patency of the aqueous outflow system.

The Goldmann equation implied that aqueous flow in living ocular tissue could be expressed in the same linear terms as that of fluid in rigid tubes, which was subsequently proven inaccurate. Nevertheless, it has served for over 50 years as an adequate description of aqueous humor dynamics for clinical applications. Recent advances in glaucoma therapeutics, namely the prostaglandin agents (described in Chapter 28), have made it necessary to revise the equation and to reinterpret the meanings of its parameters to the following equation (13) presented in a form based on IOP, using the variables of aqueous flow (Fa), uveoscleral flow (Fu), trabecular outflow facility (Ct), and episcleral venous pressure

(EVP):

Fluorophotometry

Fluorophotometry is the standard research technique by which the rate of aqueous humor flow is calculated under various circumstances, including the response to glaucoma drugs.

In brief, the fluorophotometry protocol involves instilling a given number of drops of saturated fluorescein topically, waiting for an appropriate period of time for steady state distribution of the fluorescein in the anterior segment structures of the cornea and anterior chamber, and then scanning the eye two or three times to obtain appropriate emission scans (16). Calculations are made on the basis of the change in fluorescein measured in the cornea and anterior chamber over time.

In a study of 519 subjects, there is a skewed normal distribution of aqueous humor flow measured between 8 AM and noon with an average of 2.97 (µL/m in (16). Among 180 normal subjects studied between midnight and 6 AM, there was decrease in aqueous humor flow to half of the morning flow value and with a narrower distribution of flow. A later study showed concordance of flow in normal subjects in the morning and night (17) meaning that individuals who had either low, medium, or high aqueous flow phenotypes in the morning showed the expected decrease in flow at night time, but also had a relatively low, medium, or high flow at night, respectively. This latter approach to characterize aqueous flow as a phenotype provides evidence that the factors that contribute to IOP can be studied as a quantitative trait (18). At present, there are no genetic markers for IOP variance, but genome-wide studies currently under way hold the promise of identifying such markers that may be important in identifying patients who have wide IOP fluctuation. In the future, such a molecular medicine approach (see Chapter 8) will help minimize glaucoma progression in patients with wide IOP fluctuation.

In general, aqueous humor flow decreases with age (16, 19). Fluorophotometric studies suggest that aqueous production is relatively insensitive to long-term changes in IOP (20). It

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appears that the main mechanism involved in elevated IOP is alteration in outflow facility (21), which is related to increased resistance to outflow at the trabecular meshwork to a greater extent than the uveoscleral outflow, rather than a “hyper secreter, ” but the role of high aqueous flow phenotype in la rge IOP fluctuation is not known. Resistance to aqueous outflow increases with an increase in the IOP (the physiologic basis of which is discussed in Chapter 1). The tonographic result is that the C value of an eye decreases with increasing IOP (21), which is related to trabecular outflow, also described as conventional outflow, which is discussed in the next section on tonography.

Figure 3.9 Tonography unit.

At present, there is no method to measure uveoscleral outflow, also described as unconventional outflow. The influence of unconventional outflow on the tonographic results (discussed in the next section) is not fully understood. At present, the uveoscleral outflow is calculated on the basis of measurements derived from fluorophotometry and tonography (22, 23).

Tonography

Tonography is a means of estimating the outflow facility by raising the IOP with an electronic indentation tonometer and observing the subsequent decay curve in the IOP over time, which is continuously recorded on a paper strip (Figs. 3.9 and 3.10). The elevated pressure causes an increased rate of aqueous outflow, leading to a change in the aqueous volume (V), which is inferred from Friedenwald tables (24).

In brief, the protocol involves measurements on a patient in a supine position. After measuring the IOP, a weighted tonometer raises the IOP from the baseline (P0) to a new, higher level (Pt). Depending on the

instrument, a 2- or 4-minute pressure tracing is recorded by gently applying the tonometer to the cornea and maintaining this position until a smooth tracing has been obtained. A good tracing will have fine oscillations and a gentle downward slope. If the slope is steeper or irregular during the first few seconds, which is not uncommon, the study is continued until a smooth tracing is obtained.

The slope of the tracing is estimated by placing a line through the middle of the oscillations. The change in IOP during this time is computed as an arithmetic average of pressure increments for successive halfminute intervals [Ave.(Pt — P 0)]- The scale readings are noted at the beginning and end of the tracing.

P0 and the change in scale readings over 4 minutes (T) are then used to obtain the C value from special tonographic tables derived from Grant's equation:

Figure 3.10 Tonographic tracing.

The wave components of a tonographic tracing include (a) fine oscillations, which reflect the cardiac pulse; (b) large waves, which reflect the respiratory movement; and (c) still larger, irregular waves (Traube-Hering waves), which reflect periodic oscillations in the systemic blood pressure. Cardiac irregularities (e.g., extrasystole, bigeminy) can also cause irregularities in the tonographic tracing (25). Aqueous production may decrease during the early phase of a rise in IOP, primarily because of an alteration in ultrafiltration (26). Any subsequent IOP drop in response to reduced production of aqueous creates an impression of increased outflow and is called pseudofacility. This may account for as much as 20% of the total C value. Tonography measures the total C value without distinguishing between true facility and pseudofacility.

In a study of 1379 eyes, Becker reported a mean C value of 0.28 µL/min/mm Hg in 909 healthy eyes (27). A low C value of less than 0.18 µL/min/mm Hg was found in 2.5% of healthy eyes, 65% of those with glaucoma (N= 250 eyes), and 20% of those with a family history of glaucoma (N= 220 eyes). An even lower C value, of less than 0.13 µL/min/mm Hg, was recorded for 0.15%, 3%, and 11%, respectively. The P0/C ratio was 56 in the healthy populations. The proportion of participants with a

high P0/C ratio of greater than 100 was 2.5% among healthy eyes, 95% among those with glaucoma, and 31% in those with a family history of glaucoma. An even higher P0/C ratio, of greater than 138, was

found among 0.15% of healthy eyes, 50% of those with glaucoma and 14% of those with a family history of glaucoma.

In a study of 7577 eyes, the C value was found to decrease with age, with an average of 0.29 µL/min/mm Hg for those aged 41 to 45 years, compare d with 0.25 µL/min/mm Hg in those aged 81 to 85 years (28). No differences by sex were found for any age-group.

The tonographic method has several sources of error. First, this technique was developed with several major assumptions.

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The calculations assume that only the rate of aqueous outflow changes in response to a change in IOP. However, many other ocular parameters, such as ocular blood volume (29) and ocular rigidity, also respond to pressure change, and all of them can affect the tonographic result. Ocular rigidity is an

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expression of the “ stretchability” of the eye and represents elasticity and viscoelastic properties of the eye (30, 31 and 32). An average ocular rigidity coefficient of 0.013 mmHg/µL was used for calculating the tonographic C value, which leads to a potential source of error because of significant interpatient variation in this parameter. For this reason, it is useful to check the pressure by applanation tonometry before performing the tonography and to compare this with the P0 obtained with the indentation

tonometer, to identify any major discrepancy in ocular rigidity. Another assumption was that the C value calculations from each minute did not differ significantly; however, this was shown to be invalid, with a trend toward highest values in the first minute and progressive reduction in the ensuing minutes (33).

Last, the corneal curvature was assumed as an average of 7.8 mm, but variations in the cornea may significantly influence the pressure measurements.

Second, there were some instrumentation and operating issues that contributed as a source of error. The instrument was designed with a larger hole in the electronic tonometer footplate to prevent sticking. At low scale readings, the cornea may mold into the space between the plunger and hole, pushing the plunger up and leading to falsely high pressure readings (34). During the time of these studies, variations in line voltage could produce a drift in the IOP measurements, which was minimized with line voltage stabilizers and by avoiding magnetic fields.

Third, several patient factors influence tonography studies. The IOP has been shown to drop approximately 1 mm Hg in the fellow eye while tonography is being performed on the first eye. This consensual pressure drop was once thought to have a neural cause, but it was subsequently found to be secondary to the evaporation that results from keeping the eye open for fixation during the 4-minute test (35). In addition, eye movement affected IOP measurements, which was described as a “patientrelaxation effect” during the first 15 to 20 second s after the tonometer is placed on the cornea. So, additional time was allowed for this before starting the 4-minute tracing.

Fourth, operator error, including improper cleaning leading to a sticky tonometer, calibration, or positioning of the instrument, and improper calculation of the tracing, can also lead to inaccurate results. Measurement of Episcleral Venous Pressure

Various techniques have been developed for measuring the pressure in the episcleral veins. All of these work on the principle of correlating partial collapse of the vein with the force required to achieve the alteration in blood flow (36). A pressure-chamber technique uses a thin membrane stretched over the tip of a hollow applanating head, which is filled with air or saline. The pressure in the chamber is raised until the bulging membrane produces the desired visible change in the adjacent vessel. Most of these instruments are mounted on a slitlamp, although a portable pressure transducer has been developed to measure episcleral venous pressure with a patient in various body positions (37). When comparing a torsion balance instrument and a pressure chamber technique to direct cannulation of the episcleral vein, the pressure chamber method was found to be superior to the torsion technique (38).

The normal episcleral venous pressure is generally considered to be between 8 and 11 mm Hg. Two features that significantly influence the measured pressure are the selected endpoint and the choice of vessel. When a pressure chamber technique was compared to direct cannulation, a slight indentation, rather than an intermittent or sustained collapse of the vein lumen, gave the most accurate reading (39). It has been suggested that the best point of measurement is just distal to the junction of aqueous and episcleral veins, although this junction is often difficult to ascertain and it may be more practical to take all measurements 3 mm from the limbus (36).

Episcleral venous pressure rises an average of 1.25 mm Hg with the pressure elevation during tonography (40), which is usually corrected for in the formula by adding 1.25 to P0. Episcleral venous

pressure measurements throughout tonography indicate that the rise is greatest during the first half of tonography, with a return to a nearly pretonographic level by the end of the procedure and a mean change in episcleral venous pressure during this time of 0.44 mm Hg.

KEY POINTS

Gonioscopy is an essential tool used to evaluate patients with glaucoma to assess the angle

anatomy.

High-resolution ultrasound biomicroscopy and anteriorsegment OCT are imaging methods to evaluate the drainage angle. High-resolution ultrasound biomicroscopy can evaluate structures, such as the ciliary body and suspicious masses, behind the iris.

Aqueous humor flow, trabecular outflow, uveoscleral outflow, and episcleral venous pressure are the four physiological components of IOP. Functional assessment of these dynamic components is possible using fluorophotometry tonography, and venomanometry

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11.Radhakrishnan S, Huang D, Smith SD. Optical coherence tomography imaging of the anterior chamber angle. Ophthalmol Clin North Am. 2005;18(3):375-381.

12.Ahmed IK, Lee RH. Utilization of Visante OCT for glaucoma evaluations. In: Steinert RF, Huang D, eds. Anterior Segment Optical Coherence Tomography. Thorofare, NJ: SLACK Inc.; 2008:89-106.

13.Brubaker RF. Goldmann's equation and clinical measures of aqueous dynamics. Exp Eye Res. 2004;78(3):633-637.

14.Goldmann H. Augendruck and gluakom. Die Kammer-wasservenen und das Poiseuille'sche Gesetz. Ophthalmologica. 1949;118:496-519.

15.Grant W. Tonographic method for measuring the facility and rate of aqueous flow in human eyes. Arch Ophthalmol. 1950;44:204-214.

16.Brubaker RF. Clinical measurements of aqueous dynamics: implications for addressing glaucoma. In: Civan MM, ed. The Eye's Aqueous Humor, From Secretion to Glaucoma. New York, NY: Academic Press; 1998:234-284.

17.Radenbaugh PA, Goyal A, McLaren NC, et al. Concordance of aqueous humor flow in the morning and at night in normal humans. Invest Ophthalmol Vis Sri. 2006;47(11):4860-4864.

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19.Toris CB, Koepsell SA, Yablonski ME, et al. Aqueous humor dynamics in ocular hypertensive patients. J Glaucoma. 2002;11(3):253-258.

20.Carlson KH, McLaren JW, Topper JE, et al. Effect of body position on intraocular pressure and aqueous flow. Invest Ophthalmol Vis Sci. 1987; 28(8):1346-1352.

21.Moses RA. Constant pressure applanation tonography. 3. The relationship of tonometric pressure to

rate of loss of ocular volume. Arch Ophthalmol. 1967;77(2):181-184.

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Shields > SECTION I - The Basic Aspects of Glaucoma >

4 - Optic Nerve, Retina, and Choroid

Authors: Allingham, R. Rand

Title: Shields Textbook of Glaucoma, 6th Edition Copyright ©2011 Lippincott Williams & Wilkins

> Table of Contents > SECTION I - The Basic Aspects of Glaucoma > 4 - Optic Nerve, Retina, and Choroid

4

Optic Nerve, Retina, and Choroid

Glaucoma is characterized by progressive atrophy of the optic nerve head secondary to the loss of optic

1 - Cellular and Molecular Biology of Aqueous Humor Dynamics Page 83 of 225

nerve fiber. Because it is this pathologic alteration that leads to the irreversible loss of vision, an understanding of glaucomatous optic atrophy is essential in the diagnosis and management of glaucoma. ANATOMY AND HISTOLOGY

Terminology

In the context of a discussion on glaucoma, the optic nerve head is defined as the distal portion of the optic nerve that is directly susceptible to intraocular pressure (IOP) elevation. In this sense, the optic nerve head extends anteriorly from the retinal surface to the myelinated portion of the optic nerve that begins just behind the sclera, posterior to the lamina cribrosa. The term optic nerve head is generally preferred over optic disc because the latter suggests a flat structure without depth. However, the terms disc and papilla are frequently used when referring to the portion of the optic nerve head that is clinically visible by ophthalmoscopy (1). It is the optic nerve head and nerve fiber layer containing retinal ganglion cell (RGC) axons that are most clearly associated with glaucomatous vision loss (Fig. 4.1).

General Description

The optic nerve head comprises the nerve fibers that originate in the ganglion cell layer of the retina and converge upon the nerve head from all points in the fundus. At the surface of the nerve head, these RGC axons bend acutely to exit the globe through a fenestrated scleral canal, called the lamina cribrosa. In the nerve head, the axons are grouped into approximately 1000 fascicles, or bundles, and are supported by astrocytes. There is considerable variation in the size of the optic nerve head. In one study, the diameter varied from 1.18 to 1.75 mm (2). Other studies have revealed ranges of 0.85 to 2.43 mm in the shortest diameter and 1.21 to 2.86 mm in the longest (3), or a mean of 1.88 mm vertically and 1.77 mm

horizontally (4). The disc area may range from 0.68 mm2 to 4.42 mm2 (3). In a large, population-based study, the average disc area was 2.42 mm2 (5). In a different study, the average disc area was 2.56 mm2

when measured by the Heidelberg retina tomograph (HRT) and 2.79 mm2 by the analysis of disc photographs (6). When optic nerve head area and neuroretinal rim area were determined in 36 radial 10degree segments on stereophotographs, cup area had stronger correlation with the disc area than the rim area, suggesting that correction for disc size may be more important for cup area than for rim area (7). Another study showed a positive correlation between the optic disc size and the thickness of the peripapillary retinal nerve fiber layer (RNFL) (8).

Studies using a confocal scanning laser tomograph showed that in healthy eyes the neuroretinal rim area and optic disc diameter have a higher correlation with the optic nerve head configuration than with age, sex, or refractive error (9). The diameter and the area may vary depending on the definition of the edge of the optic disc and methods of measurement (4, 10, 11). Therefore, some authors have suggested applying various formulas to correct magnification of images when comparing disc measurements on different instruments (12, 13).

The diameter of the nerve expands to approximately 3 mm just behind the sclera, where the neurons acquire a myelin

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sheath. The optic nerve head is also the site of entry and exit of the retinal vessels. This vascular system supplies some branches to the optic nerve head, although the predominant blood supply for the nerve head comes from the ciliary circulation.

Figure 4.1 A: Optic nerve head with physiologic enlarged cupping demonstrating robust, symmetric, and healthy RNFL. B: Glaucomatous optic nerve showing an inferotemporal notch and corresponding loss of the RNFL that is appreciated by “baring” of the ret inal vessels. The point of the (arrows) delimits the RNFL defect.

Figure 4.2 Divisions of the optic nerve head. A: Surface nerve fiber layer. B: Prelaminar region. C: Lamina cribrosa region. D: Retrolaminar region.

Divisions of the Optic Nerve Head

The nerve head may be arbitrarily divided into four portions from anterior to posterior (14) (Fig. 4.2). Surface Nerve Fiber Layer

The innermost portion of the optic nerve head is composed predominantly of nerve fibers. In the rhesus