Chapter 213 – Clinical Examination of Glaucoma
M. FRAN SMITH
J. WILLIAM DOYLE
• Glaucoma is a type of optic neuropathy associated with characteristic optic disc damage, which may result in certain visual field loss patterns, at least in part secondary to suboptimal intraocular pressure. The clinical examination is vital to make this diagnosis.
• Tonometry to record accurate intraocular pressures.
• Gonioscopy to identify any angle pathology.
• Optic disc examination.
• Nerve fiber layer analysis.
• Visual field examination.
• The role of tonography.
Once, glaucoma was considered a single disease entity characterized by optic nerve damage and visual loss secondary to elevated intraocular pressure. It is now understood that many different ocular disorders and processes may result in that specific pattern of optic disc damage and visual field loss called glaucoma. The clinical examination is vital to differentiate the mechanisms associated with a particular case of glaucoma.
The clinical examination in a patient who has possible glaucoma is similar to the ocular examination of any new patient. A detailed history must be taken, a thorough slit-lamp evaluation of anterior segment structures must be carried out, and special attention must be directed to the key aspects described below.
The importance of intraocular pressure (IOP) assessment in the evaluation of glaucoma has been understood for over 100 years. Digital estimation of globe firmness yielded to instrumental (Schiøtz) tonometry over the first 20 years of the twentieth century. Today, the Goldmann applanation tonometer provides the gold standard for the clinical measurement of IOP.
A tonometer uses certain physical principles to measure pressure within the globe. Basically, the force necessary to deform a globe is directly related to the pressure within that globe. Three styles of tonometer currently are in use. Indentation, or high-displacement, tonometers utilize a plunger to indent the cornea by a variable amount. This indentation displaces a significant volume of intraocular fluid at the time of corneal deformation and results in a near doubling of the IOP. Conversion tables, in turn, estimate the original IOP from the indentation tonometric value obtained. Applanation, or low-displacement, tonometers raise IOP negligibly, because they subject the eye to sufficient force only to flatten the cornea. The amount of force required to achieve a constant degree of corneal flattening is converted into IOP values. Noncontact tonometers flatten the cornea using a puff of air, and the time required to flatten the cornea is correlated to estimated IOP. Each form of tonometer has a place in the examination of eyes.
Schiøtz, in 1905, described the indentation tonometer ( Fig. 213-1 ). The plunger freely moves and is encased in a shaft that ends in a footplate, which rests on the anesthetized cornea. The movement of a lever attached to the plunger reflects the degree to which the cornea is indented—a softer globe shows greater indentation and greater lever movement across the upper scale. Schiøtz tonometers all conform to American Academy of Ophthalmology standardized physical specifications. Thus, use of the tonometer on a steel test block results in a scale reading of zero. Generally, using the standardized plunger weight of 5.5?g, normal eyes give scale readings of 5–8 units, and glaucomatous high-pressure eyes read less than 4 units. The provided conversion table is used to convert scale readings into IOP readings (mmHg or kPa).
Multiple potential sources of error are present in the use of Schiøtz tonometry. The patient must be comfortable and supine. The lids must be wide open. The examiner must take great care to ensure no external pressure is applied to the globe. Otherwise, a falsely low reading (high IOP) may be obtained. Another potential source of inaccuracy arises from differences in ocular rigidity among different eyes. Some eyes are more distensible than others; so, although the conversion tables take into account an average ocular rigidity, eyes that have a low ocular rigidity may give a falsely high Schiøtz scale reading, which is then converted
Figure 213-1 The Schiøtz tonometer in use. Notice the patient’s reclining position.
into a falsely low IOP reading. The physician always must applanate eyes known to have low scleral rigidity. Such eyes include those that have high myopia, osteogenesis imperfecta, history of strong miotic (especially cholinesterase inhibitor ) therapy, history of retinal detachment (especially vitrectomy surgery),  and history of vasodilatation therapy. Similarly, the physician must recognize that high hyperopia, extreme myopia, long-standing glaucoma, macular degeneration, and vasoconstrictor therapy are associated with high scleral rigidity. A falsely low Schiøtz reading (falsely high IOP) may be measured in these eyes.
Two other sources of error occur using Schiøtz tonometry. These include the variable expulsion of intraocular blood during the indentation  and extremes in corneal shape or thickness. Specifically, the thin cornea of a patient with keratoconus may be associated with a falsely low IOP. Indentation of a thickened cornea results in a greater displacement of intraocular fluid than occurs when a regular cornea is indented. Consequently, a falsely high IOP reading may be obtained. A steep cornea also may cause a falsely high IOP reading.  Because there are so many potential sources of error, Schiøtz tonometry largely has been replaced by applanation tonometry. Goldmann or, when portability is an issue, Perkins or Tono-Pen tonometers are popular. However, familiarity with the Schiøtz instrument remains useful. It is the most affordable instrument available for IOP estimation. As such, it is still found in many emergency rooms. Additionally, it may be sterilized and used under sterile conditions in the operating room (for example, if IOP needs to be established immediately prior to intraocular surgery, either digital pressure or the Schiøtz tonometer may be used).
Unlike in Schiøtz tonometry, in which a relatively large corneal displacement occurs, in applanation tonometry only enough force is applied to flatten the cornea, disturbing relatively little aqueous. Two types of applanation tonometry exist. In constant-force applanation tonometry, a constant force is applied to the cornea, and IOP is estimated by measurement of the diameter of the flattened corneal area. The Maklakov tonometer is based on this principle. However, the remainder of this section deals with variable-force tonometry, because investigators in Western developed countries are more familiar with it. The Goldmann tonometer is the prime example of a variable-force tonometer. Based on Fick’s law, which states that pressure within a sphere is equal to the force needed to flatten part of the sphere divided by the area flattened (P = F/A), the Goldmann tonometer measures IOP simply and reproducibly.
Many variables had to be addressed before Fick’s law could be applied to the applanation and pressure measurement of eyes. After all, Fick’s law theoretically applies only to perfect, infinitely thin, dry spheres. The cornea is not dry, thin, or perfectly round. Thus, adjustments had to be made for force application to the corneal outer surface (although IOP is directed against the inner corneal surface) for corneal astigmatism and variable corneal and scleral stiffness, and for tear capillary attraction between the tonometer and cornea. Eventually, it was determined that a corneal applanation area of diameter 3.06?mm best achieved the necessary balance among the above variables in the human eye. Also, use of this diameter value allows direct conversion, by multiplication by 10, of applanation gram force into millimeters of mercury of pressure, or multiplication by 0.133 for conversion of applanation gram force into kPa.
The Goldmann tonometer consists of a sensitive spring balance attached to a plastic biprism ( Fig. 213-2 ), which on contact with the cornea creates two half circles. These semicircles are particularly easy to view with a cobalt blue light after fluorescein application in the ocular cul-de-sac. The examiner then adjusts the spring force applied to the globe using the tonometer’s attached dial, so that the inner margins of the biprism semicircles just
Figure 213-2 The Goldmann tonometer. A, The patient at the instrument. B, Biprism semicircles just touch.
touch. When these inner margins touch, 3.06?mm of the cornea is applanated and approximately 0.05?µl of aqueous volume is displaced. As a result of the small quantity of aqueous displaced, the measured pressure (read from the dial) is probably less than 3% higher than IOP prior to applanation. However, excess fluorescein application may result in a falsely high IOP, and too little or no fluorescein use may produce a falsely low IOP.
Other factors may cause error in IOP measurement using Goldmann tonometry; these include abnormal corneal thickness and curvature, excess contact time, and improper instrument calibration. Generally, corneas thickened from edema are associated with falsely low IOP readings. Those thickened secondary to other processes (i.e., from increased collagen fibrils) may give a falsely high IOP reading.  Thin corneas usually give falsely low readings. Astigmatism greater than 3–4D causes an IOP measurement error of approximately 1?mmHg (0.13?kPa) per 4D. This potential error is avoided by using the average of two pressure readings, one taken with mires vertical and the other with mires horizontal. Alternatively, to avoid measurement error secondary to astigmatism, the tonometer biprisms may be aligned so that the red line on the prism holder is opposite the known corneal axis of least astigmatism. Another source of error is excess contact time between tonometer and eye, which is associated with a falsely low IOP and is avoided easily by using a “light” touch. A light touch has the additional advantage of sparing the eye iatrogenic corneal epithelial defects. Finally, to avoid any errors from improper instrument calibration, at least biyearly instrument calibration must be carried out.
If the above caveats are kept in mind, the Goldmann tonometer will provide decades of reliable IOP measurements. Repeated, accurate IOP measurements, with an error of about 2?mmHg (0.27?kPa) among various examiners or at different times, may be expected. Care must be taken to wipe the tonometer tip with 3% hydrogen peroxide or 70% isopropyl alcohol before it is placed on a patient’s eye. Such precautions destroy any human immunodeficiency virus present and, presumably, adenovirus and hepatitis virus, as well. Corneal epithelial defects are prevented if the tip is wiped dry with a tissue after disinfection.
The Perkins and Draeger applanation tonometers are both portable, hand-held, Goldmann-style tonometers with built-in biprisms.  They require some skill to use effectively. The Perkins tonometer is probably as accurate as the Goldmann tonometer and may be used on reclining patients ( Fig. 213-3 ). The Draeger tonometer is not used as widely as the Perkins. Another variable-force style of applanation tonometer is the pneumotonometer ( Fig. 213-4 ). It is a Mackay–Marg-type
Figure 213-3 The Perkins tonometer. This picture demonstrates its handheld portability.
Figure 213-4 The pneumotonometer.
Figure 213-5 The Tono-Pen. It is extremely portable and easy to use.
tonometer. In Mackay–Marg-style tonometers, the force measured is that necessary to keep the plunger’s flat plate flush with its surrounding sleeve, despite IOP against corneal flattening. The pneumotonometer assesses IOP via a central sensing device controlled by air pressure, while the force required to bend the cornea is transferred to a surrounding sleeve. The pneumotonometer is not portable, and the base unit is sufficiently large to discourage room-to-room transfer. The correlation between the pneumotonometer and the Goldmann instrument is good, but IOPs measured using the former tend to be overestimated. However, unlike any of the Goldmann-style tonometers, the pneumotonometer may be used to estimate IOP in eyes that have scarred and irregular corneas.
Of the Mackay–Marg-style tonometers, perhaps the Tono-Pen has gained the widest acceptance ( Fig. 213-5 ). It is highly portable and easier to use than any other portable IOP device. A strain gauge is used to create an electrical impulse as the footplate flattens the cornea. A microprocessor chip senses appropriate force curves, calculates the average of 4–10 readings, and then produces a final digital readout with variability percentages. Most investigators feel it gives accurate IOP readings in the normal range but may overestimate IOP in the low and underestimate IOP in the high ranges.  It reportedly measures IOP fairly accurately through a soft contact lens. It is a useful device for the measurement of pressure in patients for whom applanation tonometry is impossible because of a scarred or irregular cornea.
No discussion of tonometry is complete without mention of “puff tonometry.” In noncontact tonometry, a puff of air is used to flatten the cornea, with the length of time required to flatten it, as measured by an optoelectronics system, correlated with the IOP. This length of time is on the scale of milliseconds. Thus, the ocular pulse may present a significant source of 1–3?mmHg (0.13–0.40?kPa) variability in pressure. Still, noncontact tonometry is fairly accurate in the normal range of IOP. In addition, the availability of a handheld Pulsair noncontact tonometer may make screening efforts by paramedical professionals easier, because there is no risk of infection spread or corneal abrasion when using it.
ROLE OF TONOGRAPHY
Tonography measures IOP over the course of 4 minutes while a Schiøtz tonometer rests on the eye. Based on how IOP drops over this period (secondary to tonometer load displacement of aqueous), an estimate of the ease with which aqueous leaves the eye is made. This estimate is called facility of outflow, or C. For many years, tonography and estimation of outflow facility was considered a useful adjunct to routine clinical examination of patients who had open-angle glaucoma. It was used, also, to confirm positive provocative tests in angle-closure glaucoma and to diagnose outflow abnormalities, which may be masked by decreased aqueous production.
Grant originated the technique in 1950. He reported his results on 600 normal and glaucomatous eyes and felt that the reduced outflow facility seen in glaucomatous eyes accounted for the high IOP seen in glaucoma. Accordingly, Grant was one of the first physicians to publish proof that glaucoma was a disease of inadequate outflow and not of fluid overproduction. He also proposed that reduced C values could be a useful predictor in eyes suspected of being glaucomatous. However, most now feel that tonography has little diagnostic value in any individual patient. Facility of outflow values may overlap considerably between normal and glaucomatous groups.  Although a mean C value in normal eyes of 0.24–0.28?µl/min per mmHg (0.03–0.037?µl/min per kPa) is recognized, there is a wide range of normal values (0.15–0.34?µl/min per mmHg or 0.02–0.045?µl/min per kPa), and up to one third of patients with glaucoma may have a C value greater than 0.18?µl/min per mmHg (>0.024?µl/min per kPa).
Despite these concerns, it is useful to be familiar with the principles behind tonography. Grant attached an electronic tonometer to a paper strip recorder, which recorded the drop in scale units over time with the tonometer set remaining in contact with an eye. Patients with normal eyes show a slow, steady
decline in IOP over 4 minutes. In patients with glaucoma, presumably secondary to decreased outflow capabilities through the conventional system, there is a smaller decline in IOP over 4 minutes. This ease of outflow, or facility of outflow coefficient (C), is estimated by dividing the change in globe aqueous volume (V) by the time interval (T) for which the tonometer rests on the eye and the IOP change (?P) in this time ( Equation 213-1 ).
Friedenwald had established that a certain increasing volume of aqueous is displaced by indentation tonometry over several minutes. Grant’s formula simply utilizes this fact and others to arrive at an estimation of outflow facility. In practice, however, tonographic equipment comes with tables which estimate C based on initial and final tonometer readings and the quantity of tonometer weight applied over 4 minutes.
Tonography and the resultant C valve may be influenced by multiple factors. These include IOP, decrease in aqueous production secondary to tonometer-related IOP elevation (so-called pseudofacility), increase in episcleral venous pressure secondary to tonometer weight, and variable ocular rigidity. Thus, the final derived C value does not reflect rate of aqueous outflow only. To a variable degree, C is influenced by some or all of these other factors. Nonetheless, to call C the coefficient of aqueous outflow is a useful oversimplification for most purposes, and tonography even today has a place in some research settings.
Numerous avenues are open to explore IOP in the human eye, and the final IOP measured is influenced by many factors. Young children tend to have lower IOPs, with an average IOP of 8.4 ± 0.6?mmHg (1.12 ± 0.08?kPa) in infants under 1 year of age. This may be attributed partially to the influence of anesthetic agents necessary to obtain a measurement in babies. Conversely, some investigators feel that IOP tends to rise with age, perhaps related to decreased facility of outflow through the aged trabecular meshwork. This is despite an associated decrease in aqueous production with age.
Generally, IOP tends to be similar between sexes, although some investigators have noted an increase in IOP in women after the menopause. Black patients (African–Americans and African–Caribbeans) may run slightly higher IOPs than Caucasians. Those patients who have a positive family history of glaucoma tend to have higher IOPs than those who have a negative family history.
One study noted that myopes who have greater axial lengths tend to have higher IOPs, although this remains unconfirmed.
It is well established that normal IOP varies by 5?mmHg (0.7?kPa) or more during the day. In glaucoma patients who receive no treatment, diurnal variation may be in the range 10–30?mmHg (1.3–4.0?kPa),  which stresses that excessive emphasis must not be placed on a single normal pressure reading in a patient who might have glaucoma.
When changing from a sitting to a reclining position, IOP may increase by up to 9?mmHg (1.2?kPa). This change is more common in patients affected by glaucoma, especially normal-tension glaucoma. Although prolonged physical activity may be associated with lower IOP,  anything that causes a short-term strain, such as a Valsalva maneuver, may cause a jump in IOP. Hard blinking may cause a rise in IOP from 10–90?mmHg (1.3–12.0?kPa). 
As touched on briefly in the discussion of age influences above, most anesthetic agents result in a drop in IOP. Ketamine and succinylcholine are exceptions to this statement and usually cause an increase in IOP. When an attempt is made to rule out congenital glaucoma, the surgeon must be careful not to place the child under a general anesthetic, because a falsely low IOP reading may be obtained. Ketamine is the agent of choice in
Figure 213-6 Intraocular pressure distribution in the population. This distribution is not a bell curve.
such cases. Also, midazolam seems not to result in IOP elevation or depression.
Systemic hypertension, diabetes, hyperthyroidism, obesity, and Cushing’s disease may be associated with elevated IOP. Alcohol and marijuana use may lower IOP, but caffeine has virtually no effect. Tobacco use may be correlated positively with higher IOPs. 
Before moving on to further points in the clinical examination of patients with glaucoma, a brief discussion of the value of IOP measurement in the modern examination follows. At one time, ophthalmologists were taught that IOP was a “be-all and end-all” in glaucoma care. Mean IOP in whole populations was measured at 15.5 ± 2.57?mmHg (2.1 ± 0.34?kPa). Physicians initially assumed IOP values distributed themselves along a gaussian curve and that 95% of the area under the curve fell in the range 10.5–20.5?mmHg (1.4–2.7?kPa). So, for many years any IOP measurements greater than 2 standard deviations above this mean (i.e., >21?mmHg [>2.8?kPa]) were considered abnormal, and the ophthalmologist contemplated treatment as necessary to lower IOP back to normal, or less than 21?mmHg (<2.8?kPa). Of course, today it is understood that the treatment of glaucoma is not nearly so simple. First, IOP distribution does not lie along a perfect Gaussian curve but has a skewed tail toward higher IOPs ( Fig. 213-6 ).  For this reason alone, no cut off exists for normal versus abnormal IOP. In addition, most investigators now feel that the best management protocol for glaucoma patients involves setting an individual target IOP based on an individual’s particular extent of nerve damage and visual field loss. A patient who has a relatively healthy optic nerve and normal visual field may do well with a target IOP of about 28?mmHg (3.9?kPa). Another patient who suffers advanced nerve and field damage may need a target IOP of 12?mmHg (1.9?kPa), if further glaucomatous damage is (hopefully) to be avoided. There can be no absolute “safe” or “dangerous” IOPs for the general population—IOP goals must be individualized for each patient. Despite these caveats, IOP remains an easily measurable value. Accurate assessment of each individual’s IOP is indispensable, if proper care of patients with glaucoma is to ensue.
Following a detailed anterior segment examination and IOP measurement, gonioscopy is performed on all glaucoma suspects. Gonioscopy is the technique used by clinicians to view the anterior chamber angle. Although a challenge for the novice, it provides vital information to help the clinician determine the type of glaucoma present. Only after an accurate diagnosis is made can appropriate therapy be instituted. Incorrect diagnoses, made by clinicians who neglect to examine the angle, may result in improper therapy.
Figure 213-7 The Koeppe lens. This lens is used most frequently for pediatric gonioscopy during examination under anesthesia.
The anterior chamber angle is not directly visible with slit-lamp examination. As light passes from the angle to the cornea, its angle of incidence is greater than the critical angle for a cornea–air interface (46°). Thus, it is reflected normally back into the eye. Gonioscopy utilizes a contact lens to neutralize corneal refractive power, which, in turn, allows either direct or indirect visualization of angle structures.
The Koeppe lens is used for direct gonioscopy ( Fig. 213-7 ). It is a 50D concave lens which comes in adult (large diameter and smaller radius of posterior curvature) and pediatric (small diameter and larger radius of posterior curvature) versions. The patient is placed in a reclining position. Methylcellulose is applied to the underside of the contact lens. The eye is anesthetized topically, and the lens is applied to the eye. An examiner uses a hand biomicroscope with 320× magnification and a separate light source to view the angle directly.
Such an angle view is useful in that the image seen is a real one (not a reflection). If an eye has a particularly convex iris with narrowed angle, the examiner can vary the direction of view easily, to peer up and over the iris into the angle. Also, if a Koeppe lens is placed on each eye, the examiner may view both angles almost simultaneously. By switching views back and forth between eyes, determination of any subtle differences in angle depth or morphology is made. A Koeppe-style lens is used whenever goniotomy is performed.
Some disadvantages exist to the use of the Koeppe lens. The first is inconvenience if the patient has to be moved to a viewing room, in which the biomicroscope is available and the patient can be reclined. Second, the biomicroscope is somewhat unwieldy and heavy and often requires support by a cord from the ceiling. Third, the magnification obtained using this lens is suboptimal. Last, because the patient lies flat, the angle may appear artificially deep.
Two basic styles of mirrored goniolenses exist. The first, typified by the Zeiss lens, has a 9?mm corneal segment and a radius of curvature (7.72?mm) approximately that of most corneas ( Fig. 213-8 ). Thus, the lens easily couples to the cornea, using just a drop of anesthetic (or, better, a drop of high-viscosity artificial tear preparation) on the lens surface. The Zeiss lens comes with a holding fork, the Unger holder. Other Zeiss-style lenses include the Posner lens (handle attached to lens) and Sussman (finger-held) lens. All of these lenses have in each of four quadrants a mirror tilted at 64°, for ease of viewing the angle 360°. The angle view seen is indirect, through the mirror.
The patient is seated at the slit lamp. After topical anesthetic has been applied to the eye, the lens is touched to the eye, but
Figure 213-8 The Zeiss lens and Unger holder.
Figure 213-9 Portion of angle with a synechia and area of appositional closure. Angle view with and without compression gonioscopy.
barely. This allows for an undistorted angle view. Most parts of open angles are viewed with this lens easily. If the examiner finds it difficult to examine one part of the angle, the patient may be asked to look toward the mirror in use (i.e., away from that part of the angle being examined). Typically, that portion of angle comes into view. Alternatively, if the angle appears narrowed, an indentation or “compression” gonioscopy may be carried out. With this technique, gentle pressure is applied to the lens center while the suspicious portion of angle is viewed using a narrow slit beam. This extraordinarily useful technique allows easy distinction between appositional angle closure and synechial closure ( Fig. 213-9 ). Thus, if previously hidden structures, such as trabecular meshwork, become visible upon pressure application, then the:
• Area of angle closure is only appositional
• Angle closure attack may be broken temporarily by this physical opening of the chamber angle
• Laser iridectomy may allow a return to normal pressures (versus cases of synechial closure, which often eventually require trabeculectomy).
The other type of indirect goniolens is the Goldmann lens, which may have a single mirror 12?mm high and tilted 62°. Other Goldmann lenses have additional mirrors at different angles for fundus examination ( Fig. 213-10 ). A key difference is the posterior lens diameter of 12?mm with a posterior radius of curvature of 7.38?mm. A viscous solution of methylcellulose must be used to couple this lens to the cornea. Many examiners find it easier to use these lenses because the lens tends to “suck” onto the cornea, which negates the need to apply the lens to the eye
Figure 213-10 The Goldmann lens.
Figure 213-11 The normal anterior chamber angle. This is viewed through the Zeiss lens. Notice the ciliary body band, scleral spur, and trabecular meshwork.
with “just the right amount of force.” Also, the taller mirror of this lens makes it easier to view over convex irises, especially if the patient is instructed to look at the mirror. However, the methylcellulose may be messy to clean up and may prevent a further good ocular examination by the initial or subsequent examiner. Also, this lens’ large posterior diameter and short radius of curvature prevent the luxury of indentation gonioscopy.
Advantages of indirect gonioscopy over direct gonioscopy are several. Both the Zeiss-style lenses and the Goldmann lens are easier to use than the Koeppe lens. Indirect gonioscopy enjoys excellent optics and magnification at the slit lamp. With the Zeiss lens, the physician has the ability to perform indentation gonioscopy.
Gonioscopic Angle Appearance
Normal anterior chamber angles have four basic landmarks. Starting posteriorly at the base of the iris and moving anteriorly, the ciliary body, scleral spur, trabecular meshwork, and Schwalbe’s line may be identified ( Fig. 213-11 ).
When the gonioscopic examination is begun, the iris contour is examined initially. This portion of the examination is especially important in cases of plateau iris and pigmentary glaucoma, as discussed later. Most irides have a slight forward convexity. Highly hyperopic eyes may have more iris convexity. Flat or even mildly concave iris contours may be seen in myopic eyes and aphakes. Some patients who have pigmentary glaucoma and myopia show a highly characteristic concave iris contour. Apart from contour, the position at which the iris appears to insert into the ciliary body is noted. Normally, insertion appears below the scleral spur. However, in patients with plateau iris angle-closure glaucoma, iris insertion is just at the scleral spur level, with the plane of the iris further forward to the level of trabecular meshwork. Thus, angle drainage may be blocked by this peculiar anatomical arrangement. Obviously, a peripheral iridectomy serves no use in such situations, except to rule out pupillary block.
The iris normally inserts into the ciliary body. The next angle structure, the ciliary body band, may be identified easily by following a narrow slit beam of light along the iris toward the cornea. This band’s width is dependent on the location of insertion of the iris. Its color is usually dark brown.
Moving anteriorly from the ciliary body band, the scleral spur is the next identifiable structure in open angles. The scleral spur is seen as a thick, white band between the ciliary body and trabecular meshwork. It represents the posterior portion of the scleral sulcus. Occasionally, thin iris processes extend from the iris root across the scleral spur. If 360° of scleral spur can be identified, then no angle closure is present.
In front of the scleral spur is pigmented or functional trabecular meshwork. Posterior pigmented trabecular meshwork is that portion of the eye’s drain through which primary aqueous outflow passes. Actually, newborns have very little to no pigment in this portion of the meshwork. As the body ages, variable amounts of pigment accumulate here. At this level, much pathology may be found in some of the secondary forms of glaucoma (see below).
Anterior to the pigmented meshwork, often a nonpigmented, or anterior, meshwork band may be identified, just prior to Schwalbe’s line, the final major angle landmark. Schwalbe’s line marks the anterior start of the drainage angle, and the posterior-most portion of translucent cornea. Anatomically, it is a fine ridge, often with a smattering of pigment on it. As detailed above, many investigators prefer to identify angle structures by moving from posterior iris root to anterior Schwalbe’s line. However, an anterior–posterior “check” system may be used if any landmarks are unclear. Specifically, if a thin, three-dimensional slit beam is focused on cornea, at Schwalbe’s line this slit beam collapses into a two-dimensional line that runs posteriorly through angle structures as noted above. This check system is especially useful to confirm a diagnosis of angle-closure glaucoma.
Following angle examination, angle depth is recorded or graded in one of the accepted standard fashions—Shaffer system, Scheie system, or Spaeth system.
The Shaffer grading system is perhaps the simplest. Essentially, angle depth is estimated by the geometric angle formed between the posterior corneal wall and anterior iris face. A closed angle (0° geometric angle) is graded 0; narrow angles (0–10° and 10–20° geometric angles) are graded I and II, respectively; moderately open angles (30°) are graded III; and wide open angles (>40°) are graded IV ( Fig. 213-12 ).
Alternatively, some ophthalmologists use the Scheie system to record angle depth. Unfortunately, angle depth is graded in a fashion exactly opposite to that of the Shaffer system. A wide open angle is graded I, a moderately open angle with a view just to the scleral spur II, a narrow angle with view of anterior meshwork only III, and a closed angle IV. To avoid confusion, the ophthalmologist must note which gonioscopic grading system is used, if either the Scheie or Shaffer system is chosen.
The Spaeth system is perhaps the most elaborate of angle grading systems and the one preferred. It forces the examiner to examine three critical elements. First, to assess where the iris apparently inserts:
Figure 213-12 Shaffer’s angle grading system.
• A: Anterior to trabecular meshwork
• B: Behind Schwalbe’s line
• C: At scleral spur
• D: Deeply, with visible ciliary body
• E: Extremely deeply
Second, to estimate the geometric angle between cornea and iris (as with the Shaffer system), in the range 10–50°. Third, to establish the peripheral iris contour as:
• s: Steep and convex
• r: Regular (i.e., flat to mildly convex)
• q: Queer and concave
A Spaeth system classification of a moderately open angle with apparent iris insertion at the scleral spur, but which opens fully with a view of the ciliary body with compression gonioscopy, may read (C)D40r. Classification of a potentially occludable, narrow angle with a steep iris insertion just behind Schwalbe’s line, may read B20s.
COMPARISON OF GRADING SYSTEMS.
These three grading systems all are carried out using a gonioscopic lens. No acceptable substitute exists for an actual examination of the eye’s angle. Van Herick described a technique in which, theoretically, angle depth may be estimated from slit-beam examination of the far temporal cornea and anterior chamber. A thin slit beam is focused perpendicular to the temporal cornea. Anterior chamber depth is estimated relative to corneal thickness from a 60° viewing angle. A Shaffer grade I angle corresponds to an anterior chamber depth of less than one fourth of the corneal thickness, grade II and III angles correspond to one fourth to one half of the corneal thickness anterior chamber depth, and a grade IV angle corresponds to one half to full corneal thickness chamber depth. However, these estimations may miss closed and significantly narrowed angles. Additionally, use of this system instead of a gonioscopic lens means the examiner may miss potentially pertinent angle pathology (see below).
First, the angle is examined to determine if it is closed, could be closed, or widely open. Most investigators feel that if scleral spur is visible (Spaeth C–E categories), imminent closure is unlikely. If a Spaeth A or B angle is seen, the angle is either closed (with synechiae), or closure is imminent. Potential closure of a currently open angle is particularly possible if a uniformly B10–20s type angle is seen. Of course, angle depth may not be uniform for 360°. Commonly, the superior angle is the narrowest and the inferior angle the most open. Unevenness in angle depth or areas of partial closure may result from old peripheral anterior synechiae (PAS) in some quadrants. Also, a posterior iris cyst or
Figure 213-13 Uneven angle depth secondary to an iris tumor.
Figure 213-14 Small irregular peripheral anterior synechiae. After argon laser trabeculoplasty.
tumor ( Fig. 213-13 ), ciliary body tumor, or partial lens subluxation may result in uneven angle depth. If an angle is closed partially with PAS as a result of previous angle-closure attacks or from some secondary forms of glaucoma and treatment is not instituted, full angle closure and painfully high IOP may result.
Adhesions of iris to trabecular meshwork, PAS effectively block aqueous outflow where they form. In a small, irregular fashion, they frequently may form after argon laser trabeculoplasty ( Fig. 213-14 ). Most feel this type of PAS is quite different in effect from the broad-based, aqueous outflow–blocking PAS seen in angle-closure and some secondary forms of glaucoma. In primary angle-closure glaucoma, synechiae usually form superiorly first ( Fig. 213-15 ), whereas PAS of uveitic glaucoma form inferiorly first. These synechiae are broad-based, tenting adhesions across the full angle depth, which may start as a build-up of exudates in the trabecular meshwork. In neovascular glaucoma, first a fibrovascular membrane lines the angle; then broad, vessel-filled synechiae form. The PAS of iridocorneal endothelial syndrome are characterized by their extension to cornea, anterior to Schwalbe’s line. Finally, PAS may form after trauma.
After trauma, angle examination may reveal much. As noted, mild trauma may be associated with iritis and PAS formation. Moderate blunt trauma may produce tears between the longitudinal and circular muscles of the ciliary body, which result in
Figure 213-15 Broad peripheral anterior synechiae with angle closure.
Figure 213-16 Angle recession (arrows).
posterior displacement of the ciliary body, or “angle recession” ( Fig. 213-16 ). This extra deepness of the angle may be complete or partial in the affected eye. It is noted easily by comparison of the angle depth with that of the contralateral, untraumatized eye. Usually, coexisting tears in the trabecular meshwork also occur at the time of trauma, but these heal with scarring and often are indiscernible on later gonioscopic examination. Other findings on angle examination after trauma may include increased pigmentation, blood ( Fig. 213-17 ) and, rarely, foreign bodies ( Fig. 213-18 ). Cyclodialysis clefts may occur, too—these are seen as a separation of iris and ciliary body from the ciliary sulcus.
Trabecular meshwork pigmentation may vary considerably in eyes. Normal eyes may have 0 (none) to 2+ or 3+ (heavy) pigment. Most commonly, 4+ (very heavy) pigmented angles are associated with pathology. Pseudoexfoliation syndrome and pigmentary glaucoma are associated with heavy meshwork pigmentation, as well as increased pigmentation of Schwalbe’s line, and create a so-called Sampaoelesi’s line ( Fig. 213-19 ). Specks of gray–white “dandruff” also may be seen in the angles of patients who have pseudoexfoliation. Iris melanoma may cause 4+ meshwork pigmentation. Finally, if an anterior or posterior chamber lens is placed improperly, with resultant haptic–iris chafe, heavy 4+ angle pigmentation can occur.
Vasculature in the angle is worthy of careful examination. Normal vessels may become engorged with inflammation and must be differentiated from neovascularization. Normal vessels are either part of the arterial circle in the ciliary muscle or are branches of it. The branches become radial arteries of the iris; these easily viewed iris vessels usually run strictly radially and do not meander. On the other hand, the arterial circle is typically posterior to the
Figure 213-17 Blood in an angle (after trauma).
Figure 213-18 An encysted foreign body in an angle.
Figure 213-19 Darkly pigmented trabecular meshwork.
periphery of the iris and, thus, commonly is not viewed. Some normal eyes, however, demonstrate forward displaced, visible portions of this circle. These portions, like their more posteriorly located counterparts, are characterized by circumferential vessel orientation and undulating shape. These vessels virtually never attach anterior to the scleral spur. Also, congenitally abnormal vessels occasionally are seen with congenital glaucoma. Such vessels may form a hairpin loop that extends to Schwalbe’s line, but they have both ends in iris stroma and do not arborize abnormally.
Figure 213-20 Neovascularization of an angle (arrows).
To be differentiated from such vessels are neovascular vessels ( Fig. 213-20 ), which usually grow from the circumferential ciliary body artery erratically onto angle wall and iris. These tend to meander irregularly and do not follow either a circumferential or radial course as normal vessels do. Such vessels grow onto the iris surface, not into stroma (whence come normal iris vessels). Abnormal vessels grow forward across the angle, over scleral spur, onto meshwork, and even over Schlemm’s line, another key differentiating characteristic compared with normal vessels.
Neovascularization of the angle usually extends to cover the iris, although it stays within the angle initially and is accompanied by fibrous tissue ingrowth. This fibrous tissue, although invisible to gonioscopic examination, is that portion of the neovascular process which results in eventual angle contracture and closure, with increased IOP. Associated with ischemia and vascular retinopathy, this type of neovascularization usually carries the eye to blindness and phthisis if left untreated. Also, neovascularization of the angle may be seen with uveitis and Fuchs’ heterochromic cyclitis. The neovascularization associated with uveitis tends to be as aggressive and as difficult to treat as that from ischemia. Interestingly, the neovascularization seen with Fuchs’ heterochromic cyclitis may behave differently. These vessels tend to be finer, and less tendency exists to branching and a greater tendency to spontaneous bleeding. Occasionally, these fine vessels may not be associated with glaucoma, unlike the neovascularization seen from ischemia.
Before concluding a discussion of angle examination and pathology, the variations seen in normal and abnormal infant angles should be mentioned. Normal infant angles are deep and have a flat iris insertion posterior to the scleral spur. They have little pigment in a translucent trabecular meshwork, and a normal ciliary body band is present. In eyes affected by congenital glaucoma, the key finding in some eyes is an anterior insertion of the iris directly into the trabecular meshwork. This is associated with a thin ciliary band, which may be viewed through the thin peripheral iris tissue. Abnormal vessels, as previously noted, may also be seen.
Ultrasound biomicroscopy is another form of ocular imaging. A B-scan technique is used, with high-frequency transducers (50–100?MHz) to provide high-resolution imaging of the anterior segment. Resolution approaches the 20–50?µm (microscopic) level, and images of anterior segment structures are significantly sharper than those seen using conventional ultrasonography. Penetration with these transducers is limited to approximately 5?mm, but this still is sufficient to allow excellent imaging of the entire anterior segment.
Instrumentation involves the use of an ultrasonographic apparatus with a scanning head on an articulated arm ( Fig. 213-21 ).
Figure 213-21 The ultrasound biomicroscopy apparatus. (Courtesy of Dr. C. Pavlin.)
Figure 213-22 Ultrasound biomicroscopic image of an eye that has plateau iris. (Courtesy of Dr. C. Pavlin.)
An eyecup is filled with methylcellulose and applied to the reclining patient’s eye; subsequently the examiner places the probe in the eyecup. Gentle movement of the probe establishes maximal image clarity.
Ultrasound biomicroscopy has been used to clarify the relationships between the drainage angle, ciliary body, zonular apparatus, and iris in many types of glaucoma.  It is particularly useful in the examination of a patient who has plateau iris ( Fig. 213-22 ). Anterior placement of ciliary processes, which prevents peripheral iris from falling back after iridectomy, has been visualized well using this technique in these patients. Additionally, the technique has helped define the anatomy in some patients who have pigmentary glaucoma and iris concavity, and even has demonstrated elimination of iris concavity after iridectomy. Ultrasound biomicroscopy also has provided helpful clinical information in cases of pupillary block, angle recession, supraciliary effusion, and malignant glaucoma.   The technique has been useful to those who have access to it, but many consider it less a clinical aid and more a research tool by which to clarify the underlying mechanisms of disease.
OPTIC DISC, NERVE FIBER LAYER, AND VISUAL FIELDS
So important are these remaining aspects of the clinical examination, that each is discussed in separate chapters. Suffice it to say here that, usually as a result of IOP or drainage angle pathology, nearly all forms of glaucoma share a characteristic pattern of optic disc damage, with or without associated visual field
changes. Thus, no clinical examination of a potential glaucoma patient is complete without thorough disc, nerve fiber layer, and visual field analysis.
Tonometry, gonioscopy, nerve fiber layer analysis, disc examination, and visual field analysis are elements crucial to diagnosis of the individual patient’s glaucoma. These crucial aspects are incorporated into a complete ocular examination of each patient. This examination begins with a good history, which often indicates glaucoma masquerade syndromes or the diagnoses of certain secondary forms of glaucoma. Of importance are medical histories remarkable for diabetes, hypertension, stroke, migraine, or Raynaud’s or venereal disease. A surgical history of severe trauma with blood loss or gastrectomy may be significant, as may an ocular history of repeated episodes of red eye, trauma, or surgery. It is necessary to establish systemic medicines taken by the patient, whether glucocorticoids have been used, and whether the patient is aware of a family history of glaucoma. Mainly, tonography is a useful research tool.
Careful slit-lamp examination is important, too. Interstitial scars, dystrophy, guttata, keratic precipitates, endothelial pigment, a posterior membrane, and abnormal thickening must be sought in corneal examination. The nature of the anterior chamber must be established (e.g., fully deep and quiet). Iris transillumination, texture and shape, and nature of the lens capsule and lens (e.g., excessively sclerotic, in normal position) are determined. For a pseudophakic or aphakic eye, the condition of the vitreous (e.g., presence of pigment cells) is important. Posterior examination (e.g., for masses, retinal attachment, vascular events) is also key.
All of these and other pertinent aspects must be addressed by a meticulous examination. After such an examination, with special attention to the key aspects of IOP, angle nature, disc health, and visual fields (as noted above), a proper diagnosis usually may be made. Only then can attention be turned to management options.
1. Kolker AE, Hetherington J Jr. Becker–Shaffer’s diagnosis and therapy of the glaucomas, ed 5. St Louis: CV Mosby; 1983.
2. Kaiser-Kupfer MI, McCain L, Shapiro JR. Low ocular rigidity in patients with osteogenesis imperfecta. Invest Ophthalmol Vis Sci. 1981;20:807–9.
3. Drance SM. The coefficient of scleral rigidity in normal and glaucomatous eyes. Arch Ophthalmol. 1960;63:668–74.
4. Simone JN, Whitacre MM. The effect of intraocular gas and fluid volumes on intraocular pressure. Ophthalmology. 1990;97:238–43.
5. Johnson MW, Han DP, Hoffman KE. The effect of scleral buckling on ocular rigidity. Ophthalmology. 1990;97:190–5.
6. Friedenwald JS. Contribution to the theory and practice of tonometry. Am J Ophthalmol. 1937;20:985–1024.
7. Friedman E, Irvy M, Ebert E, et al. Increased scleral rigidity and age related macular degeneration. Ophthalmology. 1989;96:104–8.
8. Hetland–Eriksen J. On tonometry. 2. Pressure recordings by Schiøtz tonometry on enucleated human eyes. Acta Ophthalmol. 1966;44:12–9.
9. Foster CS, Yamamoto GK. Ocular rigidity in keratoconus. Am J Ophthalmol. 1978;86:802–6.
10. Friedenwald JS. Some problems in the calibration of tonometers. Am J Ophthalmol. 1948;31:935–44.
11. Goldmann H, Schmidt TH. Uber applanations-tonometrie. Ophthalmologica. 1957;134:221–42.
12. Ehlers N, Bramsen T, Sperling S. Applanation tonometry and central corneal thickness. Acta Ophthalmol (Copenh). 1975;53:34–43.
13. Mark HH. Corneal curvature in applanation tonometry. Am J Ophthalmol. 1973; 76:223–4.
14. Moses RA. The Goldmann applanation tonometer. Am J Ophthalmol. 1958; 46:865–9.
15. Moses RA, Lin CH. Repeated applanation tonometry. Am J Ophthalmol. 1968; 66:89–91.
16. Pepose JS, Linnette G, Lee SF, MacRae S. Disinfection of Goldmann tonometers against human immunodeficiency virus type 1. Arch Ophthalmol. 1989;107: 983–5.
17. Perkins ES. Hand-held applanation tonometer. Br J Ophthalmol. 1965;49:591–3.
18. Krieglstein GK, Waller WK. Goldmann applanation versus hand-applanation and Schiøtz indentation tonometry. Graefes Arch Klin Exp Ophthalmol. 1975;194: 11–6.
19. Jain MR, Marmion VJ. A clinical evaluation of applanation pneumotomography. Br J Ophthalmol. 1976;60:107–10.
20. West CE, Capella JA, Kaufman HE. Measurement of intraocular pressure with a pneumatic applanation tonometer. Am J Ophthalmol. 1972;74:505–9.
21. Fienkel REP, Hong YJ, Shin DH. Comparison of the Tono-Pen to the Goldmann applanation tonometer. Arch Ophthalmol. 1988;106:750–3.
22. Hessemer V, Rossler R, Jacobi KW. Tono-Pen, a new hand-held tonometer: comparison with the Goldmann applanation tonometer. Klin Monatsbl Augenheilkd. 1988;193:420–6.
23. Panek WL, Boothe WA, Lee DA, et al. Intraocular pressure measurement with the Tono-Pen through soft contact lenses. Am J Ophthalmol. 1990;109:62–5.
24. Myers KJ, Scott CA. The non-contact (“air-puff”) tonometer: variability and corneal staining. Am J Optom Physiol Opt. 1975;52:36–46.
25. Shields MB. The non-contact tonometer. Its value and limitations. Surv Ophthalmol. 1980;24:211–9.
26. Grant WM. Tonographic method for measuring the facility and rate of aqueous flow in human eyes. Arch Ophthalmol. 1950;44:204.
27. Kronfeld PC. Tonography. Arch Ophthalmol. 1952;48:393–404.
28. Podos SM, Becker B. Tonography—current thoughts. Am J Ophthalmol. 1973; 75:733–5.
29. Goethrals M, Missotten L. Intraocular pressure in children up to 5 years of age. J Pediatr Ophthalmol Strabismus. 1983;20:49–51.
30. Brubaker RF. The effect of age on aqueous humor formation in man. Ophthalmology. 1981;88:283–8.
31. Armaly MF. On the distribution of applanation pressure. I. Statistical features and the effect of age, sex, and family history of glaucoma. Arch Ophthalmol. 1965; 73:11–8.
32. Wallace J, Lovel HG. Glaucoma and intraocular pressure in Jamaica. Am J Ophthalmol. 1969;67:93–100.
33. Tomlinson A, Phillips CI. Applanation tension and axial length of the eyeball. Br J Ophthalmol. 1970;54:548–53.
34. Newell FW, Krill AE. Diurnal tonography in normal and glaucomatous eyes. Trans Am Ophthalmol Soc. 1964;62:349–74.
35. Leonard TJK, Kerr-Muir MG, Kirby GR, Hitchings RA. Ocular hypertension and posture. Br J Ophthalmol. 1983;67:362–6.
36. Lempert P, Cooper KH, Culver JF, Tredici TJ. The effect of exercise on intraocular pressure. Am J Ophthalmol. 1967;63:1673–6.
37. Biro I, Botar Z. On the behavior of intraocular tension in various sport activities. Klin Monatsbl Augenheilkd. 1962;140:23–30.
38. Coleman DJ, Trokel S. Direct-recorded intraocular pressure variations in a human subject. Arch Ophthalmol. 1969;82:637–40.
39. Maddox TS Jr, Kielar RA. Comparison of the influence of ketamine and halothane anesthesia on intraocular tensions of nonglaucomatous children. J Pediatr Ophthalmol. 1974;11:90–3.
40. Meyers EF, Krupin T, Johnson M, Zink H. Failure of nondepolarizing neuromuscular blockers to inhibit succinylcholine-induced increased intraocular pressure; a controlled study. Anesthesiology. 1978;48:149–51.
41. Williams BI, Ledinghham JG. Significance of intraocular pressure measurement in systemic hypertension. Br J Ophthalmol. 1984;68:383–8.
42. Klein BEK, Klein R, Moss SE. Intraocular pressure in diabetic persons. Ophthalmology. 1984;91:1356–60.
43. Aziz MA. The relationship of IOP to hormonal disturbance. Bull Ophthalmol Soc Egypt. 1967;60:303–22.
44. Shiose Y. The aging effect on intraocular pressure in an apparently normal population. Arch Ophthalmol. 1984;102:883–7.
45. Peczon JD, Grant WM. Glaucoma, alcohol, and intraocular pressure. Arch Ophthalmol. 1965;73:495–501.
46. Hepler RS, Frank IR. Marijuana smoking and intraocular pressure. JAMA. 1971; 217:1392.
47. Higginbotham EJ, Kilimanjaro HA, Wilensky JT, et al. The effect of caffeine on intraocular pressure in glaucoma patients. Ophthalmology. 1989;96:624–6.
48. Mehra KS, Roy PN, Khare BB. Tobacco smoking and glaucoma. Ann Ophthalmol. 1976;8:462–4.
49. Leydhecker W, Akiyama K, Neumann HG. Der intraokulare druck gesunder menschlicher augen. Klin Monatsbl Augenheilkd. 1958;133:662–70.
50. Colton T, Ederer F. The distribution of intraocular pressures in the general population. Surv Ophthalmol. 1980;25:123–9.
51. Forbes M. Gonioscopy with corneal indentation: a method for distinguishing between appositional closure and synechial closure. Arch Ophthalmol. 1966;76: 488–92.
52. Kolker AE, Hetherington J Jr, eds. Becker and Shaffer’s diagnosis and therapy of the glaucomas, ed 5. St Louis: CV Mosby; 1976.
53. Scheie HG. Width and pigmentation of the angle of the anterior chamber. Arch Ophthalmol. 1957;58:510–2.
54. Spaeth GL. The normal development of the human anterior chamber angle: a new system of descriptive grading. Trans Ophthalmol Soc U K. 1971;91:709–39.
55. van Herick W, Shaffer RN, Schwartz A. Estimation of width of angle of anterior chamber. Am J Ophthalmol. 1969;68:626–9.
56. Riley SF, Nairn JP, Maestre FA, et al. Analysis of the anterior chamber angle by gonioscopy and by ultrasound biomicroscopy. Int Ophthalmol Clin. 1994;34: 271–82.
57. Pavlin CJ. Practical application of ultrasound biomicroscopy. Can J Ophthalmol. 1995;30:225–9.
58. Pavlin CJ, Ritch R, Foster FS. Ultrasound biomicroscopy in plateau iris syndrome. Am J Ophthalmol. 1992;113:390–5.
59. Pavlin CJ, Macken P, Trope G, et al. Ultrasound biomicroscopic features of pigmentary glaucoma. Can J Ophthalmol. 1994;29:187–92.
60. Pavlin CJ, Rutnin SS, Devenyi R, et al. Supraciliary effusions and ciliary body thickening after scleral buckling procedures. Ophthalmology. 1997;104:433–8.