Pacific Glaucoma CE Optometry Yudcovitch

Glaucoma is the third most common cause of blindness in the United States, with over 120,000 legally blind from the disease. Over 3 million people in the U.S. have the diagnosis; of those diagnosed, about half have a visual impairment. Over 70% of glaucoma is of the primary open angle glaucoma (POAG) type. In addition, between 6-12 million people in the U.S. have elevated intraocular pressure (IOP), or ocular hypertension. Almost 5 million office visits per year are due to glaucoma. This course takes a procedure-based approach to provide a basic review and update on examination tests, diagnostic signs, and new instrumentation for glaucoma management.

Several risk factors for glaucoma should be considered in the case history. Ethnicity is a strong risk factor. Blacks are 3 to 6 times more likely to develop primary open angle glaucoma than are Caucasians. POAG also occurs earlier and is 6 times more likely to cause blindness. In fact, POAG is the leading cause of blindness in Blacks.(1)

A family history of glaucoma should also be pursued. Close relatives of patients with POAG have an increased prevalence of glaucoma.(2) Although genetic factors are obviously involved, the mode of inheritance is unclear. A gene associated with glaucoma, the myocilin gene, has been isolated, but only 5% of POAG cases result from mutations of this gene.(3)

A history of systemic vascular conditions such as heart disease, Reynaud’s syndrome, and migraine are especially important in determining the patient's risk for normal tension glaucoma.(4)

Increasing age also raises the risk of developing glaucoma. Myopia (particularly higher myopia) may also be a risk factor.

Visual acuities are typically not affected by glaucoma in its early or moderate stages, but may be affected in more advanced stages, particularly when the papillomacular bundle is affected.

Because glaucoma is typically a bilateral condition, a difference in pupillary response is often hard to assess, unless there is notable assymetric nerve damage between the eyes. A sluggish pupillary response to light may occur, usually in more advanced stages of the disease.

Like visual acuities and pupils, defects are not noted unless the disease is advanced. Desaturation of color may be more common than complete color vision loss in moderate stages of glaucoma.

POAG has no obvious and universal signs that can be detected using biomicroscopy. However, certain signs are associated with secondary forms of glaucoma.

Pigmentation on the corneal endothelium (e.g., Kruckenberg’s spindle), peripheral transillumination of the iris, and increased pigment in the trabcular meshwork may indicate pigmentary dispersion glaucoma.

Grey flake-like material on the anterior lens capsule in a target pattern (i.e., a central disc and peripheral ring with an intervening clear area), and loss of pupillary ruff pigment may indicate pseudoexfoliative glaucoma. (Pseudoexfoliation should not to be confused with true exfoliative material occasionally seen with 'glassblowers' cataract).

Pseudoexfoliative glaucoma is more common in patients of Northern European/Scandinavian ethnicity.

A difference in color between the irides (iris hetereochromia) may warn of a unilateral glaucoma. Iris neovascularization (rubeosis iridis), usually secondary to diabetes or vascular occlusion, may indicate neovascular glaucoma.

Iris synechiae can accompany uveitic or inflammatory glaucoma. Pupillary corectopia (irregular-shaped pupil) and/or pupillary dialysis (breakage of the iris root connection to the ciliary body) can be associated with fibrotic or neovascular changes in the anterior chamber angle, or it can result from a prior injury, potentially resulting in traumatic (angle recession) glaucoma.

A narrow anterior chamber, and/or a hazy, ‘steamy’ cornea with perilimbal injection suggests angle closure glaucoma. Opacities in the anterior lens cortex (glaucomflecken) may also result from highly elevated intraocular pressure associated with angle closure glaucoma or malignant glaucoma secondary to cataract surgery complication.

As an interesting side-note, highly elevated pressures from glaucomatocyclic crisis (Posner-Schlossman Syndrome) tend to show no markedly obvious biomicroscopic findings except for mild anterior uveitic signs. This rare condition typically affects young male adults, of which 40% are positive for white blood cell component HLA-Bw54. These patients may be completely asymptomatic.(5)

Having replaced Schiotz indentation tonometry many years ago, Goldmann applanation tonometry is considered the ‘gold standard’ in measurement of intraocular pressure. Goldmann readings are, however, influenced by factors including corneal thickness and curvature. These factors are discussed in detail below.

The Pascal Dynamic Contour Tonometer (DCT) is a newer IOP measurement device that incorporates a flexible measurement tip to evenly distribute applanation across the corneal surface. This negates the effect of differences in corneal thickness. The DCT offers the potential for obtaining true IOPs for eyes in which there has been significant corneal disruption, e.g., eyes that have had LASIK.(6)

The Proview™ tonometer (Bausch & Lomb) is a spring-based, non-electrical instrument that allows patients to monitor their own intraocular pressure at home. It uses a phosphene-based method of feedback in which a patient presses the instrument tip against upper nasal eyelid until a glowing pressure phosphene is perceived in the lower temporal field of view. The pressure against the lid at that point corresponds to IOP. IOPs obtained with the Proview have recently been found to be significantly lower than those measured with Goldmann and thus may overestimate the effects of pressure-lowering drugs.(7)

Ocular pressures between 10 and 21mmHg are considered ‘statistically normal’ with the mean value being around 16 mmHg. However at least one in six people with POAG never have pressures above 21 mmHg. Thus, there is no ‘normal’ ocular pressure; rather IOP is merely a risk factor for glaucoma. The higher the IOP, the greater the risk of glaucoma.

Ocular pressures tend to follow a diurnal curve, being higher in the early morning and lower in the evening. Patients with POAG may have wider diurnal curve than those without glaucoma. Therefore, serial tonometry, in which tonometry measurements are taken at several different times on the same day, may be useful in determining the range of ocular pressures.

When measuring the IOP, care should be taken not to apply pressure to the eye (e.g., when lifting the upper eyelid) in order to not artificially raise the pressure reading.

In general, IOP tends to increase with age by an average of about 1.2 mmHg per decade of life.

Pachymetry typically involves use of either an ultrasound or an optical probe to assess corneal thickness. It has recently become a very popular and useful procedure because of the need to adjust Goldmann IOP measures to compensate for differences in corneal thickness between patients.

Use of Pachymetry to Adjust Goldmann IOP Readings

The original calculations used to determine IOP using Goldmann applanation tonometry were based on an assumed corneal thickness of 520 microns. Central corneal thicknesses of greater than 520 microns would cause the true IOP to be overestimated (i.e., the Goldmann readings would be too high) and thicknesses of less than 520 microns would cause the IOP to be underestimated (i.e., the Goldmann readings would be too low). Although these relationships were well known, few doctors considered them when using Goldmann readings to diagnose or follow glaucoma.

Several years ago, a randomized, multi-center clinical trial called the Ocular Hypertensive Treatment Study (OHTS) was conducted to evaluate progression to glaucoma in a group of ocular hypertensives with IOPs greater than 24 mmHg and no signs of glaucoma (optic nerve cupping, visual field loss, etc.). Half the subjects were given hypotensive medication, and the other half received none. After five years, 9.5% of non-treated subjects progressed to POAG, but only 4.4% of treated subjects progressed. The study demonstrated that prophylactic treatment of ocular hypertensive patients can decrease the risk of glaucoma development.(8)

An additional goal of the OHTS was to assess a number of risk factors beyond ocular hypertension for developing glaucoma. Central corneal thickness (CCT), as measured by pachymetry, was one of the factors considered. CCT was found to be a powerful predictor for progression to POAG in the study patients; the thinner the cornea, the greater the risk of developing glaucoma.(9)

As group, Blacks had a significantly thinner corneas than did the Caucasians in the study, and this was associated with an increased risk of converting to glaucoma.(9) Similar to the thinner corneas found in the Black ocular hypertensives, Blacks in general have significantly thinner central corneas than do Caucasians.(10) They also have higher rates of glaucoma and glaucoma-related blindness.

It has been suggested that the relationship between corneal thickness and glaucoma is associated with the fact that IOP measurements of patients with thin corneas underestimate true IOP because of the applanation procedure used by the Goldmann. This might mean that thin cornea patients would not be diagnosed as readily or treated as vigorously if Goldmann IOP was the only criterion used.

(As a group, the ocular hypertensive OHTS subjects were found to have thicker corneas than normals and POAG patients, which suggests that perhaps they were grouped in this category because of an IOP overestimation.)(11)

Subsequent to the OHTS, several well-designed studies have suggested that corneal thickness is also a predictor of field loss in patients with glaucoma.(12)

These and other findings, along with development of commercially available pachymeters, have lead to renewed interest in adjusting Goldmann IOP readings to compensate for CCT. The goal of adjusting Goldmann IOPs seems to be one of allowing doctors treating glaucoma to continue using the "old" IOP numbers they are familiar with but customizing them for individual patients. Thus, an adjusted IOP of 21 mmHg would mean essentially the same for every patient regardless of race or CCT, and management (e.g., setting target pressures in adjusted IOP units) would be somewhat simplified.

Not using a CCT adjustment may mean that patients (e.g., Blacks) with thin corneas might have their true IOPs underestimated, which could lead to a delay in diagnosis, inadequate treatment, and a higher risk of blindness. Patients who have undergone LASIK or other corneal-thinning surgeries may also present with artifactually low IOPs. Conversely, patients with corneal edema, Fuch’s dystrophy, or other cornea-thickening conditions may have artifactually high IOPs. It should be noted that corneal thickness does not affect the true IOP itself, but only affects the Goldmann measured IOP.

A number of adjustment tables, such as the one shown in Table 1, which is based on the average CCT of about 550 microns for Caucasians, have been proposed. Different correction tables for use with races (e.g,. Blacks) having different mean CCTs might be needed.

Gonioscopy allows direct viewing of the angle structures using an mirror lens. Gonioscopy should be used in every case of suspected open angle glaucoma to rule out a partial narrow angle component.

Because angle configuration and structures, as well as iris insertion, can be seen during gonioscopy, gonioscopy is essential for evaluating secondary glaucomas. Pigmentation on Schwalbe’s line (called Sampolesi’s line) and/or in the trabecular meshwork may indicate pigmentary dispersion syndrome with the increased risk of pigmentary glaucoma. Likewise, pseudoexfoliative flakes in the anterior chamber angle might represent pseudoexfoliative syndrome, again with an increased risk of pseudoexfoliation glaucoma.

A gonio lens treated to withstand laser light levels can be used during the procedure of trabeculoplasty to treat pigmentary glaucoma and pseudoexfoliation glaucoma.

Variation in width of the angle structures might suggest angle recession or traumatic glaucoma. Lack of visibility of most or all of the anterior chamber angle structures suggests angle closure glaucoma. The Sussman or Posner-type gonioscopy lenses can also be used therapeutically (via corneal compressions) in cases of highly elevated IOP (over 40 mmHg) .

In some instances, the gonioscopy lens must be tilted to view over bowed or plateau iris configurations to view the angle structures. Pupillary block glaucoma, in which the pupillary margin is adherent to the anterior lens capsule and the iris bows forward (iris bombe) due to blocked aqueous flow, may also be detected using gonioscopy.

Visual field testing is currently the only functional visual test for detection and assessment of glaucoma.

Glaucoma patients can present with several types of visual field defects. However, in most cases progression of visual field defects is parallel to optic nerve head changes. The first change in the optic nerve head is usually inferior or superior rim tissue thinning that occurs on the inside edge of the rim. Because the nerve fibers that enter the optic nerve head on the inside edge of the rim originate from areas close to the disc, the earliest visual field changes are seen in the paracentral field, either in the superior or inferior field. These earliest changes are seen as small areas of depressed sensitivity (relative paracentral scotomas) between 5 and 20 degrees of fixation.

As the rim continues to thin, depressed areas enlarge and deepen circumferentially along the distribution of arcuate nerve fibers (Seidel scotoma) until they coalesce to form an arcuate-shaped defect that joins with the blind spot (Bjerrum or arcuate scotoma). Because the inferior or superior rim tissue is first involved and then followed by involvement of the opposite rim, double arcuate scotomas can develop.

A nasal step (more loss above or below the horizontal meridian in the nasal field) is frequently associated with paracentral scotomas or arcuate scotomas but may be present by itself. A temporal wedge defect (temporal to blind spot) may appear. Field loss gradually spreads to periphery and also centrally. Eventually only a small island of central vision and a temporal “sliver” are left. Overall generalized depression of sensitivity may also be an indicator, although this is not definitive for glaucoma. Since anatomically nerve fibers do not cross the horizontal raphe, glaucomatous field defects tend to obey the horizontal midline. This is in contrast to post-chiasmal field defects, which tend to obey the vertical midline.

The classic kinetic target Goldman bowl perimeter has been for the most part replaced by numerous automated computer-driven perimeters from several companies (e.g. Dicon, Synemed, Interzeag, Oculus, Medmont, etc.).

Even though all the other automated perimeters can be used to assess the visual field for glaucoma, the Carl Zeiss-Humphrey II Visual Field Analyzer is considered by many to be the current ‘standard’ of visual field testing. Several visual field testing strategies are available on this perimeter, including:

The Humphrey/Welch-Allyn Frequency-Doubling Technology (FDT) Perimeter utilizes the frequency-doubling principle to help diagnose visual field loss caused by glaucoma. A stimulus is presented that consists of alternating low spatial frequency black-white grating bars creating. The flicker effect produced by this stimulus isolates M (Magnocellular) cells in the retina and their large diameter neurons. These large neurons may be the first to die in glaucoma.

Good correlation was seen between FDT visual fields and traditional white stimulus on white background threshold visual field tests. The Humphrey Matrix is a newer field analyzer that works on the same principle as FDT, but provides a larger visual field area (same size as a 30-2 threshold test) with the same test points as a 30-2 threshold test.

Various confounding elements may cause misinterpretation of visual field results. These confounds can include: ptosis, patient fatigue, small pupils, poor alignment, trial lens holder artifacts and other diseases creating glaucoma-like patterns (e.g., retinal vascular occlusions, optic neuropathies, retinal scarring, and strokes).

Patients with early glaucomatous field loss often show variability or fluctuation of fields within a single test session and/or from session to session. Some patients give unreliable visual fields some of the time, while others give unreliable results all of the time. Multiple measurement attempts may be necessary to confirm field loss. The OHTS results suggested that to get a good baseline visual field, at least two fields taken about two weeks apart are necessary. If the fields do not show similar results, a third visual field taken several months later is useful.(16)

The automation of field testing has not eliminated the need for a skilled technician to be present during testing. The more skillful the technician, the less likely the field will be unreliable. It is necessary to ensure that the patient is properly occluded (to eliminate false positives), that the patient is looking through the appropriate trial lens (to reduce chances of false field loss or generalized sensitivity reduction), and to be sure that the trial lens is as close to the patient's eye and as well-centered as possible to prevent false arcuate scotoma artifacts. The technician must also help the patient retain fixation because excessive loss of fixation makes the visual field invalid.

Fundus photography is a common procedure used in the management of glaucoma. Stereo white-light photos are standard, with photos taken at least every two years (or more frequently if changes are noted). Red-free imaging of the nerve fiber layer is also an option. Photography can be used as adjunct to detailed stereoscopic ophthalmoscopic evaluation of the optic nerve and nerve fiber layer. Digital photographic options are now available and can be coupled with computer analysis to quantify retinal features.

The doctor may follow glaucomatous progression with dilated fundus evaluations, examining the optic nerve, vasculature, and nerve fiber layer for changes. This examination is independent of the initial eye exam, and requires detailed diagrammatic documentation.

The only disc change that is completely diagnostic of glaucomatous damage is progressive thinning of the neural rim. Typically, progressive glaucomatous neuroretinal loss occurs in a sectorial sequence, usually beginning in the inferotemporal disc quadrant and progressing to the superotemporal, the temporal horizontal, the inferonasal and finally, the superonasal sector.

The size range for a normal optic nerve head is between 1.33 to 2.66 mm in diameter, with 1.5 mm considered to be average. Because the scleral canal size determines disc size, a larger scleral canal results in a larger optic nerve head size. There are about 1.2 million neurons entering the optic nerve head and these neurons require the same surface area as they leave the eye regardless of the disc size. Thus, an anatomically large disc creates a physiologically large cup, due to the larger space left over as the neurons leave the retina in the rim tissue. Up to a point, the size of the cup reflects the size of the disc and might not indicate any specific risk of glaucoma. Blacks and Latinos tend to have larger optic nerve head sizes than Caucasians and thus have larger physiological cups.(17)

When examining a patient for the first time, making a cup/disc (c/d) ratio estimation is appropriate. If no information about the patient's c/d ratio history is available, it cannot be determined whether the cup is enlarging, and thus no information about the risk of glaucoma in that eye is available.

However, evaluation of the rim tissue will give a much better index of glaucoma "suspicion." In normal discs, the thickness of the neural rim follows the "ISN'T" rule. The inferior rim is the thickest, followed by the superior rim, the nasal rim, and the temporal rim in order of decreasing thickness.

Typically, the first change in rim tissue caused by glaucoma is thinning of the inferior or the superior rim. Therefore, if the inferior rim is thinner than the superior rim, the patient may have glaucoma and further testing is warranted.

Typically, the horizontal ratio (H) is compared to the vertical ratio (V), (e.g., H/V = 0.6/0.65), and, in a normal disc, the ratios are very similar. As indicated above, the first changes to the disc in glaucoma are thinning of the inferior or superior rim followed by thinning of the opposite rim. This leads to vertical elongation of the cup and a greater vertical than horizontal ratio. A very focal area of thinning is called notching of the rim tissue and is a key sign that glaucoma may be present.

After superior and inferior rim thinning, temporal thinning of the neuroretinal rim occurs. A temporal rim that is less than 1/8 of the diameter of the optic nerve may indicate glaucomatous excavation.

Eventually undermining of the neuroretinal rim may extend concentrically around the optic nerve, creating a ‘bean pot’ appearance with deep (1 mm or 3 diopters) cupping. Laminar dots at the base of the cup may also become elongated slits (laminate striae), especially in the superior and inferior areas, as excavation of the nerve head progresses. Eventually only a sliver of nasal rim tissue may remain, with the cup taking up the rest of the nerve head.

Depigmentation of the peripapillary region and peripapillary chorio-retinal atrophy may be associated with glaucoma. This sign is called alpha and beta atrophy. It is important to distinguish high myopic atrophy, malinserted discs, and normal variations from peripapillary atrophy associated with glaucoma.

It should be noted that certain optic nerve conditions may mimic glaucoma or be present along with glaucoma. Examples are cases of ischemic optic neuropathy, toxic neuropathy due to tobacco or alcohol, or retrograde damage of axons due to pathway lesion in the brain (e.g., pituitary adenoma). Pallor of the nerve heads can be a normal variation (mild temporal pallor) or can be caused by ischemic problems or retinal disease (e.g., retinitis pigmentosa).

Several retinal vessel signs may suggest glaucoma. Vessel kinking/bayoneting at the cup edge is a classic finding due to the undermining of the neuroretinal rim tissue in glaucoma.

Nasal migration of disc vessels may occur over time, although this may or may not be a reliable indicator of glaucoma. Vessel “bowing” in cup may help determine cup depth and size. Baring of circumlinear vessels occurs as glaucoma advances due to exposure of the retinal arterioles and venules that reside in the gradually atrophying nerve fiber layer. As the nerve fibers die, the vessels become more exposed creating sharper appearing vessels.

Other vascular changes that occur in glaucoma include overpass cupping in which vessels eventually collapse into a bared area of atrophy in the optic cup. Drance splinter hemorrhages (flame-shaped hemorrhage crossing the optic nerve edge, usually at the inferior temporal disc margin). Because Drance hemorrhages precede glaucomatous damage in the nerve fibers, they are an ominous prognostic sign.(18)

Spontaneous venous pulsation can be present in normals, but arteriolar pulsation usually indicates excessively high intraocular pressure, or excessively reduced vascular pressure.

The normal nerve fiber layer is seen as fine silver glistening striations that correspond to nerve fiber bundles. It may be more obvious in darker pigmented fundi such as those of Blacks and Asians.

Examination of the nerve fiber layer can be performed with a clear binocular indirect or high plus lens. However, a red-free filter can highlight its appearance. The nerve fiber layer is the thickest in the inferior and superior areas, due to the neurons arching around the macula coming from the temporal periphery (papilomacular bundle) in addition to the neurons coming from the inferior and superior periphery. Defects in the nerve fiber layer may be seen as dark slits or wedges that emanate from optic nerve margin. An inferior temporal wedge defect is the most obvious nerve fiber layer defect and usually corresponds with inferior temporal notching and superior visual field loss. Slit defects (slightly larger than arterioles at the disc) may also be present although these can be seen in about 10% of normals. Diffuse nerve fiber layer thinning is more common in high pressure glaucoma and corresponds to diffuse visual field loss and constriction.

Of interest, “rake” nerve fiber layer defects associated with small refractile talc bodies may indicate that the patient has a history of injected substance abuse (e.g., cocaine or heroin). Early glaucomatous-like paracentral scotomas may also appear in the visual field of these individuals, confusing the presentation with glaucoma.

Diagnostic digital imaging has become a powerful new tool in glaucoma diagnosis and management. Computerized measurement of optic disc structure/size/area, cup size/volume, retinal nerve fiber layer thickness, and macular thickness provide a detailed analysis of the optic disc and retina.

Up to 40% of a person’s nerve fiber layer can be lost before any subjective visual field loss is clinically detectable using visual field testing. A new generation of digital instruments holds promise for making glaucoma detection more sensitive so that treatment can begin before significant nerve fiber damage has occurred.

This instrument uses low-intensity polarized light to measure the thickness of the nerve fiber layer and then it compares the patients data with an internal statistical database. The less polarization, the thinner the nerve fiber layer and the more likely it is that glaucomatous nerve fiber damage has occurred. The Variable Corneal Compensator (VCC) in the instrument adjusts for corneal stromal fiber polarization in the calculation of the nerve fiber layer thickness, thus providing a baseline measurement. A new baseline is required if corneal thickness changes due to LASIK or other reasons.

The instrument determines the nerve fiber thickness in a ring around the disc margin. In normal patients, the result is a double humped curve with the humps indicating the increased thickness in the superior and inferior regions of the retina. In a glaucoma patient, the humps are flattened indicating nerve fiber layer atrophy. The instrument also uses a statistical program to assign a number between 0 and 100 indicating the probability that the patient has glaucoma. The higher the number, the more likely glaucoma is present.

Two types of instruments are available – the HRT and HRT II Models. The instruments use scanning laser deviations that produce retinal and optic nerve head elevation/depression maps. The HRT II can be adapted to provide vascular flowimetry data of the optic nerve as well.

Many parameters are calculated using HRT data. Optic disc parameters include rim area and volume, disc area and volume, and c/d ratio. The mean nerve fiber thickness at the disc margin is also calculated.

The surface area of the rim tissue is one parameter that is closely associated with a glaucoma diagnosis. This matches what is seen using ophthalmoscopy. As glaucoma progresses, neurons on the inside of the rim atrophy and the rim tissue thins. This results in less surface area being visible.

Like the HRT, the RTA uses scanning laser deviations that are translated into retinal and optic nerve head elevation/depression maps. To determine glaucomatous damage, the RTA measures retinal thickness of the central 20 degrees of the fundus. This area contains 50% of the retinal ganglion cells, which make up around 30% of the total retinal thickness. Loss of ganglion cells and nerve fibers are reflected in decreased retinal thickness.

This instrument utilizes Michelson interferometry to create a very detailed cross sectional image of the disc and retinal layers, similar to an image created by ultrasound. The thickness of the retinal nerve fiber layer in the peripapillary region is compared to a database of thicknesses from normals. In addition, the OCT analyzes changes in the retinal nerve fiber layer from one exam to another.

Because of the cross sectional nature of the image, this instrument measures not only the thickness of retinal tissue but it can also assess changes in the tissue. This is very useful for assessing macular disease such as cystoid macular edema and macular holes.

As glaucoma research continues, other testing modalities have been explored to help the clinician in diagnosing and managing patients. Tonographic measures, multifocal electroretinograms (mERGs), ultrasonography, blood flow analyzers, and evoked potential systems have shown some clinical applications.

This instrument provides a detailed image of the anatomy (and pathology) in the anterior segment including cornea, iris, sclera, and ciliary body including Schlemm’s Canal. It replaces the discontinued Humphrey Ultrasound Biomicroscope.

Several mechanisms have been postulated to explain how elevated IOP causes the optic nerve damage that occurs in POAG. Although no single mechanism can adequately explain the great variations in the disease process, one factor most likely involved is vascular perfusion of the optic nerve head. It would be valuable to know what level of IOP can blood vessels serving the optic nerve head withstand before they partially collapse and cause a decreased the blood flow to the optic nerve head. To assess this dimension of glaucoma, instrumentation to measure the Ocular Blood Flow Analyzer (OBFA) has been developed.

The OBFA is a unique instrument that uses a complex air suspension system to provide real-time ocular pulse rate/strength/flow and tonometry. Decreased ocular blood flow indicates decreased optic nerve perfusion. Results from this instrument can help to determine which patients have easily compressed disc vasculature or poor flow and are thus at increased risk for glaucoma. Ocular blood flow has been found to be significantly compromised in many eyes with normal tension glaucoma.

Another instrument that measures blood flow to the optic nerve head is the Heidelberg Retinal Flowmeter (HRF). This instrument combines the HRT II confocal scanning laser with a color doppler flowmeter. Blood volume, flow, and velocity are measured on a microvascular level.

Poorer retinal hemodynamics were found in a group of glaucoma subjects compared with the controls suggesting that changes in the circulation of the optic nerve head could be an early indicator of the glaucoma process.(19)

This relatively new instrument uses multifocal visual evoked potentials (VEPs) to detect defects in the visual field. A major advantage of the devise is that a subjective response by the patient is not required therefore the device can used for retarded or otherwise non-communicative patients. The AcuMap may also have the potential to identify glaucomatous defects earlier than conventional perimetry. The Acumap was developed in Australia and recently approved for use in the US.

New research and technologies continue to inform and assist the practitioner in the diagnosis and management of glaucoma. The optometric physician should be aware of the current practice standards and instrumentation available to help in diagnosing glaucoma and in preventing the progression of the disease and ultimately prevent vision loss.

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American Academy of Ophthalmology. Summary benchmarks for preferred practice patterns. October 2002.

American Optometric Association Clinical Practice Guideleines. Open Angle Glaucoma, April 1998 Primary Angle Closure Glaucoma, March 1997.

Pacific University College of Optometry provides On-Line CE as a service to optometrists. The college does not endorse or recommend any products, equipment, or services that might be discussed in the courses. Courses are prepared by individuals believed to be experts in their areas of specialization who are compensated for their efforts. The College relies on their expertise to produce accurate and timely courses. Questions or concerns about courses should be directed to the individual authors and/or the Continuing Education Department at the College of Optometry at kundart@pacificu.edu .

CCT (microns)	Adjustment for Measured IOP mmHg
445	+7
455	+6
465	+6
475	+5
485	+4
495	+4
505	+3
515	+2
525	+1
535	+1
545	0
555	-1
565	-1
575	-2
585	-3
595	-4
605	-4
615	-5
625	-6
635	-6
645	-7

A Review of Glaucoma Examination Procedures and New Instrumentation