Evaluating a patient with a possible diagnosis of glaucoma is a challenge. A glaucoma suspect is an individual who is at risk of losing visual function from glaucoma but in whom glaucomatous damage is not clearly evident.1 The term glaucoma suspect refers to a situation where the angle is open on gonioscopy and there is an absence of secondary causes of glaucoma such as pigment dispersion syndrome, pseudoexfoliation, inflammation, or trauma. An individual can be classified as a glaucoma suspect based on an elevated IOP (ocular hypertension), a suspicious optic disc appearance, a suspicious visual field, significant risk factors, or a combination thereof.

RISK FACTORS
Ophthalmologists have long recognized ocular hypertension (IOP>21 mm Hg) as a risk factor for glaucoma. Other factors include African American race, a family history of glaucoma, and advanced age.1 The Ocular Hypertension Treatment Study2 helped define baseline factors that increase the risk of converting to glaucoma in eyes in which the pressure is elevated and the optic disc and visual field are normal. Those risk factors include a central corneal thickness of <556 µm, a C/D >0.4, and a larger-than-average pattern standard deviation on an otherwise normal threshold visual field.3 Additional ocular and systemic risk factors are diabetes, hypertension, high myopia, cardiovascular disease, and migraine/vasospasm, all of which the practitioner must take into account.1

OPTIC DISC
When considering the disc itself, clinicians may become alert to the possibility of glaucoma owing to certain features. Increased cupping (diffuse or focal narrowing of the disc rim), asymmetric cupping, and recurrent disc hemorrhages are classic high-risk findings. Additionally, other disc types exist where the overlap between glaucomatous and nonglaucomatous discs is greater, such as occurs with tilted discs, large optic nerve heads with thin disc rims, and anomalous discs.

Traditionally, clinicians have used stereo photography both for documenting the baseline optic disc appearance and for follow-up. This technique is not useful for distinguishing glaucomatous from nonglaucomatous nerves at baseline, however. Recently, computerized optic disc imaging devices have been used for both baseline evaluation and the follow-up of discs. Practitioners have had limited success with these instruments in separating normal eyes from those with early glaucoma, but these devices provide valuable information that, in combination with other clinical information, can be quite helpful in identifying susceptible individuals.4-6 The two devices my colleagues and I use in our practice are confocal scanning laser tomography with the Heidelberg Retinal Tomograph (HRT; Heidelberg Engineering GmbH, Dossenheim, Germany) and nerve fiber layer (NFL) polarimetry with the GDx VCC (Laser Diagnostic Technologies, San Diego, CA).

PERIMETRY
Practitioners typically assess a patient's visual field with white-on-white threshold automated perimetry. A normal field does not preclude a diagnosis of glaucoma, however, because structural optic disc atrophy precedes field loss on standard threshold perimetry.7 Thus, other methods have been developed to assess “pre-perimetric” glaucoma.

Automated perimetric strategies that test a smaller subpopulation of retinal ganglion cells have the potential to detect visual field loss earlier. The tests we use in our practice are short wavelength automated perimetry (SWAP; Carl Zeiss Meditec Inc., Dublin, CA) and frequency doubling technology (Welch Allyn Medical Products, Skaneateles, NY). Various studies have shown that these methods may be able to detect visual field defects that predate those on standard perimetry by 3 to 5 years or to confirm questionable defects on standard perimetry.8,9 One of the drawbacks of SWAP is the test's variability. It is therefore important that patients who are familiar with perimetric testing and who have performed well on previous white-on-white testing be considered for these versions of functional testing. Furthermore, practitioners must confirm defects prior to initiating or escalating therapy.

PATIENT EVALUATION
The typical patient who is being evaluated as a glaucoma suspect has mixed clinical findings. The goal of the initial examination is to gather as much data as possible and to document the patient's baseline status. Based on these findings, the practitioner either prescribes treatment or follows the patient. Following are some examples of patients from my practice.

Case 1: Recurrent Disc Hemorrhages
A 57-year-old white male presented in 1995 with 20/15 UCVA OU and mild ocular hypertension. His IOP ranged between 23 and 26 mm Hg, his discs had a healthy appearance with a C/D ratio of 0.2, and his fields were normal on standard threshold perimetry. I obtained optic disc photos to document baseline and followed the patient. When he later developed a disc hemorrhage in his right eye, I initiated treatment that resulted in an IOP of 18 mm Hg OU.

Over the next 3 years, the patient's IOP gradually crept up to 22 mm Hg OU, and I observed another disc hemorrhage in his right eye. HRT and SWAP results were normal, but the presence of the hemorrhage prompted me to increase his medication in order to regain an IOP of 18 mm Hg OU.

In 2002, another disc hemorrhage occurred despite an IOP of 18 mm Hg OU. The HRT and SWAP findings were unchanged. By this time, our practice had begun using pachymetry, and I measured the patient's central corneal thickness at 502 µm OD and 505 µm OS. The thinness of the patient's corneas indicated that Goldmann applanation tonometry underestimated his IOP. I adjusted the patient's treatment to reach a target IOP in the mid-to-low teens. Thus far, I have noted no additional disc hemorrhages, and the results with SWAP and HRT have remained unchanged.

Case 2: Myopic Discs
A 66-year-old black female presented in 1990 with high myopia (-13.00 D OD and -10.50 D OS), 20/25 BCVA OU, a positive family history of glaucoma, and mild hypertension. Her IOP was in the midteens bilaterally, and a tilted disc with a posterior staphyloma was present in each eye (Figure 1A and B). I obtained baseline disc photos and threshold automated perimetry and found nonspecific changes on the field. Treatment was not initiated.
By 2003, the patient's BCVA had declined to 20/50 OU due to cataracts. On examination, her IOP remained stable, but her discs seemed more cupped compared to the baseline photos. New disc photos were obtained, and a photo-to-photo comparison showed a stable optic disc appearance. Cataract surgery resulted in 20/25 UCVA OU. Perimetry still demonstrated nonspecific loss, but the NFL evaluation using the GDx VCC was within the normal acceptable range (Figure 1C). The central corneal thickness was normal at 553 µm OD and 556 µm OS. The patient continues to be followed without treatment.


Figure 1. This patient had tilted, myopic discs with thinning of the temporal rims (A, B). Imaging with the GDx VCC showed normal NFL thickness but mild superior flattening consistent with tilted discs.


Case 3: Disc Cupping, Normal IOP
A 67-year-old black male with hypertension, adult-onset diabetes, a negative family history of glaucoma, and an exotropia with mild amblyopia in his left eye presented for a routine examination in 1999. His BCVA was 20/20 OD and 20/30 OS, and his IOP measured

12 mm Hg OD and 14 mm Hg OS. Suspicious disc cupping was present (Figure 2A and B), and the fields were borderline, especially in the patient's left eye due to his inability to maintain fixation. I obtained baseline disc photos.

By 2003, the patient's IOP had increased to between 13 and 17 mm Hg OD and between 16 and 20 mm Hg OS. I obtained new disc photos, which were stable compared to the baseline set. Repeat Humphrey Visual Field testing (Carl Zeiss Meditec Inc.) showed stability in his right eye but was unreliable in his left. Pachymetry measurements revealed thin central corneas (474 µm OD, 470 µm OS), and GDx VCC testing showed very thin NFLs bilaterally (Figure 2C). I initiated treatment.


Figure 2. This patient exhibited mild cupping in his right eye (A) and moderate cupping with a thin superior rim in his left (B). Imaging with the GDx VCC showed pronounced NFL loss at the superior and inferior poles of the optic disc (C).


Case 4: Ocular Hypertension, Small Optic Nerve Heads
A 59-year-old white female with mild ocular hypertension presented for a second opinion regarding her need for glaucoma medication. She had a negative family history of glaucoma. Her medical history was remarkable for asthma and hypertension. Her UCVA was 20/25 OU, and her untreated IOP ranged from 22 to 25 mm Hg OD and from 20 to 24 mm Hg OS. She had small, cupless optic nerve heads and borderline threshold visual fields.

The patient began treatment in 2000 but ceased it 2 years later due to multiple medication intolerances. Further evaluation with frequency doubling technology showed borderline visual field changes. Imaging with the GDx VCC found that her NFLs were within an acceptable, normal range, although thinner in her left eye (Figure 3). Pachymetry measured 599 µm OD and 595 µm OS. The patient was followed without treatment.


Figure 3. Imaging with the GDx VCC showed a normal NFL that was slightly thinner in this patient's left eye.

SUMMARY
There often is no correct answer on whether to treat a patient who is a glaucoma suspect. The clinician must assess individual risk factors, obtain good baseline studies, and discuss treatment options with the patient. The risk of glaucomatous damage must be balanced with the risk and cost of treatment. Because most glaucomatous changes will occur slowly, it is not imperative to make a treatment decision on the patient's first visit. Continued surveillance and regular follow-up is important, however, because the preservation of patients' vision is the practitioner's ultimate goal.

Eydie Miller, MD, is Clinical Associate Professor at the Scheie Eye Institute, University of Pennsylvania Health System, Philadelphia. She disclosed no financial interest in the products and companies mentioned herein. Dr. Miller may be reached at (215) 662-8188; eydie.miller@uphs.upenn.edu.

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