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Issue: April 2009 Managing Trial and Error in a Complicated Case
CONTINUING EDUCATION

Managing Trial and Error in a Complicated Case

Find out how 19 years of progress helped save this patient's vision.

This case demonstrates how much glaucoma therapy has changed since the 1990s — and why we need to keep adapting to those changes to provide the best patient care possible.

In 1992, a 44-year-old African American man with a negative ocular history presented with decreased visual acuity at near and occasional blurriness at distance. His mother had been diagnosed with primary open-angle glaucoma. I determined he had borderline high blood pressure, but he wasn't taking an antihypertensive medication.

Below are the results of my physical examination:

■ Visual acuity: 20/25 J3 at 16 inches OD; 20/25 J3 at 16 inches OS

■ Manifest refraction: OD +1.00-0.25× 090 20/20; OS +0.75-0.25×090 20/20, with an add +1.25 J1 at 16 inches

■ Pupils: PERRLA, absent relative afferent papillary defect (-RAPD)

■ Extraocular muscles: smooth and full

■ Color vision: normal on AO plates

■ Confrontation fields: full OU

■ Slit lamp exam: cornea clear OU; anterior chamber, deep and quiet OU; lens clear OU

■ IOPs: 30 mmHg OD; 48 mmHg OS

■ Gonioscopy: D-40-R OD, 1+ trabecular pigment OS E-40-R, 2-3+ pigment (Negative history of trauma reported)

■ Fundus evaluation: moderately large cup-to-disc ratio of .55/.55 for both cups, with sharp disc margins; neuroretinal rims were intact 360°. No retinal nerve fiber layer (RNFL) defects were observed

■ Media: clear OU

■ Threshold visual fields: normal and reliable using the Humphrey 24-2 program.

Deciphering the Results

Despite the patient's report to the contrary, the E-40-R, 2-3+ pigment gonioscopy measurement appeared to reflect a history of trauma OS. Average patients without narrow angles have a D-40-R configuration, without a 1+ trabecular meshwork pigment. Another important issue was his family history of glaucoma, but my biggest concern was his very high IOPs, which indicated prompt treatment, despite his average-looking cups and other normal findings.

Before choosing a treatment, I ruled out a history of chronic obstructive pulmonary disease, asthma, shortness of breath and cardiac disease. I also established that his pulse (76 beats per min.) and blood pressure (130/85) were normal. Therapies were limited in 1992, so I prescribed timolol maleate 0.5% (Timoptic, Merck & Co.) q12h OU and oral acetazolamide (Diamox Sequels, Duramed Pharmaceuticals Inc.) q12h.

Two days later, his IOPs dropped to 18 mmHg OD and 26 mmHg OS. He couldn't tolerate the acetazolamide because of significant gastrointestinal distress. I took the patient off the acetazolamide, continued him on timolol maleate 0.5% and added pilocarpine hydrochloride gel 4% (Pilopine HS, Alcon Laboratories Inc.) to be instilled in his left eye at bedtime.

More Control Needed

When the patient returned 4 weeks later, he reported excellent compliance but was experiencing reduced vision in his left eye, especially at night. His pupil was slightly miotic from the pilocarpine, but he was willing to continue with treatment to avoid surgery. His vision was corrected to 20/20 and his IOPs were in a safe range of 19 mmHg OD and 17 mmHg OS.

I continued with the same regimen and saw him 3 months later, at which time his pressures were in the upper teens and his optic nerve heads and visual fields remained unchanged.

Cloudy Vision

In November 1995, the patient returned with complaints of cloudy vision OS. He reported excellent compliance with his regimen. His visual acuity was 20/20 OD and 20/30 OS. His pupils were reactive OD, miotic and fixed OS. A slit lamp evaluation revealed a clear lens OD and a 2+ iatrogenic nuclear cataract OS, likely caused by the pilocarpine. He complained of a left-sided headache that resolved after being on pilocarpine for about 2 weeks. His IOP OS also had increased to 27 mmHg. His IOP OD was 19 mmHg. Visual fields and the nerve heads remained stable.

I added dipivefrin hydrochloride ophthalmic solution (Propine, Allergan Inc.), but this was unsuccessful because of intolerance. Next, I prescribed dorzolamide hydrochloride (Trusopt, Merck & Co.), but that failed to reduce his IOP OS. An argon laser trabeculoplasty, performed in February 1996, also wasn't successful in lowering his IOP in his left eye. His IOP OS increased to 30 mmHg within 1 month.

Few Options Remaining

Left with few options, I referred the patient for surgical trabeculectomy. The postoperative IOP was excellent in the left eye at 8 mmHg. His IOP in the right eye remained at 20 mmHg on timolol maleate 0.5%. The visual fields and optic nerve heads remained stable.

In July 1997, he presented with a chief complaint of greatly reduced vision OS. I found a dense nuclear cataract and a posterior subcapsular cataract OS. His visual acuity was now at 20/100 OS. The right lens remained clear. IOP was 21 mmHg OD and 9 mmHg OS.

The patient underwent cataract surgery, benefiting from an excellent outcome. Postoperative visual acuity was 20/20 OU (with plano OS). IOPs were 22 mmHg OD and 10 mmHg OS. The fundus was unchanged.

Constant Change

I had stabilized this patient after asking him to endure the adverse effects of three medications and two surgical procedures. But more change was about to occur.

In June 2002, the patient was asymptomatic, reporting excellent compliance with timolol maleate 0.5% OD and no visual complaints. However, the pressure in his right eye had climbed to 25 mmHg; his IOP in the left eye was 11 mm Hg with no medication.

I discontinued timolol maleate and switched him to latanoprost (Xalatan, Pfizer Inc.) OD to be taken at bedtime. This change reduced the pressure in his right eye to 14 mmHg within 4 weeks.

At this point, we'd just published the Ocular Hypertension Treatment Study (OHTS)1 and had learned of the significance of central corneal thickness (CCT). The patient's CCT was 548 microns OD and 535 microns OS.

With his history of elevated intraocular pressure, these corneal readings were thin and put him in a high-risk category, even though I hadn't realized it earlier. Had my treatment through the years been enough? The unchanged nerve heads and visual fields suggested he was fine (Figure 1). In November 2004, more than 2 years later, his pressures were 15 mmHg OD and 10 mmHg OS, and his optic nerve heads and visual fields were unchanged.

Figure 1. Despite normal-looking cups and normal visual fields, this patient required prompt treatment due to high IOPs.

Burning News

In January 2008, the patient reported that his right eye was burning and tearing excessively, and his left eye was tearing occasionally. His IOPs were 15 mmHg OD and 9 mmHg OS.

Tear breakup time was 2 seconds OU. A slit lamp evaluation uncovered superficial punctate keratitis, greater in the right eye than in the left eye. Realizing I needed to address his ocular surface irritation,2 I discontinued the latanoprost OD and replaced it with travoprost with sofZia (Travatan Z, Alcon Laboratories Inc.) to be taken at bedtime. I also added unpreserved artificial tears to be taken as needed OU.

Evidence suggests dry eye patients have fewer ocular symptoms if they use a benzalkonium chloride-free medication to prevent glaucoma progression.3

One month later, he reported that his eyes were feeling much better. Since then, I've continued with his medications. His longterm prognosis is excellent.

No Surgery Required

These new medications undoubtedly saved this patient's right eye from undergoing the same surgery as his left eye. Using today's therapeutic alternatives, we can achieve better outcomes without putting as much burden on the patient. This was true in all three cases I've presented. We just need to be diligent in our follow-up and resourceful in how we respond to our changing examination findings. OM


Dr. Bennett is director of the Glaucoma Center of Excellence at The Eye Institute and professor at the Pennsylvania College of Optometry at Salus University.

References
  1. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120:714–720; discussion 829–830.
  2. Leung EW, Medeiros FA, Weinreb RN. Prevalence of ocular surface disease in glaucoma patients. J Glaucoma. 2008;17:350–355.
  3. Fechtner RD, Budenz DL, Godfrey DG, et al. Prevalence of ocular surface disease symptoms in glaucoma patients on IOP-lowering medications. Poster presented at the annual meeting of the American Glaucoma Society, March 8, 2008, Washington, DC.
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