Article

GLAUCOMA TECHNOLOGY AND MANAGEMENT

Q: How can I integrate new diagnostic technology, and when should I move a patient to a different drug?

A: The answers have to do with need and target.

INTEGRATION

The short answer is “see a need, fill a need.” To accomplish this, consider these consensus statements from the 10th World Glaucoma Association’s (WGA-10) Consensus Series “Diagnosis of Primary Open Angle Glaucoma:”

  • “Clinical evaluation and documentation of the optic nerve head is essential for the diagnosis and the monitoring of glaucoma. . . [and] photography is effective to document glaucomatous optic disc appearance and nerve fiber layer damage. [Furthermore], imaging technologies, including optical coherence tomography (OCT), confocal scanning laser ophthalmoscopy (CSLO) and scanning laser polarimetry (SLP), provide an objective and quantitative approach to detect and monitor glaucoma.”
  • “Functional testing is essential for the evaluation, staging and monitoring of glaucoma [and] standard automated perimetry (SAP) is the reference standard for all functional testing.”

Based on these main principle points, and to most effectively diagnose and manage glaucoma in our offices, optometrists definitely need some form of structural and functional diagnostic technology, with dependable corroboration between these two technologies. In addition, O.D.s need to regularly perform reliable Goldmann applanation tonometry to help determine the risk for the development and progression of glaucoma, pachymetry to aid in putting the IOP into proper context and gonioscopy to help determine the proper diagnosis and treatment.

Regarding other more advanced technologies, WGA-10 states that there is “. . .strong evidence implicating lower corneal hysteresis as a risk factor for glaucoma development and progression. . .” Finally, OCT Angiography (OCT-A) may likely play a more prominent role in the future by helping O.D.s to better monitor for glaucomatous progression, reports a study in Ophthalmology.

Diagnosing and managing glaucoma is a dynamic puzzle with many moving pieces, and each of the above diagnostic tools helps add pieces to the puzzle. With this in mind, which critical pieces may be missing in the optometrist’s office? Which basic or advanced technology would help the O.D. better put these puzzle pieces together?

Investment updates within the practice and/or respectful collaboration with fellow colleagues who may have such testing more readily available, enable optometrists to provide the best care for glaucoma suspects and patients. For specific tips on how to use this equipment precisely, see “Integrate Devices Efficiently,” which appeared in the Glaucoma PMO series at bit.ly/GlaucomaIntegrate .

MAKING THE MOVE

The short answer is it’s all about “staying on target.” To accomplish this, consider this consensus statement from the 7th World Glaucoma Association’s (WGA-7) Consensus Series “Medical Treatment of Glaucoma:”

“The target IOP is the IOP range at which the clinician judges that the estimated rate of progression is unlikely to affect the patient’s quality of life.”

In other words, the optometrist’s goal is to prevent functional vision loss in patients now and, for some patients, decades later. With this ambitious goal in mind, optometrists need to set a dynamic target IOP range for each patient, based on the patient’s age and stage of the disease. As a very general rule for a very multifactorial disease, “For both POAG and PACG after an iridotomy, in mild glaucoma, the initial target IOP range could be kept as 15 mmHg to 17 mmHg, in moderate glaucoma, 12 mmHg to 15 mmHg and in the severe stage of glaucomatous damage, 10 mmHg to 12 mmHg,” according to a study in the Indian Journal of Ophthalmology. This initial target IOP range can be an effective guide in the O.D.’s decision process and a strong motivator for patient cooperation.

What should optometrists consider/do when the IOP is not on target? When (not if) this scenario occurs, in my mind, we must then initially consider these three very likely possibilities:

  1. The patient is not taking the drops as prescribed (either partial or complete in adherence) and/or
  2. the patient is not getting the drops in as prescribed (due to poor technique, immediately wiping eyes after instillation, etc.) and/or
  3. the drops the patient are taking simply are not working.

If the first two possibilities are the reasons, further patient education about the progressive nature of glaucoma, reviewing the technique, setting alarm clock reminders, etc., may be all that is needed to solve the problem. (For additional information on achieving patient compliance to the prescribed medication, see the sidebar “Medication Compliance Tips,” which appeared in the Glaucoma PMO series article, “Progressing Glaucoma,” at bit.ly/ProgressingGlaucoma .)

However, if the latter possibility is the reason, optometrists need to add yet another drop and/or change to one of the newer drugs to reach target IOP. In such situations, we have literally hundreds of choices to consider amongst all of the different drug classes. A caveat: With such a vast selection, it can be easy to prescribe the usual or, at the very least, hover in the clinically dangerous state of indecision.

To avoid such pitfalls, O.D.s should remember that behind every drop or prescription, there is a patient: What if that patient was your family member? What if the patient was the optometrist? With that patient-centric approach, which topical treatment(s) will best help the patient stay on target?

Optometrists can wisely and effectively, decide on the best topical treatment options, as we consider each patient individually, identify stages of the disease and the rate/risk of progression. Now, more than ever, we have more topical “tools” with which to initiate and maintain treatment. With the right tools, we can make a difference. OM

Glaucoma Drugs

ALPHA-ADRENERGIC AGONISTS:

→ Apraclonidine: 0.5% and 1% (Iopidine, Novartis and generic)

→ Brimonidine: 0.2% preserved with BAK and 0.15% non-BAK preservative and 0.1% (Alphagan P, Allergan, preserved with Purite)

BETA-BLOCKERS:

→ Beta-1 selective betaxolol hydrochloride 0.5% (generic) and 0.25% (Betoptic-S, Novartis)

→ Levobunolol hydrochloride 0.5% (Betagan, Allergan) and 0.25% and 0.5% (generic)

→ Timolol hemihydrate 0.25% and 0.5% (Betimol, Akorn)

→ Timolol maleate 0.25% and 0.5% (Timoptic, Timoptic Ocudose and Timoptic XE, Valeant Ophthalmic) and 0.5% (Istalol, Bausch + Lomb, and generic)

CARBONIC ANHYDRASE INHIBITORS:

→ Acetazolamide 125 mg and 250 mg tablets (generic) and 500 mg sustained-release capsules

→ Brinzolamide 1% (Azopt, Novartis)

→ Dorzolamide 2% (generic and Trusopt, Merck)

FIXED COMBINATION:

→ Brinzolamide/brimonidine 1%/0.2% (Simbrinza, Novartis)

→ Brimonidine 0.2%/timolol 0.5% (Combigan, Allergan)

→ Dorzolamide 2%/timolol 0.5% (generic; Cosopt and Cosopt PF, Akorn)

→ Preservative-free dorzolamide and dorzolamide/timolol (Imprimis Pharmaceuticals)

→ Netarsudil/latanoprost ophthalmic solution, 0.02%/0.005% (Rocklatan, Aerie Pharmaceuticals)

RHO-KINASE (ROCK) INHIBITOR:

→ Netarsudil ophthalmic solution 0.02% (Rhopressa, Aerie Pharmaceuticals)

PROSTAGLANDIN ANALOGUES:

→ Bimatoprost 0.03% (generic)

→ Bimatoprost 0.01% (Lumigan, Allergan)

→ Latanoprost 0.005% (generic and Xalatan, Pfizer)

→ Latanoprost ophthalmic emulsion 0.005% (Xelpros, Sun Pharma)

→ Latanoprostene bunod 0.024%, (Vyzulta, Bausch + Lomb)

→ Tafluprost 0.0015% (Zioptan, Akorn)

→ Travoprost 0.004% (generic and Travatan Z, Novartis)