Continuing Medical Education - Optometry

Three Stages of Primary Open Angle Glaucoma

STAGE 1

The first stage is increased pressure in the eye often accompanied by decrease circulation to the nerve. In this stage neither optic nerve head nor the fiber layer shows any damage, even on nerve fiber layer imaging studies. Optic nerve head hemorrhages have not been seen.

In these cases it is important to order pachymetry testing to exclude inaccurate readings on Goldmann tonometry. If the cornea, for instance is over 600 microns, the applanation reading might be overestimating the pressure. Your ocular hypertensive patient may actually be normotensive and potentially unduly alarmed by being labeled as such. Normal pachymetry is about 540 microns.

In the Ocular Hypertensive Treatment Study (OHTS) (Archives of Ophthalmology, June 2002, Kass et al.) patients with high intraocular pressures were randomized into treated and untreated groups. Study criteria were 24 to 32 in one eye and 21 to32 in the fellow eye, normal visual field testing, and normal optic disk on clinic exam and stereophotography. The goal was a pressure reduction of 20% of more and to reach an IOP of 24 or less in the treated group with commercially availably topical ocular hypotensive medications.

At 60 months into the study, 9.5% of the obsevation (untreated) group had developed glaucoma, whereas only 4.4% of the treated group had glaucomatous changes 9defined as either visual field or optic nerve defects). The study concluded:

“Although this does not imply that all patients with borderline or elevated IOP should receive medication, clinicians should consider initiating treatment for individuals with ocular hypertension who are at moderate or high risk for developing primary open angle glaucoma.”

At this stage one level, the addition of the ocular blood flow meter to my armamentarium has been welcomed and has affected my clinical decision-making. If there is asymmetric cupping (though still within normal range) and the ocular blood flow is compromised in the eye with greater cupping, that may tilt me in favor of treatment. The test is well tolerated by patients, who appreciate the extra information brought by this advanced technology.

STAGE II

In stage two, tissue damage is now seen. Clinical exam with 90 diopter ophthalmoscopy may show: abnormal optic nerve cupping as inferior notching, thinning of the neuroeretinal rim temporally, optic nerve head hemorrhages, increased visibility of the lamina cribosa or shunt vessels on the disk surface.

The retinal ganglion layer can be examined by red-free light looking for loss of nerve fibers along the superior or inferior nerve bundles. This however has shown limited usefulness and has been supplanted by nerve fiber layer (NFL) imaging studies that do both qualitative and quantitative analysis.

NLF imaging functions in four ways:

1. Confirmatory of suspicious cupping or other optic nerve abnormalities
2. Normal in presence of suspicious cupping thus making the diagnosis of glaucoma less likely
3. Abnormal in the presence of normal cupping thus making the specter of glaucoma more likely
4. Inconclusive because of corneal bifrigence problems, media irregularities such as cataracts or other issues

In early stage two, visual field changes may not yet be evident. A normal visual field in the presence of tissue damage does not rule out glaucoma by any means, as most glaucomatologists believe that a threshold of tissue damage is necessary before abnormalities arise on standard Humphrey testing. Conversely there are cases where visual field defects show up before demonstrable tissue (optic nerve) changes on clinical exam, although this is the exception, rather than the rule, in my experience.

STAGE III

In stage three, visual field changes occur. In most cases tissue damage (optic nerve cupping or NFL damage) has already occurred. It is interesting to survey patients to see if they have noticed changes in the vision. If the field loss is asymmetric, I’ll alternatively occlude each eye and ask the patient if the vision differs between each side.

I generally recommend two visual field tests for glaucoma. On the first visit, I will run a full field Armaly screening, as this studies the nasal step, arcuate, and temporal wedge areas and is relatively short. On the second visit, a 24-2 SITA is performed. Keep in mind that it makes the defects look more localized and denser than its cousin test the 24-2 Fastpack. If the SITA is normal and my clinical suspicion is high, I may later run a Fastpack. On rare occasions, I’ll order a full-field 120 testing. New technologies that utilized double frequency testing strategies have a role in early glaucoma detection, but are not yet useful in monitoring for progression.

The goal in stage three is to monitor for signs of deterioration. In stage 3, technologies such as NFL studies, and optic nerve topography studies may be more useful that ophthalmoscopy in assessing progression. In my own practice I am relying more on these types of studies and less on ophthalmoscopy or send comparison of optic nerve photography to “make the call” that progression has occurred.

We are all familiar with the vagaries of following visual fields for progression. If a change – not confirmed by pressure or optic nerve changes - is detected, the field should be repeated to verify that a new defect or worsening of an existing defect has actually occurred. There are times when one area worsens, but in the same eye a previously noted scotoma is less dense. Here, looking at the mean deviation gives a sense of the overall field loss. Co-morbid conditions such as cataract and macular degeneration must be considered in cases where visual field progression has occurred in the absence of concomitant cupping.

Despite all the technology available to monitor fields and optic nerve progression, accurate measurements of intraocular pressure do matter. The reason is simple: sometimes visual field testing, optic nerve and NFL imaging, and ocular blood flow give inconsistent or inconclusive results. Knowing our patients’ baseline pressure readings, current pressure readings, and corneal pachymetry readings is our fall-back position. In marginally controlled patients, it is often helpful to do a drug holiday to re-establish a new baseline pressure. Serial tonometry and pharmacological provocative tests still have a place in our repertoire of glaucoma testing.

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