Coverage of the the Hawaiian Eye Meeting, January, 2009
Comments in italics are the responses of the author to the information presented.
Leon Herndon, MD from Duke University presented his thoughts on the rational use of optic nerve and retinal nerve fiber layer imaging in the diagnosis and management of glaucoma patients at the Hawaiian Eye Meeting, January, 2009.
He began with a case presentation of a 73 year old Caucasian male with a diagnosis of primary open angle glaucoma (POAG) made 7 years ago and a history of treatment with laser trabeculoplasty OU and most recently glaucoma drainage device surgery OD. The patient is currently using brimonidine, timolol and travaprost OS. Visual acuity is OD=20/70, OS=20/30. Intraocular pressure (IOP) is OD=13 mmHg, OS=18. Central corneal thickness (CCT) is OD=466 microns and OS=464. The optic nerve evaluation reveals severe glaucomatous optic nerve damage with a vertical cup to disc OD=0.95, OS=0.9 to 0.95. The visual field shows the right eye to have a dense superior and inferior arcuate scotoma with a split fixation superiorly, and the left eye to have a dense inferior arcuate scotoma with a superior nasal step. An OCT was ordered that showed the right eye to have severe superior and inferior nerve fiber layer (NFL) thinning and the left eye to have severe superior and moderate inferior NFL loss. The question he poses is: “How does imaging help in this patient?”
We know from large scale glaucoma clinical trials that structural loss can precede visual field loss. For example, in the Ocular Hypertension Treatment Study, an endpoint of progression from ocular hypertension to glaucoma was defined as a change in optic nerve cupping (structure), or a change in visual field (function), or both. Of those participants that showed progression to an endpoint, 55% were based on optic nerve changes alone, 35% on visual field alone, and 10% on both. Thus, if we were to rely on visual field testing for progression, we would have missed over half of those patients that progressed to glaucoma.
Actually, this brings up several interesting points. The first is the one just stated, that structural changes precede functional changes in a majority of patients. However, the structural changes here are expert evaluation of glaucomatous changes in the appearance of the optic nerve, not glaucoma imaging. Some may argue that changes in the RNFL actually precede optic nerve cupping, so that this percentage may be underestimated. Another point is that over one third of subjects actually showed a worsening on standard achromatic perimetry (white on white visual field testing) prior to any notable change in the optic nerve. The last notable finding was the very poor concordance of visual field and optic nerve progression (only 10%!).
The well known structure versus function curve in glaucoma represents current thinking of many experts on the progression of glaucoma (see figure 1). As time passes on the x axis, the RNFL exhibits damage first, followed closely by optic nerve changes. Only after some time has passed does the visual field begin to show damage. As the disease progresses to advanced stages, the RNFL and optic nerve bottom out, but the visual field continues to show a measurable decline until blindness. Thus, glaucoma imaging modalities may have their greatest use in early and moderate disease, where they are able to detect the presence and progression of early disease. Once severe damage has occurred, however, the RNFL is so damaged that measuring it will likely add little information for patient management.
Figure 1: Structure Function Relationship in Glaucoma
Dr. Herndon then presented information from the Ophthalmic Technology Assessment Committee report on advanced glaucoma imaging by lead author Shan Lin in the journal Ophthalmology. This evidence based review examined available published studies on the HRT 2, Stratus OCT, and GDX VCC and the ability to aid in the diagnosis of glaucoma and detection of progression. They found no level one evidence, but several level two studies showing no difference in one device versus another in ability to diagnosis glaucoma and detect progression. Several studies such as (Medeiros IOVS) have shown that the sensitivity of the devices to detect glaucoma increase with severity of the disease. This makes sense, as the more advanced glaucoma cases are easily distinguished from normals. However, the ability to detect progression may be decreased in more advanced disease, as test variability increases with increasing damage (Ortega, IOVS).
He concluded with a case presentation of a patient that may be more appropriate for initial and follow up imaging. The patient is a 36 year old female with high myopia who was found to have elevated IOP by a referring optometrist. Visual acuity is 20/20 OU, IOP OD=17mmHg, OS=20, CCT OD=592, OS=592. The optic disc evaluation shows a cup to disc ratio of 0.4 OD and 0.5 OS. The visual field is normal OU, and the OCT shows a full RNFL OU. Advanced imaging technology may be better suited for distinguishing normal from pre-perimetric glaucoma or for following progression in mild or moderate glaucoma.
It makes sense to use glaucoma imaging in cases where it is likely to aid in diagnosis or treatment decisions based on progression. As Dr Herndon suggested, there is little utility in advanced cases of optic nerve damage. Indeed, reimbursement for glaucoma imaging is already under scrutiny from private health insurers and may become so by Medicare as well. This is in response to the sudden explosion in billing for these procedures as more ophthalmologists are purchasing the devices. Longitudinal studies that show the usefulness of imaging in glaucoma diagnosis and progression need to be performed in order to provide evidence based support for their continued use. Until then, rational use of the technology in those patients that are likely to benefit from it is our responsibility.
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