Progression of glaucoma

Letters to the Editor Progression of Glaucoma Dear Editor: We read with interest Jonas et al’s findings that age, a thin neuroretinal rim, and a ␤-zone are risk factors for progression of glaucoma.1 We note, however, that intraocular pressure (IOP), a recognized risk factor for glaucoma, was not considered in the analysis. We feel this study would hold more relevance to glaucoma management if the IOP had been analyzed as a risk factor for disc progression. Optic disc progression is ultimately associated with visual field progression. AGIS 7 states that “low IOP is associated with a reduced progression of visual field defect.2 If IOP has not been excluded as the cause, how can we assume that the disc progression was related to the disc morphology? Could the disc morphology be a consequence of the pathology (which may be a relatively elevated IOP)? The authors stated that all patients had an IOP of ⬍21 mmHg on the day of examination. However, this gives no indication of the actual IOP relative to a particular disc. Neither do we know how the IOP varied over the duration of the study, and it’s relationship with the individual discs. AGIS 7 states that the lower the IOP, the less chance of progression. Patients with an IOP of 12 mmHg are less likely to have progression of disc and visual field defects than patients with an IOP of 20 mmHg. It would be helpful to know if the discs that progressed were in eyes with an IOP in the upper range, or whether disc morphology is an independent risk factor. JOANNA M. KOPPENS ANTHONY J. KING Nottingham, United Kingdom References 1. Jonas JB, Martus P, Budde WM, et al. Small neuroretinal rim and large parapapillary atrophy as predictive factors for progression of glaucomatous optic neuropathy. Ophthalmology 2002;109:1561–7. 2. AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol 2000;130:429 – 40.

Author reply Dear Editor: We completely agree with Drs Koppens and King that intraocular pressure is a main risk factor for progression of glaucoma, as has also been shown by AGIS.1 Concerning the comments raised by Drs Koppens and King with respect to our article, the main question may be whether the morphologic predictors became irrelevant after adjustment for intraocular pressure. Having reanalyzed our data, we have found that none of the significant morphologic predictors as described in the article became statistically insignificant after adjustment for intraocular pressure. Additionally, odds ratios related to the different morphologic predictors did not change after adjustment for intraocular pressure. This sug-

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gests that, besides intraocular pressure as shown in preceding studies,1 a small neuroretinal rim and a large ␤-zone of parapapillary atrophy may be predictive factors for progression of chronic open-angle glaucoma. It also agrees with other studies2– 4 in which an advanced stage of glaucoma was found to be a predictive factor for further progression of the disease. JOST B. JONAS, MD WIDO M. BUDDE, MD ANSELM JUNEMANN, MD JOCHEN HAYLER, MD Erlangen, Germany PETER MARTUS Berlin, Germany References 1. AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. Relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol 2000; 130:429 – 40. 2. Araie M, Sekine M, Suzuki Y, Koseki N. Factors contributing to the progression of visual field damage in eyes with normaltension glaucoma. Ophthalmology 1994;101:1440 – 4. 3. AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 12. Baseline risk factors for sustained loss of visual field and visual acuity in patients with advanced glaucoma. Am J Ophthalmol 2002;134:499 –512. 4. Tezel G, Siegmund KD, Trinkaus K, et al. Clinical factors associated with progression of glaucomatous optic disc damage in treated patients. Arch Ophthalmol 2001;119:813– 8.

Interface Fluid after LASIK Dear Editor: Dr Hamilton et al1 presented the important clinical picture of a clear fluid-filled space in the cornea between the flap and stromal bed after LASIK associated with high intraocular pressure. In their discussion they state that “the role of endothelial function in developing interface fluid associated with elevated intraocular pressure is uncertain.” To clarify this issue further, and to expand the differential diagnosis, I describe herein two patients who had developed interface fluid pockets that look very similar to the clinical presentation by Dr Hamilton et al (Fig 1), but these were associated with low endothelial cell counts, with normal intraocular pressures. Both of these patients had had corneal transplantation and had LASIK due to high levels of anisometropia. In one of the patients the endothelial cell count was uncountable before the surgery. The other patient had an endothelial cell count of 678 cells/mm2. It appears that the flap interface is an area for potential fluid collection, both from high intraocular pressure and from endothelial cell dysfunction. A similar clinical picture can occur in patients who have steroid-induced glaucoma after LASIK or who have endothelial cell dysfunction before or after LASIK. These cases of high pressure after LASIK are extremely important from a clinical standpoint.