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Journal Français d'Ophtalmologie
Volume 40, n° 4
pages e121-e123 (avril 2017)
Doi : 10.1016/j.jfo.2016.01.018
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Progression of visual field defect in an unilateral glaucoma patient after an unilateral photorefractive keratectomy
Glaucome unilatéral chez un patient opéré de laser de surface sur un seul œil

N. Saib , B. Le Du, C. Virevialle, J. Akesbi, J.-P. Nordmann
 Hôpital des Quinze-Vingts, 28, rue de Charenton, 75012 Paris, France 

Corresponding author.

The growing popularity and development of refractive surgery in recent years have brought accuracy of intraocular pressure (IOP) measurement to the fore. Goldmann applanation tonometry and pneumatonometer have limitations and several sources of error have been described. These include variations in corneal biomechanics, central corneal thickness (CCT) and corneal curvature (CC). The reduction of measurement IOP after refractive surgery may lead to an increasing problem in glaucoma diagnosis and management in the future. To date, we report the first case of progression in unilateral visual field defect after an unilateral photorefractive keratectomy (PRK).

Case presentation

A 60-year-old man presented to the hospital Quinze-Vingts with an unilateral glaucoma. He was operated at 41-year-old by unilateral photorefractive keratectomy (PRK) on the right eye. The correction before surgery was on the right eye –7.25 (160°, –1) and on the left eye –6 (0°, –1.50) the programmation of the excimer laser was –9 D on the right eye, he did not want to operate the left eye because of the loss of near vision. There was no family history of glaucoma, no traumatism, no pseudoexfoliation syndrome and no pigmentary dispersion. On examination, the uncorrected-visual acuity without correction in right eye was 0 LogMAR and distance visual acuity with contact lens (–6.50 D) in left eye was 0 LogMAR. The intraocular pressure measurements with pneumatonometer was 13mmHg in right eye and 19mmHg in left eye and with the Goldmann applanation tonometer was 14mmHg in right eye and 18mmHg in left eye without treatment. The pachymetry was 465μm for right eye and 533μm for left eye. In gonioscopy, angle was wide open in the both eye. The examination of the optic nerve found a cup/disc ratio at 0.6 on the right eye with optic nerve superior notch and at 0.5 on the left eye (Figure 1).

Figure 1

Figure 1. 

Optic nerve photography.


The visual field 24-2 and 10-2 found an inferior arcuate scotoma of Bjerrum on the right eye and was normal for the left eye (Figure 2). The FDT Matrix was strictly normal for the left eye.

Figure 2

Figure 2. 

Humphrey 24:2 and 10:2 visual field for right eye.


The OCT RNFL reported a loss of Superior RNFL thickness on the right eye and normal RNFL thickness for the left eye, the macular retinal ganglion cell analysis reported a loss of thickness on the right eye and normal on the left eye (Figure 3). The Ocular Response Analyser detected loss of biomechanical corneal on the right eye: corneal hysteresis (CH) 8.5mmHg, corneal resistance factor (CRF) 7.5mmHg, Goldmann-correlated IOP (IOPg) 11.2mmHg, corneal-compensated IOP (IOP cc) 14.3mmHg. On the left eye, CH 10.9mmHg, CRF 11.2mmHg, IOP g 16.6mmHg, IOP cc 16.4mmHg. The echodoppler of the trunks supraaortics and the cerebral MRI were normal. Topical bitherapy by bimatoprost 0.3mg/ml and Timolol 5mg/ml once daily was started in right eye. Timolol was stopped because of bradycardia induced. Eighteen months after induction of bimatoprost 0.3mg/ml, the intraocular pressure with Goldmann applanation was 13mmHg in the right eye and 15mmHg in the left eye. On the visual field, visual scotoma worsen in the right eye: the mean deviation of the 10-2 Humphrey visual field study increased from –7.09dB to –8.37dB. The visual field was normal in left eye. Decision of selective laser trabeculoplasty on right eye has been taken and bimatoprost 0.3mg/ml was started in left eye for prevention because of the gravity of glaucoma in right eye in this young patient.

Figure 3

Figure 3. 

OCT RNFL and Macular retinal ganglion cell analysis of each eye.



Progression of a visual field defect has already been reported after Laser-Assisted In Situ Keratomileusis (LASIK). As for glaucoma development associated with LASIK, there are several reports of secondary steroid-induced glaucoma [1, 2] and the pressure elevation during the suction ring used during laser in situ keratomileusis may have precipitated optic nerve head ischemia and visual field defect [2, 3, 4, 5]. To date, it is the first case report of progression in a visual field defect after PRK. Three tracks of physiopathology are possible for this case. Firstly, the normal-tension glaucoma or high myopia glaucoma, but it is strictly an unilateral glaucoma and there is not early sign of glaucoma in the controlateral eye. Secondly, secondary steroid-induced glaucoma, but there are no evidence of a long-term treatment with corticosteroid and glaucoma scotoma still evolve slightly in time without corticosteroid; it is unlikely that short treatment of corticosteroid could generate chronic trabecular meshwork damage. Thirdly, the modification of biomechanical cornea (reduction of CH) induced by refractive surgery could induce fragility of all tissue of eyeball, distension of all intraocular tissue: cornea, sclera, cribriform plate and promote glaucoma. After refractive surgery, IOP measurements are lower than preoperatively, because of the reduction of cornea thickness and modification of biomechanical cornea and can lead to diagnosis‘s delay. Glaucoma, a leading cause of preventable blindness, has a high prevalence among myopic patients, the primary population undergoing refractive surgery. In this case, there was a discrepancy between the optic nerve damage, lowly in OCT RNFL, and visual field which was hardly hit. This underlines the importance of visual field and ganglion cells study. Inspection of the optic nerve prior and after refractive surgery may allow identification of some of the patients who are at risk, if any doubts exist, visual field should be performed.

Disclosure of interest

The authors declare that they have no competing interest.


Hamilton D.R., Manche E.E., Rich L.F., Maloney R.K. Steroid-induced glaucoma after laser in situ keratomileusis associated with interface fluid Ophthalmology 2002 ;  109 : 659-665 [cross-ref]
Shaikh N.M., Shaikh S., Singh K., Manche E. Progression to end-stage glaucoma after laser in situ keratomileusis J Cataract Refract Surg 2002 ;  28 : 356-359 [cross-ref]
Inoue K., Hashida S., Tajima Y., Wakakura M., Inoue J., Tomita G. Progression of visual field defect in a normal-tension glaucoma patient after laser in situ keratomileusis Eye 2004 ;  18 : 850-853 [cross-ref]
Bushley D.M., Parmley V.C., Paglen P. Visual field defect associated with laser in situ keratomileusis Am J Ophthalmol 2000 ;  129 : 668-671 [inter-ref]
Weiss H.S., Rubinfeld R.S., Anderschat J.F. LASIK associated visual field loss in a glaucoma suspect Arch Ophthalmol 2001 ;  119 : 774-775

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