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Refractory intraocular pressure increase after photorefractive keratectomy
case
reports
Refractory intraocular pressure increase after photorefractive keratectomy Yair Levy, MD, Limor Hefetz, MD, David Zadok, MD, David Krakowski, MD, Pinhas Nemet, MD ABSTRACT A patient with developmental angle anomaly developed a corticosteroid-induced refractory increase in intraocular pressure (lOP) after photorefractive keratectomy (PRK). Trabeculectomy was required to reduce the pressure. Although rare, corticosteroid-induced refractory lOP increase is a serious complication of PRK and may necessitate trabeculectomy. More frequent monitoring of lOP in post-PRK patients and a re-evaluation of postoperative treatment are indicated. J Cataract Refract Surg
1997; 23:593-594
A
lthough photo refractive keratectomy (PRK) is considered a relatively safe treatment for myopia,l assuming appropriate patient selection, its safety remains a matter of concern. We report a case in which a patient developed a refractory increase in intraocular pressure (lOP) after PRK.
Case Report A 35-year-old man with no family history of glaucoma had PRK (Aesculap Meditec Mel 60 excimer laser) in the left eye for a cycloplegic refraction of - 5.25 -1.00 X 20. Preoperative evaluation included uncorrected and best spectaclecorrected visual acuities, applanation tonometry, slitlamp inspection, retinoscopy, fundus examination, pachymetry, and corneal topography. Topical dexamethasone (0.1 %) four times daily in the left eye was given after surgery. One month later, lOP was 18 mm Hg in the right eye and 40 mm Hg in the left eye. Uncorrected visual acuity in the left eye was 20/25. Biomicroscopy of the left eye's anterior segment was normal except for mild corneal haze. The cupto-disc was unchanged (0.3 bilaterally). Gonioscopy disclosed From the Department ofOphthalmology, AssafHarofeh Medical Center, Zerifin, and Sackler School ofMedicine, Tel Aviv University, Israel. Reprint requests to Yair Levy, MD, Department ofOphthalmology, Assaf Harofeh Medical Center, Zerifin 70300, Israel
a wide open angle in both eyes, with multiple prominent iris processes inserted in the trabeculum, obscuring the scleral spur. The dexamethasone was discontinued. Timolol 0.5% and dipivefrin 0.1 % were given rwice a day in the left eye, and oral acetazolamide 250 mg four times a day was started. Despite treatment, lOP in the left eye remained uncontrolled, with spikes to 57 mm Hg. Computerized visual field examination revealed reduced sensitivity (mean deviation -7.95) in that eye. Therefore, trabeculectomy was performed 12 months after PRK. Six months later, lOP in the left eye was below 15 mm Hg with the patient taking topical timolol 0.5% rwice daily. Best spectacle-corrected visual acuity was 20/20.
Discussion Most clinical PRK trials include a topical steroid regimen for several months postoperatively. 1 Corticosteroid-induced increase in lOP is a prevalent, early postoperative complication of PRK, occurring in from 8 to 32% of treated eyes. 1,2 In most cases, lOP decreases when steroids are discontinued and beta blockers instilled. To the best of our knowledge, this is the first report of a refractory increase in lOP induced by corticosteroid treatment after PRK in a myopic patient with developmental angle anomaly. Kim and coauthors3 described
J CATARACT REFRACT SURG-VOL 23, MAY 1997
593
CASE REPORTS: LEVY
two eyes in the same patient that required filtration surgery 10 and 11 months after PRK because of a steroidinduced refractory increase in lOP with development of visual field defect and glaucomatous cupping. This patient did not have anomalous angle morphology. The etiology of the refractory increase in lOP in our patient was probably multifactorial and included local ocular corticosteroid treatment, myopia, and developmental angle anomaly. Permanent lOP rise after a few weeks of topical steroid use has been reported. 3 ,4 T opical corticosteroid administration in an eye with developmental angle anomaly may aggravate or induce irreversible glaucoma. 5 Cessation of steroids and antiglaucoma treatment in patients with developmental angle anomaly usually does not reduce lOP, eventually necessitating surgery.5 Some ophthalmologists report using dexamethasone 0.1% after PRK. 6 - 8 However, most now treat post-PRK patients with fluorometholone 0.1 %. Fluorometholone, a poorly penetrating topical steroid, has less pressure-raising effect than dexamethasone. 9 Gonioscopy is not routinely performed before PRK, nor is normal angle morphology considered an eligibility criterion. 1,10 Recognition and diagnosis of developmental angle anomaly are not always obvious because structural changes may be subtle. Thus, while gonioscopy before PRK is recommended, there is no conclusive evidence that it should be mandatory for patient selection. Early detection of lOP increase and prompt treatment are recommended to prevent these complications. We suggest measuring lOP in post-PRK patients no more than 2 weeks after corticosteroid treatment initiation. In addition, we recommend replacing dexametha-
594
sone with fluorometholone or another poorly penetrating topical steroid in the postoperative management of PRK patients.
References 1. Seiler T, Holschbach A, Derse M, et al. Complications of myopic photorefractive keratectomy with the excimer laser. Ophthalmology 1994; 101:153-160 2. Machat Tayfour F. Photorefractive keratectomy for myopia: preliminary results in 147 eyes. Refract Corneal Surg 1993; 9(suppl):SI6-S19 3. Kim ]H, Sah Wl, Hahn TW, Lee yc. Some problems after photorefractive keratectomy.] Refract Corneal Surg 1994; 1O(suppl):S226-S230 4. Spiers F. A case of irreversible steroid-induced rise in intraocular pressure. Acta Ophthalmol 1965; 43:419422 5. Ticho U, Ben-Dor D. Developmental glaucoma aggravated by topical steroids. Ann Ophthalmol 1971; 3:1257-1259 6. Seiler T, McDonnell P]. Excimer laser photorefractive keratectomy. Surv Ophthalmol1995; 40:89-118 7. Epstein D, Fagerholm P, Hamberg-Nystrom H, Tengroth B. Twenty-four-month follow-up of excimer laser photorefractive keratectomy for myopia; refractive and visual acuity results. Ophthalmology 1994; 101: 15581563 8. Gartry DS, Kerr Muir MG, Marshall ]. Excimer laser photorefractive keratectomy: 18 month follow-up. Ophthalmology 1992; 99:1209-1219 9. Fairbairn WD, Thorson]C. Fluorometholone; anti-inflammatory and intraocular pressure effects. Arch Ophthalmol1971; 86:138-141 10. Sher NA, Chen V, Bowers RA, et al. The use of the 193-nm excimer laser for myopic photo refractive keratectomy in sighted eyes; a multicenter study. Arch Ophthalmol1991; 109:1525-1530
n,
J CATARACT REFRACT SURG-VOL 23, MAY 1997
reports
Refractory intraocular pressure increase after photorefractive keratectomy Yair Levy, MD, Limor Hefetz, MD, David Zadok, MD, David Krakowski, MD, Pinhas Nemet, MD ABSTRACT A patient with developmental angle anomaly developed a corticosteroid-induced refractory increase in intraocular pressure (lOP) after photorefractive keratectomy (PRK). Trabeculectomy was required to reduce the pressure. Although rare, corticosteroid-induced refractory lOP increase is a serious complication of PRK and may necessitate trabeculectomy. More frequent monitoring of lOP in post-PRK patients and a re-evaluation of postoperative treatment are indicated. J Cataract Refract Surg
1997; 23:593-594
A
lthough photo refractive keratectomy (PRK) is considered a relatively safe treatment for myopia,l assuming appropriate patient selection, its safety remains a matter of concern. We report a case in which a patient developed a refractory increase in intraocular pressure (lOP) after PRK.
Case Report A 35-year-old man with no family history of glaucoma had PRK (Aesculap Meditec Mel 60 excimer laser) in the left eye for a cycloplegic refraction of - 5.25 -1.00 X 20. Preoperative evaluation included uncorrected and best spectaclecorrected visual acuities, applanation tonometry, slitlamp inspection, retinoscopy, fundus examination, pachymetry, and corneal topography. Topical dexamethasone (0.1 %) four times daily in the left eye was given after surgery. One month later, lOP was 18 mm Hg in the right eye and 40 mm Hg in the left eye. Uncorrected visual acuity in the left eye was 20/25. Biomicroscopy of the left eye's anterior segment was normal except for mild corneal haze. The cupto-disc was unchanged (0.3 bilaterally). Gonioscopy disclosed From the Department ofOphthalmology, AssafHarofeh Medical Center, Zerifin, and Sackler School ofMedicine, Tel Aviv University, Israel. Reprint requests to Yair Levy, MD, Department ofOphthalmology, Assaf Harofeh Medical Center, Zerifin 70300, Israel
a wide open angle in both eyes, with multiple prominent iris processes inserted in the trabeculum, obscuring the scleral spur. The dexamethasone was discontinued. Timolol 0.5% and dipivefrin 0.1 % were given rwice a day in the left eye, and oral acetazolamide 250 mg four times a day was started. Despite treatment, lOP in the left eye remained uncontrolled, with spikes to 57 mm Hg. Computerized visual field examination revealed reduced sensitivity (mean deviation -7.95) in that eye. Therefore, trabeculectomy was performed 12 months after PRK. Six months later, lOP in the left eye was below 15 mm Hg with the patient taking topical timolol 0.5% rwice daily. Best spectacle-corrected visual acuity was 20/20.
Discussion Most clinical PRK trials include a topical steroid regimen for several months postoperatively. 1 Corticosteroid-induced increase in lOP is a prevalent, early postoperative complication of PRK, occurring in from 8 to 32% of treated eyes. 1,2 In most cases, lOP decreases when steroids are discontinued and beta blockers instilled. To the best of our knowledge, this is the first report of a refractory increase in lOP induced by corticosteroid treatment after PRK in a myopic patient with developmental angle anomaly. Kim and coauthors3 described
J CATARACT REFRACT SURG-VOL 23, MAY 1997
593
CASE REPORTS: LEVY
two eyes in the same patient that required filtration surgery 10 and 11 months after PRK because of a steroidinduced refractory increase in lOP with development of visual field defect and glaucomatous cupping. This patient did not have anomalous angle morphology. The etiology of the refractory increase in lOP in our patient was probably multifactorial and included local ocular corticosteroid treatment, myopia, and developmental angle anomaly. Permanent lOP rise after a few weeks of topical steroid use has been reported. 3 ,4 T opical corticosteroid administration in an eye with developmental angle anomaly may aggravate or induce irreversible glaucoma. 5 Cessation of steroids and antiglaucoma treatment in patients with developmental angle anomaly usually does not reduce lOP, eventually necessitating surgery.5 Some ophthalmologists report using dexamethasone 0.1% after PRK. 6 - 8 However, most now treat post-PRK patients with fluorometholone 0.1 %. Fluorometholone, a poorly penetrating topical steroid, has less pressure-raising effect than dexamethasone. 9 Gonioscopy is not routinely performed before PRK, nor is normal angle morphology considered an eligibility criterion. 1,10 Recognition and diagnosis of developmental angle anomaly are not always obvious because structural changes may be subtle. Thus, while gonioscopy before PRK is recommended, there is no conclusive evidence that it should be mandatory for patient selection. Early detection of lOP increase and prompt treatment are recommended to prevent these complications. We suggest measuring lOP in post-PRK patients no more than 2 weeks after corticosteroid treatment initiation. In addition, we recommend replacing dexametha-
594
sone with fluorometholone or another poorly penetrating topical steroid in the postoperative management of PRK patients.
References 1. Seiler T, Holschbach A, Derse M, et al. Complications of myopic photorefractive keratectomy with the excimer laser. Ophthalmology 1994; 101:153-160 2. Machat Tayfour F. Photorefractive keratectomy for myopia: preliminary results in 147 eyes. Refract Corneal Surg 1993; 9(suppl):SI6-S19 3. Kim ]H, Sah Wl, Hahn TW, Lee yc. Some problems after photorefractive keratectomy.] Refract Corneal Surg 1994; 1O(suppl):S226-S230 4. Spiers F. A case of irreversible steroid-induced rise in intraocular pressure. Acta Ophthalmol 1965; 43:419422 5. Ticho U, Ben-Dor D. Developmental glaucoma aggravated by topical steroids. Ann Ophthalmol 1971; 3:1257-1259 6. Seiler T, McDonnell P]. Excimer laser photorefractive keratectomy. Surv Ophthalmol1995; 40:89-118 7. Epstein D, Fagerholm P, Hamberg-Nystrom H, Tengroth B. Twenty-four-month follow-up of excimer laser photorefractive keratectomy for myopia; refractive and visual acuity results. Ophthalmology 1994; 101: 15581563 8. Gartry DS, Kerr Muir MG, Marshall ]. Excimer laser photorefractive keratectomy: 18 month follow-up. Ophthalmology 1992; 99:1209-1219 9. Fairbairn WD, Thorson]C. Fluorometholone; anti-inflammatory and intraocular pressure effects. Arch Ophthalmol1971; 86:138-141 10. Sher NA, Chen V, Bowers RA, et al. The use of the 193-nm excimer laser for myopic photo refractive keratectomy in sighted eyes; a multicenter study. Arch Ophthalmol1991; 109:1525-1530
n,
J CATARACT REFRACT SURG-VOL 23, MAY 1997