Choroidal neovascularization in a young, healthy eye after LASIK

Size: px

Start display at page:

Download "Choroidal neovascularization in a young, healthy eye after LASIK"

Claude Gordon
5 years ago
Views:

1 Optometry (2010) 81, Choroidal neovascularization in a young, healthy eye after LASIK Bharti Bathija-Lala, O.D., a Sherry J. Bass, O.D., a Richard J. Madonna, O.D., a and Alan Dayan, M.D. b a State University of New York State College of Optometry, New York, New York; and b New York Eye and Ear Infirmary, New York, New York. KEYWORDS Choroidal neovascularization; Laser-in-situ keratomileusis (LASIK); Myopia, macular hemorrhage Abstract BACKGROUND: Choroidal neovascularization (CNV) is associated with age-related macular degeneration (AMD), degenerative myopia, angioid streaks, presumed ocular histoplasmosis syndrome, and numerous other ocular and systemic conditions. Idiopathic CNV is also a common form of the condition. However, CNV has rarely been noted after laser-assisted in situ keratomileusis (LASIK) and a cause-and-effect relationship has not been found. A case of CNV after uneventful LASIK is reported here, along with a literature review of previously reported cases and suggested pathophysiology. A link between LASIK and CNV is sought. METHODS: A case report of CNV in a young, healthy eye after uneventful LASIK is presented. Review of the pertinent literature reporting a relationship between LASIK and CNV was conducted through 2007, and few studies are reported after CONCLUSION: To date, there is anecdotal evidence of CNV after LASIK. The incidence from prior reports ranges from 0.003% to 0.33%. However, a causal link cannot be disregarded and merits further study. Each patient undergoing LASIK warrants a thorough preoperative dilated fundus examination, including a thorough examination of the macula. This occurrence, albeit rare, should be considered for inclusion in the refractive surgery consent form. Optometry 2010;81: Choroidal neovascularization (CNV) involves new, fragile blood vessel growth that may leak, spontaneously involute, or scar over. CNV may occur in any retinal location: subfoveal, juxtafoveal, or extrafoveal. The most visually devastating is subfoveal because it is the most difficult to manage. 1 The development of CNV is associated with a number of retinal conditions, primarily age-related macular degeneration (AMD), degenerative myopia, angioid streaks, and Disclosure: The authors have no financial or other relationships that might lead to a conflict of interest. Corresponding author: Bharti Bathija-Lala, O.D., Mabrypark Place, Alpharetta, Georgia bbathija@gmail.com presumed ocular histoplasmosis syndrome (POHS). After AMD, idiopathic CNV is the second most common etiology. 2 Reports of CNV after laser-assisted in situ keratomileusis (LASIK) are rare. Table 1 lists the cases of CNV after LASIK in patients without and with predisposing factors. Table 2 lists the cases of macular involvement without CNV. Case report A 23-year-old white woman with no ocular or health history presented for a LASIK consultation. Her best-corrected visual acuity (VA) was 20/20 in both the right and left eyes. Cycloplegic refraction showed diopters (D) in each /$ - see front matter Ó 2010 American Optometric Association. All rights reserved. doi: /j.optm

2 Table 1 CNV after LASIK in patients with and without predisposing factors Study Year Preoperative prescription Age (y) Sex Predisposing factors Time s/p LASIK Eye CNV location Treatment Outcome NO PREDISPOSING FACTORS Saeed et al Pinto et al x180 20/ x155 20/ / /25 Arevalo SE 20/ SE 20/ / / / / / / VA? VA? Arevalo et al ,916 cases Chen et al x7 37 M 3 mo O.S. Subfoveal 6/60 64 M AMD 3 mo O.S. Extrafoveal Argon then PDT 20/ F 3 wk O.S. Subfoveal None 20/50 28 F None 3 y O.D. Subfoveal PDT x 3 20/ F None 3 y O.D. Subfoveal PDT 20/40 47 F Focal RPE 4 y O.S. Subfoveal PDT x 2 20/100 atrophy O.S. 38 F None 5 y O.S. Subfoveal PDT 20/ F None 2 y O.S. Subfoveal PDT x 2 20/200 None 2 y O.S. Juxtafoveal Vitrectomy-retinotomy CF 32 M None 4 wk OU Subfoveal OU x179 Maturi et al d OU Subfoveal; Lacquer cracks PREDISPOSING FACTORS Ellies et al /50 32 F None 4 d O.S. Mac Heme (-) CNV Sobha et al / x125 6/ F Fuch s spot 1 d O.D. Subfoveal. 20/200 Federovic et al Moderate myopia 61 M O.D. perifoveal spot 12 wk O.D. OU Extrafoveal PDTx2 Scarring 8 wk O.S. Ruiz-Moreno et al /50 41 M 2 y O.D. Extrafoveal Argon 20/ /20 O.S /20 30 F O.D. Juxtafoveal CNV O.S. Lacquer cracks 3mo 9mo OU Subfoveal Juxtafoveal Argon O.S. 20/800 20/ OU 20/50 36 M 1 y O.S. Subfoveal Excision 20/200 Note. Table shows patients who had choroidal neovascularization after LASIK. These patients include those with and without predisposing factors for the development of CNV. eye; OU 5 both eyes; s/p 5 status post; SE 5 spherical equivalent; CF 5 counting fingers. 20/80 O.D. 5 right eye; O.S. 5 left Bathija-Lala et al Issue Highlight 633

$634 Optometry, Vol 81, No 12, December 2010 Table 2 Macular complications, excluding CNV, after LASIK Study Year Refractive error Age Sex Luna et al. 13 1999 216.75 10.75x180 216.50 10.$

3 634 Optometry, Vol 81, No 12, December 2010 Table 2 Macular complications, excluding CNV, after LASIK Study Year Refractive error Age Sex Luna et al x x55 Ruiz-Moreno, SE 20/32 Montero et al SE 20/28 Singhvi et al Principe et al MACULAR HEMES/INVOLVEMENT Predisposing factors 31 M 1 d 17 d Time after LASIK Eye Macula Final VA OU OU mac hemes 1 venous congestion 37 F 2 mo O.D. Mac heme 1 Lacquer crack (-) CNV RPE CSR OU atrophy OU 36 F O.S. Mac Heme (-) CNV 20/60 20/50 Note. Table shows other complications that occurred in the macula of patients who underwent LASIK. These patients did not have choroidal neovascularization. O.D. 5 right eye; O.S. 5 left eye; OU 5 both eyes; CSR 5 central serous retinopathy. 20/25 20/25 eye. The anterior segment structures were normal. Central corneal thickness (CCT) was 518 mm in the right eye and 525 mm in the left eye. Examination of the retinas did not find any macular or peripheral abnormalities in either eye. She subsequently underwent uneventful, simultaneous bilateral LASIK. At her 1-day postoperative visit, her uncorrected VA was 20/20 in the right eye and 20/25 in the left eye, which was correctable to 20/20 with D sphere. At her 6-week follow-up visit, her uncorrected VA in the right eye was still 20/20 but was best corrected to only 20/60 in the left eye. She noted that the Snellen optotypes appeared wavy. The patient was not aware of this decrease in vision. Amsler grid testing of the left eye found a 3 area of metamorphopsia slightly superior to fixation. The corneal flaps and anterior segment were found to be normal in both eyes. A dilated fundus examination found a serous macular detachment with a greenish-grey pigmented area inferior to the macula in the left eye (see Figure 1). Fluorescein angiography (FA) found a classic, juxtafoveal choroidal neovascular net inferonasal to the fovea in the left eye (see Figure 2). The right eye was normal. Ocular coherence tomography (OCT) of the left eye found a highly reflective area above the retinal pigment epithelium inferonasal to the fovea with an overlying serous detachment (see Figure 3). Accordingly, the left eye was treated with 1 course of photodynamic therapy (PDT) and an intravitreal injection of triamcinolone acetonide. Over the next 4 weeks, the fluid resorbed, and the VA in the left eye improved to 20/25, but the macula retained a mottled pigmentary appearance (see Figure 4). Further follow-up over a 2-year period has not found any additional recurrence in the left eye and no similar development in the right eye. Currently, her VA in the left eye has stabilized to 20/20 (see Figure 5). Discussion Review of the literature divides cases of CNV after LASIK into those with no predisposing factors and those with predisposing factors. Predisposing factors include, but are not limited to, (1) high myopia, (2) angioid streaks, (3) AMD, (4) prior retinal laser treatment, (5) age-related macular mottling, (6) Fuch s spot, (7) lacquer cracks, and (8) POHS. CNV after LASIK: no predisposing factors Patients without predisposing factors in whom CNV develops after LASIK ranged in age from 27 to 64 years. Figure 1 Macular fluid and an area of green grey pigmentation inferonasal to the fovea in the left eye with visual acuity of 20/60.

Bathija-Lala et al Issue Highlight 635 The patients in whom CNV developed included both myopes and hyperopes, although the preponderance of cases was found in the moderate myopes.

$The CNV developed anywhere from 1 day to 5 years after LASIK and tended to present as subfoveal membranes. Preoperative refractive errors ranged from 14.00 D to 216.$

4 Bathija-Lala et al Issue Highlight 635 The patients in whom CNV developed included both myopes and hyperopes, although the preponderance of cases was found in the moderate myopes. The incidence of CNV after LASIK in these studies ranged from 0.003% to 0.33%. 6 None of the above studies reported the CCT values of the affected patients. Proposed mechanism of development of CNV after LASIK Figure 2 Fluorescein angiography shows a small classic subfoveal choroidal neovascular membrane in the left eye. The CNV developed anywhere from 1 day to 5 years after LASIK and tended to present as subfoveal membranes. Preoperative refractive errors ranged from D to D, with the majority of cases taking place in the moderate myopes Of interest, in the Arevalo 6 (2000) study of 29,916 cases, only 1 patient had CNV, representing an incidence of 0.003%, and this patient had a hyperopic refractive error (see Table 1). CNV: predisposing factors and macular involvement Patients with predisposing factors to CNV ranged in age from 30 to 61 years and had preoperative refractive errors from D to D. Predisposing factors in these studies included Fuch s spot, lacquer cracks, POHS, and previous CNV. Patients with macular involvement had macular hemorrhages, lacquer cracks, venous congestion, and central serous retinopathy, but no CNV. Their ages ranged from 31 to 37 years with preoperative refractive errors ranging from D to D (see Table 2). Of the cases cited in the Table 1, 1 factor occurred in both the hyperopic and myopic patient: CNV developed after LASIK. Although a direct cause effect relationship is unclear, 2 major mechanisms have been proposed to explain the development of CNV after LASIK. The LASIK procedure can be divided into 3 major phases. The first phase involves the creation of the flap with a microkeratome, which requires a temporary but significant increase in intraocular pressure. The second phase involves photocoagulation of the stromal bed, and the third phase is repositioning of the flap. It is during the first 2 phases in which the eye is stressed the most that the answer may lie. Phase 1: flap creation. It is postulated that the increase in eye pressure during flap formation creates a mechanical force, a tangential stress, which may encourage or enhance breaks in Bruch s membrane with subsequent development of CNV. According to the manufacturer of the microkeratome, it is believed that eye pressure has to exceed 65 mmhg to create the vacuum allowing the microkeratome ring to suction onto the cornea. 12 It has been proposed that the suction ring may exert its effect up to 4 mm posterior to the limbus. 6 Thus, LASIK can be thought of as a trauma to the eye in the form of increased intraocular pressure (IOP) delivering a blow to the retina. Maturi et al. 8 utilizes LaPlace s law (T 5 PR/2) to explain the relationship between macular hemorrhages and CNV after LASIK. An increase in wall tension (T) will increase axial length (R 5 half of axial length). Maturi Figure 3 OCT shows a serous detachment and highly reflective area above the retinal pigment epithelium.

8 cite a private communication in which they report that IOP (P) increases to 100 mmhg, and not 65 mmhg, during the creation of the flap.

5 636 Optometry, Vol 81, No 12, December 2010 Figure 4 20/25. The left eye 4 weeks after treatment with PDT and 1 intravitreal injection of Kenalog. The serous detachment has resolved, and visual acuity is et al. 8 cite a private communication in which they report that IOP (P) increases to 100 mmhg, and not 65 mmhg, during the creation of the flap. This results in a 27% greater wall tension than some myopic eyes may be able to tolerate. The increased tension, caused by the increased eye pressure, may cause breaks in Bruch s membrane with subsequent hemorrhaging and CNV in the macula. Sobha et al. 10 stated that hyperopic patients generally do not have any predisposition for the development of CNV. Typically, they have no breaks in Bruch s membrane or other factors associated with CNV growth. However, the patient in their report was 61 years old and therefore had age as an influencing factor. The patient may have had subclinical age-related weakening of Bruch s membrane. They postulate that the pressure differential caused by the microkeratome may be the etiologic agent for inducing growth of CNV. Ruiz-Moreno et al. 12 believe that a myopic fundus has retinal abnormalities related to the elongation of axial length that predispose the development of CNV. For example, they note that lacquer cracks are found in 83% of eyes with CNV. On average, the growth rate of CNV is 10 mm per day. 12 In their patient, CNV developed 8 months after LASIK, but given its size, the CNV should have appeared earlier, i.e., 4 months postoperatively. Because of this time discrepancy, Ruiz-Moreno et al. 12 believe the CNV may be related to the existing degenerative myopia and not to LASIK. However, they too offer a similar theory of increased IOP as a possible etiology in their patient. Phase 2: photoablation of the stromal bed. The other proposed mechanism is that of the creation of acoustic waves. Pulsed ablation of the stromal bed by the laser sets up acoustic stress waves along the axis of the eye. These shock waves travel from the anterior segment through the posterior segment. Ruiz-Moreno et al. 12 states that the stress wave amplitudes reach a maximum pressure focus of 100 atmospheres in the posterior lens and anterior vitreous. The pressure focus then dissipates to less than 10 atmospheres by the time it reaches the retina or posterior segment. Even at 10 atmospheres, this acoustic shock wave may be responsible for creating disruptions in Bruch s membrane, thereby facilitating CNV growth in some patients. Sobha et al. 10 supported the findings of Ruiz-Moreno et al., 12 citing the incidence of CNV after photorefractive keratectomy as 0.01% and 0.33% after LASIK. Sobha et al. 10 speculate that the difference in incidence may be attributed to the different modality used to perform the procedure. Influence of central corneal thickness Figure 5 Two years later, the left eye remains quiescent with no recurrences. Persistent pigment abnormalities remain inferonasally, but visual acuity is maintained at 20/20. Although none of the cited studies reported central corneal thickness (CCT) or investigated its role in the development of CNV after LASIK in their patients, our patient is notable for

6 Bathija-Lala et al Issue Highlight 637 having a CCT that is thinner than average. The question remains whether a thinner-than-average cornea represents another risk factor for the development of CNV after LASIK because it may be less resilient to the stresses placed on the eye by the flap creation and photoablation. Because thin corneas place some eyes at risk for glaucoma, 17 such eyes may also be at risk for retinal problems, especially when stressed, as during LASIK. Further studies may be warranted. Other posterior segment complications after LASIK In addition to CNV, other posterior segment complications 18 have been reported after LASIK. These include retinal tears and retinal detachment, posterior vitreal detachment, 17 increased neovascularization in proliferative diabetic retinopathy, 22 and ischemic complications of other vascular disease. 2 These changes are postulated to be caused by a transient elongation of the axial length during ring suction. Conclusion Millions of LASIK procedures have been performed worldwide, and a majority of these are successful. The incidence of post-lasik CNV is very low, ranging from 0.003% to 0.33%. 6 The causal link between CNV development after LASIK has not been proven but cannot be disregarded. Although rare, more studies of this relationship are warranted. 23 A detailed preoperative dilated fundus examination, with careful attention to the macula, should be done on every patient undergoing LASIK. In light of the cited studies, it is worthwhile to note that even a low myope with no risk factors reportedly had CNV after LASIK. Although most complications after LASIK are associated with the flap and corneal interface, 24 the inclusion of the development of CNV, however unlikely, on the consent form, should be considered. Alternatives such as cataract surgery with replacement with a PC IOL 25 may be more suitable for patients with high refractive errors and thin corneas, although this procedure is not without retinal risk. In addition, patients with preexisting risk factors for CNV, e.g., Fuch s spot, atrophic macular degeneration, diabetic retinopathy, or POHS, should be counseled on the increased possibility of CNV development after LASIK and may also want to consider alternative refractive surgery options. As for the healthy, young eye with no predisposing factors, the development of CNV, albeit rare, can occur, and patients should be counseled accordingly. References 1. Browning DJ, Fraser CM. Ocular conditions associated with peripapillary subretinal neovascularization: Their relative frequencies and associated conditions. Ophthalmology 2005;112: Alexander L. Primary care of the posterior segment, Third ed. Spain: McGraw-Hill; Saeed M, Poon W, Goyal S, et al. Choroidal neovascularization after laser in situ keratomileusis in a patient with low myopia. J Cataract Refract Surg 2004;30(12): Pinto RVB, Smiddy WE, Culbertson W. Choroidal neovascularization following laser in situ keratomileusis. Ophthalmic Surg Laser Imaging 2005;35(1): Arevalo JF. Retinal complications after laser-assisted in situ keratomileusis (LASIK). Curr Opin Opthalmol 2004;15: Arevalo JF, Ramirez E, Suarez E, et al. Incidence of vitreoretinal pathologic conditions within 24 months after laser in situ keratomileusis. Ophthalmology 2000;107(12): Chen YC, Ma DHK, Yang KJ, et al. Bilateral choroidal neovascularization after laser-assisted in situ keratomileusis. Retina 2001;21(2): Maturi RJ, Kitchens JW, Spitzberg DH, et al. Choroidal neovascularization after LASIK. J Cataract Refract Surg 2003;19(4): Ellies P, Pietrinin D, Lumbroso L, et al. Macular hemorrhage after laser in situ keratomileusis for high myopia. J Cataract Refract Surg 2000;26(6): Sobha S, Rajan MS, Jackson H. Choroidal neovascularization following hyperopic LASIK surgery. Clin Exp Ophthalmol 2004;32: Federovich I, Mehr DS, Akduman L. Choroidal neovascularization after laser in situ keratomileusis in a patient with presumed ocular histoplasmosis syndrome. Eur J Ophthalmol 2004;14(3): Ruiz-Moreno JM, Perez-Santonja JJ, Alio JL. Choroidal neovascularization in myopic eyes after laser-assisted in situ keratomileusis. Retina 2001;21(21): Luna JD, Reviglio VE, Juarez CP. Bilateral macular hemorrhage after laser in situ keratomilesis. Graefe s Arch Clin Exp Ophthalmol 1999; 237: Ruiz-Moreno JM, Montero J, Alio JL. Lacquer crack formation after LASIK. Ophthalmology 2003;110(8): Singhvi A, Dutta M, Sharma N, et al. Bilateral serous macular detachment following laser in situ keratomileusis. Am J Ophthalmol 2004; 138: Principe AH, Lin DY, Small KW, et al. Macular hemorrhage after laser in situ keratomileusis with femtosecond laser flap creation. Am J Ophthalmol 2004;138: Gordon MO, Beiser JA, Brandt JD, et al, for the Ocular Hypertension Treatment Study Group. The ocular hypertension treatment study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120: Luna JD, Artal MN, Reviglio VE, et al. Vitreoretinal alteration following laser in situ keratomileusis: clinical and experimental studies. Graefe s Arch Clin Exp Ophthalmol 2001;239: Arevalo JF, Ruiz-Moreno JM, Fernandez CF, et al. Photodynamic therapy with verteporfin for subfoveal choroidal neovascular membranes in highly myopic eyes after laser in situ keratomileusis. Ophthalmic Surg Laser Imaging 2005;35(1): Flaxel CJ, Choi YH, Sheety M, et al. Proposed mechanism for retinal tears after LASIK. Ophthalmology 2003;110(8): Mostafavi D, Fekrat S, Toth CA, et al. Letter to editor: LASIK and vitreous pathology after LASIK. Ophthalmology 2002;109: Ghanbari H, Ahmadieh H. Aggravation of proliferative diabetic retinopathy after laser in situ keratomileusis. J Cataract Refract Surg 2003;29: Bailey CS. Editorial response to Choroidal neovascularization after laser in situ keratomileusis in a patient with low myopia. J Cataract Refract Surg 2005;31: Stulting RD, Carr JD, Thompson KP, et al. Complications of laser in situ keratomileusis for the correction of myopia. Ophthalmology 1999; 106: Lowenstein A, Goldstein M, Lazar M. Retinal pathology occurring after excimer laser surgery or phakic intraocular lens implantation: Evaluation of possible relationship. Surv Ophthalmol 2002;17:

Retina Conference. Janelle Fassbender, MD, PhD University of Louisville Department of Ophthalmology and Visual Sciences 09/04/2014

Retina Conference. Janelle Fassbender, MD, PhD University of Louisville Department of Ophthalmology and Visual Sciences 09/04/2014 Retina Conference Janelle Fassbender, MD, PhD University of Louisville Department of Ophthalmology and Visual Sciences 09/04/2014 Subjective CC/HPI: 64 year old Caucasian female referred by outside ophthalmologist