- Email: [email protected]
Light-Induced Maculopathy from the Operating Microscope in Extracapsular Cataract Extraction and Intraocular Lens Implantation
Light-Induced Maculopathy from the Operating Microscope in Extracapsular Cataract Extraction and Intraocular Lens Implantation H. RICHARD MCDONALD, MD, A. RODMAN IRVINE, MD
Abstract: A characteristic macular lesion has been noted in six patients who underwent extracapsular cataract extraction with posterior chamber lens implantation. The lesion appeared similar to that which other investigators have produced in monkeys as a response to the coaxial illumination of the operating microscope. On the first or second postoperative day, the lesion appeared as an oval area of mild yellow-white discoloration of the retina; gradually it developed mottled pigmentation over the next few weeks. The pigmentary changes were often subtle, but fluorescein angiography revealed a characteristic sharply circumscribed lesion. In most of our patients the lesion was just above or below the foveola, so that central vision returned to normal, but a paracentral scotoma was present. These findings should encourage the clinician to heed the warnings of those laboratory studies which have shown the phototoxic potential of the operation microscope's unfiltered coaxial illumination and force us to re-examine our filters and operating techniques. [Key words: cataract extraction, light, light-induced, maculopathy, operational microscope, phototoxic, retinal damage by light.] Ophthalmology 90:945-951,
1983
The toxic effects of light on the retina have been well documented. 1- 6 Recently, the phototoxic potential of several common ophthalmic instruments has been shown in experimental animals. 7- 12 The present report describes findings in patients who underwent extracapsular cataract extraction with implantation of a posterior chamber lens and whom we believe manifest evidence of macular light toxicity secondary to the coaxial illu-
From the Department of Ophthalmology, University of California, San Francisco, California. Presented at the Eighty-seventh Annual Meeting of the American Academy of Ophthalmology, San Francisco, California, October 30-November 5, 1982. Reprint requests to A. Rodman Irvine, MD, U-490, University of California Department of Ophthalmology, San Francisco, CA 94143. 0161-6420/83/0800/0945/$1.15 ©American Academy of Ophthalmology
mination of the operating microscope. The lesions closely resemble those produced experimentally by Hochheimer et al in rhesus monkeys 11 and are, to the best of our knowledge, the first reported cases of clinical light toxicity from the operating microscope.
CASE REPORTS All cases were operated upon with a standard ceiling mounted Zeiss Operating Microscope with a 30-watt bulb. They were done by senior residents who had each performed over 15 lens implantations prior to the current cases. After a "can opener" style anterior capsulotomy and expression of the nucleus, cortical material was removed with a closed microsurgical approach using an infusion-aspiration tip. The posterior capsule was then carefully "polished" with a diamond-
945
OPHTHALMOLOGY • AUGUST 1983 • VOLUME 90 • NUMBER 8
coated irrigating cannula. The lens implant was inserted under an air bubble and the wound was closed with interrupted sutures. The surgical operating times, as recorded in the anesthetic records, varied between 1 hour 15 minutes and 1 hour 30 minutes. One faculty member (AI) served as responsible surgeon and performed the postoperative care on the first three cases. Once the maculopathy was recognized in these cases, the fourth, fifth, and sixth cases were picked up when they were sent to the fluorescein Angiography Unit by the other surgeons. It is of note that the pigment epithelial changes were subtle enough in these last three cases that they had not been noted clinically prior to the angiography, and there was no suspicion of a light-induced maculopathy by the referring surgeon. Case 1. This 60-year-old woman underwent uncomplicated extracapsular cataract extraction and implantation of a Kratzstyle posterior chamber lens on February 15, 1982. One week after surgery, the patient was noted to have a questionable, faint retinal pigment epithelial change in the superior macula. This was thought at that time to be a possible shallow RPE detachment. This area of retinal pigment epithelial change took on a striking, mottled pattern over the next several months. Vision required several months to improve but 5 months after surgery acuity was 20/30 with a refraction of -1 .00 sphere with + 1.50 cyclinder axis 150. Tangent screen perimetry at this time revealed an oval scotoma inferior to fixation (Fig 1). fluorescein angiography revealed a sharply defined elliptical area of mottled fluorescein transmission corresponding to the area of pigment epithelial change (Fig 1). Case 2. This 82-year-old woman underwent an uncomplicated extracapsular cataract extraction with implantation of a Sinskey style posterior chamber lens on February 9, 1982. Two weeks after surgery it was noted that there was a subtle oval area of pigment epithelial change superior to the fovea. Again, the vision seemed a bit slow recovering, but by 41f2 months after surgery acuity was 20/30 with a refraction of - 2.50 with a +0.75 cyclinder axis 60. fluorescein angiography at this time revealed a similar area of irregular fluorescein transmission superior to the fovea corresponding to the area of retinal pigment epithelial granularity seen ophthalmoscopically. Tangent screen perimetry at this time revealed a scotoma inferior to fixation (Fig 2).
Fig I. Case I: A, fundus photo shows oval, sharply defined area of pigment mottling just above the fovea.
Fig 2. Case 2: A, fundus photo shows a subtle pigment mottling in an oval area superior to the fovea.
Fig 3. Case 3: A, fundus photo shows an oval area of pigment mottling just below the fovea.
946
Fig 3. B, fluorescein angiography in the arteriovenous stage accentuates the pigment lesion.
OS
Name :
MP
lsopters:
3/ 2000
Date : 7-19-82
Fig 1. B, fluorescein angiography shows fluorescein transmission and
blockage limited to the focal area of pigment mottling.
Fill 1. C, tangent screen field shows a dense paracentral scotoma corresponding with the pigment lesion.
OD
c
NameWH
Fig 2. B, fluorescein angiography makes the focal oval area of pigment
mottling obvious.
Date
lsopters
3/ 2000
7-19 -82
Fig 2. C, tangent screen field shows a dense paracentral scotoma.
90/30
0/30
180/30
270/30
Fig 3. C, the late stage of the angiogram shows cystoid macular edema. This was the only patient showing such edema in this series.
Fig 3. D, automated perimetry with the Octopus<~> instrument reveals a dense scotoma superior to fixation corresponding with the pigment lesion.
947
OPHTHALMOLOGY •
AUGUST 1983 •
VOLUME 90 •
NUMBER 8
Fig 4. Case 4: A, fundus photo shows subtle area of pigment mottling inferior to the fovea and just above the inferotemporal vein.
Fig 4. B, fluorescein angiogram accentuates the area of pigment mottling.
Case 3. This 71-year-old white man underwent uncomplicated extracapsular cataract extraction and implantation of a Sinskey style posterior chamber lens on June 7, 1982. Eleven days after surgery the patient was noted to have an oval area of apparent pallor inferior to the fovea. Two months after surgery, fundus photography revealed a very subtle area of irregular retinal pigment epithelial atrophy in this area. Fluorescein angiography revealed a sharply defined oval area of patchy fluorescein transmissions similar to that in the two preceeding patients. This patient, however, also exhibited cystoid macular edema. Visual acuity at this time was 20/100 with a refraction of - 1.00 sphere with +3.00 cyclinder axis 90. Tangent screen and octopus automated perimetry showed a scotoma superior to fixation (Fig 3). Case 4. This 65-year-old man underwent uncomplicated extracapsular cataract extraction and implantation of a Shearing style posterior chamber lens on June 18, 1982. Six weeks after surgery visual acuity was best corrected to 20/100. No macular lesion was recognized, but he was referred for fluorescein angiography to rule out the possible presence of cystoid macular edema. The fluorescein angiography showed no cystoid macular edema but revealed an oval area of irregular fluorescein transmission inferior to the fovea, identical to that in the initial three patients. The fundus photography revealed a very subtle area of irregular pigment epithelial atrophy corresponding to the area of fluorescein transmission (Fig 4). Case 5. This 80-year-old woman underwent uncomplicated extracapsular cataract extraction and implantation of a Shearing type posterior chamber lens on March 3, 1982. Whereas the patient's initial postoperative course was uncomplicated and vision was 20/30, approximately 4 months following surgery visual acuity had dropped to 20/80. In order to determine whether this drop was due to opacification of the posterior capsule or to cystoid macular edema, fluorescein angiography was ordered. The fluorescein angiogram again revealed an oval sharply defined area of irregular fluorescein transmission similar to that seen in the preceeding four patients. It was only
after seeing the fluorescein angiogram, that a careful examination of the fundus revealed a corresponding area of subtle pigment epithelial mottling (Fig 5). Case 6. This 62-year-old man underwent uncomplicated extracapsular cataract extraction and implantation of a Sinskey style posterior chamber lens on June 16, 1982. After attaining early visual recovery, the patient developed a sudden decrease in acuity three months postoperatively with anterior ischemic optic neuropathy. Fluorescein angiography on September 14, 1982 revealed in addition to the ischemic optic nerve, the same characteristic oval, mottled transmission patterns seen in the other patients (Fig 6).
948
DISCUSSION Phototoxic damage to the retina has been an area of avid investigation for 20 years. In 1965, Noell found that the retina of rats could be damaged by light of moderate intensity. Histologically, he found simultaneous destruction of the retinal pigment epithelium and the photoreceptors. 1 Kuwahara and Gorn showed that, depending on the duration and nature of the light exposure, retinal damage could vary from total destruction of the entire retina to minimal changes in the photoreceptors.2 Tso conducted light and electron microscopic studies on rhesus monkeys who had been exposed to the light of an indirect ophthalmoscope for 1 hour.6 He described the ensuing maculopathy in three stages: ( 1) an initial retinal edema with damage to the photoreceptors and retinal pigment epithelium; (2) macrophagic influx to the subretinal region; and (3) apparent regeneration of photoreceptor outer segments over areas of depigmented and proliferated retinal pigment epithelium at 3 to 5 months.
MCDONALD AND IRVINE • LIGHT-INDUCED MACULOPATHY
Fig 5. Case 5: A, Fundus photography was difficult due to capsular opacification but an area of pigment mottling is present above the fovea just below the superior temporal arcade.
Fig 5. B, fluorescein angiography makes the focal pigment abnormality much more obvious.
Fig 6. Case 6: A, fundus photography shows an area of pigment mottling just temporal to the fovea, as well as pale swelling of the optic nerve.
Fig 6. B, fluorescein angiography accentuates the area of pigment change temporal to the fovea. Leakage from the ischemic disc is also seen.
More recently, other ophthalmic instruments have been found capable of producing damaging effects on the retina. Fuller et al, and more recently Myers and Bonner, studied retinal phototoxicity induced in the monkey by the fibroptic endoilluminators normally used for vitrectomy surgery. 8 •13 Friedman and Kuwahara showed retinal damage from a 15-minute exposure to an indirect ophthalmoscope. 3 Hochheimer et al described retinal damage caused by light exposure from the slit lamp and operating microscope. 11 The phototoxic potential of the operating microscope is particularly distressing. Calkins and Hochheimer calculated the retinal exposures from several operating microscopes and found the average retinal irradiance produced to be five times greater than that produced by the average indirect ophthalmoscope. 9 •10 They evaluated the effect of several microscopes on the retina and cal-
culated theoretical "safe-times" for their use, using the American National Standards Institute's guidelines for the safe use oflasers. They predicted the maximum permissible exposures (MPE) would be reached in from 250 seconds! Hochheimer showed that irreversible damage could be done to a rhesus monkey retina by exposing it to a light of an operating microscope for 1 hour. 11 The lesions produced were oval, discrete areas of pigment epithelial mottling that bore a striking resemblance to the lesions found in our patients. The spectrum of the offending light source appears to be important. Shorter wave lengths, those in the UV, near UV, and blue range, seem more damaging to the retina than the longer wave lengths. Most of the near ultraviolet light is normally filtered by the crystalline lens; therefore, aphakic eyes are more susceptible to pho-
949
OPHTHALMOLOGY •
AUGUST 1983 •
Fig 7. Fluorescein angiogram of a rhesus monkey three weeks post phacoemulsification and posterior chamber lens implantation (30 minutes) followed by 30 minutes extra exposure to the coaxial illumination of the microscope (total 60-minute exposure). An oval area of mottled hyperfluorescence is present just above the fovea.
totoxicity. Ham found that the retinas of aphakic rhesus monkeys were six times more sensitive to light of 350 and 325 nanometers wave lengths than to blue light. 15 Due to the transmission of near UV light by polymethylmethacrylate, pseudophakic eyes would be expected to behave like aphakic eyes. In fact, Mainster has demonstrated that the pseudophakic eye is more susceptible to retinal damage from UV light sources than the normal eye. 12 It should be noted, however, that the emission spectrum of the coaxial illuminator of the Zeiss operating microscope contains no appreciable light below 400 nanometers. 17·18 The operating microscope has been in widespread use for cataract extraction for over 15 years. One must ask how it is possible that photic macular damage from the operating microscope is only now being recognized. Perhaps one factor is the nature of the operation. It is only recently that the residents at the University of California Medical Center have begun doing a significant number of extracapsular lens extractions by using the closed irrigation-aspiration technique along with lens implantation. It is possible that the presence of the pseudophakos is an important factor, with the pseudophakos acting to focus the illuminating light on the retina during wound closure. It is also possible that the relatively long time spent in careful cleaning of all cortical material from the posterior capsule prior to implantation of the pseudophakos is the more important factor. It should be stressed that we have found evidence of this maculopathy in only a small percentage of those patients on whom we have performed extracapsular lens extraction and posterior chamber lens implantation. Finally, the lesion is very easily missed as it is usually asymptomatic and the fundus changes are often subtle and easily dismissed as due to aging. In most of our patients, fluorescein angiography was necessary in order to appreciate the unique and characteristic pattern of retinal pigment epithelial change. It would seem this lesion may not be 950
VOLUME 90 •
NUMBER 8
rare. Once we had learned to recognize it in our own patients, three more cases from other surgeons (case 46) were seen in our Eye Photography Unit within 2 months. Recently we have duplicated this lesion experimentally (Fig 7). We perf01med an extracapsular cataract extraction and implantation of a posterior chamber lens in an adult rhesus monkey. This surgery required 30 minutes. We then removed the air bubble and continued to shine the operating microscope light into the eye for another 30 minutes to total 60 minutes exposure. Fundus photos taken on the first preoperative day revealed an oval area of yellow-white retinal edema just superior to the fovea. Fluorescein angiography 3 weeks after surgery clearly demonstrated the same oval area of mottled hypertluorescence seen in our patients. This lesion appeared identical to the lesions demonstrated by Hochheimer in phakic monkeys who had undergone 60 minutes exposure to the operating microscope.11 Since our patients appear to be asymptomatic, one may ask whether this lesion has clinical significance. We believe it may be in part fortuitous that the lesions were located either above or below the foveola in our patients rather than crossing it. This could depend upon the tilt of the eye and of the operating microscope at the time of surgery. It may also be due to an increased threshold for photic damage in the center of the fovea, as demonstrated in monkeys by Lawwill and co-workers. 19 Nonetheless, the sharply defined scotomas persisting over 5 months after surgery in several of our patients certainly attest to the damaging affect of this lesion on visual function. Despite the fact that aphakic cystoid macular edema was described prior to use of the operating microscope, some recent authors have speculated that a large percentage of modem cases of aphakic cystoid macular edema are related to ph ototoxicity from the illumination source of the operating microscopeY· 16 We have found no association between the apparent light induced maculopathy in our patients and aphakic or pseudophakic cystoid macular edema. Only one of our six patients with light-induced maculopathy showed cystoid macular edema on fluorescein angiography, and most of those patients who have developed pseudophakic cystoid macular edema following extracapsular lens extraction and posterior chamber implantation at our Medical Center over the past year have not shown this characteristic oval lesion of light-induced maculopathy. The finding of maculopathy, presumably related to the coaxial illumination of the operating microscope, in this small series of patients, should force all clinicians to heed recent laboratory studies warning of potential dangers of the illuminating sysems in ophthalmic instruments. The gap between the laboratory and the operating room has now been bridged, and the findings in the former have proven relevant clinically. This necessitates study of more effective filters for our ophthalmic instruments and forces us to re-examine our surgical techniques in relation to their potential for retinal photic and thermal toxicity.
MCDONALD AND IRVINE •
ACKNOWLEDGMENT Bruce W. Morris and Michael H . Narahara performed the ophthalmic photography.
REFERENCES 1. Noell WK, Walker VS, Kang BS, Berman S. Retinal damage by light in rats. Invest Ophthalmol 1966; 5:450- 73. 2. Kuwabara T, Gorn RA. Retinal damage by visible light; an electron microscopic study. Arch Ophthalmol 1968; 79:69- 78. 3. Friedman E, Kuwabara T. The retinal pigment epithelium. IV. The damaging effects of radiant energy. Arch Ophthalmol1968; 80:26579. 4. Gorn RA, Kuwabara T. Retinal damage by visible light; a physiologic study. Arch Ophthalmol1967; 77:115-8. 5. Lanum J: The damaging effects of light on the retina. Empirical findings, theoretical and practical implications. Surv Ophthalmol 1978; 22:221-49. 6. Tso MOM: Photic maculopathy in rhesus monkey: a light and electron microscopic study. Invest Ophthalmol 1973; 12:17-34. 7. Tso MOM, Fine BS, Zimmerman LE: Photic maculopathy produced bJ: the indirect ophthalmoscope. I. Clinical and histopathologic study. Am J Ophthalmol 1972; 73:686- 99.
LIGHT-INDUCED MACULOPATHY
8. Fuller D. Machemer R, Knighton RW. Retinal damage produced by intraocular fiber optic light. Am J Ophthalmol 1978; 85:519-37. 9. Calkins JL, Hbchheimer BF. Retinal light exposure from operation microscopes. Arch Ophthalmol 1979; 97:2363-7. 10. Calkins JL, Hochheimer BF, D'Anna SA. Potential hazards from specific ophthalmic devices. Vision Res 1980; 20:1039-53. 11. Hochheimer BF, D' Anna SA, Calkins JL. Retinal damage from light. Am J Ophthalmol1979; 88:1039- 44. 12. Mainster MA. Spectral transmittance of intraocular lenses and retinal damage from intense light sources. Am J Ophthalmol1978; 85:16770. 13. Meyers SM, Bonner FR. Retinal irradiance from vitrectomy endoilluminators. Am J Ophthalmol1982; 94:26-9. 14. Sperling HG. Are ophthalmologists exposing their patients to dangerous light levels? Invest Ophthalmol Vis Sci 1980; 19:989-90. 15. Ham WT Jr. Mueller HA, Ruffolo JJ Jr, et al. Action spectrum for retinal injury from near-ultraviolet radiation in the aphakic monkey. Am J Ophthalmol 1982; 93:299-306. 16. Henry MM,Henry LM, Henry LM: A possible cause of chronic cystic maculopathy. Ann Ophthalmol1977; 9:455- 7. 17. Keates RH, Genstler DE: UV radiation . Ophthalmic Surg 1982; 13:327. 18. Henry MM. Henry LM, Henry LM. Carl Zeiss Bulletin. May 11 , 1981 . 19. Lawwill T, Crockett S, Currier G. Retinal damage secondary to chronic light exposure, thresholds and mechanisms. Doc Ophthalmol1977; 44:379-402.
951
Abstract: A characteristic macular lesion has been noted in six patients who underwent extracapsular cataract extraction with posterior chamber lens implantation. The lesion appeared similar to that which other investigators have produced in monkeys as a response to the coaxial illumination of the operating microscope. On the first or second postoperative day, the lesion appeared as an oval area of mild yellow-white discoloration of the retina; gradually it developed mottled pigmentation over the next few weeks. The pigmentary changes were often subtle, but fluorescein angiography revealed a characteristic sharply circumscribed lesion. In most of our patients the lesion was just above or below the foveola, so that central vision returned to normal, but a paracentral scotoma was present. These findings should encourage the clinician to heed the warnings of those laboratory studies which have shown the phototoxic potential of the operation microscope's unfiltered coaxial illumination and force us to re-examine our filters and operating techniques. [Key words: cataract extraction, light, light-induced, maculopathy, operational microscope, phototoxic, retinal damage by light.] Ophthalmology 90:945-951,
1983
The toxic effects of light on the retina have been well documented. 1- 6 Recently, the phototoxic potential of several common ophthalmic instruments has been shown in experimental animals. 7- 12 The present report describes findings in patients who underwent extracapsular cataract extraction with implantation of a posterior chamber lens and whom we believe manifest evidence of macular light toxicity secondary to the coaxial illu-
From the Department of Ophthalmology, University of California, San Francisco, California. Presented at the Eighty-seventh Annual Meeting of the American Academy of Ophthalmology, San Francisco, California, October 30-November 5, 1982. Reprint requests to A. Rodman Irvine, MD, U-490, University of California Department of Ophthalmology, San Francisco, CA 94143. 0161-6420/83/0800/0945/$1.15 ©American Academy of Ophthalmology
mination of the operating microscope. The lesions closely resemble those produced experimentally by Hochheimer et al in rhesus monkeys 11 and are, to the best of our knowledge, the first reported cases of clinical light toxicity from the operating microscope.
CASE REPORTS All cases were operated upon with a standard ceiling mounted Zeiss Operating Microscope with a 30-watt bulb. They were done by senior residents who had each performed over 15 lens implantations prior to the current cases. After a "can opener" style anterior capsulotomy and expression of the nucleus, cortical material was removed with a closed microsurgical approach using an infusion-aspiration tip. The posterior capsule was then carefully "polished" with a diamond-
945
OPHTHALMOLOGY • AUGUST 1983 • VOLUME 90 • NUMBER 8
coated irrigating cannula. The lens implant was inserted under an air bubble and the wound was closed with interrupted sutures. The surgical operating times, as recorded in the anesthetic records, varied between 1 hour 15 minutes and 1 hour 30 minutes. One faculty member (AI) served as responsible surgeon and performed the postoperative care on the first three cases. Once the maculopathy was recognized in these cases, the fourth, fifth, and sixth cases were picked up when they were sent to the fluorescein Angiography Unit by the other surgeons. It is of note that the pigment epithelial changes were subtle enough in these last three cases that they had not been noted clinically prior to the angiography, and there was no suspicion of a light-induced maculopathy by the referring surgeon. Case 1. This 60-year-old woman underwent uncomplicated extracapsular cataract extraction and implantation of a Kratzstyle posterior chamber lens on February 15, 1982. One week after surgery, the patient was noted to have a questionable, faint retinal pigment epithelial change in the superior macula. This was thought at that time to be a possible shallow RPE detachment. This area of retinal pigment epithelial change took on a striking, mottled pattern over the next several months. Vision required several months to improve but 5 months after surgery acuity was 20/30 with a refraction of -1 .00 sphere with + 1.50 cyclinder axis 150. Tangent screen perimetry at this time revealed an oval scotoma inferior to fixation (Fig 1). fluorescein angiography revealed a sharply defined elliptical area of mottled fluorescein transmission corresponding to the area of pigment epithelial change (Fig 1). Case 2. This 82-year-old woman underwent an uncomplicated extracapsular cataract extraction with implantation of a Sinskey style posterior chamber lens on February 9, 1982. Two weeks after surgery it was noted that there was a subtle oval area of pigment epithelial change superior to the fovea. Again, the vision seemed a bit slow recovering, but by 41f2 months after surgery acuity was 20/30 with a refraction of - 2.50 with a +0.75 cyclinder axis 60. fluorescein angiography at this time revealed a similar area of irregular fluorescein transmission superior to the fovea corresponding to the area of retinal pigment epithelial granularity seen ophthalmoscopically. Tangent screen perimetry at this time revealed a scotoma inferior to fixation (Fig 2).
Fig I. Case I: A, fundus photo shows oval, sharply defined area of pigment mottling just above the fovea.
Fig 2. Case 2: A, fundus photo shows a subtle pigment mottling in an oval area superior to the fovea.
Fig 3. Case 3: A, fundus photo shows an oval area of pigment mottling just below the fovea.
946
Fig 3. B, fluorescein angiography in the arteriovenous stage accentuates the pigment lesion.
OS
Name :
MP
lsopters:
3/ 2000
Date : 7-19-82
Fig 1. B, fluorescein angiography shows fluorescein transmission and
blockage limited to the focal area of pigment mottling.
Fill 1. C, tangent screen field shows a dense paracentral scotoma corresponding with the pigment lesion.
OD
c
NameWH
Fig 2. B, fluorescein angiography makes the focal oval area of pigment
mottling obvious.
Date
lsopters
3/ 2000
7-19 -82
Fig 2. C, tangent screen field shows a dense paracentral scotoma.
90/30
0/30
180/30
270/30
Fig 3. C, the late stage of the angiogram shows cystoid macular edema. This was the only patient showing such edema in this series.
Fig 3. D, automated perimetry with the Octopus<~> instrument reveals a dense scotoma superior to fixation corresponding with the pigment lesion.
947
OPHTHALMOLOGY •
AUGUST 1983 •
VOLUME 90 •
NUMBER 8
Fig 4. Case 4: A, fundus photo shows subtle area of pigment mottling inferior to the fovea and just above the inferotemporal vein.
Fig 4. B, fluorescein angiogram accentuates the area of pigment mottling.
Case 3. This 71-year-old white man underwent uncomplicated extracapsular cataract extraction and implantation of a Sinskey style posterior chamber lens on June 7, 1982. Eleven days after surgery the patient was noted to have an oval area of apparent pallor inferior to the fovea. Two months after surgery, fundus photography revealed a very subtle area of irregular retinal pigment epithelial atrophy in this area. Fluorescein angiography revealed a sharply defined oval area of patchy fluorescein transmissions similar to that in the two preceeding patients. This patient, however, also exhibited cystoid macular edema. Visual acuity at this time was 20/100 with a refraction of - 1.00 sphere with +3.00 cyclinder axis 90. Tangent screen and octopus automated perimetry showed a scotoma superior to fixation (Fig 3). Case 4. This 65-year-old man underwent uncomplicated extracapsular cataract extraction and implantation of a Shearing style posterior chamber lens on June 18, 1982. Six weeks after surgery visual acuity was best corrected to 20/100. No macular lesion was recognized, but he was referred for fluorescein angiography to rule out the possible presence of cystoid macular edema. The fluorescein angiography showed no cystoid macular edema but revealed an oval area of irregular fluorescein transmission inferior to the fovea, identical to that in the initial three patients. The fundus photography revealed a very subtle area of irregular pigment epithelial atrophy corresponding to the area of fluorescein transmission (Fig 4). Case 5. This 80-year-old woman underwent uncomplicated extracapsular cataract extraction and implantation of a Shearing type posterior chamber lens on March 3, 1982. Whereas the patient's initial postoperative course was uncomplicated and vision was 20/30, approximately 4 months following surgery visual acuity had dropped to 20/80. In order to determine whether this drop was due to opacification of the posterior capsule or to cystoid macular edema, fluorescein angiography was ordered. The fluorescein angiogram again revealed an oval sharply defined area of irregular fluorescein transmission similar to that seen in the preceeding four patients. It was only
after seeing the fluorescein angiogram, that a careful examination of the fundus revealed a corresponding area of subtle pigment epithelial mottling (Fig 5). Case 6. This 62-year-old man underwent uncomplicated extracapsular cataract extraction and implantation of a Sinskey style posterior chamber lens on June 16, 1982. After attaining early visual recovery, the patient developed a sudden decrease in acuity three months postoperatively with anterior ischemic optic neuropathy. Fluorescein angiography on September 14, 1982 revealed in addition to the ischemic optic nerve, the same characteristic oval, mottled transmission patterns seen in the other patients (Fig 6).
948
DISCUSSION Phototoxic damage to the retina has been an area of avid investigation for 20 years. In 1965, Noell found that the retina of rats could be damaged by light of moderate intensity. Histologically, he found simultaneous destruction of the retinal pigment epithelium and the photoreceptors. 1 Kuwahara and Gorn showed that, depending on the duration and nature of the light exposure, retinal damage could vary from total destruction of the entire retina to minimal changes in the photoreceptors.2 Tso conducted light and electron microscopic studies on rhesus monkeys who had been exposed to the light of an indirect ophthalmoscope for 1 hour.6 He described the ensuing maculopathy in three stages: ( 1) an initial retinal edema with damage to the photoreceptors and retinal pigment epithelium; (2) macrophagic influx to the subretinal region; and (3) apparent regeneration of photoreceptor outer segments over areas of depigmented and proliferated retinal pigment epithelium at 3 to 5 months.
MCDONALD AND IRVINE • LIGHT-INDUCED MACULOPATHY
Fig 5. Case 5: A, Fundus photography was difficult due to capsular opacification but an area of pigment mottling is present above the fovea just below the superior temporal arcade.
Fig 5. B, fluorescein angiography makes the focal pigment abnormality much more obvious.
Fig 6. Case 6: A, fundus photography shows an area of pigment mottling just temporal to the fovea, as well as pale swelling of the optic nerve.
Fig 6. B, fluorescein angiography accentuates the area of pigment change temporal to the fovea. Leakage from the ischemic disc is also seen.
More recently, other ophthalmic instruments have been found capable of producing damaging effects on the retina. Fuller et al, and more recently Myers and Bonner, studied retinal phototoxicity induced in the monkey by the fibroptic endoilluminators normally used for vitrectomy surgery. 8 •13 Friedman and Kuwahara showed retinal damage from a 15-minute exposure to an indirect ophthalmoscope. 3 Hochheimer et al described retinal damage caused by light exposure from the slit lamp and operating microscope. 11 The phototoxic potential of the operating microscope is particularly distressing. Calkins and Hochheimer calculated the retinal exposures from several operating microscopes and found the average retinal irradiance produced to be five times greater than that produced by the average indirect ophthalmoscope. 9 •10 They evaluated the effect of several microscopes on the retina and cal-
culated theoretical "safe-times" for their use, using the American National Standards Institute's guidelines for the safe use oflasers. They predicted the maximum permissible exposures (MPE) would be reached in from 250 seconds! Hochheimer showed that irreversible damage could be done to a rhesus monkey retina by exposing it to a light of an operating microscope for 1 hour. 11 The lesions produced were oval, discrete areas of pigment epithelial mottling that bore a striking resemblance to the lesions found in our patients. The spectrum of the offending light source appears to be important. Shorter wave lengths, those in the UV, near UV, and blue range, seem more damaging to the retina than the longer wave lengths. Most of the near ultraviolet light is normally filtered by the crystalline lens; therefore, aphakic eyes are more susceptible to pho-
949
OPHTHALMOLOGY •
AUGUST 1983 •
Fig 7. Fluorescein angiogram of a rhesus monkey three weeks post phacoemulsification and posterior chamber lens implantation (30 minutes) followed by 30 minutes extra exposure to the coaxial illumination of the microscope (total 60-minute exposure). An oval area of mottled hyperfluorescence is present just above the fovea.
totoxicity. Ham found that the retinas of aphakic rhesus monkeys were six times more sensitive to light of 350 and 325 nanometers wave lengths than to blue light. 15 Due to the transmission of near UV light by polymethylmethacrylate, pseudophakic eyes would be expected to behave like aphakic eyes. In fact, Mainster has demonstrated that the pseudophakic eye is more susceptible to retinal damage from UV light sources than the normal eye. 12 It should be noted, however, that the emission spectrum of the coaxial illuminator of the Zeiss operating microscope contains no appreciable light below 400 nanometers. 17·18 The operating microscope has been in widespread use for cataract extraction for over 15 years. One must ask how it is possible that photic macular damage from the operating microscope is only now being recognized. Perhaps one factor is the nature of the operation. It is only recently that the residents at the University of California Medical Center have begun doing a significant number of extracapsular lens extractions by using the closed irrigation-aspiration technique along with lens implantation. It is possible that the presence of the pseudophakos is an important factor, with the pseudophakos acting to focus the illuminating light on the retina during wound closure. It is also possible that the relatively long time spent in careful cleaning of all cortical material from the posterior capsule prior to implantation of the pseudophakos is the more important factor. It should be stressed that we have found evidence of this maculopathy in only a small percentage of those patients on whom we have performed extracapsular lens extraction and posterior chamber lens implantation. Finally, the lesion is very easily missed as it is usually asymptomatic and the fundus changes are often subtle and easily dismissed as due to aging. In most of our patients, fluorescein angiography was necessary in order to appreciate the unique and characteristic pattern of retinal pigment epithelial change. It would seem this lesion may not be 950
VOLUME 90 •
NUMBER 8
rare. Once we had learned to recognize it in our own patients, three more cases from other surgeons (case 46) were seen in our Eye Photography Unit within 2 months. Recently we have duplicated this lesion experimentally (Fig 7). We perf01med an extracapsular cataract extraction and implantation of a posterior chamber lens in an adult rhesus monkey. This surgery required 30 minutes. We then removed the air bubble and continued to shine the operating microscope light into the eye for another 30 minutes to total 60 minutes exposure. Fundus photos taken on the first preoperative day revealed an oval area of yellow-white retinal edema just superior to the fovea. Fluorescein angiography 3 weeks after surgery clearly demonstrated the same oval area of mottled hypertluorescence seen in our patients. This lesion appeared identical to the lesions demonstrated by Hochheimer in phakic monkeys who had undergone 60 minutes exposure to the operating microscope.11 Since our patients appear to be asymptomatic, one may ask whether this lesion has clinical significance. We believe it may be in part fortuitous that the lesions were located either above or below the foveola in our patients rather than crossing it. This could depend upon the tilt of the eye and of the operating microscope at the time of surgery. It may also be due to an increased threshold for photic damage in the center of the fovea, as demonstrated in monkeys by Lawwill and co-workers. 19 Nonetheless, the sharply defined scotomas persisting over 5 months after surgery in several of our patients certainly attest to the damaging affect of this lesion on visual function. Despite the fact that aphakic cystoid macular edema was described prior to use of the operating microscope, some recent authors have speculated that a large percentage of modem cases of aphakic cystoid macular edema are related to ph ototoxicity from the illumination source of the operating microscopeY· 16 We have found no association between the apparent light induced maculopathy in our patients and aphakic or pseudophakic cystoid macular edema. Only one of our six patients with light-induced maculopathy showed cystoid macular edema on fluorescein angiography, and most of those patients who have developed pseudophakic cystoid macular edema following extracapsular lens extraction and posterior chamber implantation at our Medical Center over the past year have not shown this characteristic oval lesion of light-induced maculopathy. The finding of maculopathy, presumably related to the coaxial illumination of the operating microscope, in this small series of patients, should force all clinicians to heed recent laboratory studies warning of potential dangers of the illuminating sysems in ophthalmic instruments. The gap between the laboratory and the operating room has now been bridged, and the findings in the former have proven relevant clinically. This necessitates study of more effective filters for our ophthalmic instruments and forces us to re-examine our surgical techniques in relation to their potential for retinal photic and thermal toxicity.
MCDONALD AND IRVINE •
ACKNOWLEDGMENT Bruce W. Morris and Michael H . Narahara performed the ophthalmic photography.
REFERENCES 1. Noell WK, Walker VS, Kang BS, Berman S. Retinal damage by light in rats. Invest Ophthalmol 1966; 5:450- 73. 2. Kuwabara T, Gorn RA. Retinal damage by visible light; an electron microscopic study. Arch Ophthalmol 1968; 79:69- 78. 3. Friedman E, Kuwabara T. The retinal pigment epithelium. IV. The damaging effects of radiant energy. Arch Ophthalmol1968; 80:26579. 4. Gorn RA, Kuwabara T. Retinal damage by visible light; a physiologic study. Arch Ophthalmol1967; 77:115-8. 5. Lanum J: The damaging effects of light on the retina. Empirical findings, theoretical and practical implications. Surv Ophthalmol 1978; 22:221-49. 6. Tso MOM: Photic maculopathy in rhesus monkey: a light and electron microscopic study. Invest Ophthalmol 1973; 12:17-34. 7. Tso MOM, Fine BS, Zimmerman LE: Photic maculopathy produced bJ: the indirect ophthalmoscope. I. Clinical and histopathologic study. Am J Ophthalmol 1972; 73:686- 99.
LIGHT-INDUCED MACULOPATHY
8. Fuller D. Machemer R, Knighton RW. Retinal damage produced by intraocular fiber optic light. Am J Ophthalmol 1978; 85:519-37. 9. Calkins JL, Hbchheimer BF. Retinal light exposure from operation microscopes. Arch Ophthalmol 1979; 97:2363-7. 10. Calkins JL, Hochheimer BF, D'Anna SA. Potential hazards from specific ophthalmic devices. Vision Res 1980; 20:1039-53. 11. Hochheimer BF, D' Anna SA, Calkins JL. Retinal damage from light. Am J Ophthalmol1979; 88:1039- 44. 12. Mainster MA. Spectral transmittance of intraocular lenses and retinal damage from intense light sources. Am J Ophthalmol1978; 85:16770. 13. Meyers SM, Bonner FR. Retinal irradiance from vitrectomy endoilluminators. Am J Ophthalmol1982; 94:26-9. 14. Sperling HG. Are ophthalmologists exposing their patients to dangerous light levels? Invest Ophthalmol Vis Sci 1980; 19:989-90. 15. Ham WT Jr. Mueller HA, Ruffolo JJ Jr, et al. Action spectrum for retinal injury from near-ultraviolet radiation in the aphakic monkey. Am J Ophthalmol 1982; 93:299-306. 16. Henry MM,Henry LM, Henry LM: A possible cause of chronic cystic maculopathy. Ann Ophthalmol1977; 9:455- 7. 17. Keates RH, Genstler DE: UV radiation . Ophthalmic Surg 1982; 13:327. 18. Henry MM. Henry LM, Henry LM. Carl Zeiss Bulletin. May 11 , 1981 . 19. Lawwill T, Crockett S, Currier G. Retinal damage secondary to chronic light exposure, thresholds and mechanisms. Doc Ophthalmol1977; 44:379-402.
951