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Retinal Light Damage and Eye Surgery
Ophthalmology
Volume 103, Number,4, April 1996
symptom-free 9 months later. These patients were treated between 9 and 12 weeks after cataract surgery, and hypotropia did not exceed 13 prism diopters in primary position before treatment. In the other two patients, this therapy failed. The injections were performed 4 and 6 months after surgery, and deviations in primary position of gaze before treatment were 16 and 25 prism diopters, respectively. Although the efficacy of Botulinum toxin injection in these patients remains to be established, it could be an effective therapy in some patients, especially when the vertical deviation is not very large and the length of time after cataract surgery not excessive. Would it seem reasonable to recommend this management? We congratulate the authors on this report, especially for the detailed and clear explanations of the clinical exami nation. JAIME TEJEDOR, MD JOSE M. RODRIGUEZ SANCHEZ, MD Madrid, Spain References I. Hamed LM. Strabismus presenting after cataract surgery.
Ophthalmology 1991 ;98:247-52. 2. Hamed LM, Mancuso A. Inferior rectus muscle contracture syndrome after retrobulbar anesthesia. Ophthalmology 1991 ;98: 1506-12. 3. Grimmett MR, Lambert SR. Superior rectus muscle overaction after cataract extraction. Am J OphthaImol 1992; 114: 72-80. 4. Hamilton SM, Elsas FJ, Dawson TL. A cluster of patients with inferior rectus restriction following local anesthesia for cataract surgery. J Pediatr OphthaImol Strabismus 1993;30: 288-91. 5. Ong-Tone L, Pearce WG. Inferior rectus muscle restriction after retrobulbar anesthesia for cataract extraction. Can J Ophthalmol 1989;24:162-5. 6. de Faber J-THN, von Noorden GK. Inferior rectus muscle palsy after retrobulbar anesthesia for cataract surgery. Am J Ophthalmol 1991; 112:209-11. 7. Esswein MB, von Noorden GK. Paresis of a vertical rectus muscle after cataract extraction. Am J OphthaImol 1993;116:424-30.
Author's reply
Dear Editor: Drs. Tejedor and Rodriguez Sanchez describe five patients with vertical diplopia immediately after cataract surgery. These patients later were shown to have contracture of the inferior rectus muscle. They note that this appears to contlict with our observation that the onset of diplopia may be delayed when anesthetic myotoxicity produces subsequent muscle contracture. The key to this apparent contradiction is the authors' observation that they did not examine the patients personally until several months after surgery. We believe that in these five patients, an immediate inferior rectus muscle paresis occurred secondary to the death of muscle cells caused by the anesthetic agent, producing a hypertropia of the surgical eye, with vertical diplopia when the patch was removed. Days to weeks later, as fibroblasts proliferated and contracted, the paresis
546
changed to a contracture, producing a hypotropia of the surgical eye, again with vertical diplopia. Capo and Guyton 1 have documented this change from paresis to contracture of a superior rectus muscle after retrobulbar anesthesia in a 74-year-old woman. She had vertical diplopia the day after surgery and showed a hypotropia in the surgical eye, lasting at least 2 weeks. Six months later, a large hypertropia was present secondary to apparent contracture of the superior rectus muscle. The patient was not aware of the "reversal" of her vertical diplopia. The change from hypotropia to hypertropia (or viceversa), while obvious to a strabismus specialist, is not likely to be recognized by a patient or a cataract surgeon, especially if the initial deviation is small. We agree that Botulinum toxin injections might be used to treat mild inferior rectus muscle contracture. However, treatment of inferior rectus muscle contracture secondary to anesthetic myotoxicity is not analogous to treatment of, for example, a neurogenic lateral rectus muscle paresis. In a patient with a sixth nerve paresis, Botulinum toxin is injected into a normal medial rectus muscle to counteract paresis of the antagonist lateral rectus muscle. In a patient with hypotropia secondary to anesthetic myotoxicity, Botulinum toxin is injected into an abnormal, scarred, contractured inferior rectus muscle, and the results may be less predictable. The best results probably will be obtained with Botulinum toxin if, as Drs. Tejedor and Rodriguez Sanchez suggest, the deviation is relatively small, which to us means that the cluster of contracting fibroblasts involves only a small segment of the inferior rectus muscle. DAVID HUNTER, MD, PHD Baltimore, Maryland Reference
I. Capo H, Guyton DL. Ipsilateral hypertropia after cataract surgery. Ophthalmology (in press).
Retinal Light Damage and Eye Surgery Dear Editor: In the recent editorial entitled, "Retinal Light Damage and Eye Surgery" (Ophthalmology 1995;102:1741-2), Dr. Minckler emphasizes that photic maculopathy from operating microscopes is multifactoral in etiology, and that no generally accepted guidelines or standards exist regarding protection from this injury. The author stresses minimizing both exposure time and light intensity as the principle means of avoiding photic injury. These concepts are ideal, but clinical ophthalmologists generally are unaware of the light intensity produced by their own operating microscope or the frequency with which they generate photic injuries. Although many ophthalmologists take steps to limit surgical light exposure, it is the illumination intensity of the microscope, not the duration of exposure, that is easiest for the surgeon to control. As yet, operating microscope intensity is not quantified for clinical use, requiring the surgeon to merely guess at a reasonable intensity level while performing ocular surgery.
Letters to the Editor The illumination intensity of the operating microscope has been measured and correlated with the incidence of photic maculopathy in three clinical investigations to date. The Zeiss OpMi-6 operating microscope reported by Byrnes et aI' was measured at 55 mW/cm 2 and created photic injuries in 28% of 43 patients undergoing extracapsular cataract surgery (resident and staff surgeons). The shortest overall exposure creating a photic injury was 37 minutes, not 55 minutes as indicated in the editorial. All exposures greater than 110 minutes resulted in photic injury. In a subsequent article, Byrnes et at2 reported no photic injuries in 37 patients undergoing resident phacoemulsification surgery using a Zeiss OpMi-6 FR microscope measured at 39 mW/cm2 • The coaxial exposure times were shorter than the first study (15-80 minutes) due to differences in surgical technique and the use of indirect illumination during portions of the surgery. In a follow-up study recently completed at this institution (unpublished data), no photic injuries were detected in 38 patients undergoing phacoemulsification surgery (resident and staff surgeons) using the Zeiss Retroskop 3 microscope at 33 m W /cm2 illumination intensity. Coaxial illumination exposures ranged from 16 to 71 minutes with additional portions of the surgery performed using indirect illumination. In none of these controlled studies did the surgeons believe that illumination was insufficient or unsafe to perform the procedure. Although differences in surgical technique may account for some of the reduced incidence in photic injuries cited in the last two studies, the dramatic reduction in the incidence value is most likely due to reduced illumination levels and shorter coaxial exposures compared with the first study. To improve our understanding of retinal light hazard, it is imperative that the illumination intensity of surgical microscopes be quantified so that ophthalmologists may develop a reference on which to base surgical safety. Ideally, spectral measurements also should be obtained because blue light has been shown to be more damaging than longer wavelength light. 3,4 The surgeon's clinical impression of microscope brightness from day to day is not sufficient to establish safe illumination settings. In our own experience, we have seen as much as a 66% difference in illumination intensity preference among ophthalmologists. All ophthalmologists should continue to limit unnecessary light exposure during surgery using the methods of shielding or indirect illumination as outlined in the editorial. Facilities with the ability to measure illumination intensity of their operating microscope should compare their values with those cited above and record surgical variables associated with photic injuries. Until we begin to actually quantify and standardize microscope intensity and spectral output, we will be unable to develop an understanding of the threshold at which photic injuries occur. GORDON A. BYRNES, MD DAVID O. MAZUR, MD SHARON A. MILLER, MSEE Bethesda, Maryland
References 1. Byrnes GA, Antoszyk AN, Mazur DO, et al. Photic macu-
lopathy after extracapsular cataract surgery: a prospective study. Ophthalmology 1992;99:731-8. 2. Byrnes GA, Chang B, Loose I, et al. Prospective incidence of photic maculopathy after cataract surgery. Am J Ophthalmo1 1995;119:231-2. 3. FDA Public Health Advisory: Retinal photic injuries from operating microscopes during cataract surgery, Center for Devices and Radiological Health, Food and Drug Administration, Rockville, MD 20857, October, 1995. 4. American Conference of Government Industrial Hygienists Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices (ACGIH, Cincinnati,OH, 1994). Editor's reply
Thank you for clarifying for readers that the shortest "reported" overall exposure time for creation of photic maculopathy after cataract extraction in your series was 37 not 55 minutes, which was correctly cited from a previous article.' The "shortest" overall operating time reported to cause photic injury to the retina is a useful parameter for concerned surgeons, but must be kept in perspective because it is highly likely that such injuries have occurred after much less overall light exposure in "vulnerable" eyes. Your comments about reduced illumination clearly lessening the risk of photic maculopathy are well taken. With regard to the possibility of increased vulnerability of glaucomatous eyes to photic maculopathy, I neglected to cite a recent quantitative study in primary open-angle glaucoma eyes that did not show disease-related photoreceptor loss. 2 Even if the outer retina remains intact in advanced glaucoma, increased risk of photic maculopathy during glaucoma or combined cataract and glaucoma surgery seems reasonable because of ganglion cell loss. Any photoreceptor injury created during surgery in glaucomatous eyes may still be disproportionately harmful. DON MINCKLER, MD Editor-in-Chief References 1. Boldrey EE, Ho BT, Griffith RD. Retinal burns occurring at cataract extraction. Ophthalmology 1984;91:1297-302. 2. Kendell KR, Quigley HA, Kerrigan LA, et al. Primary openangle glaucoma is not associated with photoreceptor loss. Invest Ophthalmol Vis Sci 1995;36:200-5.
The "Poor Man's" Corneal Shield and Retinal Light Protector Dear Editor: We applaud your December editorial revisiting the topic of retinal light damage during eye surgery (Ophthalmology 1995;102:1742-3). This is of great concern in the glaucoma population and cannot be over emphasized. While protecting the cornea during the surgical procedure is always of concern for anterior segment surgeons, potential
547
Volume 103, Number,4, April 1996
symptom-free 9 months later. These patients were treated between 9 and 12 weeks after cataract surgery, and hypotropia did not exceed 13 prism diopters in primary position before treatment. In the other two patients, this therapy failed. The injections were performed 4 and 6 months after surgery, and deviations in primary position of gaze before treatment were 16 and 25 prism diopters, respectively. Although the efficacy of Botulinum toxin injection in these patients remains to be established, it could be an effective therapy in some patients, especially when the vertical deviation is not very large and the length of time after cataract surgery not excessive. Would it seem reasonable to recommend this management? We congratulate the authors on this report, especially for the detailed and clear explanations of the clinical exami nation. JAIME TEJEDOR, MD JOSE M. RODRIGUEZ SANCHEZ, MD Madrid, Spain References I. Hamed LM. Strabismus presenting after cataract surgery.
Ophthalmology 1991 ;98:247-52. 2. Hamed LM, Mancuso A. Inferior rectus muscle contracture syndrome after retrobulbar anesthesia. Ophthalmology 1991 ;98: 1506-12. 3. Grimmett MR, Lambert SR. Superior rectus muscle overaction after cataract extraction. Am J OphthaImol 1992; 114: 72-80. 4. Hamilton SM, Elsas FJ, Dawson TL. A cluster of patients with inferior rectus restriction following local anesthesia for cataract surgery. J Pediatr OphthaImol Strabismus 1993;30: 288-91. 5. Ong-Tone L, Pearce WG. Inferior rectus muscle restriction after retrobulbar anesthesia for cataract extraction. Can J Ophthalmol 1989;24:162-5. 6. de Faber J-THN, von Noorden GK. Inferior rectus muscle palsy after retrobulbar anesthesia for cataract surgery. Am J Ophthalmol 1991; 112:209-11. 7. Esswein MB, von Noorden GK. Paresis of a vertical rectus muscle after cataract extraction. Am J OphthaImol 1993;116:424-30.
Author's reply
Dear Editor: Drs. Tejedor and Rodriguez Sanchez describe five patients with vertical diplopia immediately after cataract surgery. These patients later were shown to have contracture of the inferior rectus muscle. They note that this appears to contlict with our observation that the onset of diplopia may be delayed when anesthetic myotoxicity produces subsequent muscle contracture. The key to this apparent contradiction is the authors' observation that they did not examine the patients personally until several months after surgery. We believe that in these five patients, an immediate inferior rectus muscle paresis occurred secondary to the death of muscle cells caused by the anesthetic agent, producing a hypertropia of the surgical eye, with vertical diplopia when the patch was removed. Days to weeks later, as fibroblasts proliferated and contracted, the paresis
546
changed to a contracture, producing a hypotropia of the surgical eye, again with vertical diplopia. Capo and Guyton 1 have documented this change from paresis to contracture of a superior rectus muscle after retrobulbar anesthesia in a 74-year-old woman. She had vertical diplopia the day after surgery and showed a hypotropia in the surgical eye, lasting at least 2 weeks. Six months later, a large hypertropia was present secondary to apparent contracture of the superior rectus muscle. The patient was not aware of the "reversal" of her vertical diplopia. The change from hypotropia to hypertropia (or viceversa), while obvious to a strabismus specialist, is not likely to be recognized by a patient or a cataract surgeon, especially if the initial deviation is small. We agree that Botulinum toxin injections might be used to treat mild inferior rectus muscle contracture. However, treatment of inferior rectus muscle contracture secondary to anesthetic myotoxicity is not analogous to treatment of, for example, a neurogenic lateral rectus muscle paresis. In a patient with a sixth nerve paresis, Botulinum toxin is injected into a normal medial rectus muscle to counteract paresis of the antagonist lateral rectus muscle. In a patient with hypotropia secondary to anesthetic myotoxicity, Botulinum toxin is injected into an abnormal, scarred, contractured inferior rectus muscle, and the results may be less predictable. The best results probably will be obtained with Botulinum toxin if, as Drs. Tejedor and Rodriguez Sanchez suggest, the deviation is relatively small, which to us means that the cluster of contracting fibroblasts involves only a small segment of the inferior rectus muscle. DAVID HUNTER, MD, PHD Baltimore, Maryland Reference
I. Capo H, Guyton DL. Ipsilateral hypertropia after cataract surgery. Ophthalmology (in press).
Retinal Light Damage and Eye Surgery Dear Editor: In the recent editorial entitled, "Retinal Light Damage and Eye Surgery" (Ophthalmology 1995;102:1741-2), Dr. Minckler emphasizes that photic maculopathy from operating microscopes is multifactoral in etiology, and that no generally accepted guidelines or standards exist regarding protection from this injury. The author stresses minimizing both exposure time and light intensity as the principle means of avoiding photic injury. These concepts are ideal, but clinical ophthalmologists generally are unaware of the light intensity produced by their own operating microscope or the frequency with which they generate photic injuries. Although many ophthalmologists take steps to limit surgical light exposure, it is the illumination intensity of the microscope, not the duration of exposure, that is easiest for the surgeon to control. As yet, operating microscope intensity is not quantified for clinical use, requiring the surgeon to merely guess at a reasonable intensity level while performing ocular surgery.
Letters to the Editor The illumination intensity of the operating microscope has been measured and correlated with the incidence of photic maculopathy in three clinical investigations to date. The Zeiss OpMi-6 operating microscope reported by Byrnes et aI' was measured at 55 mW/cm 2 and created photic injuries in 28% of 43 patients undergoing extracapsular cataract surgery (resident and staff surgeons). The shortest overall exposure creating a photic injury was 37 minutes, not 55 minutes as indicated in the editorial. All exposures greater than 110 minutes resulted in photic injury. In a subsequent article, Byrnes et at2 reported no photic injuries in 37 patients undergoing resident phacoemulsification surgery using a Zeiss OpMi-6 FR microscope measured at 39 mW/cm2 • The coaxial exposure times were shorter than the first study (15-80 minutes) due to differences in surgical technique and the use of indirect illumination during portions of the surgery. In a follow-up study recently completed at this institution (unpublished data), no photic injuries were detected in 38 patients undergoing phacoemulsification surgery (resident and staff surgeons) using the Zeiss Retroskop 3 microscope at 33 m W /cm2 illumination intensity. Coaxial illumination exposures ranged from 16 to 71 minutes with additional portions of the surgery performed using indirect illumination. In none of these controlled studies did the surgeons believe that illumination was insufficient or unsafe to perform the procedure. Although differences in surgical technique may account for some of the reduced incidence in photic injuries cited in the last two studies, the dramatic reduction in the incidence value is most likely due to reduced illumination levels and shorter coaxial exposures compared with the first study. To improve our understanding of retinal light hazard, it is imperative that the illumination intensity of surgical microscopes be quantified so that ophthalmologists may develop a reference on which to base surgical safety. Ideally, spectral measurements also should be obtained because blue light has been shown to be more damaging than longer wavelength light. 3,4 The surgeon's clinical impression of microscope brightness from day to day is not sufficient to establish safe illumination settings. In our own experience, we have seen as much as a 66% difference in illumination intensity preference among ophthalmologists. All ophthalmologists should continue to limit unnecessary light exposure during surgery using the methods of shielding or indirect illumination as outlined in the editorial. Facilities with the ability to measure illumination intensity of their operating microscope should compare their values with those cited above and record surgical variables associated with photic injuries. Until we begin to actually quantify and standardize microscope intensity and spectral output, we will be unable to develop an understanding of the threshold at which photic injuries occur. GORDON A. BYRNES, MD DAVID O. MAZUR, MD SHARON A. MILLER, MSEE Bethesda, Maryland
References 1. Byrnes GA, Antoszyk AN, Mazur DO, et al. Photic macu-
lopathy after extracapsular cataract surgery: a prospective study. Ophthalmology 1992;99:731-8. 2. Byrnes GA, Chang B, Loose I, et al. Prospective incidence of photic maculopathy after cataract surgery. Am J Ophthalmo1 1995;119:231-2. 3. FDA Public Health Advisory: Retinal photic injuries from operating microscopes during cataract surgery, Center for Devices and Radiological Health, Food and Drug Administration, Rockville, MD 20857, October, 1995. 4. American Conference of Government Industrial Hygienists Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices (ACGIH, Cincinnati,OH, 1994). Editor's reply
Thank you for clarifying for readers that the shortest "reported" overall exposure time for creation of photic maculopathy after cataract extraction in your series was 37 not 55 minutes, which was correctly cited from a previous article.' The "shortest" overall operating time reported to cause photic injury to the retina is a useful parameter for concerned surgeons, but must be kept in perspective because it is highly likely that such injuries have occurred after much less overall light exposure in "vulnerable" eyes. Your comments about reduced illumination clearly lessening the risk of photic maculopathy are well taken. With regard to the possibility of increased vulnerability of glaucomatous eyes to photic maculopathy, I neglected to cite a recent quantitative study in primary open-angle glaucoma eyes that did not show disease-related photoreceptor loss. 2 Even if the outer retina remains intact in advanced glaucoma, increased risk of photic maculopathy during glaucoma or combined cataract and glaucoma surgery seems reasonable because of ganglion cell loss. Any photoreceptor injury created during surgery in glaucomatous eyes may still be disproportionately harmful. DON MINCKLER, MD Editor-in-Chief References 1. Boldrey EE, Ho BT, Griffith RD. Retinal burns occurring at cataract extraction. Ophthalmology 1984;91:1297-302. 2. Kendell KR, Quigley HA, Kerrigan LA, et al. Primary openangle glaucoma is not associated with photoreceptor loss. Invest Ophthalmol Vis Sci 1995;36:200-5.
The "Poor Man's" Corneal Shield and Retinal Light Protector Dear Editor: We applaud your December editorial revisiting the topic of retinal light damage during eye surgery (Ophthalmology 1995;102:1742-3). This is of great concern in the glaucoma population and cannot be over emphasized. While protecting the cornea during the surgical procedure is always of concern for anterior segment surgeons, potential
547