Leave a comment

Chapter 142 – Light Toxicity and Laser Burns

Chapter 142 – Light Toxicity and Laser Burns









• Damage to the retina produced by any type of light source.



• Mechanism of damage is usually photochemical.

• Thermal enhancement of retinal damage is possible.

• Potential causes of photic retinopathy include solar eclipse, welding arc, lightning, ophthalmic instruments, laser.



• Delayed appearance of the lesion after the injury by hours to days.

• Variable recovery of vision.

• Severity of damage proportional to increased duration and intensity of exposure.





There are a variety of methods to prevent damage to structures of the eye, which may be induced by light sources. Breakdown of the intrinsic ocular protective mechanisms or exposure to external high-risk conditions can produce light or photic damage to the retina. The development and degree of photic damage to the retina depends on numerous factors including the preexisting ocular anatomy and the parameters of the light source (including wavelength, duration, and power).


The electromagnetic spectrum encompasses a broad range of radiation ( Fig. 142-1 ). The eye primarily perceives radiation in the optical spectrum, which is comprised of visible (400–760?nm), ultraviolet (UV, 200–400?nm), and infrared (IR, >760?nm) wavelengths. Radiation in this region can be produced by many sources such as the sun, artificial lighting, ophthalmic instruments, and lasers.

The tissue effects of light may be classified as mechanical, thermal, or photochemical. These effects are determined by the irradiance (W/cm2 ) from the light source, the wavelength of incident light, the duration of exposure, and the absorption of target tissue.[1] Mechanical injury results from high irradiance, short-duration exposures in the nanosecond ( 10-9 sec) to picosecond (10-12 sec) range. The energy produced strips electrons from molecules and disintegrates the target tissue into a collection of ions and electrons, known as plasma. This is the mechanism of photodisruption produced by the neodymium: yttrium–aluminum–garnet (Nd:YAG) laser. At a moderate irradiance and exposure duration greater than 1?µsec, thermal effects result from a critical temperature rise in the target tissue. An elevation of retinal temperature by 10–20°C produces protein denaturation and enzyme inactivation, which results in coagulation, cellular necrosis, and hemostasis. [2] [3] Long visible wavelengths and IR radiation produce thermal injury to the retina and choroid during retina laser photocoagulation. Photochemical or phototoxic effects occur with low-to-moderate irradiances below coagulation thresholds and with short wavelengths, in particular UV and visible blue wavelengths. Damage to cellular components occurs at temperatures too low to cause thermal destruction, which may account for a delay of 24–48 hours before the appearance of a lesion. Absorption of a photon by the outer electrons produces an excited molecular state, which can drive a chemical reaction. Because the energy per photon is inversely proportional to its wavelength, short-wavelength photons have more energy to induce a photochemical reaction. Long-wavelength visible light also can induce photochemical changes when tissues are sensitized by an exogenous photosensitizer. At intermediate values of irradiance and exposure, more than one of the above mechanisms may be in effect to produce tissue damage.

Light must penetrate the ocular media in order to interact with the retina. The ocular media transmit 75–90% of electromagnetic radiation in the range of 400–1064?nm.[4] Several mechanisms exist to reduce retinal light exposure. The cornea absorbs most UV-B (280–315?nm) and UV-C (<280?nm), as well as some IR radiation, and reflects up to 60% of incident light that is not perpendicular to its surface.[4] The lens absorbs most UV-A (315–400?nm) and visible blue wavelengths. Intrinsic ocular defenses against retinal light damage include xanthophyll absorption of near-UV and blue light to protect the photoreceptors, temperature control by the choroidal circulation, intracellular molecular detoxification of free radicals and toxic molecules, and retinal pigment epithelium (RPE)-mediated photoreceptor renewal.[5] Physiological protective mechanisms include the eyebrow ridge, squint and blink reflexes, the aversion response, and pupillary miosis. Light damage to the retina may occur when protective mechanisms are impaired, such as with surgical alterations to the eye or with deliberate gazing at a light source. Young patients may be at increased risk due to more efficient transmission of light through the ocular media.


Photic retinopathy is a nonspecific term that refers to light-induced retinal damage. It is most often due to inadvertent exposure. Retinal damage induced by solar viewing and the operating microscope is typically photochemical and may be enhanced by elevated tissue temperature and increased blood oxygen tension.[6] Increased chorioretinal pigmentation facilitates light absorption in the RPE and choroid, which may elevate the background retinal temperature and thermally enhance photochemical damage. It has been hypothesized that retinal defenses against toxic free radicals from light and oxygen are overwhelmed by supranormal light exposure. Damage manifests as a disorder of RPE and photoreceptor outer segments.[7] Retinal phototoxic injury originally was believed to be permanent; however, visual recovery has been noted in cases of solar retinopathy, welding arc maculopathy, and operating microscope phototoxicity. Mild photochemical damage may not be symptomatic or visible ophthalmoscopically, so clinical reports appear to represent the more severe





Figure 142-1 The electromagnetic spectrum. This includes the spectrum of electromagnetic radiation, the optical part of the spectrum and the visible part of the spectrum.

injuries. The extent of retinal injury and the likelihood of visual recovery depend on multiple factors, including the location and area of exposed retina, the duration, intensity, and spectrum of the light source, and host susceptibility factors, such as age, nutritional status, ocular pigmentation, and core temperature.

Solar Retinopathy

Solar retinopathy refers to retinal injury induced by direct or indirect solar viewing. Other names for this entity include foveomacular retinitis, photoretinitis, photomaculopathy, and eclipse retinopathy. The harmful effects of solar viewing have been recognized for centuries. Foveomacular retinitis was characterized initially as a syndrome of bilateral decreased vision and foveal lesions in military persons. A history of solar viewing was elicited subsequently from most of these patients.[8] Solar retinopathy also has been associated with religious sun gazing, solar eclipse observing, telescopic solar viewing, sunbathing, psychiatric disorders, and the use of psychotropic drugs.[9] Solar radiation damages the retina through photochemical effects, which may be enhanced by elevated tissue temperature. Direct solar observation through a 3?mm pupil produces a 4°C temperature rise, which is below thermal damage thresholds.[3] Sustained solar viewing for more than 90 seconds through a constricted pupil exceeds the threshold for photochemical retinal damage.[10] Solar observation through a dilated 7?mm pupil produces a 22°C increase in retinal temperature, which is above photocoagulation thresholds.[3]

Symptoms usually develop 1–4 hours after solar exposure and include unilateral or bilateral decreased vision, metamorphopsia, central or paracentral scotomata, chromatopsia, photophobia, afterimage, and periorbital ache. Visual acuity ranges from 20/40 to 20/200 acutely. A small yellow spot with a gray margin may be noted in the foveolar or parafoveolar area shortly after exposure ( Fig. 142-2 ). This discoid lesion measures up to 200?µm in diameter and corresponds to the retinal image of the sun.[3] [9] In mild cases, a lesion may not be visible ophthalmoscopically. Histopathology of the acute solar lesion demonstrates injury to the RPE with necrosis, detachment, irregular pigmentation, and minimal change to the photoreceptors.[11] Fluorescein angiography may be normal or reveal transmission defects due to RPE irregularities ( Fig. 142-3 ). Leakage of fluorescein rarely is noted during the acute stage.

The yellow lesion is replaced by a permanent focal depression, with RPE mottling or a lamellar hole during the weeks following injury. Vision usually improves to 20/20–20/40 within 6 months, although scotomata and metamorphopsia can persist. Multiple areas of RPE mottling may represent previous episodes of sun gazing.

Numerous factors may affect and increase the susceptibility of the retina to photic damage. These include the interval and spectrum of solar exposure, a reduction in the ozone layer, atmospheric conditions, the distance from the sun, telescopic viewing, pupil dilatation, elevated body temperature, increased chorioretinal pigmentation, clarity of the ocular media, and preexisting retinal disease. Emmetropes and hyperopes may be at increased risk caused by effective focusing of light on the retina.[5] Systemic photosensitizing agents, such as tetracycline, hematoporphyrins, and psoralen, may predispose to photochemical damage.

The term eclipse retinopathy specifically describes macular damage that occurs as a result of viewing a solar eclipse. The visual morbidity associated with the full solar eclipse on August 11, 1999, was evaluated. The majority of patients sought treatment within 2 days of viewing the eclipse. An abnormal macular appearance was reported in 84% of those evaluated. The visual morbidity is usually, but not always, temporary. There were no cases of continued visual loss or symptoms after 6 months in a series of 70 cases.[12] In another report, four patients had persistent symptoms 7 months after eclipse viewing. [13] Evaluation of the mechanism of retinal damage following eclipse and excessive light exposure in albino rats demonstrated irreversible neuronal







Figure 142-2 Solar retinopathy of both eyes. In the right eye (A) and in the left eye (B), of the same patient. (Courtesy of William E. Benson, MD.)



Figure 142-3 Fluorescein angiography of solar retinopathy in the left eye. Transmission hyperfluorescence corresponds to the retinal pigment epithelium defect. (Courtesy of William E. Benson, MD.)

apoptosis of retinal cells and gliovascular responses.[14] Cellular apoptosis is an irreversible process, which could account for permanent visual impairment, while the activation of the non-neuronal glial and endothelial cells may be responsible for the more transient clinical symptoms.

No specific therapy exists for solar retinopathy. Further episodes of solar viewing should be discouraged. Eclipse viewing should be discouraged unless there is adequate use of the proper protective eyewear. Commercially available tested solar filters with high-quality absolute visible, UV, and IR light are recommended for eclipse observation. Public health education may reduce visual morbidity. Oral corticosteroids have been used to treat acute lesions, but a beneficial effect has not been demonstrated conclusively because vision often improves spontaneously.

Welding Arc Exposure

Welding arcs emit radiation, and the most common injury produced is keratitis due to UV absorption by the cornea. Retinal injury is rare but can occur after a welding arc is viewed without proper ocular protection.[15] The retinal temperature increase is below photocoagulation thresholds; thus, injury is produced by photochemical effects from UV and short blue wavelength exposure. Symptoms include unilateral or bilateral decreased vision, scotomata, and metamorphopsia. The respective appearances of the retinal lesion and clinical course are similar to those of solar retinopathy. A yellow edematous lesion occurs acutely in the fovea, which is replaced over time by an RPE irregularity or a pseudomacular hole. No effective therapy exists. Vision usually improves with time, although some patients experience a permanent loss of vision.

Lightning Retinopathy

Lightning maculopathy describes acute visual loss and macular changes that occur after one is injured by lightning. The visual loss to light perception may be severe. Lesions described include macular edema, macular hole, cyst, or a solar retinopathy-like picture, cataract, retinal detachment, retinal artery occlusions, and relative afferent pupillary defect.[16] Visual recovery often occurs over time, even with severe maculopathy. High-dose intravenous methylprednisolone treatment may play a role in recovery of vision, because its use has been associated with reversal of lightning-induced blindness in two cases.[17]

Retinal Phototoxicity From Ophthalmic Instruments

Ophthalmologists use a variety of powerful light sources for diagnostic and therapeutic purposes. Retinal injury in humans has been described following exposure to light produced by the operating microscope and fiberoptic endoillumination. Iatrogenic phototoxicity has been reported after cataract extraction, epikeratophakia, combined anterior segment procedures, and vitreous surgery.[7] The most frequently cited cause of ophthalmic instrument phototoxicity is the operating microscope. The associated injury was described initially after uncomplicated extracapsular cataract extraction.[18] A wide range in the incidence of operating microscope phototoxicity has been reported, up to 28% in a prior study. In one series, 7% of 135 patients having cataract operations demonstrated operating microscope phototoxicity, while there were no cases in a prospective study of 37 cataract surgeries.[19] [20] This range is likely due to variations in the intensity of microscope illumination, surgical technique, cataract density, and duration of surgery. The mechanism of intraoperative phototoxicity is photochemical but may be thermally enhanced. Because operating microscopes generate little UV radiation, photochemical damage probably is caused by short-wavelength visible







Figure 142-4 Acute retinal phototoxicity 2 weeks after cataract surgery. A, Perifoveal fluorescein mottling in the early stage angiogram. B, Modest fluorescein leakage and retinal pigment mottling in the late phase. Visual acuity is 20/60. (Courtesy of Gordon A. Byrnes, MD.)





Figure 142-5 Chronic retinal phototoxicity in the left eye. A, Visual acuity is 20/50 (6/15). A well-defined area of retinal pigment epithelium mottling is present. The patient also has congenital retinal venous tortuosity. B, Fluorescein angiogram reveals blocking and transmission defects without late fluorescein leakage. (Both courtesy of Gordon A. Byrnes, MD.)

blue and green light. The incorporation of UV and IR filters in the intraocular lens (IOL) and microscope may reduce the risk of photic and thermal effects, respectively. Human photic retinal injury has been produced in a blind phakic eye after 60 minutes of operating microscope light exposure, despite the presence of UV and IR filters, which demonstrates that filters do not prevent damage completely.[21]

Few patients manifest symptoms after operating microscope damage, and the level of vision depends on the size and location of the lesion. A foveal lesion can produce severe permanent vision loss, while an eccentric lesion is compatible with good vision and a pericentral scotoma that corresponds to the lesion’s location. Immediately after exposure, there is little to no clinical evidence of macular pathology. Within 24–48 hours, a yellow lesion measuring 0.5–2.0 disc diameters at the level of the RPE is found and retinal edema may be present. Retinal damage often is inferior to the fovea due to rotation of the globe by a superior rectus bridle suture, microscope tilt, and displacement of the microscope field over the superior limbus. Injury may occur at or superior to the fovea during vitreous surgery or when a superior rectus bridle suture is not used. The shape of the lesion matches that of the surgical illuminating source. A tungsten filament in the operating microscope produces a horizontal, oval lesion, while the fiberoptic illuminator produces a round lesion. Fluorescein angiography of the acute lesion reveals fluorescein leakage at the level of the RPE ( Fig. 142-4 ), which may simulate the appearance of choroidal neovascularization. Over subsequent weeks, the yellow lesion fades and is replaced by permanent areas of RPE clumping and atrophy ( Fig. 142-5 , A), which correspond angiographically to blocking and transmission defects, respectively ( Fig. 142-5 , B). Other long-term sequelae include postoperative erythropsia and retinal surface wrinkling.



Choroidal neovascularization has been reported adjacent to an area of operating microscope photic damage at 18 months after cataract surgery.[22] In primates, sub-RPE neovascularization in areas of photic damage has been reported after 2–5 years.[23] Mild light-induced retinal injuries may be overlooked, because subtle postoperative pigmentary changes may be attributable to other causes. Operating microscope light exposure has been implicated in the development of post–cataract extraction cystoid macular edema, but this association has not been demonstrated conclusively. [7]

Histopathological studies of acute human photic lesions produced after 60 minutes of operating microscope exposure prior to enucleation for malignant melanoma revealed RPE and photoreceptor damage.[24] In primates, early photic lesions demonstrate photoreceptor damage and disruption of RPE tight junctions; the latter is noted clinically by fluorescein leakage through the RPE.[23] Regeneration of photoreceptor outer segments was noted in primates 3–5 months after injury. This may account for the recovery of vision after phototoxic injury noted in some human eyes.

Operating microscope phototoxicity has been associated with multiple surgical factors, including increased microscope brightness, wavelength of light exposure, prolonged surgical duration, and surgical technique. Although the duration of surgery has decreased with phacoemulsification, phototoxic retinal lesions still may occur. Retinal phototoxic lesions after short-duration cataract surgery (defined as surgery less than 30 minutes) were associated with a final refraction within 1.0D of emmetropia and with diabetic retinopathy.[25] The risk of photic damage may increase after IOL insertion, which can focus the incoming light on the retina; however, photic injury has been described without IOL insertion. Patient susceptibility factors include increased body temperature and blood oxygenation, chorioretinal pigmentation, preexisting maculopathy, pupillary dilatation, diabetes mellitus, retinal vascular disease, deficiencies of either ascorbic acid or vitamin A, and hydrochlorothiazide use.

No specific treatment is available for acute lesions, but spontaneous visual improvement usually occurs within a few months. The prognosis for visual recovery appears to be good, even when phototoxic lesions involve the macula. Various methods recommended to decrease the risk of phototoxicity include reduction of microscope coaxial illumination and operative time, use of IR and UV filters in the microscope and IOL, placement of an air bubble in the anterior chamber to defocus the light, and use of an eclipse filter or corneal cover to block light from entering the pupil when the incision is sutured.

The irradiance produced by the indirect ophthalmoscope and fundus camera are lower than experimentally determined retinal injury thresholds.[26] The total energy delivered to the eye is less under nonoperative than operative conditions. These instruments have not been shown to produce acute retinal injury in humans; however, prolonged exposure to the indirect ophthalmoscope has produced lesions in primates. The cumulative effect of repeated examination is unknown, and it is recommended that retinal examinations be performed with the minimal illumination required.


The relationship between environmental light exposure and age-related macular degeneration (AMD) remains speculative. It has been suggested that the cumulative effect of repeated mild photic injury during life may contribute to retinal and RPE degeneration in AMD. An association between long-term solar exposure and AMD was suggested when AMD was found to be less common in patients who have nuclear cataract formation.[27] Histopathological studies of acute photic injury in animals reveal damage to the RPE and photoreceptors in the macular region, which is at the same tissue depth and geographical location as changes observed in AMD.[23] Solar observation in humans acutely damages the RPE and produces RPE pigmentary irregularities, which are similar in appearance to those in AMD, although the diffuse thickening of Bruch’s membrane noted in AMD does not occur with solar damage.[11] The relationship between light and AMD has been evaluated using epidemiological studies. In a population-based study of Chesapeake Bay watermen, no association was found between cumulative UV-A or UV-B exposure and mild or advanced AMD.[28] An association was noted between blue or visible light exposure over the preceding 20 years and the risk of developing advanced AMD (defined as exudative neovascular disease or geographical atrophy).[29] In the Beaver Dam Eye Study, no association was found between the estimated ambient UV-B exposure and AMD.[30] The amount of outdoor leisure time in summer was associated with increased retinal pigmentation in men and late AMD in both men and women. The use of hats and sunglasses was inversely associated with the prevalence of soft, indistinct drusen.

Although some association may exist between visible light exposure and AMD, no study has yet demonstrated conclusively a relationship between long-term UV light exposure and AMD. Until the relationship between light and AMD is more clearly defined, sunglasses to filter UV and blue light may be considered for individuals, especially those at risk, such as pseudophakes and aphakes without UV-protective intraocular lenses and individuals with decreased ocular pigmentation or at risk of developing AMD.[5]


Laser applications in industrial, military, and laboratory situations account for a number of cases of accidental retinal injury. Retinal damage results from either direct exposure to the laser or its reflections. It usually occurs when the laser is fired inadvertently and an individual without ocular protection is in the vicinity of the laser. Although this type of injury often can be avoided by wearing proper eye protection, goggles may impair vision and the ability to perform fine tasks, such as alignment of the laser. The type of retinal damage depends on the laser parameters; the mechanism may be thermal, mechanical, or photochemical. Damage ranges from a small, subtle lesion to extensive hemorrhage and disruption of the retina and choroid. Accidental foveal photocoagulation can produce immediate loss of vision up to 20/200, with a foveal cyst or yellow discoloration of the RPE ( Fig. 142-6 ). Long-term evaluation may reveal RPE irregularities,



Figure 142-6 Inadvertent foveal laser burn from an Nd:YAG laser. Snellen visual acuity is 20/200. (Courtesy of Carmen A. Puliafito, MD.)



epiretinal membrane, macular hole, and gliosis. Recovery of vision is variable and is related to the extent and location of the initial injury.[31] Corticosteroids have been used to treat laser-induced retinal injuries, although their benefit is unproved.

In the ophthalmology setting, laser operators and persons in the laser area are at risk from laser light scattered from optical interfaces, such as contact lenses and mirrors. Lasers for photocoagulation contain filters to protect the operator and are positioned in the slit lamp or operating microscope before laser energy is produced. The risk to others in the vicinity of the laser is related to the distance from the laser—protective goggles should be worn by all. Decreased color discrimination in a tritan color-confusion axis has been noted in ophthalmologists who use the argon blue–green laser.[32] This may be due to long-term exposure to reflections from the argon blue aiming beam. Many photocoagulators now employ either a red or green aiming beam to minimize operator risk.


Laser pointers are low-energy lasers with output powers either less than 1 milliwatt (mW) (class 2 devices) or between 1 and 5?mW (class 3A devices). Most of the common class 3A laser pointers have power outputs that are 2?mW or less. In contrast, class 3B lasers used by ophthalmologists for retinal therapy have output powers up to or greater than 100?mW. The use and availability of laser pointers to the general public has become quite common. There is a potential for misuse of and inadvertent ocular exposure to these handheld lasers. As well, the emitted red beam may produce visual distraction or simulate a weapon-aiming beam. There are very few reports of presumed retinal damage caused by laser pointers. [33] [34] [35] [36] The mechanism of injury is not clear, but it appears due to thermal chorioretinal damage, because the longer red 650?nm- or 635?nm-wavelength light emitted from a laser pointer should not produce significant retinal phototoxicity.[37] Damage manifests as transient visual abnormalities and macular RPE disturbances that correspond to window defect hyperfluorescence on fluorescein angiography.[33] Acute uniocular reduction in vision to 20/40 with two small pericentral scotomata and a hypopigmented ring-shaped foveal lesion was described in a 19-year-old woman after deliberate staring into a commercial class 2 laser pointer for 10 seconds. [33] Visual acuity improved to 20/20 and visual field returned to normal within 8 weeks, but a subjective decrease in brightness and foveal RPE disturbances persisted. Retinal injury was not demonstrated in three patients after class 3A laser pointer retinal exposure (parameters 1?mW, 2?mW, or 5?mW for up to 15 minutes’ duration to foveal and juxtafoveal locations) prior to enucleation for uveal melanoma. Other than transient afterimages for minutes, there was no specific laser-induced ocular damage noted with ophthalmoscopy, angiography, or histology. [38] Thus, it appears to be difficult to produce ocular injury with a laser pointer without deliberate inappropriate, prolonged, foveal exposure. Factors such as patient age, preexisting maculopathy, and clarity of the ocular media likely play a role in determining retinal susceptibility to damage.





1. Mainster MA, Ham WT, DeLori FC. Potential retinal hazards. Instrument and environmental light sources. Ophthalmology. 1983;90:927–32.


2. Priebe LA, Cain CP, Welch AJ. Temperature rise required for the production of minimal lesions in the Macaca mulatta retina. Am J Ophthalmol. 1975;79:405–43.


3. White TJ, Mainster MA, Wilson PW, Tips JH. Chorioretinal temperature increases from solar observation. Bull Math Biophys. 1971;33:1–17.


4. Boettner EA, Wolter JR. Transmission of the ocular media. Invest Ophthalmol. 1962;1:776–83.


5. Mainster M. Light and macular degeneration: a biophysical and clinical perspective. Eye. 1987;1:304–10.


6. Lanum J. The damaging effects of light on the retina. Empirical findings. Theoretical and practical implications. Surv Ophthalmol. 1978;22:221–49.


7. Michels M, Sternberg P Jr. Operating microscope-induced retinal phototoxicity: pathophysiology, clinical manifestations and prevention. Surv Ophthalmol. 1990;34:237–52.


8. Cordes FC. A type of foveo-macular retinitis observed in the U.S. Navy. Am J Ophthalmol. 1944;27:803–16.


9. Yannuzzi LA, Fisher YL, Krueger A, Slatker J. Solar retinopathy; a photobiological and geophysical analysis. Trans Am Ophthalmol Soc. 1987;85:120–58.


10. Sliney DH, Wolbarsht ML. Safety with lasers and other optical sources. A comprehensive handbook. New York: Plenum; 1980.


11. Tso MOM, LaPiana FG. The human fovea after sungazing. Trans Am Acad Ophthalmol Otolaryngol. 1975;79:788–95.


12. Michaelides M, Rajendram R, Marshall J, Keightley S. Eclipse retinopathy. Eye. 2001;15:148–151.


13. Wong SC, Eke T, Ziakas NG. Eclipse burns: a prospective study of solar retinopathy following the 1999 solar eclipse. Lancet. 2001;357:199–200.


14. Thanos S, Heiduschka P, Romann I. Exposure to a solar eclipse causes neuronal death in the retina. Graefes Arch Klin Exp Ophthalmol. 2001;239(10):794–800.


15. Naidoff MA, Sliney DH. Retinal injury from a welding arc. Am J Ophthalmol. 1974;77:663–8.


16. Lee MS, Gunton KB, Fischer DH, Brucker AJ. Ocular manifestations of a remote lightning strike. Retina. Am J Ophthalmol. 2002;22:808–10.


17. Norman ME, Younge BR. Association of high-dose intravenous methylprednisolone with reversal of blindness from lightning in two patients. Ophthalmology. 1999;106:743–5.


18. McDonnell HR, Irvine AR. Light-induced maculopathy from the operating microscope in extracapsular cataract extraction and intraocular lens implantation. Ophthalmology. 1983;90:945–51.


19. Khwarg SG, Linstone FA, Daniels SA, et al. Incidence, risk factors, and morphology in operating microscope light retinopathy. Am J Ophthalmol. 1987;103: 255–63.


20. Byrnes GA, Chang B, Loose I, et al. Prospective incidence of photic maculopathy after cataract surgery. Am J Ophthalmol. 1995;119:231–2.


21. Robertson DM, McLaren JW. Photic retinopathy from the operating microscope. Arch Ophthalmol. 1989;107:373–5.


22. Leonardy NJ, Dabbs CK, Sternberg P Jr. Subretinal neovascularization after operating microscope burn. Am J Ophthalmol. 1990;109:224–5.


23. Tso MOM, Woodford BJ. Effect of photic injury on the retinal tissues. Ophthalmology. 1983;90:952–63.


24. Green WR, Robertson DM. Pathologic findings of photic retinopathy in the human eye. Am J Ophthalmol. 1991;112:520–7.


25. Kleinmann G, Hoffman P, Schechtman E, Pollack A. Microscope-induced retinal phototoxicity in cataract surgery of short duration. Ophthalmology. 2002;109:334–8.


26. Robertson DM, Erikson GJ. The effect of prolonged indirect ophthalmoscopy on the human eye. Am J Ophthalmol. 1979;87:652–60.


27. Sperduto RD, Hiller R, Seigel D. Lens opacities and senile maculopathy. Arch Ophthalmol. 1981;99:1004–8.


28. West SK, Rosenthal FS, Bressler NM, et al. Exposure to sunlight and other risk factors for age-related macular degeneration. Arch Ophthalmol. 1989;107:875–9.


29. Taylor HR, West S, Munoz B, et al. The long-term effects of visible light on the eye. Arch Ophthalmol. 1992;110:99–104.


30. Cruickshanks KJ, Klein R, Klein BEK. Sunlight and age-related macular degeneration. The Beaver Dam Eye study. Arch Ophthalmol. 1993;111:514–8.


31. Thach AB, Lopez PF, Snady-McCoy LC, et al. Accidental Nd:YAG laser injuries to the macula. Am J Ophthalmol. 1995;119:767–73.


32. Berninger TA, Canning CR, Gunduz K, et al. Using argon laser blue light reduces ophthalmologists color contrast sensitivity. Arch Ophthalmol. 1989;107:1453–8.


33. Sell CH, Bryan JS. Maculopathy from handheld diode laser pointer. Arch Ophthalmol. 1999;117:1557–8.


34. Zamir E, Kaiserman I, Chowers I. Laser pointer maculopathy. Am J Ophthalmol. 1999;127:728–9.


35. McGhee CNJ, Crain JP, Moseley H. Laser pointers can cause permanent retinal injury if used inappropriately. Br J Ophthalmol. 2000;84:229–230.


36. Mainster MA, Timberlake GT, Warren KA, Sliney DH. Pointers on laser pointers. Ophthalmology. 1997;104:1213–4.


37. Mainster MA, Reichel E. Transpupillary thermotherapy for age-related macular degeneration: long-pulse photocoagulation, apoptosis and heat shock proteins. Ophthalmic Surg Lasers. 2000;31:359–73.


38. Robertson DM, Lim TH, Salomao DR, et al. Laser pointers and the human eye: a clinicopathologic study. Arch Ophthalmol. 2000;118:1686–91.


Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s

%d bloggers like this: