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Retinal Injury Due to Industrial Laser Burns
Retinal Injury Due to Industrial
Laser Burns
EDWIN E. BOLDREY, MD,* HUNTER L. LITTLE, MD,* MILTON FLOCKS, MD,* ARTHUR V ASSILIADIS, PhDt
Abstract: Ocular industrial laserbui'hs in seven patients were analyzed as to cause, severity, and type of injury. Ocular damage ranged from minimal retinal burns to extensive areas of damage with commotio retinae and vitreous hemorrhage. Visual loss ranged from complete recovery without residual defect to a profound decrease in central acuity. The kinds of lasers causing these injuries were neodymium YAG, argon, krypton, and rhodamine dye. Severity of injury was related to several factors . Some degree of carelessness was involved in all injuries. [Key words: laser, laser accidents, macular hole, retinal laser burns, retinal trauma, vitreous hemorrhage.] Ophthalmology 88: 101-1 07, 1981
Although industrial use of lasers has become widespread over the last 20 years, only seven instances of ocular injury caused by their use have been reported in the ophthalmic literature. Perhaps by being located near a center of computer and laser industry, the authors have accumulated seven additional cases which are the subject of this report.
CASE REPORTS Case 1. On June 27, 1979, a 31 -year-old white man with five years experience with lasers sustained a neodymium laser burn to the left eye, causing an immediate dense central scotoma. Examination later that day showed visual acuity to be 20/20 in the right eye and 20/300 in the left with scanning. Tangent screen field showed an absolute central scotoma and central distortion and blockage was seen with Amsler grid. Slit-lamp examination was normal. Fundus examination showed a blood clot overlying the fovea with two boatshaped preretinal and vitreous hemorrhages along the infratemporal arcade (Fig IA). A \.-2-disc diameter area of dense retinal edema centered around the fovea, and more diffuse edema of the retina involved a 2.S x 3-disc diameter From the Division of Ophthalmology, Stanford University School of Medicine,' and Metricon, Mountain View, California.t Presented at the Eighty-Fifth Annual Meeting of the American Academy of Ophthalmology, Chicago, November 4, 1980. Reprint requests to Edwin E .Boldrey, MD, Palo Alto Medical Clinic , 300 Homer Avenue, Palo Alto, CA 94301 .
0161-6420/8110200/01011$00.85
area of the macula. Fluorescein angiography showed blockage by the hemorrhages but no leak was seen and no retinal capillary damage could be demonstrated. By nine days the hemorrhage had partially resorbed and a full thickness SOO-Mm retinal hole could be seen. By six weeks retinal edema had cleared and the retina at the margin of the hole had elevated approximately 100 to 200 Mm. No hyperplasia of the retinal pigment epithelium was noted but several yellow dots were seen through the hole at the level of the pigment epithelium. Fluorescein angiography showed only transmission fluorescence . By three months all findings were unchanged (Fig IB). Circumstances of injury were as follows: The patient was working on a commercial laser production line adjusting a laser through an opening in its top; this location required him to lean over the laser during beam alignment. In this position his safety glasses slid up, allowing the laser beam to pass underneath. The beam was reportedly being reflected from a piece of test paper in a plastic bag, a normal procedure during beam alignment, when the patient heard a snap and saw a bright afterimage which lasted for 20 minutes before fading to a central scotoma. The laser was neodymium YAG with a wave length of 1.06 Mm and a power of I,SOO mW. Beam diameter was Soo Mm with a pulse duration of 0.1 seconds and a rate of about 10 pulses per second. Case 2. On January 10, 1977, a 32-year-old white man with nine years experience with lasers was injured in the left eye by a neodymium Y AG laser causing the immediate onset of photopsias, pain, and visual blur. One day after injury visual acuity was 20/20 in each eye, and tangent screen visual field showed a Bjerrum scotoma inferiorly in the left eye . Slit-lamp examination was normal. Fundus examination showed a ¥.I-disc diameter area of retinal edema with a possible small central hole located just
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Figs lA-B. Case 1. A, left, appearance on day of injury. Note commotio retinae and preretinal and vitreous hemorrhage. B, right, appearance three months following injury. Macular hole with local detachment is present.
Figs 2A-B. Case 2. A, left, appearance one day after injury. Note retinal burn and preretinal hemorrhage. B, right, appearance at three months. Yellow deposits in the scar and a nerve fiber layer defect between the scar and optic nerve are visible.
below the supratemporal arcade I-disc diameter from the optic nerve (Fig 2A). A small blood clot overlying the edema was connected to diffuse vitreous blood in the inferior midperiphery. By two weeks, faint edema of the nerve fiber layer extended from the impact site towards the optic nerve and vitreous blood had almost cleared. By six weeks, most retinal edema had cleared and a few yellow spots at the level of the retinal pigment epithelium could be seen within the retinal hole. By three months, the yellow deposits had increased and nerve fiber layer thinning could be seen extending from the optic nerve past the laser impact site (Fig 2B). Visual acuity was 20/20 on all visits. Circumstances of injury were as follows: A laser had been custom-designed and built by the patient and others for his company. During modifications, a special beam-turning prism had been added which incidentally had produced known stray reflections. Plans to block these reflections had
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not been carried out. The patient, who was not wearing safety glasses, had just entered the room to help align the beam when he felt a "pop" and a sudden pain which lasted a few moments and which was associated with many photopsias and floaters. The laser was Q-switched neodymium Y AG with wave length of 1.06ILm and peak power of 1 mW (6 mJ per pulse). Pulse duration was 6 nsec with 10 pulses per second. Beam diameter was estimated as 1.5 to 3 mm. Case 3. On December 9, 1979, a 27-year-old graduate student with three years experience with lasers sustained a neodymium laser burn to his left eye causing an immediate central scotoma. One day after injury, best visual acuity was 20/20 in the right eye and 20/100 in the left. A central scotoma was demonstrable both on tangent screen and on Amsler grid. Examination showed a }4-disc diameter area of partially coagulated blood underneath the retina at fixation. There
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Figs 3A-D. Case 3. A, top leji, one day after injury. Note blood under the macula. B, top right, fluorescein angiography reveals an intact perifoveal capillary network silhouetted by subretinal hemorrhage. C, bottom left, angiography at six-weeks shows only window defect at scar. D, bottom right, four months after injury. Hemorrhage has cleared and paracentral scar is present.
was a tiny spot of retinal necrosis at the nasal edge of the fovea. No vitreous blood was seen (Fig 3A). By the fifth day, visual acuity was 20150. Fluorescein angiography showed a normal perifoveal capillary bed without leakage or damage, with choroidal fluorescence completely blocked by subretinal hemorrhage (Fig 3B). By three weeks, acuity was still 20150 but most subretinal blood had resorbed. The macular retinal pigment epithelium appeared slightly mottled and a ring of pigment could be seen immediately nasal to fixation. By six weeks visual acuity was 20/25. Amsler grid showed II1z squares of distortion immediately temporal to fixation. Repeat fluorescein angiography revealed only window-defect fluorescence at the site of laser impact (Fig 3C). By four months acuity was 20/20 -3 and a scotoma was visible to the patient only during Amsler grid testing. The pigmented scar was unchanged (Fig 3D). Circumstances of injury were as follows: The patient had assembled an experimental laser and had removed a beam
block while making adjustments. As he leaned over, he saw a flash in his peripheral vision and instinctively turned his eye towards the flash. There was an immediate central scotoma and decrease in visual acuity. He was not wearing safety glasses at the time of injury. The laser was pulsed neodymium Y AG with a wave length of 1.06 fLm and a power of 1 mJ with 50 to 100 kW peak power. Beam diameter was 2.5 mm and duration was 20 nsec, pulsing at probably 10 pulses per second. Case 4. On April 15, 1971, a 31-year-old white man with many years experience with lasers was struck in the left eye with an argon laser beam, causing an immediate paracentral visual blur. One day after injury, examination showed visual acuity to be 20115 in the right eye and 20/20 in the left, with a one degree 1/1000/W paracentral scotoma demonstrable infratemporal to fixation. Amsler grid showed the corresponding scotoma to be % of a square across. Examination
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Figs 4A-D. Initial appearance of smaller retinal bums. A, top left, case 4; B, lOp right, case 5; C, bottom left, case 6; D, bottom right, case 7. Note small central spot of coagulation necrosis in each case. All patients had final visual acuity of 20/20 and a faint pigmented scar at the burn site.
revealed a densely white round area of coagulative necrosis 50 to 100 JLm across at the level of the retinal pigment epithelium and deep sensory retina superonasal to the fovea (Fig 4A). Fluorescein angiography showed no demonstrable retinal or choroidal leak. By the fifth day visual acuity was still 20/20 and retinal edema was unchanged. By the 12th day visual acuity was 20115 -2 and edema had resolved, leaving a juxtafoveal depression in the retina. By the 27th day the paracentral scotoma was approximately Y.l Amsler square across. A slightly pigmented spot was present at the burn site. By two months, no defects were demonstrable on Amsler grid testing although the tiny area of pigmentation persisted. The findings were unchanged 16 months postinjury. Circumstances of injury were as foIlows: Without wearing his safety glasses , the patient was inspecting a clear glass laser beam splitter for dust particles as part of the normal production line procedure. During this examination, laser power was accidentaIly turned on by another person, causing the beam to strike the patient's eye.
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The laser was continuous wave argon with wave lengths of 4,880 and 5,145 A . Power incident on the cornea was 70 mW and beam diameter was 1.4 mm. The exposure duration depended on the blink reflex of the patient, estimated as being 0.125 seconds. Case 5. On April 21, 1978, a 24-year-old white man with five months experience with lasers was struck in the right eye with an argon laser beam, causing an immediate visual blur and scotoma. Three days after injury, examination showed visual acuity to be 20/20 -2 in the right eye and 20/15 in the left . Goldmann and tangent screen visual fields were normal, but Amsler grid showed a smaIl central area of blur approximately 2 squares across. Retinal examination revealed a tiny white spot of coagulative necrosis at the supranasal margin of the fovea surrounded by a 0.2 disc diameter area of subretinal blood and fluid which was in turn surrounded by an area of retinal edema approximately 0.3 disc diameters across (Fig 4B). No vitreous hemorrhage was noted and slit-lamp examination was normal.
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By one week postlnJury, visual acuity had dropped to
20/25 , and so the patient was treated with 60 mg of oral
Prednisone daily for five days. By the 11th day, visual acuity had improved to 20/15 and retinal edema had disappeared. Pigment clumping was noted which remained unchanged thereafter. One month postinjury, Amsler grid distortion had shrunk to cover only the square immediately temporal and tangential to fixation; this had not changed at the patient's last examination, eight months following injury. Circumstances of injury were as follows: The patient was working without safety glasses on a laser production line aligning a laser. He had bent over the laser to adjust the beam when a reflection from a Brewster window struck his eye , causing him temporarily to see a flash towards which he instinctively looked, bringing on the injury. The laser was continuous wave argon with wave lengths of 4,880 and 5,145 A. Power was 500 mW . Reflection from the Brewster window was estimated to be less than or equal to 25 mW. Beam diameter at the time of injury was probably less than 1 mm. Case 6. On August 27, 1979, a 34-year-old white man with six years experience with lasers was injured in the left eye with a rhodamine dye laser, causing an immediate visual blur and scotoma. One day after injury visual acuity was 20/30 in the right eye and 20/25 in the left. Tangent screen field showed the left eye to have a 211000/W scotoma with the corresponding Amsler grid defect being approximately 2 squares across. Examination of the left eye showed a pale area of coagulative necrosis 50 to 100 JLm in diameter at the nasal edge of the fovea at the level of the retinal pigment epithelium and deep retina (Fig 4C). No hemorrhages were noted. Examination of the right eye showed an area of retinal pigment epithelium atrophy and clumping approximately 100 JLm across at the temporal edge of the fovea. By the eighth day, retinal edema had improved considerably, visual acuity then being 20/25 in the right eye and 20/20 in the left. Amsler grid showed the left eye scotoma to have shrunken to cover approximately V2 square, a size that persisted through later examinations . .On this visit also, a scotoma was found in the right eye on Amsler grid, there being I square across immediately nasal to fixation. This did not change on subsequent examinations. By two weeks all edema had disappeared and retinal pigment epithelial clumping had developed. Examinations at one and three months revealed no additional changes and by 3V2 months the patient was unaware of his scotoma except during testing. A pre-employment eye examination done 5V2 years prior to injury showed vision to be 20/20 +2 in both eyes with a normal tangent screen visual field and a normal Amsler grid examination in both eyes. The patient was unaware of any other episodes of laser eye injury . Circumstances of injury were as follows: Without wearing safety glasses the patient was adjusting a laser which had been constructed at his place of employment. While attaching a piece of cardboard to the laser to block a known light leak the beam struck his eye, causing him to see an orange flash followed by an immediate scotoma and blur. The laser was rhodamine pulsed dye with a wave length of approximately 5,920 to 5,940 A. Power was 0.2 mJ (20 kW power) with a beam diameter of 6 mm . Beam duration was 10 nsec with a rate of 10 pulses per second. Case 7. On February 13, 1979, a 35-year-old white man with 16 years experience with lasers was struck in the right eye with a beam from a krypton ion laser, resulting in an immediate visual blur and scotoma.
One day after injury visual acuity was 20/20 tangentially. Visual field showed a one degree paracentral scotoma with a 2/ 1000/W spot which could also be demonstrated as V2square scotoma on Amsler grid testing . A densely white , round spot of coagulative necrosis approximately 50 JLm in diameter was located tangential to the nasal edge of the fovea at the level of the retinal pigment epithelium and deep sensory retina (Fig 4D). No hemorrhage was noted. Fluorescein angiography revealed only slight local fluorescence. By the eighth day edema had disappeared, leaving a tiny area of depigmentation which remained unchanged during the 16 month follow-up period as did the visual field defect. The Amsler grid defect resolved in eight days to mere blurring of the lines , stabilizing at that point. Circumstances of injury were as follows : The patient was assembling a production line laser and, although not wearing safety glasses, he had removed a safety screen to align the beam . The beam was focused on ajet of ethylene glycol and dimethyl sulfoxide solution when a bubble in the stream deflected the beam towards the patient's eye, causing the injury. The laser was continuous wave krypton ion with a wave length of6,471 and 6,742 A and power of approximately 5 W. The portion of the beam reflected to the patient ' s eye is unknown. Beam diameter in the fluid was 30 JLm.
DISCUSSION The first ophthalmologic reports of industrial ocular injury caused by laser were those in 1965 by Rathkey, 1 by Blancard et aI,2 and by Jacobson and McLean. 3 Since then, three additional cases have been reported.4--6 All seven injuries were caused by ruby lasers and four of the five patients in whom visual acuity was recorded had final vision markedly reduced from normal. In addition, one patient suffered a macular hole and two had preretinal and vitreous hemorrhages. Other cases have been mentioned in nonmedical publications. 7-10 The final visual acuities described in this report were much better than in the previously reported cases. All but one of the eyes reported here reached or maintained 20/20, though usually with a paracentral scotoma. These excellent final visual results, coupled with the discovery of a previously unrecognized laser burn in the second eye of one patient, (patient 6) leads one to speculate that more laser injuries occur than are reported and that many burns are of a low level of severity and produce minimal symptoms. Reports to the authors by some patients of others with laser eye injuries reinforces this impression. Careful clinical examination of the less severe burns in this series showed the burn level to be at the retinal pigment epithelium (RPE) and choroid making these -similar to clinically applied laser burns in this regard. Follow-up examinations showed that the lesions followed the usual course of clinically applied burns, stabilizing for the most part after two to six weeks. Somewhat later repair did occur in patient 4 in whom improvement in and finally complete disappearance of the scotoma occurred by two months postinjury, 105
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clearing which could be accounted for by displacement of receptor cells into the irradiated area as described by Marshall and Mellerio l l in experimental laser bums or by outer segment regeneration. Evidence that injury is primarily to the RPE and choroid was found in patient 3, in whom subretinal hemorrhage blocked choroidal fluorescence, allowing an excellent fluorescein angiographic view of the retinal capillaries. These appeared to have been unaffected by the injury in that neither dye leakage nor vessel distortion nor closure was seen. Following resorption of subretinal hemorrhage, visual acuity in this patient returned froin 20/100 to 20/20. Although it has been shown that short laser pulses require less energy to produce damage,I2-15 the cases presented here do not confirm previous reports that, in actual laser accidents, severity of injury is by far the greatest with very short pulses. 16 In this series, all three patients injured by lasers with pulses of 20 nsec or less recovered 20/20 acuity, and the one patient with permanent loss of central vision was injured by a laser beam of 0.1 seconds duration, a relatively long pulse. Nor did this series confirm the report that retinal hemorrhage in accidental laser bums greatly increases the possibility of loss of vision. 16 Although subretinal hemorrhage from other causes can carry a poor visual prognosis, after the subretinal blood in patients 3 and 5 resorbed, vision returned to 20/20. Vitreous and preretinal blood in patient 2 did not interfere with visual acuity because of its paracentral location. Preretinal and vitreous blood in patient 1 was associated with permanent visual loss, but this loss was related to the macular hole caused by the bum rather than to the hemorrhage itself. It must be concluded that the presence of blood under the macula or in the vitreous in the absence of other retinal damage does not necessarily mean visual acuity will suffer. Comparison of energy levels in cases in this report with energy levels in experimental laser bums can be
of interest. It has been shown that to produce a minimum lesion in Rhesus monkeys, Q-switched (ultra-short) neodymium pulses require at least 160 p,J of energy,12-15 while a pulse length of 0.1 sec requires energy of at least 6.5 mJ. 13 These values vary with changes in laser wavelength. 12-15 Although extrapolation to human retinas from animals is difficult, the human retina appears to be less sensitive to laser radiation than Rhesus retina. For example, limited measurements using intentional Q-switched (ultra-short) beams in human retinas showed a minimum lesion to be obtained at 4 mJ ,12.13 a ratio of 25:1 to minimum Rhesus damage level (MRDL) in ultra-short neodymium bums. In experimental human retinal bums limited by the blink reflex, estimated to be 125 msec, with argon laser a minimum lesion occurred at about 35 mW.13 When compared with a MRDL of 5 mW for these longer visible bums, a ratio of 7: 1 for minimum lesion in these longer bums is obtained. It should be noted that, while useful, these ratios are based on only a limited number of human bums and are therefore not exact. Comparison with MRDL using the above-mentioned ratios for minimal lesions in the human eye would cause one to predict a minimal lesion in the cases of neodymium bum, patients 1, 2, and 3 (Table 1). In all three cases, however, damage was far more severe than predicted, so that, assuming the MRDL is meaningful in human injury, one must conclude that multiple exposures were received by each of these patients. This is probable because all three lasers were pulsing at a high rate and because the blink reflex was not a factor , neodymium laser being at an invisible wavelength. In addition, damage would be more severe in all three cases because the long-wave length of a neodymium beam would cause it to be focused most sharply on the retina when the eye is accommodated to about one meter, the probable situation at the time of these accidents.
Table 1. Laser Exposures
Case 1 2 3 4 5 6 7
Pulse Length 0.1 sec, 10 6 nsec, 10 20 nsec, 10 Blink reflex Blink reflex 10 nsec, 10 Blink reflex
pps pps pps pps
Exposure
Ratio of Exposure Dose to Minimum Rhesus Damage Level (MRDL)*
Ratio of Exposure Dose To HEW Accessible Emission Limit (AELr
150 mJ 6 mJ 1 mJ 70mW ",,25mW 0.2 mJ
23 38 6 14 ",,5 31
24 6,000 1,000 48 ",,17 1,000
?
* In order to compare exposure dose with MRDL and with AEL, certain assumptions are necessary . In all except cases 5 and 7, it is assumed that the full laser power entered the eye. In case 1 this assumption is made because scatter or reflection from the plastic or paper would be unlikely to be of sufficient energy to cause significant damage . In case 4, the power of the beam at the cornea was measured . In case 5, because the amount of reflection from a Brewster window is known to be small , it was estimated that less than 25 mW entered the eye . Calculations in case 7 have confirmed that injury is possible from Fresnel reflections from a bubble. HEW = Department of Health, Education , and Welfare. pps = pulses per second.
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The remaining cases involved lasers whose emission is visible and whose exposure length was therefore limited by the blink reflex. In patients 4 and 5, the ratio to MRDL is at a level that when compared with the appropriate MRDL ratio would allow us to predict a minimal lesion, which in each case is what is found. The injury level in patient 7 is hard to predict because the size of the reflecting bubble and therefore the power density of the reflected beam is unknown. In patient 6, a more severe injury would have been predicted than occurred. Explanation for this less-thanexpected degree of damage is probably related to the multifactorial nature of these bums. In all of these cases, it is the authors' impression that severity of injury is related to a combination of several factors, including location of the bum, pupillary size, accomodative state of the eye and choroidal pigmenta" tion as well as spot size on the retina, amount of the beam entering the eye, pulse duration, pulse repetition rate, and laser type. No factor by itself seemed to be of absolute importance. If comparisons are made between MRDL and the Department of Health, Education, and Welfare's accessible emission limits (AEL),17 obvious differences are noted (Table 1). These differences can be attributed to different levels of importance which have been assigned to the duration of the laser pulse, and because a safety factor has been built into the AEL. For example, in cases 2,3, and 6, the three cases with extremely short laser pulse lengths, the extremely large ratio of exposure to AEL means that for these very short pulsed lasers a wide safety margin appears to have been included in the AEL. Examination of the circumstance
tion model lasers whose manufacture had been completed, such lasers would seem to be relatively safe when in use under usual conditions with normal safety precautions. Second, since all cases involved persons in close physical proximity to the laser, those working at a distance would appear to be considerably safer even though a laser beam can travel great distances without significant energy loss. Reinforcing this impression, Sliney and Wolbarsht have calculated the chance of a random 2-mm beam striking a single 7-mm pupil at 100 m distance to be only 1 in 105 • 16
REFERENCES 1. Rathkey AS. Accidental laser burn of the macula. Arch Ophthalmol 1965; 74:346-8. 2. Blancard P, Sorato M, Blonk K, Iris L, et al. A propos d'une photo-coagulation maculaire par laser, accidentelle. Ann Oculist 1965; 198:263-4. 3. Jacobson JH, McLean JM. Accidental laser retinal burns. Arch Ophthalmol 1965; 74:882. 4. Curtin TL, Boyden DG. Reflected laser beam causing accidental burn of retina. Am J Ophthalmol 1968; 65:188-9. 5. Henkes HE, Zuidema H. Accidental laser coagulation of the central fovea. Ophthalmologica 1975; 171 :15-25. 6. Zweng HC. Accidental Q-switched laser lesion of human macula. Arch Ophthalmol 1967; 78:596-9. 7. Armstrong CEo Eye injuries in some modern radiation environments. J Am Optom Assoc 1970; 41 :55-62. 8. Accidental laser exposure. Health and Safety Information, Issue No 322, US Atomic Energy Commission, Washington, DC, December 15, 1972. 9. Decker CD. Accident victim's view. Laser Focus 1977; 13:6. 10. ILS employee regains central vision lost for a month after laser accident. Laser Focus 1977; 13:21-2. 11. Marshall J, Mellerio J. Disappearance of retino-epithelial scar tissue from ruby laser photocoagulations. Exp Eye Res 1971;
12:173-4. 12. Vassiliadis A, Zweng HC, Peppers NA, et al. Thresholds of laser eye hazards. Arch Environ Health 1970; 20: 161. 13. Vassiliadis A, Rosan RC, Zweng HC. Research on ocular laser thresholds. SRI Project 7191 Report, Stanford Research Institute, Menlo Park, CA, August 1969. 14. Vassiliadis A, et al. Investigation of laser damage to ocular tissues. SRI Project 6680 Report, Stanford Research Institute, Menlo Park, CA, March 1968. 15. Vassiliadis A, Zweng HC, Dedrich KG: Ocular laser threshold investigations. SRI Project 8209 Report, Stanford Research Institute, Menlo Park, CA, January 1971. 16. Sliney D, Wolbarsht ML. Safety with Lasers and Other Optical Sources. New York: Plenum Press, 1980; 488-510. 17. Regulations for the administration and enforcement of the radiation control for health and safety act of 1968. HEW Publication (FDA) 79-8035 US Department of Health, Education, and Welfare, Food and Drug Administration, Bureau of Radiological Health, Rockville, MD, 1978.
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Laser Burns
EDWIN E. BOLDREY, MD,* HUNTER L. LITTLE, MD,* MILTON FLOCKS, MD,* ARTHUR V ASSILIADIS, PhDt
Abstract: Ocular industrial laserbui'hs in seven patients were analyzed as to cause, severity, and type of injury. Ocular damage ranged from minimal retinal burns to extensive areas of damage with commotio retinae and vitreous hemorrhage. Visual loss ranged from complete recovery without residual defect to a profound decrease in central acuity. The kinds of lasers causing these injuries were neodymium YAG, argon, krypton, and rhodamine dye. Severity of injury was related to several factors . Some degree of carelessness was involved in all injuries. [Key words: laser, laser accidents, macular hole, retinal laser burns, retinal trauma, vitreous hemorrhage.] Ophthalmology 88: 101-1 07, 1981
Although industrial use of lasers has become widespread over the last 20 years, only seven instances of ocular injury caused by their use have been reported in the ophthalmic literature. Perhaps by being located near a center of computer and laser industry, the authors have accumulated seven additional cases which are the subject of this report.
CASE REPORTS Case 1. On June 27, 1979, a 31 -year-old white man with five years experience with lasers sustained a neodymium laser burn to the left eye, causing an immediate dense central scotoma. Examination later that day showed visual acuity to be 20/20 in the right eye and 20/300 in the left with scanning. Tangent screen field showed an absolute central scotoma and central distortion and blockage was seen with Amsler grid. Slit-lamp examination was normal. Fundus examination showed a blood clot overlying the fovea with two boatshaped preretinal and vitreous hemorrhages along the infratemporal arcade (Fig IA). A \.-2-disc diameter area of dense retinal edema centered around the fovea, and more diffuse edema of the retina involved a 2.S x 3-disc diameter From the Division of Ophthalmology, Stanford University School of Medicine,' and Metricon, Mountain View, California.t Presented at the Eighty-Fifth Annual Meeting of the American Academy of Ophthalmology, Chicago, November 4, 1980. Reprint requests to Edwin E .Boldrey, MD, Palo Alto Medical Clinic , 300 Homer Avenue, Palo Alto, CA 94301 .
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area of the macula. Fluorescein angiography showed blockage by the hemorrhages but no leak was seen and no retinal capillary damage could be demonstrated. By nine days the hemorrhage had partially resorbed and a full thickness SOO-Mm retinal hole could be seen. By six weeks retinal edema had cleared and the retina at the margin of the hole had elevated approximately 100 to 200 Mm. No hyperplasia of the retinal pigment epithelium was noted but several yellow dots were seen through the hole at the level of the pigment epithelium. Fluorescein angiography showed only transmission fluorescence . By three months all findings were unchanged (Fig IB). Circumstances of injury were as follows: The patient was working on a commercial laser production line adjusting a laser through an opening in its top; this location required him to lean over the laser during beam alignment. In this position his safety glasses slid up, allowing the laser beam to pass underneath. The beam was reportedly being reflected from a piece of test paper in a plastic bag, a normal procedure during beam alignment, when the patient heard a snap and saw a bright afterimage which lasted for 20 minutes before fading to a central scotoma. The laser was neodymium YAG with a wave length of 1.06 Mm and a power of I,SOO mW. Beam diameter was Soo Mm with a pulse duration of 0.1 seconds and a rate of about 10 pulses per second. Case 2. On January 10, 1977, a 32-year-old white man with nine years experience with lasers was injured in the left eye by a neodymium Y AG laser causing the immediate onset of photopsias, pain, and visual blur. One day after injury visual acuity was 20/20 in each eye, and tangent screen visual field showed a Bjerrum scotoma inferiorly in the left eye . Slit-lamp examination was normal. Fundus examination showed a ¥.I-disc diameter area of retinal edema with a possible small central hole located just
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Figs lA-B. Case 1. A, left, appearance on day of injury. Note commotio retinae and preretinal and vitreous hemorrhage. B, right, appearance three months following injury. Macular hole with local detachment is present.
Figs 2A-B. Case 2. A, left, appearance one day after injury. Note retinal burn and preretinal hemorrhage. B, right, appearance at three months. Yellow deposits in the scar and a nerve fiber layer defect between the scar and optic nerve are visible.
below the supratemporal arcade I-disc diameter from the optic nerve (Fig 2A). A small blood clot overlying the edema was connected to diffuse vitreous blood in the inferior midperiphery. By two weeks, faint edema of the nerve fiber layer extended from the impact site towards the optic nerve and vitreous blood had almost cleared. By six weeks, most retinal edema had cleared and a few yellow spots at the level of the retinal pigment epithelium could be seen within the retinal hole. By three months, the yellow deposits had increased and nerve fiber layer thinning could be seen extending from the optic nerve past the laser impact site (Fig 2B). Visual acuity was 20/20 on all visits. Circumstances of injury were as follows: A laser had been custom-designed and built by the patient and others for his company. During modifications, a special beam-turning prism had been added which incidentally had produced known stray reflections. Plans to block these reflections had
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not been carried out. The patient, who was not wearing safety glasses, had just entered the room to help align the beam when he felt a "pop" and a sudden pain which lasted a few moments and which was associated with many photopsias and floaters. The laser was Q-switched neodymium Y AG with wave length of 1.06ILm and peak power of 1 mW (6 mJ per pulse). Pulse duration was 6 nsec with 10 pulses per second. Beam diameter was estimated as 1.5 to 3 mm. Case 3. On December 9, 1979, a 27-year-old graduate student with three years experience with lasers sustained a neodymium laser burn to his left eye causing an immediate central scotoma. One day after injury, best visual acuity was 20/20 in the right eye and 20/100 in the left. A central scotoma was demonstrable both on tangent screen and on Amsler grid. Examination showed a }4-disc diameter area of partially coagulated blood underneath the retina at fixation. There
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Figs 3A-D. Case 3. A, top leji, one day after injury. Note blood under the macula. B, top right, fluorescein angiography reveals an intact perifoveal capillary network silhouetted by subretinal hemorrhage. C, bottom left, angiography at six-weeks shows only window defect at scar. D, bottom right, four months after injury. Hemorrhage has cleared and paracentral scar is present.
was a tiny spot of retinal necrosis at the nasal edge of the fovea. No vitreous blood was seen (Fig 3A). By the fifth day, visual acuity was 20150. Fluorescein angiography showed a normal perifoveal capillary bed without leakage or damage, with choroidal fluorescence completely blocked by subretinal hemorrhage (Fig 3B). By three weeks, acuity was still 20150 but most subretinal blood had resorbed. The macular retinal pigment epithelium appeared slightly mottled and a ring of pigment could be seen immediately nasal to fixation. By six weeks visual acuity was 20/25. Amsler grid showed II1z squares of distortion immediately temporal to fixation. Repeat fluorescein angiography revealed only window-defect fluorescence at the site of laser impact (Fig 3C). By four months acuity was 20/20 -3 and a scotoma was visible to the patient only during Amsler grid testing. The pigmented scar was unchanged (Fig 3D). Circumstances of injury were as follows: The patient had assembled an experimental laser and had removed a beam
block while making adjustments. As he leaned over, he saw a flash in his peripheral vision and instinctively turned his eye towards the flash. There was an immediate central scotoma and decrease in visual acuity. He was not wearing safety glasses at the time of injury. The laser was pulsed neodymium Y AG with a wave length of 1.06 fLm and a power of 1 mJ with 50 to 100 kW peak power. Beam diameter was 2.5 mm and duration was 20 nsec, pulsing at probably 10 pulses per second. Case 4. On April 15, 1971, a 31-year-old white man with many years experience with lasers was struck in the left eye with an argon laser beam, causing an immediate paracentral visual blur. One day after injury, examination showed visual acuity to be 20115 in the right eye and 20/20 in the left, with a one degree 1/1000/W paracentral scotoma demonstrable infratemporal to fixation. Amsler grid showed the corresponding scotoma to be % of a square across. Examination
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Figs 4A-D. Initial appearance of smaller retinal bums. A, top left, case 4; B, lOp right, case 5; C, bottom left, case 6; D, bottom right, case 7. Note small central spot of coagulation necrosis in each case. All patients had final visual acuity of 20/20 and a faint pigmented scar at the burn site.
revealed a densely white round area of coagulative necrosis 50 to 100 JLm across at the level of the retinal pigment epithelium and deep sensory retina superonasal to the fovea (Fig 4A). Fluorescein angiography showed no demonstrable retinal or choroidal leak. By the fifth day visual acuity was still 20/20 and retinal edema was unchanged. By the 12th day visual acuity was 20115 -2 and edema had resolved, leaving a juxtafoveal depression in the retina. By the 27th day the paracentral scotoma was approximately Y.l Amsler square across. A slightly pigmented spot was present at the burn site. By two months, no defects were demonstrable on Amsler grid testing although the tiny area of pigmentation persisted. The findings were unchanged 16 months postinjury. Circumstances of injury were as foIlows: Without wearing his safety glasses , the patient was inspecting a clear glass laser beam splitter for dust particles as part of the normal production line procedure. During this examination, laser power was accidentaIly turned on by another person, causing the beam to strike the patient's eye.
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The laser was continuous wave argon with wave lengths of 4,880 and 5,145 A . Power incident on the cornea was 70 mW and beam diameter was 1.4 mm. The exposure duration depended on the blink reflex of the patient, estimated as being 0.125 seconds. Case 5. On April 21, 1978, a 24-year-old white man with five months experience with lasers was struck in the right eye with an argon laser beam, causing an immediate visual blur and scotoma. Three days after injury, examination showed visual acuity to be 20/20 -2 in the right eye and 20/15 in the left . Goldmann and tangent screen visual fields were normal, but Amsler grid showed a smaIl central area of blur approximately 2 squares across. Retinal examination revealed a tiny white spot of coagulative necrosis at the supranasal margin of the fovea surrounded by a 0.2 disc diameter area of subretinal blood and fluid which was in turn surrounded by an area of retinal edema approximately 0.3 disc diameters across (Fig 4B). No vitreous hemorrhage was noted and slit-lamp examination was normal.
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By one week postlnJury, visual acuity had dropped to
20/25 , and so the patient was treated with 60 mg of oral
Prednisone daily for five days. By the 11th day, visual acuity had improved to 20/15 and retinal edema had disappeared. Pigment clumping was noted which remained unchanged thereafter. One month postinjury, Amsler grid distortion had shrunk to cover only the square immediately temporal and tangential to fixation; this had not changed at the patient's last examination, eight months following injury. Circumstances of injury were as follows: The patient was working without safety glasses on a laser production line aligning a laser. He had bent over the laser to adjust the beam when a reflection from a Brewster window struck his eye , causing him temporarily to see a flash towards which he instinctively looked, bringing on the injury. The laser was continuous wave argon with wave lengths of 4,880 and 5,145 A. Power was 500 mW . Reflection from the Brewster window was estimated to be less than or equal to 25 mW. Beam diameter at the time of injury was probably less than 1 mm. Case 6. On August 27, 1979, a 34-year-old white man with six years experience with lasers was injured in the left eye with a rhodamine dye laser, causing an immediate visual blur and scotoma. One day after injury visual acuity was 20/30 in the right eye and 20/25 in the left. Tangent screen field showed the left eye to have a 211000/W scotoma with the corresponding Amsler grid defect being approximately 2 squares across. Examination of the left eye showed a pale area of coagulative necrosis 50 to 100 JLm in diameter at the nasal edge of the fovea at the level of the retinal pigment epithelium and deep retina (Fig 4C). No hemorrhages were noted. Examination of the right eye showed an area of retinal pigment epithelium atrophy and clumping approximately 100 JLm across at the temporal edge of the fovea. By the eighth day, retinal edema had improved considerably, visual acuity then being 20/25 in the right eye and 20/20 in the left. Amsler grid showed the left eye scotoma to have shrunken to cover approximately V2 square, a size that persisted through later examinations . .On this visit also, a scotoma was found in the right eye on Amsler grid, there being I square across immediately nasal to fixation. This did not change on subsequent examinations. By two weeks all edema had disappeared and retinal pigment epithelial clumping had developed. Examinations at one and three months revealed no additional changes and by 3V2 months the patient was unaware of his scotoma except during testing. A pre-employment eye examination done 5V2 years prior to injury showed vision to be 20/20 +2 in both eyes with a normal tangent screen visual field and a normal Amsler grid examination in both eyes. The patient was unaware of any other episodes of laser eye injury . Circumstances of injury were as follows: Without wearing safety glasses the patient was adjusting a laser which had been constructed at his place of employment. While attaching a piece of cardboard to the laser to block a known light leak the beam struck his eye, causing him to see an orange flash followed by an immediate scotoma and blur. The laser was rhodamine pulsed dye with a wave length of approximately 5,920 to 5,940 A. Power was 0.2 mJ (20 kW power) with a beam diameter of 6 mm . Beam duration was 10 nsec with a rate of 10 pulses per second. Case 7. On February 13, 1979, a 35-year-old white man with 16 years experience with lasers was struck in the right eye with a beam from a krypton ion laser, resulting in an immediate visual blur and scotoma.
One day after injury visual acuity was 20/20 tangentially. Visual field showed a one degree paracentral scotoma with a 2/ 1000/W spot which could also be demonstrated as V2square scotoma on Amsler grid testing . A densely white , round spot of coagulative necrosis approximately 50 JLm in diameter was located tangential to the nasal edge of the fovea at the level of the retinal pigment epithelium and deep sensory retina (Fig 4D). No hemorrhage was noted. Fluorescein angiography revealed only slight local fluorescence. By the eighth day edema had disappeared, leaving a tiny area of depigmentation which remained unchanged during the 16 month follow-up period as did the visual field defect. The Amsler grid defect resolved in eight days to mere blurring of the lines , stabilizing at that point. Circumstances of injury were as follows : The patient was assembling a production line laser and, although not wearing safety glasses, he had removed a safety screen to align the beam . The beam was focused on ajet of ethylene glycol and dimethyl sulfoxide solution when a bubble in the stream deflected the beam towards the patient's eye, causing the injury. The laser was continuous wave krypton ion with a wave length of6,471 and 6,742 A and power of approximately 5 W. The portion of the beam reflected to the patient ' s eye is unknown. Beam diameter in the fluid was 30 JLm.
DISCUSSION The first ophthalmologic reports of industrial ocular injury caused by laser were those in 1965 by Rathkey, 1 by Blancard et aI,2 and by Jacobson and McLean. 3 Since then, three additional cases have been reported.4--6 All seven injuries were caused by ruby lasers and four of the five patients in whom visual acuity was recorded had final vision markedly reduced from normal. In addition, one patient suffered a macular hole and two had preretinal and vitreous hemorrhages. Other cases have been mentioned in nonmedical publications. 7-10 The final visual acuities described in this report were much better than in the previously reported cases. All but one of the eyes reported here reached or maintained 20/20, though usually with a paracentral scotoma. These excellent final visual results, coupled with the discovery of a previously unrecognized laser burn in the second eye of one patient, (patient 6) leads one to speculate that more laser injuries occur than are reported and that many burns are of a low level of severity and produce minimal symptoms. Reports to the authors by some patients of others with laser eye injuries reinforces this impression. Careful clinical examination of the less severe burns in this series showed the burn level to be at the retinal pigment epithelium (RPE) and choroid making these -similar to clinically applied laser burns in this regard. Follow-up examinations showed that the lesions followed the usual course of clinically applied burns, stabilizing for the most part after two to six weeks. Somewhat later repair did occur in patient 4 in whom improvement in and finally complete disappearance of the scotoma occurred by two months postinjury, 105
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clearing which could be accounted for by displacement of receptor cells into the irradiated area as described by Marshall and Mellerio l l in experimental laser bums or by outer segment regeneration. Evidence that injury is primarily to the RPE and choroid was found in patient 3, in whom subretinal hemorrhage blocked choroidal fluorescence, allowing an excellent fluorescein angiographic view of the retinal capillaries. These appeared to have been unaffected by the injury in that neither dye leakage nor vessel distortion nor closure was seen. Following resorption of subretinal hemorrhage, visual acuity in this patient returned froin 20/100 to 20/20. Although it has been shown that short laser pulses require less energy to produce damage,I2-15 the cases presented here do not confirm previous reports that, in actual laser accidents, severity of injury is by far the greatest with very short pulses. 16 In this series, all three patients injured by lasers with pulses of 20 nsec or less recovered 20/20 acuity, and the one patient with permanent loss of central vision was injured by a laser beam of 0.1 seconds duration, a relatively long pulse. Nor did this series confirm the report that retinal hemorrhage in accidental laser bums greatly increases the possibility of loss of vision. 16 Although subretinal hemorrhage from other causes can carry a poor visual prognosis, after the subretinal blood in patients 3 and 5 resorbed, vision returned to 20/20. Vitreous and preretinal blood in patient 2 did not interfere with visual acuity because of its paracentral location. Preretinal and vitreous blood in patient 1 was associated with permanent visual loss, but this loss was related to the macular hole caused by the bum rather than to the hemorrhage itself. It must be concluded that the presence of blood under the macula or in the vitreous in the absence of other retinal damage does not necessarily mean visual acuity will suffer. Comparison of energy levels in cases in this report with energy levels in experimental laser bums can be
of interest. It has been shown that to produce a minimum lesion in Rhesus monkeys, Q-switched (ultra-short) neodymium pulses require at least 160 p,J of energy,12-15 while a pulse length of 0.1 sec requires energy of at least 6.5 mJ. 13 These values vary with changes in laser wavelength. 12-15 Although extrapolation to human retinas from animals is difficult, the human retina appears to be less sensitive to laser radiation than Rhesus retina. For example, limited measurements using intentional Q-switched (ultra-short) beams in human retinas showed a minimum lesion to be obtained at 4 mJ ,12.13 a ratio of 25:1 to minimum Rhesus damage level (MRDL) in ultra-short neodymium bums. In experimental human retinal bums limited by the blink reflex, estimated to be 125 msec, with argon laser a minimum lesion occurred at about 35 mW.13 When compared with a MRDL of 5 mW for these longer visible bums, a ratio of 7: 1 for minimum lesion in these longer bums is obtained. It should be noted that, while useful, these ratios are based on only a limited number of human bums and are therefore not exact. Comparison with MRDL using the above-mentioned ratios for minimal lesions in the human eye would cause one to predict a minimal lesion in the cases of neodymium bum, patients 1, 2, and 3 (Table 1). In all three cases, however, damage was far more severe than predicted, so that, assuming the MRDL is meaningful in human injury, one must conclude that multiple exposures were received by each of these patients. This is probable because all three lasers were pulsing at a high rate and because the blink reflex was not a factor , neodymium laser being at an invisible wavelength. In addition, damage would be more severe in all three cases because the long-wave length of a neodymium beam would cause it to be focused most sharply on the retina when the eye is accommodated to about one meter, the probable situation at the time of these accidents.
Table 1. Laser Exposures
Case 1 2 3 4 5 6 7
Pulse Length 0.1 sec, 10 6 nsec, 10 20 nsec, 10 Blink reflex Blink reflex 10 nsec, 10 Blink reflex
pps pps pps pps
Exposure
Ratio of Exposure Dose to Minimum Rhesus Damage Level (MRDL)*
Ratio of Exposure Dose To HEW Accessible Emission Limit (AELr
150 mJ 6 mJ 1 mJ 70mW ",,25mW 0.2 mJ
23 38 6 14 ",,5 31
24 6,000 1,000 48 ",,17 1,000
?
* In order to compare exposure dose with MRDL and with AEL, certain assumptions are necessary . In all except cases 5 and 7, it is assumed that the full laser power entered the eye. In case 1 this assumption is made because scatter or reflection from the plastic or paper would be unlikely to be of sufficient energy to cause significant damage . In case 4, the power of the beam at the cornea was measured . In case 5, because the amount of reflection from a Brewster window is known to be small , it was estimated that less than 25 mW entered the eye . Calculations in case 7 have confirmed that injury is possible from Fresnel reflections from a bubble. HEW = Department of Health, Education , and Welfare. pps = pulses per second.
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The remaining cases involved lasers whose emission is visible and whose exposure length was therefore limited by the blink reflex. In patients 4 and 5, the ratio to MRDL is at a level that when compared with the appropriate MRDL ratio would allow us to predict a minimal lesion, which in each case is what is found. The injury level in patient 7 is hard to predict because the size of the reflecting bubble and therefore the power density of the reflected beam is unknown. In patient 6, a more severe injury would have been predicted than occurred. Explanation for this less-thanexpected degree of damage is probably related to the multifactorial nature of these bums. In all of these cases, it is the authors' impression that severity of injury is related to a combination of several factors, including location of the bum, pupillary size, accomodative state of the eye and choroidal pigmenta" tion as well as spot size on the retina, amount of the beam entering the eye, pulse duration, pulse repetition rate, and laser type. No factor by itself seemed to be of absolute importance. If comparisons are made between MRDL and the Department of Health, Education, and Welfare's accessible emission limits (AEL),17 obvious differences are noted (Table 1). These differences can be attributed to different levels of importance which have been assigned to the duration of the laser pulse, and because a safety factor has been built into the AEL. For example, in cases 2,3, and 6, the three cases with extremely short laser pulse lengths, the extremely large ratio of exposure to AEL means that for these very short pulsed lasers a wide safety margin appears to have been included in the AEL. Examination of the circumstance
tion model lasers whose manufacture had been completed, such lasers would seem to be relatively safe when in use under usual conditions with normal safety precautions. Second, since all cases involved persons in close physical proximity to the laser, those working at a distance would appear to be considerably safer even though a laser beam can travel great distances without significant energy loss. Reinforcing this impression, Sliney and Wolbarsht have calculated the chance of a random 2-mm beam striking a single 7-mm pupil at 100 m distance to be only 1 in 105 • 16
REFERENCES 1. Rathkey AS. Accidental laser burn of the macula. Arch Ophthalmol 1965; 74:346-8. 2. Blancard P, Sorato M, Blonk K, Iris L, et al. A propos d'une photo-coagulation maculaire par laser, accidentelle. Ann Oculist 1965; 198:263-4. 3. Jacobson JH, McLean JM. Accidental laser retinal burns. Arch Ophthalmol 1965; 74:882. 4. Curtin TL, Boyden DG. Reflected laser beam causing accidental burn of retina. Am J Ophthalmol 1968; 65:188-9. 5. Henkes HE, Zuidema H. Accidental laser coagulation of the central fovea. Ophthalmologica 1975; 171 :15-25. 6. Zweng HC. Accidental Q-switched laser lesion of human macula. Arch Ophthalmol 1967; 78:596-9. 7. Armstrong CEo Eye injuries in some modern radiation environments. J Am Optom Assoc 1970; 41 :55-62. 8. Accidental laser exposure. Health and Safety Information, Issue No 322, US Atomic Energy Commission, Washington, DC, December 15, 1972. 9. Decker CD. Accident victim's view. Laser Focus 1977; 13:6. 10. ILS employee regains central vision lost for a month after laser accident. Laser Focus 1977; 13:21-2. 11. Marshall J, Mellerio J. Disappearance of retino-epithelial scar tissue from ruby laser photocoagulations. Exp Eye Res 1971;
12:173-4. 12. Vassiliadis A, Zweng HC, Peppers NA, et al. Thresholds of laser eye hazards. Arch Environ Health 1970; 20: 161. 13. Vassiliadis A, Rosan RC, Zweng HC. Research on ocular laser thresholds. SRI Project 7191 Report, Stanford Research Institute, Menlo Park, CA, August 1969. 14. Vassiliadis A, et al. Investigation of laser damage to ocular tissues. SRI Project 6680 Report, Stanford Research Institute, Menlo Park, CA, March 1968. 15. Vassiliadis A, Zweng HC, Dedrich KG: Ocular laser threshold investigations. SRI Project 8209 Report, Stanford Research Institute, Menlo Park, CA, January 1971. 16. Sliney D, Wolbarsht ML. Safety with Lasers and Other Optical Sources. New York: Plenum Press, 1980; 488-510. 17. Regulations for the administration and enforcement of the radiation control for health and safety act of 1968. HEW Publication (FDA) 79-8035 US Department of Health, Education, and Welfare, Food and Drug Administration, Bureau of Radiological Health, Rockville, MD, 1978.
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