Retinal From Joseph
L.
Light Exposure Operation Microscopes
Calkins, MD, Bernard
F.
Hochheimer, MS
\s=b\ Several popular surgical microscopes were measured for source radiance. A method has been devised for calculating patient retinal exposure from these instruments. Retinal irradiance is seen to be surprisingly high, assuming dilated pupils and clear media. It ranges from 0.10 to 0.97 W/sq cm. This is one to ten times higher than that produced by an indirect ophthalmoscope. There is evidence linking light exposure during surgery to cystoid maculopathy (Irvine-Gass
syndrome). (Arch Ophthalmol 97:2363-2367, 1979) Oince the introduction of the opera^ tion
microscope
for
ophthalmic
surgery 25 years ago,' the basic optical design of popular models has changed very little. The illuminating systems
used, however, have undergone sev¬ eral revisions. Internal, or "coaxial," illumination has become almost uni¬ versal. To provide better illumination, manufacturers have tried to increase the brightness of the internal light sources. However, in addition to providing greater useful illumination, a brighter source also produces a highAccepted
for publication May 21, 1979. From The Wilmer Institute, The Johns Hopkins University Hospital, Baltimore (Dr Calkins), and The Applied Physics Laboratory, Laurel, Md
(Mr Hochheimer).
Presented at the 36th clinical meeting of the Residents Association of the Wilmer Ophthalmological Institute, April 22, 1977. Reprint requests to The Wilmer Institute, Johns Hopkins University, 601 N Broadway, Baltimore, MD 21205 (Dr Calkins).
er
retinal irradiance. This poses the
question of whether or not this light is hazardous to the patient's retina. Even though a great deal has appeared in the literature about the advantages of microsurgery, practi¬ cally nothing has been written about what happens to the light after it enters the patient's eye. We analyze this problem in this article. We describe a means of measuring and calculating the retinal irradiance likely to be received by a patient from the light source of several commonly encountered operation microscopes. These levels are then compared with light levels of similar spectral content known to be hazardous in monkey retinas. A further comparison is made
with American National Standards Institute (ANSI) laser safety stan¬ dards2 for light exposure. Figure 1 demonstrates the manner in which a typical microscope forms an image on the patient's retina of its internal light source, which may be either a lamp filament or a fiberoptic bundle termination. MATERIALS AND METHODS Four operation microscopes (Zeiss) in daily usage at The Wilmer Institute, Balti¬ more, were measured by the scheme shown in Fig 2. Lamp voltages were turned up to maximum, since the operating room nurses stated that they are usually used at maxi¬ mum level. Their illuminating systems produce a real image of the fiberoptic cable termination from about 2 to 10 cm in front of the microscope's objective lens. We care¬ fully measured the area of this trapezoidshaped "hot spot" by projecting its image
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the floor with a +8-diopter trial case lens. The area was traced and measured with a planimeter, subtracting regions where fibers were inactive. Only the active helical component of the filament was measured for instrument 6. These were reduced by the square of the linear magni¬ fication involved in the projection. We substituted this area, A, into the equation shown in Fig 2 along with the radiometer reading, Ha,r, and the distance, d. This produced the average radiance, N, of the hot spot image, in watts per steradiansquare centimeter (W/sr-sq cm). Another on
operation microscope (Weck-JFH) was available on loan; hence, it was included in our series of measurements (instrument 5). Also, a single instrument from the animal laboratory (Zeiss OpMi 1) with a nonfiberoptic internal source was measured (instru¬ ment 6). All six microscopes are detailed in
Table 1. As shown by the equation in Fig 1, we then estimated the retinal irradiance, Hr„, where Apuol, is the effective pupillary area, assumed to be dilated to 7 mm. It is also assumed for this calculation that the hot spot is focused on the retina, through clear media, in order to simulate a "worst-case" condition. Exceptions to the worst-case situation are also considered in our discus¬ sion. All measurements were made using a radiometer (EG & G model 550) with a type A silicon detector head, which passes approximately the same wavelengths as does the ocular media (flat response, ± 5%, from 450 to 1,000 nm, trailing to zero by 340 nm and 1,120 nm using the radiometrie filter). All readings were corrected for ambient illumination that persisted after the direct beam was blocked. We assumed that the index of refraction, n, of the vitreous is 1.33, the distance of the pupil¬ lary plane from the retina is 2.15 cm, and
Operating Microscope
Vitreous:
n=
1.33 (Index of Refraction)
t
0.9 (Transmission)
=
Image of Fiber Bundle
Illuminator, With Radiance Retinal Image of Irradiance (H„.)
H„,= N Patient's
Eye 2.15
Fig 1.—Surgical microscope light
Operating Microscope
source
forms
image
on
cm
patient's retina. the transmission, t, of clear ocular media is 90%. It is necessary to correct for index of refraction in the equation of Fig 1 because our radiometrie measurements were made in air (index 1.00), whereas the retina to be receiving the light is "under water." The conservation of radiance theorem states that N/n2 is constant along the observation
Image of Fiber Illuminator,
Bundle
=
With Measured Area A
path through
Measured Irradiance,
W/sq
d2 A
cm
Ha„ Radiometer
Fig
2— Method of
measuring
radiance
Table
(N)
of hot spot,
or
(Reading, Halr) light source image.
1.—Operation Microscope Light
specular optical system.
a
The ocular media is assumed to constitute a specular system prior to absorption of light at the retinal level. This, of course, would not be valid for hazy media. Even for cases where the source image is not focused sharply on the retina, our proposed analysis is valid, provided the patient's pupil is completely filled with light (for a given bundle of rays). In other words, the patient's pupil must act as the limiting stop in the system. This implies that the hot spot aerial image in front of the microscope must have a relatively large size, and it holds true for emmetropie, myopic, and some hyperopic subjects for at least the central portion of the retinal image. For high hyperopic and aphakic
Source Characteristics Hot
Spot Image
of Source
Distance Above Instrument
Description Zeiss OpMi 1 with external fiberoptic source and 200-mm objective Same as (1) Same as (1) Zeiss OpMi 6 zoom with external flberoptics and 175-mm objective Troutman-Weck-JKH zoom with dual flberop¬ tics and 150-mm objective Zeiss OpMi 1 with Internal bulb and 200-mm
objective
"Values shown
are
Operative Field, cm
Hot
Dimensions, cm*
27f
2.96, 1.35 2.40, 1.20 4.04, 1.29
15
2.66, 0.86
11
Area, sq
cm
Spot
Radiance, W/sr-sq cm
3.38 2.60 5.02
1.70
1.94
3.90
(each bundle)
0.74 0.81
1.10 12
1.37, 0.96
16
1.87, 0.70
maximum and minimum,
tlnside microscope housing.
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1.09
6.50
7.30
Table 2.—Retinal
Exposure
From
Microscope Light Sources
Proportion of 7-mm Pupil Instrument
of
Type Eyes Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic
Threshold for
Retinal
Filled With Light, % 100
Irradiance, W/sq cm 0.230 0.190 0.100 0.085 0.110 0.059 0.510 0.280
83 100 85 100 54 100 54 100
Visible Retinal
Change, mint
15.0
21.0 26.0
29.0 34.0 27.0
49.0 57.0 44.0
49.0
82.0 9.5 17.0 5.7 8.3 5.0 14.0
4.6Í 10.0
2.1Î 3.7Ì 18Î 8.5t
0.860 0.590 0.970 0.340
68 100 35
Safe Time, s" 13.0
*Safe time indicates time to reach maximum permissible exposure.'
fSee text for discussion. tSince safe time is less than 10
s,
nonequilibrium equation is used: safe time
subjects, however, the pupil would not be completely filled (for the central or axial
as viewed from the retina). Therefore, a correction factor is included in Table 2, which is based on the solid angle subtended by the source hot spot at the patient's far point plane. Where this projection intercepts the patient's pupil¬ lary plane, a computation of the percent¬ age of pupillary area filled is included, assuming +12 diopters of aphakia.
rays
·
RESULTS
Table 1 lists the measured values for corresponding microscopes. The radiance of the hot spot (aerial source image) varies from 0.74 to 7.3 W/sr-sq cm.
Calculated Hrel, or retinal irra¬ diance values, are shown in Table 2 for corresponding refractive errors. The retinal irradiance likely to be received by the patient is seen to vary for emmetropie and myopic patients from 0.10 to 0.97 W/sq cm; for aphakic patients, it varies from 0.085 to 0.59
W/sq
cm.
The column labelled "safe time" indicates how long exposure at this level of Hrel must be continuously maintained before the ANSI laser safety guidelines- are exceeded. That is, the retinal maximal permissible exposure (MPE) of 2.92 joules/sq cm is reached at the time indicated under the safe time column. This safe time is seen to vary from 1.8 to 29 s for emmetropie and myopic patients and from 3.7 to 49 s for aphakics. A final column is included in Table 2 to show how long it takes at the corresponding retinal irradiance val¬ ues before one might postulate that an ophthalmoscopically detectable retinal change might occur in 50% of the subjects so exposed. We placed this level at 292 joules/sq cm, or 100 times
=
1.68
(H„t)
H„, indicates retinal irradiance.
the MPE. The rationale for this will be discussed. For emmetropie or myopic patients with clear media and dilated pupils, one can see that ophthalmoscopically visible changes might occur after a range of five to 49 minutes for the various microscopes tested. For aphakic patients, using the same
assumptions, one might expect to see something after 8.3 to 82 minutes of continuous, uninterrupted exposure. COMMENT
This article reports the optical reti¬ nal irradiance likely to be received by a patient from a typical operation microscope if his pupil is dilated 7 mm, his media are clear, and he has spher¬ ical myopia of —3.7 to —9.1 diopters (which allows the light source hot spot to focus sharply on his retina). The analysis is valid for other refractive states as well because of the large size of the aerial hot spot image. However, as refractive error becomes extremely
hyperopic (eg, aphakic subjects), only the central regions of the exposed
retinal area would have the retinal irradiances predicted by our analysis as shown in Table 2. The edges of the approximately 1.5-disc-diameter reti¬ nal area exposed would fall off in irradiance level for high hyperopes. However, since the principal issue we are addressing here is safety, we must strive to modify our illuminators so that no portion of the retinal expo¬ sure region exceeds a "safe" level, whatever that level is determined to be. We are therefore obligated to consider what the worst-case situation would be and avoid it if possible. Following this line of reasoning, all readings taken were maximum read¬ ings, in the sense that the detector head was positioned so as to get a
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maximum reading, holding its dis¬ tance from the source constant. Also, in the case of operation microscope 5, the brighter of the two fiberoptic cables was rotated as it plugs into the lamp housing to achieve a maximum brightness. Perhaps if we had ad¬ justed the fiberoptic cables on the other units they could have achieved a higher peak also. Minimum readings for any given radiometrie measure¬ ment plane were usually about 60% of the maximum, so an average field might be considered to be about 80% of the values indicated in Table 2 for retinal irradiance, even though the maximum shown does apply for at least one location on the retina at any given time. To evaluate the potential hazard to the retina from combined thermal and direct phototoxic effects of these white light (noncoherent) sources, two approaches may be taken. One can compare these computed retinal expo¬ sures with similar exposures from white light sources known to have produced lesions; or one can correlate these values with the laser safety guidelines, granting a certain similar¬ ity between noncoherent and coherent light damage mechanisms. The first approach is the most disturbing when one considers that ophthalmoscopically visible retinal le¬ sions have been produced in monkey eyes by white light sources with roughly the same light exposures that the patient may, under certain condi¬ tions, receive from an operation microscope. Fuller et al' demonstrated that a white light fiberoptic probe inside a monkey eye, with a calculated retinal irradiance of 0.22 W/sq cm, produced ophthalmoscopically visible retinal changes in 15 to 20 minutes (or
joules/sq cm). The five operation microscopes our study were capable of
at 198 to 264
fiberoptic
tested in retinal irradiance values ranging from 0.1 to 0.86 W/sq cm, over retinal areas of comparable size (with com¬
parable spectral content).
Hochheimer et al1 aimed an opera¬ tion microscope at an anesthetized, dilated monkey's eye for one hour. Retinal irradiance was measured at 1.76 W/sq cm by the method describ¬ ed in this article, or nearly 6,320 joules/sq cm. A large macular scar was produced, which failed to re¬ solve ophthalmoscopically over nine months. Extensive damage, as noted by fluorescein angiography, persisted as well. Friedman and Kuwabara' exposed monkey retinas to the indirect oph¬ thalmoscope (20-D lens) for 15 min¬ utes. The following day whitening was evident and histologie changes were marked. Their estimate of reti¬ nal irradiance was 0.27 W/sq cm (giv¬ ing 243 joules/sq cm). Numerous other examples in the literature"" suggest that retinal changes can be induced by white light of the order of magnitude discussed in this report. Fortunately, most thresh¬ old changes seem to reverse with no
apparent sequelae.
We believe the ANSI guidelines for laser safety- are very useful for putting retinal exposure levels in perspective. The power in watts per square centimeter on the retina multi¬ plied by the number of seconds of exposure gives the total energy (or integrated retinal irradiance) in joules per square centimeter. For exposures from 10 s to 2.75 hours, one can calcu¬ late from the extended source section of the guidelines (using our equation in Fig 1) that 2.92 joules/sq cm is the MPE at the retinal level. For example, for instrument 4 (Table 2) the retinal irradiance is shown to be 0.28 W/sq cm for an aphakic patient. To find out how long exposure has to be to reach the retinal MPE of 2.92 joules/sq cm, the follow¬ ing equation is used: safe time t,,,.,, 2.92 cm _ joules/sq _2_= in 4 0.28 W/sq cm =
=
s
The MPE is intended to lie two orders of magnitude below the thresh¬ old for a 50% probability of producing an ophthalmoscopically visible retinal burn in a series of monkeys. The rationale for this factor of 100 safety margin is as follows"1 (F. A. Ander¬ son, PhD, oral communication, May "
1978).
A large variation in threshold existed among the different monkeys included in the data used for formu¬ lating the laser safety guidelines. Thus, one order of magnitude below the 50-50 visible threshold was the approximate location of the lower 95% confidence limit of the data. So, even if one assumes that no damage occurs that cannot be seen with an ophthal¬ moscope
(an unlikely situation), by
a factor of ten safety small percentage of cases would still show an ophthalmoscopical¬ ly visible lesion. Thus, another factor of ten is required to "protect" these cases. Another way of looking at it is that, in the "average" monkey, given the 50-50 threshold for a visible burn, an exposure of one tenth of this value would produce histologically evident
choosing only
margin,
a
changes (even though an ophthal¬ moscopically visible lesion would not be present). At a factor of 1/100 of this threshold one would see changes at the electron microscopic level (even though histologie changes would not be evident). This level is the MPE level, and is considered safe, even though electron microscopically de¬ tectable changes could be produced in the individual of average susceptibili¬ ty. Of course, for a more susceptible
individual at the lower end of the distribution curve, the MPE repre¬ sents the histologie change level. For the results given in Table 2, safe time is the time required to reach the MPE. For exposures longer than this, one presumably risks the occur¬ rence of some retinal or retinal
pigment epithelium (RPE) changes,
however miniscule or reversible they might be. Undoubtedly, many changes do occur that reverse completely in
healthy individuals; otherwise,
we
would all have been much more acute¬ ly aware of light-induced damage by now. However, it is much more tenuous to assume that diseased or aged maculae will recover fully or
rapidly.
Since the ANSI guidelines began with the 50-50 threshold for a visible retinal lesion in monkeys and worked downward by a factor of 100 to arrive at the MPE, we think it is useful to go in the opposite direction. That is, we take their value for the MPE, and multiply it by 100 to arrive at a ball¬ park figure for a 50-50 visible lesion threshold for that single monkey that has average susceptibility. This does not mean that for the exposure times indicated in the final column of Table 2, a patient will acquire a retinal lesion. It merely implies that if the patient's retina has about the same
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susceptibility as the hypothetical av¬ erage monkey, then as a result of this
exposure, he has a 50% chance of at least some retinal change that can be detected ophthalmoscopi¬ cally at some time up to about five
getting
days later.
One could argue that laser guide¬ lines are inappropriate for noncoher¬ ent (white light) sources, and indeed they are. However, there is a mount¬ ing body of evidence that, for the time domain of relevance here, in the visi¬ ble spectrum, comparative threshold values seem in fairly close agreement (whether xenon lamp, carbon arc, helium-neon, ruby, or argon la¬
ser)."-" In fact, there is good reason to suspect that light sources (coherent or noncoherent) that emit more heavily
toward the blue end may have a high¬ probability of producing retinal changes than even the laser safety standards would suggest. Sperling" produced extensive histologie damage to the RPE in monkeys with a blue (463 nm) noncoherent light H,.,., of 0.01 mW/sq cm to 0.1 mW/sq cm for 60 minutes. The integrated retinal irra¬ diance would, thus, be less than 0.36 joules/sq cm or around an order of magnitude less than the MPE level. Ham and co-workers'" produced oph¬ visible retinal thalmoscopically changes in a monkey with the 441.6nm line from a helium-cadmium laser at 30 mW/sq cm 1,000 s 30 joules/sq cm, or about an order of magnitude less than our proposed visi¬ ble change threshold of 292 joules/sq er
=
cm.
In a real clinical situation, of course, the "worst-case" situation assumed in Tables 1 and 2 may not apply. A single patch of retina is not usually exposed continuously because the eye is mov¬ ing somewhat, and instruments, as well as the surgeon's hands, interrupt the beam frequently. This mechanism may well be responsible for protecting numerous maculae from thermal light damage. That is, as long as the MPE is not exceeded (for strictly thermal effects), interrupting the beam might allow the retina to cool down momen¬ tarily. Subthreshold thermal exposure, as such, presumably has no cumulative effects. However, the direct phototoxic (nonthermal) effects caused pri¬ marily by the blue end of the spectrum may well be cumulative, even when exposure is less than the MPE, or safe time. Also, the patient is somewhat protected when his pupil is not dilated. If the pupil is only 3 mm, instead of the 7 mm assumed 'throughout this
report, retinal irradiance would be
18% of that indicated. One could then assume that the "safe time" column values of Table 1 could be multiplied by 5.4. This would apply for the final column of Table 2 as well. If the cornea, lens, or vitreous are hazy, some of the light will be scat¬ tered or absorbed, lessening the hazard potential. No attempt has yet been made to analyze this, nor have we attempted to evaluate the poten¬ tial hazard to a retina that is detached. When much of this data was presented at the Wilmer meetings in 1977, many participants raised the question, "If this light source is really unsafe, why don't we see retinal damage from it clinically?" We would submit that we may indeed be seeing it in the form of cystoid maculopathy (Irvine-Gass syn¬ drome) and accelerated macular de¬ generation following surgery. Henry et al'" were the first to implicate the surgical overhead lamps and operation
(3/7)-'
or
microscope as contributing to or caus¬ ing cystoid maculopathy. They noted a marked increase in cystoid maculopa¬ thy when they began using 10-0 mono-
filament suture to close their cataract wounds. They attributed this to the prolonged operative time (and there¬ fore prolonged light exposure); also, overhead lights were directed toward the macula. Knowing the quantity of light the patient might, in some cases, receive during routine microsurgery, we must conclude that if it is not causing cystoid maculopathy, then it must be causing some other frequently en-
countered retinal condition. Since 40% to 50% of routine cataract extractions are followed by cystoid maculopa¬ thy,'718 which does not seem to corre¬ late consistently with vitreous trac¬ tion, age, sex, complications, medica¬ tions, or hypotony,17 a correlation with light exposure appears to be a fruitful area for further investigation. One final article is worth mention¬ ing in this regard. Tso et al1" exposed anesthetized monkeys to an indirect ophthalmoscope using a 20-D lens for one hour. In addition to other changes, by five days following exposure gross and histologie retinal edema of all retinal layers had developed in many eyes. After one month, macular lesions became elevated, with numer¬
pigment-laden macrophages in subretinal spaces (between photoreceptors and RPE and between RPE and Bruch's membrane). Photorecep¬ tor regeneration is also reported in their articles.6 We have measured retinal irra¬ diance values likely to be achieved by indirect ophthalmoscopes-" under sim¬ ilar circumstances. We would guess that approximately 0.12 W/sq cm, on the average, was received by their monkeys. For one hour, a total expo¬ sure might then be estimated at 432 joules/sq cm. What has not been real¬ ized previously is that instrument 6 (Table 1), a surgical microscope that is widely available, is capable of reach¬ ing this same level after only 7.5 minutes of operative time. Surely there is enough proof of high light levels causing retinal edema, and now, of such high light levels being easily available in the routine microsurgical environment, to warrant further inous
vestigation.
In summary, there appears to be
an
urgent need for further revision of the illuminating system of operation mi¬
croscopes. No
minating
a
one would consider illu¬ normal retina with an
indirect ophthalmoscope continually for 15 minutes; yet the average microscope produces over five times greater retinal irradiance than does the average indirect ophthalmo¬ scope.-" The same level reached by an average indirect ophthalmoscope on a medium voltage setting in 15 minutes (61 joules/sq cm) is reached by opera¬ tion microscope 6 (Table 2) after only one minute (worst-case conditions are assumed for both instruments). We would urge manufacturers to develop a "safe" illuminating system for microsurgery. We as ophthalmol¬ ogists should stop requesting brighter and brighter light sources. Ideally, a safe source should extend the safe time to perhaps 45 minutes, and elim¬ inate much of the blue end of the spectrum, if that can be done without interfering with useful visibility. Until we have such a source readily available, it makes sense to block the pupil, whenever possible, especially during wound closure. This might be done by placing a tiny piece of opaque or diffusing material on the cornea. Merely turning down the light intensity on the microscope repre¬ sents a drop in the bucket. This might only double the safe time; eg, instead of 10 s, one might have 20 s of safe time.
This
study
was
tutes of Health
supported by
National Insti¬
grant ROÍ EY 01312.
References 1. Littman H: A new operation microscope. Klin Monatsbl Augenheilkd 124:473-476, 1954. 2. American National Standard for the Safe Use of Lasers. ANSI publication Z136.1-1973. New York, American National Standards Institute, 1973. 3. Fuller D, Machemer R, Knighton RW: Retinal damage produced by intraocular fiber optic light. Am J Ophthalmol 85:519-537, 1978. 4. Hochheimer BF, D'Anna SA, Calkins JL: Retinal damage from light. Am J Ophthalmol, to be published. 5. Friedman E, Kuwabara T: The retinal pigment epithelium: IV. The damaging effects of radiant energy. Arch Ophthalmol 80:265-279, 1968. 6. Tso MO: Photic maculopathy in rhesus monkey, a light and electron microscopic study. Invest Ophthalmol 12:17-34, 1973. 7. Cavonius CR, Elgin S, Robbins DO: Thresholds for damage to the human retina by white light. Exp Eye Res 19:543-548, 1974. 8. Dawson WW, Herron WL: Retinal illumination during indirect ophthalmoscopy: Subsequent dark adaptation. Invest Ophthalmol 9:89-96,
1970. 9. Noell WK, Walker VS, Kang BS, et al: Retinal damage by light in rats. Invest Ophthalmol 5:450-472, 1966. 10. Anderson FA: Biological Bases for and Other Aspects of a Performance Standard for Laser Products. US Department of Health, Education, and Welfare, publication (FDA) 75-8004, July 1974. 11. VanPelt WF, Payne WR, Peterson RW: A Review of Selected Bioeffects Thresholds for Various Spectral Ranges of Light. US Department of Health, Education, and Welfare, publication (FDA) 74-8010, June 1973. 12. Geeraets WJ, Ham WT Jr, Williams RC, et al: Laser versus light coagulator: A funduscopic and histologic study of chorioretinal injury as a function of exposure time. Fed Proc 24:S-48, 1965. 13. Sliney DH, Freasier BC: Evaluation of optical radiation hazards. Appl Opt 12:1-24, 1973. 14. Sperling HG: Functional changes and cellular damage associated with two regimes of moderately intense blue light exposure in Rhesus
Downloaded From: http://archopht.jamanetwork.com/ by a New York University User on 06/20/2015
monkey retina. Abstract presented at the Association for Research in Vision and Ophthalmology spring meeting, Sarasota Fla, May 5, 1978. 15. Ham WT, Mueller HA, Sliney DH: Retinal sensitivity to damage from short wavelength light. Nature 260:153-155, 1976. 16. Henry MM, Henry LM, Henry LM: A possible cause of chronic cystic maculopathy. Ann Ophthalmol 9:455-457, 1977. 17. Hitchings RA, Chisholm IH, Bird AC: Aphakic macular edema: Incidence and pathogenesis.
Invest Ophthalmol 14:68-72, 1975. 18. Irvine AR, Bresky R, Crowder BM, et al: Macular edema after cataract extraction. Ann Ophthalmol 3:1234-1240, 1971. 19. Tso MO, Fine BS, Zimmerman LE: Photopic maculopathy produced by the indirect ophthalmoscope: I. Clinical and histopathologic study. Am J Ophthalmol 73:686-699, 1972. 20. Calkins JL, Hochheimer BF: Retinal light exposure from ophthalmoscopes, slit lamps, and overhead surgical lamps: An analysis of potential hazards. Invest Ophthalmol Vis Sci, to be
published.
L.
Light Exposure Operation Microscopes
Calkins, MD, Bernard
F.
Hochheimer, MS
\s=b\ Several popular surgical microscopes were measured for source radiance. A method has been devised for calculating patient retinal exposure from these instruments. Retinal irradiance is seen to be surprisingly high, assuming dilated pupils and clear media. It ranges from 0.10 to 0.97 W/sq cm. This is one to ten times higher than that produced by an indirect ophthalmoscope. There is evidence linking light exposure during surgery to cystoid maculopathy (Irvine-Gass
syndrome). (Arch Ophthalmol 97:2363-2367, 1979) Oince the introduction of the opera^ tion
microscope
for
ophthalmic
surgery 25 years ago,' the basic optical design of popular models has changed very little. The illuminating systems
used, however, have undergone sev¬ eral revisions. Internal, or "coaxial," illumination has become almost uni¬ versal. To provide better illumination, manufacturers have tried to increase the brightness of the internal light sources. However, in addition to providing greater useful illumination, a brighter source also produces a highAccepted
for publication May 21, 1979. From The Wilmer Institute, The Johns Hopkins University Hospital, Baltimore (Dr Calkins), and The Applied Physics Laboratory, Laurel, Md
(Mr Hochheimer).
Presented at the 36th clinical meeting of the Residents Association of the Wilmer Ophthalmological Institute, April 22, 1977. Reprint requests to The Wilmer Institute, Johns Hopkins University, 601 N Broadway, Baltimore, MD 21205 (Dr Calkins).
er
retinal irradiance. This poses the
question of whether or not this light is hazardous to the patient's retina. Even though a great deal has appeared in the literature about the advantages of microsurgery, practi¬ cally nothing has been written about what happens to the light after it enters the patient's eye. We analyze this problem in this article. We describe a means of measuring and calculating the retinal irradiance likely to be received by a patient from the light source of several commonly encountered operation microscopes. These levels are then compared with light levels of similar spectral content known to be hazardous in monkey retinas. A further comparison is made
with American National Standards Institute (ANSI) laser safety stan¬ dards2 for light exposure. Figure 1 demonstrates the manner in which a typical microscope forms an image on the patient's retina of its internal light source, which may be either a lamp filament or a fiberoptic bundle termination. MATERIALS AND METHODS Four operation microscopes (Zeiss) in daily usage at The Wilmer Institute, Balti¬ more, were measured by the scheme shown in Fig 2. Lamp voltages were turned up to maximum, since the operating room nurses stated that they are usually used at maxi¬ mum level. Their illuminating systems produce a real image of the fiberoptic cable termination from about 2 to 10 cm in front of the microscope's objective lens. We care¬ fully measured the area of this trapezoidshaped "hot spot" by projecting its image
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the floor with a +8-diopter trial case lens. The area was traced and measured with a planimeter, subtracting regions where fibers were inactive. Only the active helical component of the filament was measured for instrument 6. These were reduced by the square of the linear magni¬ fication involved in the projection. We substituted this area, A, into the equation shown in Fig 2 along with the radiometer reading, Ha,r, and the distance, d. This produced the average radiance, N, of the hot spot image, in watts per steradiansquare centimeter (W/sr-sq cm). Another on
operation microscope (Weck-JFH) was available on loan; hence, it was included in our series of measurements (instrument 5). Also, a single instrument from the animal laboratory (Zeiss OpMi 1) with a nonfiberoptic internal source was measured (instru¬ ment 6). All six microscopes are detailed in
Table 1. As shown by the equation in Fig 1, we then estimated the retinal irradiance, Hr„, where Apuol, is the effective pupillary area, assumed to be dilated to 7 mm. It is also assumed for this calculation that the hot spot is focused on the retina, through clear media, in order to simulate a "worst-case" condition. Exceptions to the worst-case situation are also considered in our discus¬ sion. All measurements were made using a radiometer (EG & G model 550) with a type A silicon detector head, which passes approximately the same wavelengths as does the ocular media (flat response, ± 5%, from 450 to 1,000 nm, trailing to zero by 340 nm and 1,120 nm using the radiometrie filter). All readings were corrected for ambient illumination that persisted after the direct beam was blocked. We assumed that the index of refraction, n, of the vitreous is 1.33, the distance of the pupil¬ lary plane from the retina is 2.15 cm, and
Operating Microscope
Vitreous:
n=
1.33 (Index of Refraction)
t
0.9 (Transmission)
=
Image of Fiber Bundle
Illuminator, With Radiance Retinal Image of Irradiance (H„.)
H„,= N Patient's
Eye 2.15
Fig 1.—Surgical microscope light
Operating Microscope
source
forms
image
on
cm
patient's retina. the transmission, t, of clear ocular media is 90%. It is necessary to correct for index of refraction in the equation of Fig 1 because our radiometrie measurements were made in air (index 1.00), whereas the retina to be receiving the light is "under water." The conservation of radiance theorem states that N/n2 is constant along the observation
Image of Fiber Illuminator,
Bundle
=
With Measured Area A
path through
Measured Irradiance,
W/sq
d2 A
cm
Ha„ Radiometer
Fig
2— Method of
measuring
radiance
Table
(N)
of hot spot,
or
(Reading, Halr) light source image.
1.—Operation Microscope Light
specular optical system.
a
The ocular media is assumed to constitute a specular system prior to absorption of light at the retinal level. This, of course, would not be valid for hazy media. Even for cases where the source image is not focused sharply on the retina, our proposed analysis is valid, provided the patient's pupil is completely filled with light (for a given bundle of rays). In other words, the patient's pupil must act as the limiting stop in the system. This implies that the hot spot aerial image in front of the microscope must have a relatively large size, and it holds true for emmetropie, myopic, and some hyperopic subjects for at least the central portion of the retinal image. For high hyperopic and aphakic
Source Characteristics Hot
Spot Image
of Source
Distance Above Instrument
Description Zeiss OpMi 1 with external fiberoptic source and 200-mm objective Same as (1) Same as (1) Zeiss OpMi 6 zoom with external flberoptics and 175-mm objective Troutman-Weck-JKH zoom with dual flberop¬ tics and 150-mm objective Zeiss OpMi 1 with Internal bulb and 200-mm
objective
"Values shown
are
Operative Field, cm
Hot
Dimensions, cm*
27f
2.96, 1.35 2.40, 1.20 4.04, 1.29
15
2.66, 0.86
11
Area, sq
cm
Spot
Radiance, W/sr-sq cm
3.38 2.60 5.02
1.70
1.94
3.90
(each bundle)
0.74 0.81
1.10 12
1.37, 0.96
16
1.87, 0.70
maximum and minimum,
tlnside microscope housing.
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1.09
6.50
7.30
Table 2.—Retinal
Exposure
From
Microscope Light Sources
Proportion of 7-mm Pupil Instrument
of
Type Eyes Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic Myopic, emmetropie Aphakic
Threshold for
Retinal
Filled With Light, % 100
Irradiance, W/sq cm 0.230 0.190 0.100 0.085 0.110 0.059 0.510 0.280
83 100 85 100 54 100 54 100
Visible Retinal
Change, mint
15.0
21.0 26.0
29.0 34.0 27.0
49.0 57.0 44.0
49.0
82.0 9.5 17.0 5.7 8.3 5.0 14.0
4.6Í 10.0
2.1Î 3.7Ì 18Î 8.5t
0.860 0.590 0.970 0.340
68 100 35
Safe Time, s" 13.0
*Safe time indicates time to reach maximum permissible exposure.'
fSee text for discussion. tSince safe time is less than 10
s,
nonequilibrium equation is used: safe time
subjects, however, the pupil would not be completely filled (for the central or axial
as viewed from the retina). Therefore, a correction factor is included in Table 2, which is based on the solid angle subtended by the source hot spot at the patient's far point plane. Where this projection intercepts the patient's pupil¬ lary plane, a computation of the percent¬ age of pupillary area filled is included, assuming +12 diopters of aphakia.
rays
·
RESULTS
Table 1 lists the measured values for corresponding microscopes. The radiance of the hot spot (aerial source image) varies from 0.74 to 7.3 W/sr-sq cm.
Calculated Hrel, or retinal irra¬ diance values, are shown in Table 2 for corresponding refractive errors. The retinal irradiance likely to be received by the patient is seen to vary for emmetropie and myopic patients from 0.10 to 0.97 W/sq cm; for aphakic patients, it varies from 0.085 to 0.59
W/sq
cm.
The column labelled "safe time" indicates how long exposure at this level of Hrel must be continuously maintained before the ANSI laser safety guidelines- are exceeded. That is, the retinal maximal permissible exposure (MPE) of 2.92 joules/sq cm is reached at the time indicated under the safe time column. This safe time is seen to vary from 1.8 to 29 s for emmetropie and myopic patients and from 3.7 to 49 s for aphakics. A final column is included in Table 2 to show how long it takes at the corresponding retinal irradiance val¬ ues before one might postulate that an ophthalmoscopically detectable retinal change might occur in 50% of the subjects so exposed. We placed this level at 292 joules/sq cm, or 100 times
=
1.68
(H„t)
H„, indicates retinal irradiance.
the MPE. The rationale for this will be discussed. For emmetropie or myopic patients with clear media and dilated pupils, one can see that ophthalmoscopically visible changes might occur after a range of five to 49 minutes for the various microscopes tested. For aphakic patients, using the same
assumptions, one might expect to see something after 8.3 to 82 minutes of continuous, uninterrupted exposure. COMMENT
This article reports the optical reti¬ nal irradiance likely to be received by a patient from a typical operation microscope if his pupil is dilated 7 mm, his media are clear, and he has spher¬ ical myopia of —3.7 to —9.1 diopters (which allows the light source hot spot to focus sharply on his retina). The analysis is valid for other refractive states as well because of the large size of the aerial hot spot image. However, as refractive error becomes extremely
hyperopic (eg, aphakic subjects), only the central regions of the exposed
retinal area would have the retinal irradiances predicted by our analysis as shown in Table 2. The edges of the approximately 1.5-disc-diameter reti¬ nal area exposed would fall off in irradiance level for high hyperopes. However, since the principal issue we are addressing here is safety, we must strive to modify our illuminators so that no portion of the retinal expo¬ sure region exceeds a "safe" level, whatever that level is determined to be. We are therefore obligated to consider what the worst-case situation would be and avoid it if possible. Following this line of reasoning, all readings taken were maximum read¬ ings, in the sense that the detector head was positioned so as to get a
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maximum reading, holding its dis¬ tance from the source constant. Also, in the case of operation microscope 5, the brighter of the two fiberoptic cables was rotated as it plugs into the lamp housing to achieve a maximum brightness. Perhaps if we had ad¬ justed the fiberoptic cables on the other units they could have achieved a higher peak also. Minimum readings for any given radiometrie measure¬ ment plane were usually about 60% of the maximum, so an average field might be considered to be about 80% of the values indicated in Table 2 for retinal irradiance, even though the maximum shown does apply for at least one location on the retina at any given time. To evaluate the potential hazard to the retina from combined thermal and direct phototoxic effects of these white light (noncoherent) sources, two approaches may be taken. One can compare these computed retinal expo¬ sures with similar exposures from white light sources known to have produced lesions; or one can correlate these values with the laser safety guidelines, granting a certain similar¬ ity between noncoherent and coherent light damage mechanisms. The first approach is the most disturbing when one considers that ophthalmoscopically visible retinal le¬ sions have been produced in monkey eyes by white light sources with roughly the same light exposures that the patient may, under certain condi¬ tions, receive from an operation microscope. Fuller et al' demonstrated that a white light fiberoptic probe inside a monkey eye, with a calculated retinal irradiance of 0.22 W/sq cm, produced ophthalmoscopically visible retinal changes in 15 to 20 minutes (or
joules/sq cm). The five operation microscopes our study were capable of
at 198 to 264
fiberoptic
tested in retinal irradiance values ranging from 0.1 to 0.86 W/sq cm, over retinal areas of comparable size (with com¬
parable spectral content).
Hochheimer et al1 aimed an opera¬ tion microscope at an anesthetized, dilated monkey's eye for one hour. Retinal irradiance was measured at 1.76 W/sq cm by the method describ¬ ed in this article, or nearly 6,320 joules/sq cm. A large macular scar was produced, which failed to re¬ solve ophthalmoscopically over nine months. Extensive damage, as noted by fluorescein angiography, persisted as well. Friedman and Kuwabara' exposed monkey retinas to the indirect oph¬ thalmoscope (20-D lens) for 15 min¬ utes. The following day whitening was evident and histologie changes were marked. Their estimate of reti¬ nal irradiance was 0.27 W/sq cm (giv¬ ing 243 joules/sq cm). Numerous other examples in the literature"" suggest that retinal changes can be induced by white light of the order of magnitude discussed in this report. Fortunately, most thresh¬ old changes seem to reverse with no
apparent sequelae.
We believe the ANSI guidelines for laser safety- are very useful for putting retinal exposure levels in perspective. The power in watts per square centimeter on the retina multi¬ plied by the number of seconds of exposure gives the total energy (or integrated retinal irradiance) in joules per square centimeter. For exposures from 10 s to 2.75 hours, one can calcu¬ late from the extended source section of the guidelines (using our equation in Fig 1) that 2.92 joules/sq cm is the MPE at the retinal level. For example, for instrument 4 (Table 2) the retinal irradiance is shown to be 0.28 W/sq cm for an aphakic patient. To find out how long exposure has to be to reach the retinal MPE of 2.92 joules/sq cm, the follow¬ ing equation is used: safe time t,,,.,, 2.92 cm _ joules/sq _2_= in 4 0.28 W/sq cm =
=
s
The MPE is intended to lie two orders of magnitude below the thresh¬ old for a 50% probability of producing an ophthalmoscopically visible retinal burn in a series of monkeys. The rationale for this factor of 100 safety margin is as follows"1 (F. A. Ander¬ son, PhD, oral communication, May "
1978).
A large variation in threshold existed among the different monkeys included in the data used for formu¬ lating the laser safety guidelines. Thus, one order of magnitude below the 50-50 visible threshold was the approximate location of the lower 95% confidence limit of the data. So, even if one assumes that no damage occurs that cannot be seen with an ophthal¬ moscope
(an unlikely situation), by
a factor of ten safety small percentage of cases would still show an ophthalmoscopical¬ ly visible lesion. Thus, another factor of ten is required to "protect" these cases. Another way of looking at it is that, in the "average" monkey, given the 50-50 threshold for a visible burn, an exposure of one tenth of this value would produce histologically evident
choosing only
margin,
a
changes (even though an ophthal¬ moscopically visible lesion would not be present). At a factor of 1/100 of this threshold one would see changes at the electron microscopic level (even though histologie changes would not be evident). This level is the MPE level, and is considered safe, even though electron microscopically de¬ tectable changes could be produced in the individual of average susceptibili¬ ty. Of course, for a more susceptible
individual at the lower end of the distribution curve, the MPE repre¬ sents the histologie change level. For the results given in Table 2, safe time is the time required to reach the MPE. For exposures longer than this, one presumably risks the occur¬ rence of some retinal or retinal
pigment epithelium (RPE) changes,
however miniscule or reversible they might be. Undoubtedly, many changes do occur that reverse completely in
healthy individuals; otherwise,
we
would all have been much more acute¬ ly aware of light-induced damage by now. However, it is much more tenuous to assume that diseased or aged maculae will recover fully or
rapidly.
Since the ANSI guidelines began with the 50-50 threshold for a visible retinal lesion in monkeys and worked downward by a factor of 100 to arrive at the MPE, we think it is useful to go in the opposite direction. That is, we take their value for the MPE, and multiply it by 100 to arrive at a ball¬ park figure for a 50-50 visible lesion threshold for that single monkey that has average susceptibility. This does not mean that for the exposure times indicated in the final column of Table 2, a patient will acquire a retinal lesion. It merely implies that if the patient's retina has about the same
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susceptibility as the hypothetical av¬ erage monkey, then as a result of this
exposure, he has a 50% chance of at least some retinal change that can be detected ophthalmoscopi¬ cally at some time up to about five
getting
days later.
One could argue that laser guide¬ lines are inappropriate for noncoher¬ ent (white light) sources, and indeed they are. However, there is a mount¬ ing body of evidence that, for the time domain of relevance here, in the visi¬ ble spectrum, comparative threshold values seem in fairly close agreement (whether xenon lamp, carbon arc, helium-neon, ruby, or argon la¬
ser)."-" In fact, there is good reason to suspect that light sources (coherent or noncoherent) that emit more heavily
toward the blue end may have a high¬ probability of producing retinal changes than even the laser safety standards would suggest. Sperling" produced extensive histologie damage to the RPE in monkeys with a blue (463 nm) noncoherent light H,.,., of 0.01 mW/sq cm to 0.1 mW/sq cm for 60 minutes. The integrated retinal irra¬ diance would, thus, be less than 0.36 joules/sq cm or around an order of magnitude less than the MPE level. Ham and co-workers'" produced oph¬ visible retinal thalmoscopically changes in a monkey with the 441.6nm line from a helium-cadmium laser at 30 mW/sq cm 1,000 s 30 joules/sq cm, or about an order of magnitude less than our proposed visi¬ ble change threshold of 292 joules/sq er
=
cm.
In a real clinical situation, of course, the "worst-case" situation assumed in Tables 1 and 2 may not apply. A single patch of retina is not usually exposed continuously because the eye is mov¬ ing somewhat, and instruments, as well as the surgeon's hands, interrupt the beam frequently. This mechanism may well be responsible for protecting numerous maculae from thermal light damage. That is, as long as the MPE is not exceeded (for strictly thermal effects), interrupting the beam might allow the retina to cool down momen¬ tarily. Subthreshold thermal exposure, as such, presumably has no cumulative effects. However, the direct phototoxic (nonthermal) effects caused pri¬ marily by the blue end of the spectrum may well be cumulative, even when exposure is less than the MPE, or safe time. Also, the patient is somewhat protected when his pupil is not dilated. If the pupil is only 3 mm, instead of the 7 mm assumed 'throughout this
report, retinal irradiance would be
18% of that indicated. One could then assume that the "safe time" column values of Table 1 could be multiplied by 5.4. This would apply for the final column of Table 2 as well. If the cornea, lens, or vitreous are hazy, some of the light will be scat¬ tered or absorbed, lessening the hazard potential. No attempt has yet been made to analyze this, nor have we attempted to evaluate the poten¬ tial hazard to a retina that is detached. When much of this data was presented at the Wilmer meetings in 1977, many participants raised the question, "If this light source is really unsafe, why don't we see retinal damage from it clinically?" We would submit that we may indeed be seeing it in the form of cystoid maculopathy (Irvine-Gass syn¬ drome) and accelerated macular de¬ generation following surgery. Henry et al'" were the first to implicate the surgical overhead lamps and operation
(3/7)-'
or
microscope as contributing to or caus¬ ing cystoid maculopathy. They noted a marked increase in cystoid maculopa¬ thy when they began using 10-0 mono-
filament suture to close their cataract wounds. They attributed this to the prolonged operative time (and there¬ fore prolonged light exposure); also, overhead lights were directed toward the macula. Knowing the quantity of light the patient might, in some cases, receive during routine microsurgery, we must conclude that if it is not causing cystoid maculopathy, then it must be causing some other frequently en-
countered retinal condition. Since 40% to 50% of routine cataract extractions are followed by cystoid maculopa¬ thy,'718 which does not seem to corre¬ late consistently with vitreous trac¬ tion, age, sex, complications, medica¬ tions, or hypotony,17 a correlation with light exposure appears to be a fruitful area for further investigation. One final article is worth mention¬ ing in this regard. Tso et al1" exposed anesthetized monkeys to an indirect ophthalmoscope using a 20-D lens for one hour. In addition to other changes, by five days following exposure gross and histologie retinal edema of all retinal layers had developed in many eyes. After one month, macular lesions became elevated, with numer¬
pigment-laden macrophages in subretinal spaces (between photoreceptors and RPE and between RPE and Bruch's membrane). Photorecep¬ tor regeneration is also reported in their articles.6 We have measured retinal irra¬ diance values likely to be achieved by indirect ophthalmoscopes-" under sim¬ ilar circumstances. We would guess that approximately 0.12 W/sq cm, on the average, was received by their monkeys. For one hour, a total expo¬ sure might then be estimated at 432 joules/sq cm. What has not been real¬ ized previously is that instrument 6 (Table 1), a surgical microscope that is widely available, is capable of reach¬ ing this same level after only 7.5 minutes of operative time. Surely there is enough proof of high light levels causing retinal edema, and now, of such high light levels being easily available in the routine microsurgical environment, to warrant further inous
vestigation.
In summary, there appears to be
an
urgent need for further revision of the illuminating system of operation mi¬
croscopes. No
minating
a
one would consider illu¬ normal retina with an
indirect ophthalmoscope continually for 15 minutes; yet the average microscope produces over five times greater retinal irradiance than does the average indirect ophthalmo¬ scope.-" The same level reached by an average indirect ophthalmoscope on a medium voltage setting in 15 minutes (61 joules/sq cm) is reached by opera¬ tion microscope 6 (Table 2) after only one minute (worst-case conditions are assumed for both instruments). We would urge manufacturers to develop a "safe" illuminating system for microsurgery. We as ophthalmol¬ ogists should stop requesting brighter and brighter light sources. Ideally, a safe source should extend the safe time to perhaps 45 minutes, and elim¬ inate much of the blue end of the spectrum, if that can be done without interfering with useful visibility. Until we have such a source readily available, it makes sense to block the pupil, whenever possible, especially during wound closure. This might be done by placing a tiny piece of opaque or diffusing material on the cornea. Merely turning down the light intensity on the microscope repre¬ sents a drop in the bucket. This might only double the safe time; eg, instead of 10 s, one might have 20 s of safe time.
This
study
was
tutes of Health
supported by
National Insti¬
grant ROÍ EY 01312.
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1970. 9. Noell WK, Walker VS, Kang BS, et al: Retinal damage by light in rats. Invest Ophthalmol 5:450-472, 1966. 10. Anderson FA: Biological Bases for and Other Aspects of a Performance Standard for Laser Products. US Department of Health, Education, and Welfare, publication (FDA) 75-8004, July 1974. 11. VanPelt WF, Payne WR, Peterson RW: A Review of Selected Bioeffects Thresholds for Various Spectral Ranges of Light. US Department of Health, Education, and Welfare, publication (FDA) 74-8010, June 1973. 12. Geeraets WJ, Ham WT Jr, Williams RC, et al: Laser versus light coagulator: A funduscopic and histologic study of chorioretinal injury as a function of exposure time. Fed Proc 24:S-48, 1965. 13. Sliney DH, Freasier BC: Evaluation of optical radiation hazards. Appl Opt 12:1-24, 1973. 14. Sperling HG: Functional changes and cellular damage associated with two regimes of moderately intense blue light exposure in Rhesus
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monkey retina. Abstract presented at the Association for Research in Vision and Ophthalmology spring meeting, Sarasota Fla, May 5, 1978. 15. Ham WT, Mueller HA, Sliney DH: Retinal sensitivity to damage from short wavelength light. Nature 260:153-155, 1976. 16. Henry MM, Henry LM, Henry LM: A possible cause of chronic cystic maculopathy. Ann Ophthalmol 9:455-457, 1977. 17. Hitchings RA, Chisholm IH, Bird AC: Aphakic macular edema: Incidence and pathogenesis.
Invest Ophthalmol 14:68-72, 1975. 18. Irvine AR, Bresky R, Crowder BM, et al: Macular edema after cataract extraction. Ann Ophthalmol 3:1234-1240, 1971. 19. Tso MO, Fine BS, Zimmerman LE: Photopic maculopathy produced by the indirect ophthalmoscope: I. Clinical and histopathologic study. Am J Ophthalmol 73:686-699, 1972. 20. Calkins JL, Hochheimer BF: Retinal light exposure from ophthalmoscopes, slit lamps, and overhead surgical lamps: An analysis of potential hazards. Invest Ophthalmol Vis Sci, to be
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