A mild accidental laser injury.A 21-year-old female technician accidentally looked into the exit apertureof a repetitively pulsed infrared Nd:YAG 1064-nm target designation laser.The technician reported seeing 2 or 3 yellowish flashes at the time of thelaser exposure. Visual acuity in her left eye was 20/50 a few hours afterthe accident and 20/200 two days later; visual acuity returned to 20/15 twomonths after the injury. A, Four days after the accident, there is fovealedema, surrounding subretinal hemorrhage, and several small, hypopigmentedretinal pigment epithelium lesions. B, One month after the accident, fovealedema and subretinal hemorrhage have resolved, and a small area of fovealretinal pigment epithelium degeneration has developed.
A severe accidental laser injury.A 20-year-old male technician deliberately viewed the output of a laser rangefinderdespite reading warning labels and undergoing laser safety training. He reportedimmediate vision loss in his right eye, with some improvement after 5 minutes.He sought medical assistance 18 hours after the injury, at which time visualacuity was 20/150 OD, where there was a macular and vitreous hemorrhage. Thevitreous hemorrhage cleared, and his visual acuity returned to 20/70 duringthe next month. After the accident, visual acuity was 20/40 OD at 1 year and20/30 OD at 2 years. A, Ten weeks after the injury, there is a full-thicknessmacular hole with surrounding retinal pigment epithelium depigmentation inthe right eye. B, Fluorescein angiography documents a prominent foveal windowdefect due to retinal pigment epithelium atrophy. C, Optical coherence tomographydocuments a macular hole with increased reflectivity at its base. This increasedreflectivity is a characteristic of laser-induced macular holes.45 Itis caused by choriocapillaris scarring, so the prognosis for visual improvementafter macular surgery may be worse for laser-induced than idiopathic macularholes.45
Mainster MA, Stuck BE, Brown J. Assessment of Alleged Retinal Laser Injuries. Arch Ophthalmol. 2004;122(8):1210-1217. doi:10.1001/archopht.122.8.1210
Accidental retinal laser injuries are easily diagnosed when there areknown laser sources, typical macular injuries, and visual deficits consistentwith retinal findings. Decisions are more difficult when retinal findingsare subtle or absent, despite reported visual problems and somatic complaints.Inaccurate diagnosis of an ocular laser injury can precipitate a costly, lengthysequence of medical and legal problems. Analysis of laser-tissue interactionsand the characteristics of unambiguous retinal laser injuries provide 6 keyquestions to facilitate difficult diagnoses. Case reports demonstrate theusefulness of answering these questions before making diagnostic decisions.Retinal laser lesions that cause serious visual problems are readily apparentophthalmoscopically and angiographically. Accidental, intentional, or clinicalretinal laser lesions do not cause chronic eye, face, or head pains. Diagnosisof a retinal laser injury should be evidence based, not a matter of conjectureor speculation.
It is well understood that accidental momentary exposure to an ordinaryflashlight beam is annoying but safe. Accidental momentary exposure to a low-powerlaser pointer beam is also annoying but safe, yet it can evoke fear or outragein some people.1- 5 Untowardresponses to real or imagined laser exposures can have complex social andpsychiatric explanations or more practical fiscal motivations. Ophthalmologistsmay be called on to determine whether a retinal laser injury is responsiblefor symptoms that reportedly follow an actual or perceived laser exposureincident. The proper analysis of those situations requires a clear understandingof the organic and psychophysical consequences of actual laser injuries, particularlywhen real but unrelated ophthalmic and systemic problems are present to confoundthe analysis.
Exposure to UV radiation (200-400 nm), visible light (400-700 nm), andinfrared radiation (700-10 000 nm) can damage the eye.6- 9 Transmissionand absorption of optical radiation by ocular media depend on the wavelengthof the incident UV radiation, visible light, or infrared radiation.10 Wavelength, pulse duration, spot size, and irradiance(power density, or laser power divided by area) determine the magnitude andlateral extent of temperature rises in exposed tissue produced by incidentlaser beams.11,12 Cornea and lensrefraction produce retinal irradiances for laser beams that are up to 105 times greater than their corneal irradiances.13 Laserradiation can damage the eye by photomechanical, photothermal, or photochemicalmechanisms.8,9,14- 16 Itis useful to differentiate between these mechanisms, but more than one effectmay be involved in any particular injury.
Photomechanical injuries are caused by extremely high laser irradiancesin very brief laser exposures ranging from hundreds of femtoseconds (10− 15 seconds) to microseconds (10− 6 seconds).Tissue is fragmented, perforated, or distorted immediately by a photomechanicalinjury.Clinical examples include photodisruption in Nd:YAGlaser capsulotomy, photoablation in excimer laser keratorefractive surgery,and photovaporization in holmium:YAG laser thermokeratoplasty for hyperopia.Powerful Q-switched industrial or military lasers can cause severeretinal injuries when their radiation is absorbed in the retinal pigment epithelium(RPE) and underlying choroid.17- 23 Intypical, accidental retinal injuries, rapid tissue expansion causes hemorrhageand prominent, permanent retinal scars.
Thermal laser injuries are produced by high laser irradiances in briefexposures ranging from microseconds to several seconds. Tissue protein coagulationoften causes immediate or delayed blanching of the laser impact site and adjacenttissue. Clinical examples include argon laser panretinal photocoagulationand trabeculoplasty. Barely visible retinal photocoagulation lesions are associatedwith retinal temperature increases of 10°C.12,24- 28 Typicalclinical photocoagulation lesions are associated with much higher retinaltemperature increases (40°C-60°C).12,24,27,28 Accidentalcornea, iris, and crystalline lens injuries have been reported in clinicalphotocoagulation.29- 34 Accidentalretinal laser lesions that produce substantial vision loss are apparent ophthalmoscopicallyor angiographically.17- 23
Photochemical injuries occur when prolonged optical radiation exposurecauses phototoxic chemical reactions in affected tissues8,16,35- 37 orwhen a previously administered exogenous photosensitizer is activated by anappropriate light source.38 Clinical examplesinclude solar and operating microscope maculopathy and verteporfin photodynamictherapy for age-related macular degeneration. Viewing intense light is veryuncomfortable. Natural protective responses, such as squinting, pupillaryconstriction, and looking away from uncomfortably brilliant light sources,protect people from phototoxic retinal injuries, except in highly unusual,prolonged viewing circumstances, such as unprotected solar eclipse observationor welding arc viewing with a defective protective filter.6,9,39
It is estimated that fewer than 15 retinal injuriesworldwide each year are caused by industrial and military lasers.17,22,40- 44 Inmost actual laser eye injuries, the laser source is known, typical chorioretinaldamage occurs, there is an unambiguous temporal relationship between a laserincident and the onset of visual abnormalities that are well correlated withretinal findingsand retinal abnormalities remodel after the incidentin a manner commensurate with their severity.
Laser eye injuries can be prevented by appropriate laser safety eyewearuse. Unfortunately, laser safety glasses or goggles partially restrict vision,interfering with visually demanding laboratory, industrial, or military tasks.In addition, laser safety goggles can be uncomfortable and can fog in hotand humid environments. Most industrial accidents occur when a misfired laserbeam enters an unshielded bystander's eye. Military injuries typically occurwhen a laser rangefinder or target designator beam is inadvertently or inappropriatelyviewed by an unprotected user or onlooker (Figure 1 and Figure 2).46,47 An ordinary laser pointer is safe,unless a user chooses to stare at its uncomfortable brilliant light for morethan 10 seconds at close range, despite eye hazard labels warning users toavoid eye exposure.1- 5 Anteriorsegment eye injuries from lasers are rare because UV and infrared lasers thatproduce radiation with considerable corneal or crystalline lens absorptionare typically used in well-controlled medical or industrial devices or environments.Most ocular laser accidents are caused by powerful Q-switched lasers thatproduce serious retinal injuries.19,20,22,42
The severity of initial vision loss after a retinal laser injury dependson the distance of the laser impact site from the center of the fovea, theextent of chorioretinal disruption, and the amount of chorioretinal bleeding.Victims of visually significant retinal laser injuries typically experiencesudden, severe decreased vision in one or, less commonly, both eyes. Theyusually notice a bright flash of light even with invisible laser beams, followedby an immediate decrease in the vision of affected eyes. They occasionallyhear a loud popping sound during a Q-switched chorioretinal laser injury.Vision may improve over several days to months. Visual prognosis is excellentif retinal findings are minor or do not involve the fovea. If the resultsof Amsler grid testing are abnormal, findings stabilize within a few months.These findings are consistent, stable, and well correlated with retinal findingsin cooperative patients.
Momentary pain may occur at the time of ocular laser injury, but onlyrarely. This pain does not persist, just as it does not persist after clinicalretinal photocoagulation. Noninjurious laser exposures and most laser injuriesare painless, but rubbing an eye after a laser exposure can cause a painfultransient corneal abrasion that individuals may attribute to laser exposure.Self-inflicted corneal abrasions are responsible for reported painful visionlosses in children after laser pointer exposures.5
The most common initial clinical finding after an industrialor military Q-switched laser injury is prominent vitreous and/or chorioretinalhemorrhage from blood vessels ruptured by tissue distortion (Figure 2).17,20- 22,40 Thenumber and size of blood vessels damaged at the laser impact site determinethe extent of initial hemorrhage.23 The locationof the vessels and the structural integrity of adjacent tissue determine howeffectively blood is tamponaded locally.23 Largeretinal areas can be rendered dysfunctional if blood spreads laterally intosubhyaloid, subretinal, or sub-RPE spaces. Persistence of hemorrhage intosubretinal spaces can cause photoreceptor deterioration.48 Retinalholes and scarring can occur at the impact site (Figure 1 and Figure 2).17,20- 22,40
Fundus photography, fluorescein angiography, and opticalcoherence tomography are invaluable for determining whether retinal injuryis present after a laser incident and, if so, whether visual complaintsare consistent with documented retinal abnormalities. Acute photomechanicalinjuries typically produce a hypofluorescent spot at the laser impact sitecaused by vitreous or associated chorioretinal hemorrhage. As the hemorrhageresolves, a hyperfluorescent window defect may develop at the site owing toRPE damage (Figure 2), with hyperfluorescentstaining of any fibrosis that develops after the injury. An RPE discontinuityor elevation is commonly seen on optical coherence tomograms immediately afterand subsequent to photomechanical injuries (Figure 2). Acute photocoagulation lesions typically have a hypofluorescentcenter with a surrounding ring of faint hyperfluorescence. If a photocoagulationlesion is sufficiently small, there may be only a tiny hyperfluorescent spotat the injury site. Fluorescein leakage in the form of staining or poolingof dye at photocoagulation sites in late angiogram frames is common immediatelyafter an injury. Acute photochemical lesions may have no angiographic abnormalities(as in mild solar maculopathy) or early hyperfluorescence with late leakage(as in operating microscope injuries).9 Visuallysignificant phototoxic lesions eventually produce angiographically apparentRPE abnormalities.
Retinal photography and fluorescein angiography should be performedas soon as possible after a suspected laser injury because there may be subvisiblelesions if laser exposure variables are below thresholds for ophthalmoscopicallyapparent lesions. These tests are also important for dating chorioretinalfindings and for determining whether concurrent systemic disease rather thanlaser injury could be their cause. Indocyanine green angiography may alsobe useful, particularly if it is performed using scanning laser ophthalmoscopy.
If there is no vitreous and/or chorioretinal hemorrhage to obscure thesite, an acute laser injury is likely to produce a lesion with some fluoresceinpooling or staining, whereas an ordinary window defect on an angiogram performedwithin a week of a laser incident is more likely to be due to previous trauma,inflammation, or other natural processes. The possibility of preexisting orconcurrent eye or systemic problems makes it important to obtain a completemedical history and review of systems in cases of possible retinal laser injury,in addition to carefully reviewing copies of past medical records and retinalimaging if available.
Incidental angiographic findings should not be overinterpreted.For example, tiny RPE window defects occur routinely in angiograms with normalfindings. In a small series of 50 consecutive fluorescein angiograms reviewedby one of us (M.A.M.), two thirds of the contralateral normal eyes of individualswith unilateral retinal problems had 1 or more tiny RPE window defects. TheRPE is its own record of a lifetime of infection, trauma, inflammation, andother natural events. A few scattered RPE imperfections are neither surprisingnor conclusively diagnostic of laser injury.
The diagnosis of a laser injury can have considerable legal, financial,and medical consequences. It should be based on objective medical evidencerather than on unscientific speculation. Medicolegal problems arise when aninjury is alleged but objective findings are absent, within normal limits,or explainable by unrelated medical problems. The ease of diagnosing an actuallaser injury is directly proportional to its severity. The answers to 6 facilitatingquestions are useful for diagnosing less severe or absent injuries after areal or imagined laser accident (Table 1). If the answer to question 1 is "no," then no visually significantlaser injury has occurred. If the answers to all 6 questions are "yes," thena laser injury has almost certainly occurred.
Proper evaluation of a laser injury demands an exhaustive review ofsystems and medical history to rule out ocular or systemic causes for theophthalmic and somatic complaints ascribed to a purported laser exposure.In suggestible or otherwise susceptible individuals, pain can represent anindividual's somatization of a perceived although not organic ocular injury.Differentiating the psychiatric, financial, or other origins of nonorganicdisorders is a challenging problem,49- 60 butperceived ocular injuries with no demonstrable tissue damage are not reallaser injuries.
An 11-year-old girl stared at a red laser pointer beam held close toher right eye for more than 10 seconds to satisfy the curiosity of classmateson a school bus who wanted to know if her pupil would constrict.61 Sheexperienced no pain but developed decreased vision and a central scotoma immediatelyin her right eye. Three weeks later, a retinal evaluation revealed centralfoveal pigment mottling with corresponding faint hyperfluorescence on fluoresceinangiography. These findings became less prominent during the next 3 monthsas her scotoma resolved, and her uncorrected visual acuity returned to 20/25OD, the same as in her unaffected left eye. She had no other ocular abnormalitiesin her right eye. In addition, this patient had no recent history of infection,inflammation, or mechanical trauma and no contributory past systemic or ocularhistory.
This 11-year-old girl probably experienced a 5-mW, 10-second, 50-µmretinal spot diameter exposure that produced a 6° to 10° retinal temperaturerise with a retinal irradiance of 160 W/cm2 of diode 635-nm redlight.5,62 In comparison, clinicalphotocoagulation for diabetic retinopathy can be performed with a 200-mW,0.2-second, 200-µm retinal spot diameter exposure that produces a 40°to 60° retinal temperature rise with a retinal irradiance of 325 W/cm2 of argon laser 514-nm green radiation.62 Subvisiblelesion transpupillary thermotherapy for occult choroidal neovascularizationin age-related macular degeneration can be performed with an 800-mW, 60-second,3-mm retinal spot diameter exposure that produces a 10° retinal temperaturerise with a retinal irradiance of 7.5 W/cm2 of diode laser 810-nminfrared radiation.62
Laser pointers sold in the United States are required to have an outputpower less than 5 mW.1,2,5,63 Accidentalmomentary laser pointer exposure is safe because it is terminated in lessthan 0.25 second by normal aversion responses to uncomfortably brilliant light.1,2,5,64,65 Prolongedviewing of a laser pointer beam for more than 10 seconds is potentially harmful,1 which is the reason that these devices have warninglabels. Retinal irradiance produced by a laser pointer held close to the eyeis high because much of its power enters the eye and is concentrated intoa small retinal spot. Conversely, heat conduction cools small retinal spotsmore effectively than large ones, so retinal temperature rises for small-spot,10-second laser pointer and large-spot, 60-second transpupillary thermotherapyexposures are comparable.11,24,62 Thus,the most likely mechanism for the documented retinal damage caused by thislaser pointer exposure is threshold transpupillary thermotherapy–typephotocoagulation. In this case, the answers to all 6 diagnostic questionsgiven in Table 1 are "yes,"and this episode is a case of laser injury.
A prankster with a laser pointer momentarily exposed a middle-aged workerto the beam of an ordinary laser pointer from a distance of 9 m. The worker'svisual acuity after the incident was 20/20 OU. In the 4 years after the episode,the worker developed headaches, progressive photophobia, and severe sharpand longer-lasting dull eye pains. His photophobia was disabling even whenwearing sunglasses at ordinary indoor illumination levels. Visual field testsinitially documented unilateral hemianopsia, although findings from magneticresonance imaging were normal. Fluorescein angiography and eye examinationsby numerous ophthalmologists immediately after and subsequent to the episodedid not identify organic disease other than dry eye syndrome. The worker wasthen seen by a neuro-ophthalmologist, who diagnosed him as having photo-oculodyniasyndrome66 and attributed the origin of hispain, photophobia, and headaches to previous laser pointer exposure. The prankster'sfoolishness, the neuro-ophthalmologist's speculation that momentary laserpointer exposure can cause photo-oculodynia syndrome, and the worker's excellentemployment record and reported absence of health or occupational problemsbefore the incident probably influenced the defendant to settle this worker'sdamage claims out of court.
Laser pointers are poor optical devices that contain a simple, inexpensivelens that collimates its diode laser's divergent, astigmatic beam. Assumingthat a laser pointer beam has a full 5-mW output and a standard beam divergenceof 1.5 milliradian, only 7% of the laser beam would enter a 4-mm-diameterpupil at a distance of 9 m. This exposure would produce a physiologic retinaltemperature rise of only 0.4°C, which could not cause retinal injury.Furthermore, at a distance of 9 m from an artificial pupil, a laser pointercan be aimed through a 7-mm aperture at best only 25% of the time (B.E.S.,D. J. Lund, BS, H. Zwick, PhD, D. A. Stamper, MS, P. R. Edsall, BS, J. W.Molchany, BS, unpublished data, 1999). Normal head movements and hand movementsreduce any retinal exposure even more, so a laser pointer injury from a distanceof 9 m is impossible without pupillary dilation and mechanically restrainingand aligning both the laser pointer aperture and the observer's pupil formore than 10 seconds.
We could find only a single article66 inthe medical literature on photo-oculodynia syndrome, which is described as"a category of chronic eye pain triggered by even minor ocular trauma, whenthere is no evidence of ongoing tissue damage or inflammation." The term wasproposed as an alternative to the standard term "photophobia."66 Only6 individuals with this condition were described in the article,66 3of whom reported less discomfort after cervical sympathetic ganglion block.There is no scientific basis for the neuro-ophthalmologist's speculation thata complex ocular pain syndrome could be induced by brief, nondamaging lightexposure. If that were the case, there would be millions of people with photo-oculodyniasyndrome due to flash photography and laser eye surgery. In this case, theanswers to diagnostic questions 1 and 6 in the Table 1 are "no," and this episode is not a case of laser injury.
A young male soldier viewing the exit aperture of a laser rangefinderthat he was holding accidentally exposed his right eye to several powerfulQ-switched, 1064-nm laser pulses.20 He reportedno pain but noticed an immediate decrease in vision in his right eye. Ophthalmicexamination 24 hours later revealed vitreous hemorrhage overlying 2 retinalholes in his right fovea. Fluorescein angiography 5 days after the incidentdocumented 3 prominent chorioretinal lesions with surrounding hyperfluorescence.Central macular scarring progressed in his right eye, and his visual acuity18 months after the laser exposure was 20/400 OD.
Military Q-switched laser rangefinders and target designators are hazardousdevices with radiation outputs that far exceed maximum permissible exposurelevels.20,44,63 Injuriesto users and bystanders continue to occur infrequently despite careful precautionsand safety training. In this case, the answers to all 6 diagnostic questionsin the Table 1 are "yes," andthis episode is a case of laser injury.
A 40-year-old male soldier observed 3 red light pulses emitted in 3seconds by a tank approximately 3 km from his helicopter. He reported oculardiscomfort for approximately an hour after the mission. These symptoms wererelieved by acetaminophen use and did not recur. His visual acuity was 20/20OU after the incident and when tested several times during the next 5 years.The soldier experienced metamorphopsia 7 years after the episode. He soughtmedical care 2 years later, concerned that he might be going blind from alaser exposure. When examined at that time, his uncorrected visual acuitywas 20/20 OD and 20/50 OS, improvable to 20/20 OS, where his responses wereslower. Findings from anterior segment examination were normal, but therewere numerous yellow flecks in each macula, approximately 50 to 100 µmin longest lateral extent. A foveal fleck was present in both eyes. Earlyfluorescein angiogram frames documented that the flecks had central hypofluorescencewith a surrounding zone of hyperfluorescence. The hyperfluorescence fadedin later images.
The soldier did not undergo a thorough retinal examination or retinalimaging studies until 9 years after the tank observation incident. At thattime, ophthalmoscopy and fluorescein angiography documented pattern RPE dystrophy.67- 69 We know of no scientificevidence to suggest that this problem is caused or accelerated by light exposure.The tank that the soldier observed was probably equipped with a Q-switchedruby laser (694.3-nm, red) rangefinder. Q-switched retinal laser injuriestypically cause immediate vision loss and a prominent, permanent chorioretinalscar. The soldier did not have vision loss after the incident or a chorioretinalscar consistent with laser injury. Furthermore, the type of ruby laser rangefinderknown to be on the kind of tank he observed produces a retinal exposure farbelow international safety standards at a 3-km viewing distance.63,70 Inthis case, the answers to questions 1 and 6 in the Table 1 are "no," and this episode is not a case of laser injury.
A middle-aged photographer had pain from a corneal abrasion after takingphotographs of a ship. He surmised that there had been a laser device on theship and that a laser injury had caused his discomfort. His visual acuitywas 20/20 OU after the episode. A retina specialist found 3 tiny (10- to 20-µm)RPE window defects in one eye on a fluorescein angiogram and ascribed themto laser injury. Findings from optical coherence tomography were normal. Amslergrid test results were highly variable, and the locations of grid abnormalitiesand RPE defects were inconsistent.
During the next 5 years, the photographer developed chronic headaches,photophobia, blurred vision, and nighttime driving and reading difficulties.He reported episodes of monocular diplopia. He also reported a constellationof terrible, intermittently disabling, periodic, and chronic eye and facepains. The initial retina specialist ascribed all these symptoms to laserinjury. He also diagnosed a laser exposure in one of the photographer's companionspresent at the incident who reported similar symptoms but had completely normalfindings on retinal examination and fluorescein angiograms.
A review of the photographer's voluminous medical history several yearsafter the episode revealed dry eye syndrome, map-dot-fingerprint corneal dystrophy,temporomandibular joint syndrome, iritis, conjunctivitis, migratory arthritis,plantar fasciitis, chronic low back pain, epididymitis, and recurrent diarrhea.Most of the systemic problems predated the purported laser incident. New RPEdefects developed after the incident. The photographer had not been diagnosedpreviously as having reactive arthritis (Reiter syndrome),71 whichcan produce small RPE defects.72,73 Noevidence of laser injury was found in the years after the incident by 17 otherophthalmologists, including 5 neuro-ophthalmologists and 8 retina specialists.A trial was held 5 years after the incident in which the retina specialistwho made the initial diagnosis steadfastly maintained that all the photographer'ssymptoms were due to retinal laser injury. A jury ruled against the photographer'sclaim for damages against the ship owner.
No laser was ever identified in this case despite a search of the ship.A costly, time-consuming chain of events was precipitated by the initial retinaspecialist's (1) failure to attach significance to an association betweenthe photographer's symptoms and his complex past medical history, (2) quickdiagnosis of a laser injury, (3) subsequent attribution of the photographer'sgrowing list of pains and visual complaints to a laser injury, and (4) diagnosisof laser exposure in the photographer's associate based on symptoms in theabsence of retinal or angiographic abnormalities. As noted previously herein,the few tiny RPE defects on which the initial diagnosis was based are common.Even if these defects were due to threshold laser effects, they could nothave caused the photographer's reported problems or millions of patients wouldbe afflicted with similar problems after routine retinal laser surgery. Inthis case, the answer to question 1 in the Table 1 is "yes." Regarding question 2, there were angiographicfindings but no optical coherence tomography abnormalities. The answers toquestions 3, 4, and 5 are "no." Question 6 cannot be answered because therewas no known laser source. The patient had real complaints, but they werecaused by preexisting autoimmune problems rather than by laser injury.
Accidental laser injuries are rare. Complaints of laser injuries aremore numerous. The ease of laser injury diagnosis is proportional to the severityof the injury. In ambiguous cases, subtle retinal findings should have excellentvisual prognoses and clinical outcomes. Absence of a retinal lesion does notprove absence of laser exposure. Nonetheless, retinal laser lesions that causeserious visual problems are readily apparent ophthalmoscopically and angiographically.They remodel in the months that follow an injury. Actual retinal laser injuriesdo not cause chronic eye, face, or head pains. Thus, pains in the months thatfollow a real or imagined retinal laser injury are nonorganic or the resultof regional or systemic problems unrelated to the laser incident. Fundus photography,fluorescein angiography, and optical coherence tomography should be performedas quickly as possible after a laser incident to document findings for analysisand comparison with subsequent tests.
The legal system has an uneasy relationship with "science" and "truth."Facts are welcomed by the attorneys of plaintiffs and defendants only whenthey support their clients' biases and best interests. Medical "experts" arehired to advocate opinions that are often unrelated to evidenced-based medicalpractice. Juries struggle to separate reality from fiction. Attorneys maycraft convincing cases for "victims" who claim severe pain and vision losseven when they have no physical evidence of injury. Patients with severe nonorganicproblems of psychiatric origin or organic problems originating from problemsunrelated to an injury may be dissuaded from solving these problems by hopesof financial gain.
A clinician's intransigence and misunderstanding of laser injury characteristicscan be powerful allies of tort attorneys. When retinal laser injuries arealleged but uncertain because objective findings are minimal or absent, laserinjury diagnosis should be deferred pending completion of a rigorous reviewand analysis of relevant laser devices and the purported victim's medicalhistory, clinical course, ophthalmic examination findings, and retinal imagingstudy results. Such a review and analysis may take weeks or months to completeauthoritatively. Hasty diagnoses should be avoided because they can createserious and lengthy medical, legal, and social issues. The 6 key diagnosticquestions given in the Table 1 providea framework for evaluating potential laser injuries. The diagnosis of a laserinjury should be evidence based, not a matter for speculation or conjecture.Retinal laser injuries do not cause chronic pain, and visually significantretinal laser injuries are apparent ophthalmoscopically and angiographically.
Correspondence: Martin A. Mainster, PhD, MD, Department of Ophthalmology,University of Kansas Medical School, 3901 Rainbow Blvd, Mail Stop 3009, KansasCity, KS 66160-7379 (firstname.lastname@example.org).
Submitted for publication August 4, 2003; final revision received February12, 2004; accepted March 25, 2004.
This study was supported in part by the Kansas Lions Sight FoundationInc (Manhattan).