The emergence of high resolution optical coherence tomography (OCT) along with evidence showing
beneficial effects of anti-inflammatory drugs for retinal edema and neovascularization suggests a rational
plan for the diagnosis and management of patients with acute laser eye injury. We review the results of
recent experiments we conducted to evaluate treatment of laser lesions followed by reports of two cases of
acute laser eye injury with foveal involvement. The initial presentation of these cases was notable for the
lack of significant abnormalities on fluorescein angiography whereas OCT readily disclosed the size and
extent of retinal involvement from exposure to laser energy. Prompt referral of these cases resulted in rapid
initiation of medical therapy which included a 10-14 day combined course of steroid and non-steroidal anti-inflammatory
medication. An initial decrease in Snellen visual acuity of approximately two lines (20/25- to
20/30) was noted on presentation. In both cases, a measurable improvement of visual acuity was noted by
two weeks post injury. The use of anti-inflammatory medication may enhance the initial recovery of vision
and reduce the likelihood of longer term retinal complications from scarring and neovascularization.
The diagnosis of a laser-induced eye injury occurring in occupational or military environments is often complicated by confounding symptoms, the possibility of pre-existing pathology, and/or a lack of visual deficits that can be clearly associated with a specific incident. Two recent cases are described that illustrate the importance of a thorough differential diagnosis when coexisting retinal pathologies are present with potentially different (e.g. laser or disease) etiologies. Indocyanine green angiography (ICG) and ocular coherence tomography (OCT) used in combination with standard ophthalmic imaging can provide helpful insights as to the etiology of these lesions. Vascular choroidal abnormalities such as hemangiomas or occult histoplasmosis infection can produce findings that can mimic the leakage that may be evident from neovascular membranes associated with laser injury. Further evaluation with OCT and conventional fluorescein angiography (FA) is helpful to look for the classic signature of retinal disruption and retinal pigment layer changes that are often present in association with laser injury. Furthermore, a careful situational assessment of a potential laser exposure is important to confirm the diagnosis of laser-induced eye injury.
Due to the increasing number of optic systems that military personnel are exposed, the development of countermeasures for laser eye injury is of significant concern. Recent reports in the literature suggest some benefit form the use of Light Emitting Diode (LED) therapy on the retina that received a toxic insult. The purpose of this study was to compare retinal cell survival and multifocal electroretinography (mfERG) in a laser retinal injury model following treatment with LED photoillumination. Control and LED array (670 nm) illuminated cynomolgus monkeys received macular Argon laser lesions (514 nm, 130 mW, 100 ms). LED array exposure was accomplished for 4 days for a total dose of 4 J/cm2 per day. Baseline and post-laser exposure mfERGs were performed on most of the subjects. Ocular tissues were collected from four animals at Day 4 poast laser exposure and from two animals at 4 months post laser exposure. The tissues were processed for plastic embedding. Retinal cell counts were performed on the lesion sections. Analysis of Variance (ANOVA) results yielded no significant difference in the sparing of photoreceptors, inner nuclear and ganglion cells between the control and LED illuminated subjects. Although pathology showed no significant support for diode therapy, our early mfERG observations previously reported suggested a more rapid functional recovery. Since there is still no uniform therapy for laser retinal injury, research is continuing to determine novel therapies that may provide retinal cell sparing and functional retinal return.
There is no uniformly accepted objective method to diagnose the functional extent of retinal damage following laser eye injury and there is no uniform therapy for laser retinal injury. J.T. Eells, et al, reported the use of Light Emitting Diodes (LED) photoillumination (670 nm) for methanol-induced retinal toxicity in rats. The findings indicated a preservation of retinal architecture, as determined by histopathology and a partial functional recovery of photoreceptors, as determined by electroretinogram (ERG), in the LED exposed methanol-intoxicated rats. The purpose of this study is to use multifocal electroretinography (mfERG) to evaluate recovery of retinal function following treatment with LED photoillumination in a cynomolgus monkey laser retinal injury model. Control and LED array (670 nm) illuminated animals received macular Argon laser lesions (514 nm, 130 mW, 100 ms). LED array exposure was accomplished for 4 days for a total dose of 4 J/cm2 per day. Baseline and post-laser exposure mfERGs were performed. mfERG results for five animals post-laser injury but prior to treatment (Day 0) showed increased implicit times and P1 waveform amplitudes when compared to a combined laboratory normal and each animal's baseline normal values. In general, preliminary mfERG results of our first five subjects recorded using both the 103-hexagon and 509-hexagon patterns indicate a more rapid functional recovery in the LED illuminated animal as compared to the control by the end of the fourth day post-exposure. Research is continuing to determine if this difference in functional return is seen in additional subjects and if statistical significance exists.
Purpose: To determine funduscopic criteria that will help predict when bridging choroidal neovascular (CNV) complexes will develop after laser retinal trauma and to define early preventive treatment targets.
Methods: Ten rhesus monkeys were used and retinal lesions were produced by Nd:YAG exposures (20ns, 1-2mJ, 1064nm, min. spot size) simulating human accidental laser trauma to the central fundus. Funduscopy and fluorescein/ICG angiography were conducted at day 1, 4, and 14, and at 2 and 4 months, and animals terminated for histologic evaluation. Predisposition for bridging fibrovascular complexes was evaluated for single lesions, two small lesions showing coalescing hemorrhages, and multiple lesions involved with large field subretinal and vitreous hemorrhages.
Results: Elevated CNVs were present in all single lesions with confined subretinal hemorrhages. All lesion sets that showed initial and small coalescing subretinal hemorrhages formed bridging CNV scars. No bridging CNVs occurred in lesion sets involving a vitreous hemorrhage adjacent to a confined, but small subretinal hemorrhage. In large field subretinal hemorrhages involving multiple laser lesions, complex CNV formation occurred. Extensive secondary photoreceptor losses occurred in confined hemorrhage and CNV zones.
Conclusion: Trauma presenting with evidence of coalescing and confined subretinal hemorrhages between two adjacent lesions has a high chance of forming choroidal neovascular bridge complexes between the involved lesions. CNV formation may be related to the long residence time, break down products, and clearance processes of extravasated blood. Removal of trapped blood and curtailing angiogenesis and cellular proliferation may be helpful treatment strategies.
Purpose: To evaluate long term deficits in human color discrimination induced by accidental laser macular damage and assess potential for recovery of color vision deficits.
Methods: Nine laser accident cases (Q-switched Neodymium) presenting initially with confined or vitreous macular hemorrhage were evaluated with the Farnsworth-Munsell 100 Hue test within 2 days to 3 months post exposure. Both total as well as partial errors in the blue/yellow (B/Y) and red/green (R/G) regions were assessed. Independent assessment of axis orientation and complexity were obtained via a Fourier series expansion of error scores. Comparisons of both total and partial B/Y and R/G errors were made with age matched normal subjects, idiopathic and juvenile onset macular holes. Confocal Scanning Laser Ophthalmoscopy and Optical Coherence Tomography characterized the presence of retinal traction, intraretinal scar, macular thickness and macular hole formation.
Results: Comparison of exposed and non-exposed age matched individuals were significant (P<.001) for both total and partial errors. In four cases where macular injury ranged from mild scar to macular hole, color discrimination errors achieved normal levels in 1 to 12 months post exposure. A mild tritan axis, dominant B/Y ("blue/yellow") errors, and retinal traction were observed in a macular hole case. At 12 months post exposure, traction about the hole disappeared, and total and partial errors were normal. Where damage involved a greater degree of scarring, retinal traction and multiple injury sites, long term recovery of total and partial error recovery was retarded with complex axis makeup. Single exposures in the paramacula produced tritan axes, while multiple exposures within and external to the macula increased total and partial R/G ("red/green") error scores. Total errors increased when paramacular hole enlargement induced macular traction. Such hole formation produced significant increases in total errors, complex axis formation and increased amplitude in higher Fourier error expansion components.
Conclusion: Color discrimination losses reflect the distribution of different cone systems in and about the macula and their selective loss. When secondary damage is minimal, color discrimination deficits recover within 12 months post exposure. When macular scarring and retinal traction are severe, recovery is significantly retarded. Laser induced macular holes may affect color discrimination less when retinal scar and traction are small but may become equivalent with that of idiopathic and juvenile species when scar and traction are severe.
Choroidal perfusion was evaluated following the creation of a laser induced macular hole in a nonhuman primate model. Two Rhesus monkeys underwent macular exposures delivered by a Q-switched Nd:YAG laser. The lesions were evaluated with fluorescein angiography and indocyanine green (ICG) angiography . Each lesion produced vitreous hemorrhage and progressed to a full thickness macular hole. ICG angiography revealed no perfusion of the choriocapillaris beneath the lesion centers. Histopathologic evaluation showed replacement of the choriocapillaris with fibroblasts and connective tissue. Nd:YAG, laser-induced macular holes result in long term impairment of choroidal perfusion at the base of the hole due to choroidal scarring and obliteration of the choriocapillaris.
Thirty-seven New Zealand Red rabbits were either dosed with methyiprednisolone sodium succinate (MP, n18) about 20 nun before laser irradiafion, or they were left untreated (n=19). Dosing with MP was tapered at 30, 30, 20, 20, and 10 mg/kg/day for five consecutive days. Retinas were irradiated with a multi-lime argon laser to produce retinal injuries (grid of 16 lesions/eye) near hemorrhaging levels (285 mW/lOmsec, 290 ?m retinal spot size). A variety of funduscopic and histologic assessments were made for hemorrhagic and non-hemorrhagic lesions from 10 miii to 6 mo after injury. Fluorescein angiography showed that non-hemorrhagic control lesions stopped leaking at 3d post injury, but MPtreated lesions leaked for 2-4 days longer. After MP treatment, funduscopic lesion areas were similar to controls during the first 24 h then became smaller by 1 mo. After 1 mo, MP-treated lesions increased in area while controls became reduced. Histologic analysis showed no effect on reduction of neutrophils (PMN) in MP-treated lesions over controls at 3 hr. At 24 hi, retinal PMN values in hemorrhagic lesions ofthe MP group were elevated (p<0.05) while monocyte/macrophage counts were reduced (p<0.05) compared to control. At 4d, MP impeded replacement oflost retinal tissue, and contributed to retinal hole development at 1 mo followed by extensive enhancement of chorio-retinal scarring at 6 mo. In severe laser-induced retinal trauma, the immunosuppressive effects of high dose MP therapy contributed to a variety of untoward wound healing outcomes, thereby suggesting caution in its use to treat similar injuries in humans.
The rising number ofapplications ofultrashort laser systems presents new challenges in laser safety. Retinal damage studies have demonstrated that less energy is required to create a retinal burn for pulses shorter than one nanosecond than for pulses longer than one nanosecond. 1-3 Furthermore, as laser systems become more complex, the potential for accidental injury increases. In this paper we report the accidental injury from a Ti:Sapphire amplifier system delivering 100 picosecond pulses. The circumstances leading to the binocular injury included the use of inadequate eye protection, a defective amplifier crystal and the very dim appearance of 800 nm light. Ophthalmologists evaluating patients with laser eye injury should be prepared to discuss the physiology ofthe injury and prognosis with their patients.
The increasing number oflaser applications in military and industrial settings has resulted in a rising number of laser eye injuries. Laser-induced macular holes are one type of injury, usually caused by accidental exposure to radiation from a Q-switched Nd:YAG laser operating at 1 064 nm. Laser-induced macular holes share many features with idiopathic macular holes. Optical coherence tomography was employed in the evaluation oftwo patients with laserinduced macular holes. Tomographic features were compared with those found in patients with idiopathic macular holes. An animal model of laser-induced macular hole was also evaluated in order to elucidate the histologic correlation ofthe OCT findings.
Two Q-switched military accident cases involving foveal retinal damage were followed for at least two years with a variety of morphological and functional diagnostic techniques. Both cases demonstrated remarkable recovery of visual acuity and contrast sensitivity within 1 to 4 months post exposure. Early deficits in visual acuity, sine wave contrast sensitivity, various measures of color vision, and focal electrophysiological measures all showed remarkable recovery. With the use of a scanning laser ophthalmoscope (SLO), we were able to further evaluate the retinal preference threshold contrast targets and found that small targets requiring foveal resolution were initially placed superior and slightly temporal to the damaged fovea in these eyes, even though visual acuity in these eyes was 20/15 or better. In one of these cases, a return to foveal functionality was demonstrated even though the fovea appeared lightly scarred small test targets were placed at its center for detection. In the second case, the PRL stayed superior temporal. Attempts to force target resolution in this area were unsuccessful. These findings suggest a more active role of neural retinal plasticity in the damage recovery process as well as caution in assuming that all such injuries will exhibit such plasticity.
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