From the Vitreo-Retinal Unit, Al-Bahar Eye Center, Ibn-Sina Hospital, Safat, Kuwait.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Seemant Raizada, Vitreo-Retinal Unit, Al-Bahar Eye Center, Ibn-Sina Hospital, P.O.Box-25427, Safat-13115, Kuwait.
The increased use of lasers in industry, science and medicine has led to increase in number of accidental laser injury to the eye.1–4 Laser may interfere with vision temporarily or permanently depending on the wavelength, power and duration of exposure. Commonest reported cause of accidental laser injury is by laser pointers though it rarely causes permanent visual disturbance or loss. Laser poses a significant threat to vision in modern industrial and military operations. Anti-personnel lasers have been designed that can cause intentional blindness. Accidental blinding can also result from other types of lasers used on the battlefield, such as range-finders and anti-material lasers.4 Retinal laser injuries are easily diagnosed when there are known laser sources, typical macular injuries, and visual deficits consistent with retinal findings. Lasers that are capable of producing blindness operate within specific wavelength parameters and include visible and near infrared lasers. Patients who suffer from laser eye injuries usually complain of flash blindness, followed by transient or permanent visual loss.
We report two cases of retinal injury suspected to be caused by exposure to laser outside hospital setting.
A 27-year-old man reported to retina clinic with a complaint of decrease in vision in right eye for a period of 2 days. He was employed as an inventory clerk in the fire arms store in an army base. He gave a history of alleged exposure to some kind of strong light when he was handling an electronic item. According to him, he was looking for the serial number on that object to record in the inventory register. Since he was a civilian employed in the store, he did not know what that object was. On examination, his visual acuity was 20/400 in right eye and 20/20 in left eye. Slit lamp examination was unremarkable. Intraocular pressure was 16 mm Hg in both eyes. Fundus examination revealed clear media in right eye with normal disc. In the macular area, there were 6 whitish round lesions starting from fovea and going inferio-temporal. (Figs. 1A and 1B). The retina was edematous and there was a streak of hemorrhage around the lesions. Left eye fundus was within normal limits. Fluorescein angiography (FFA) showed blocked fluorescence in the early phases (Fig. 1C) and mild staining of the lesions in later phases (Fig. 1D). Visual field mapping in right eye showed central scotoma. Optical Coherence Tomography (OCT) readings were unremarkable. No active treatment was advised and the patient was asked to follow up. When last seen 6 months post-laser injury, his best corrected visual acuity was 20/200 in right eye and 20/20 in left eye. Slit lamp examination was unremarkable. Fundus examination showed juxta foveal scars at the level of retinal pigment epithelium (RPE) in right eye. There was no evidence of choroidal neovascular membrane (CNVM) on FFA.
Figure 1. (A, B) Six Whitish Round Lesions in Macular Area Starting from Fovea and Going Inferio-Temporal. (C) Fluorescein Angiography Showed Blocked Fluorescence in the Early Phases. (D) Mild Staining of the Lesions in Later Phrases.
A 33-year-old man was seen in casualty unit after his complaint of decrease in vision in right eye due to alleged exposure to the laser beam emitted from a red laser pointer. Patient stated that he was in a shop in scrap yard and he directed the device to his eye. He stared into the red light to check if it was working. The case was seen by an ophthalmologist in a peripheral clinic few hours after the alleged laser injury but his complete examination and assessment was done in a tertiary center 6 days after the injury. On examination, his vision was 20/40 in right eye and 20/20 in the left eye. Slit lamp examination was unremarkable. Intra ocular pressure was 18 mm Hg. Fundus examination revealed grayish white spot close to fovea in right eye (Figs. 2A and 2B). Fundus examination in left eye was normal. Amsler grid study in the right eye revealed a central scotoma involving the central 2 degrees of vision. Anterior segment was normal in both eyes. Fundus examination of the right eye by an ophthalmoscope revealed pigment clumping in the central fovea with loss of the central foveal reflex. FFA of the right eye demonstrated a mild early transmission defect in the foveal region without late staining (Figs. 2C and 2D). Fluorescein pattern in the left eye was normal. The patient refused to follow up in the tertiary center (Retina Clinic) as he felt he was fine and was following up with ophthalmologist near his residence. His recent reported (7 months after alleged laser injury to retina) vision was 20/20 in right eye with no scotoma in visual field assessment. Slit lamp examination was unremarkable. Fundus examination in right eye showed juxta foveal RPE mottling (personal communication with treating ophthalmologist).
Figure 2. (A, B) Fundus Examination Revealed a Grayish White Spot Close to Fovea in the Right Eye. (C, D) Fluorescein Angiography of the Right Eye Demonstrated a Mild Early Transmission Defect in the Foveal Region Without Late Staining.
A number of retinal injuries are caused by industrial and military lasers7,8 each year worldwide. Light-induced damage to the retina occurs through three general mechanisms involving thermal, mechanical, or photochemical effects. In most actual laser eye injuries, the laser source is known, typical chorio-retinal damage occurs, there is an unambiguous temporal relationship between a laser incident and the onset of visual abnormalities that are well correlated with retinal findings. Exposure to UV radiation (200 to 400 nm), visible light (400 to 700 nm), and infrared radiation (700 to 10 000 nm) can damage the eye.9–10 Trauma, inflammation, and some chorioretinal conditions can produce retinal findings similar to threshold laser injuries.11 Wavelength, pulse duration, spot size, and irradiance (power density, or laser power divided by area) determine the magnitude and lateral extent of temperature rise in exposed tissue by incident laser beams.11 Lasers are classified in the following four categories. Class 1 systems are deemed eye safe. Class 2 systems must emit visible radiation (400 to 780 nm) and have an upper limit of output power of 1 mW. Class 3 systems are divided into 3A and 3B, with upper limits of emission of 5 mW and 500 mW, respectively. 3A systems are supposed to be safe because blinking and aversion responses will ensure that insufficient energy enters the eye and hence do not cause irreversible damage. Class 3B systems have the potential to cause significant eye damage. Class 4 systems have a radiant emission in excess of 500 mW and are capable of causing serious irreversible damage. Ophthalmic surgical lasers are Class 4 systems.
Our first case was an example of accidental retinal injury by a laser device used in military war-fare. Lasers are used to mark the targets for the laser-guided munitions. They are also used in tactical training (Multiple Integrated Laser Engagement System-MILES) and to point small arms while using night vision goggles. Laser range finders and target designators emit levels of light that are capable of causing blindness. The way it was described by the patient seemed that it was most probably a range finder. A laser range-finder is a device that uses a laser beam to determine the distance to a reflective object. The common form of laser range-finder operates on the time of flight principle by sending a laser pulse in a narrow beam towards the object and measuring the time taken by the pulse to be reflected off the target and returned to the sender. Most range finders are Q-switched, Neodynium:YAG (Nd:YAG) laser of 1064 nm wavelength. Harrris et al.4 reported 10 cases of accidental laser eye injury from US army between 1984 and 2000. In his series, he found that none of the patients were wearing any eye protection goggles. Inadequate training to the military personnel and faulty equipment design were major factors causing this injury. Roider et al.12 reported a case of macular injury by a range finder. This patient later on developed a CNVM, which is a known late complication in retinal laser injury. Douglas et al.13 reported a case of spontaneous closure of macular hole following accidental laser injury. Our patient did not develop any of the above-mentioned complications when seen last 6 months postexposure to laser. But his vision remained low at 20/200 with formation of an RPE scar.
Case number 2 had an accidental exposure to an alleged laser device in junk yard shop. We asked the patient to go back to that shop to bring that laser device, but by that time that device had already been bought by some other unsuspecting individual. It could have been a red laser pointer but potential laser pointer injuries require willing participants who choose to endure the discomfort of prolonged fixation of brilliant light. The clinical examination and circumstantial evidence of looking into a suspected laser device and sudden decrease in vision following exposure to unknown light prompted us to diagnose it as a possible laser injury. Fundus examination and fluorescein angiogram of the right eye also indicated towards a recent retinal damage. It has been reported by studies on experimental animal models that there is a possibility of retinal photocoagulation in an eye with clear ocular media by staring at a class 3A laser beam for more than 10 seconds.14 Unfortunately, children may do this as a part of a game and hence are at greater risk for laser injury because of their clear ocular media. Clive et al.15 reported a case of 11-year-old girl with macular injury due to handheld diode laser pointer. This girl presented with 20/60 vision in the affected eye, which improved to 20/25 over a period of 11 months. Luttrull et al.16 reported a case of alleged laser injury by a laser pointer in a 34 year old man who deliberately gazed into a laser pointer beam for 30 seconds. The patient reported a transient central scotoma in affected eye though his visual acuity was 20/20. Most diode laser pointers provide 635, 650, or 670 nm red light. More expensive 532 nm green light laser pointers use a diode-pumped, frequency-doubled, neodymium-crystal laser. Permanent visual loss in unlikely due to laser pointer but with millions of inexpensive laser pointers being manufactured with variable quality control, they cannot be inspected individually. Hence, some maybe mislabeled as class 3A laser devices even though they have output powers ranging from 6 to more than 10 mW. Another possibility of the source of laser in case number 2 could be by laser used in military warfare. Kuwait as such is not involved in any direct military confrontation, but is close to Iraq where active combat situation exist. It is quite possible that some military warfare find their way into the local junk market.
Not much is available in published literature regarding treatment for retinal laser injuries in human subjects. The main focus of all the reported treatment modalities is towards the abolishment of CNVM, which is a late sequela of laser injury. It has been reported that Photodynamic therapy (PDT) and intra vitreal injection of Ranibizumab are useful in cases with laser-induced CNVM in monkeys.17 The data indicate that an intravitreal ranibizumab injection in combination with PDT causes a greater reduction in angiographic leakage than PDT alone in experimental choroidal neovascularization. Roider et al.12 in a case of accidental range finder laser injury with vitreous hemorrhage, injected 50 micrograms of tissue plasminogen activator (TPA) and 0.5 mL pure C2F6 in the vitreous. The authors concluded that intravitreal injection of TPA and C2F6 do not show a clear benefit to such laser lesions. Our cases did not have any of the above-mentioned clinical features (CNVM or vitreous hemorrhage) so no treatment was advised to the patients. A number of other medical treatments are also reported in animal experimental models. Rosner et al.18 developed a rat model for studying the efficacy of neuro-protective compounds in ameliorating laser-induced retinal damage. Four compounds were evaluated: the corticosteroid methylprednisolone, the glutamate-receptor blocker MK-801, the anti-oxidant enzyme superoxide dismutase, and the calcium-overload antagonist flunarizine. The authors concluded that Methylprednisolone and MK-801 reduce laser-induced retinal damage, whereas both superoxide dismutase and flunarizine were ineffective. There are other reports also, indicating effectiveness of steroids and non steroidal anti inflammatory drugs (NSAIDS)19,20 in laser-induced retinal injury. Certain new drugs like lumiracoxib21 (a highly selective cyclo-oxygenase-2 (COX-2) inhibitor that exhibits anti-inflammatory and antiangiogenic properties), squalamine lactate22 (a novel aminosterol with antineoplastic and antiangiogenic activity), and recombinant anti-vascular endothelial growth factor fusion protein23 are reported to be useful in restricting or inhibiting CNVM induced by laser retinal injury.
Majority of these studies are conducted in laboratory on experimental animal models. Though they maybe useful in human subjects, there use is largely empirical.
No active management or intervention was advised in both our cases. Both the cases were followed up and were last seen at about 6 months postinjury. On last examination, both cases showed juxta foveal scars with no evidence of choroidal neovascular membrane. Laser retinal damage should be suspected in any patient with visual complaints after obvious exposure to unknown strong light. The treatment for laser-induced retinal injuries is limited and hence prevention is essential.
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- Roider J, Buesqen P, Hoerauf H, Schimidt-Erfurth U, Laqua H, Birnqruber R. Macular injury by a military range finder. Retina. 1999; 19(6):531–535. doi:10.1097/00006982-199911000-00009 [CrossRef]
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- Husain Deeba, Kim Ivana, Gauthier Danny, Lane Anne Marie, et al. Safety and Efficacy of Intravitreal Injection of Ranibizumab in Combination With Verteporfin PDT on Experimental Choroidal Neovascularization in the Monkey. Arch Ophthalmol. 2005;123:509–516. doi:10.1001/archopht.123.4.509 [CrossRef]
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- Brown J Jr, Hacker H, Schuschereba ST, Zwick H, Lund DJ, Stuck BE. Steroidal and non-steroidal anti-inflammatory medications can improve photoreceptor survival after laser retinal photocoagulation. Ophthalmology. 2007Oct;114(10):1876–1883 doi:10.1016/j.ophtha.2007.04.035 [CrossRef]
- Ciulla TA, Criswell MH, Danis RP, Fronheiser M, Yuan P, Cox TA, Csaky KG, Robinson MR. Choroidal neovascular membrane inhibition in a laser treated rat model with intraocular sustained release triamcinolone acetonide microimplants. Br J Ophthalmol. 2003Aug;87(8):1032–1037. doi:10.1136/bjo.87.8.1032 [CrossRef]
- Hu W, Criswell MH, Ottlecz A, Cornell TL, Danis RP, Lambrou GN, Ciulla TA. Oral administration of lumiracoxib reduces choroidal neovascular membrane development in the rat laser-trauma model. Retina. 2005Dec;25(8):1054–1064 doi:10.1097/00006982-200512000-00015 [CrossRef]
- Ciulla TA, Criswell MH, Danis RP, Williams JI, McLane MP, Holroyd KJ. Squalamine lactate reduces choroidal neovascularization in a laser-injury model in the rat. Retina. 2003Dec;23(6):808–814 doi:10.1097/00006982-200312000-00011 [CrossRef]
- Zhang M, Zhang J, Yan M, Li H, Yang C, Yu D. Recombinant anti-vascular endothelial growth factor fusion protein efficiently suppresses choridal neovasularization in monkeys. Mol Vis. 2008;14:37–49