Class 3A laser pointer‐induced retinal damage captured on optical coherence tomography

Editor, Laser pointers are common gifts from pharmaceutical representatives. These enterprising individuals may even give them to children, believing them to be safe toys. Many articles in leading medical journals have reiterated their safety (Mensah et al. 1998). However, other reports have suggested otherwise. This report illustrates the first published case of laser-induced retinal damage captured by optical coherence tomography (OCT) (Stratus OCT; Zeiss, Jena, Germany). A 38-year-old, male, oriental consultant physician attended clinic following exposure to a Class 3A commercial laser pointer (< 5 mW, 825–880-nm wavelength). This was an accidental injury inflicted by his 4-year-old son which comprised two illuminations lasting 1–2 seconds each in the right eye, from a position temporal to the subject's visual axis. He noticed a paracentral scotoma with best corrected visual acuity of 6/12 (right), 6/6 (left), improving to 6/6 (right) with no improvement in the left with pinhole. The patient had mild keratoconus, but no other medical history. Slit-lamp biomicroscopy revealed a normal anterior segment. Dilated fundoscopy showed a raised macula and a pale lesion nasal to the fovea (Fig. 1). Fluorescein angiography showed two hyperfluorescent spots increasing in intensity nasal to the fovea (Fig. 2). Serous retinal detachment was revealed by OCT (Fig. 3). Colour fundus photograph in the right eye. Fluorescein angiogram in the right eye. Ocular coherence tomography in the right eye on presentation. This lesion persisted at the 2-month follow-up (Fig. 4). Ocular coherence tomography in the right eye at 2 months. Retinal damage due to laser pointers is not insignificant as previously stated (Mensah et al. 1998). Retinal pigment epithelial changes seen following illumination are a sign of destruction, even if most changes do not result in symptomatic change (Zamir et al. 1999). This is analogous to injuries that occur elsewhere in the body and which do not cause loss in function. Luckily, as seen in previously published cases, symptoms tend to resolve and most return to normal, with little if any residual effect. However, threshold retinal burns in rhesus monkeys can be achieved at levels as low as 1.0–4.4 mW for 1 second (Ham et al. 1970). Those suggestions that laser pointers are ‘safe’ have either relied on theoretical discussion based on the physics of the eye and the laser, or on subjective measurements of visual function. Clinicopathological studies have shown inconclusive retinal changes from red (870 nm) laser pointer exposure, whereas green (532 nm) laser pointer exposure of 60 seconds duration revealed clinically and pathologically distinguishable damage similar to that caused by solar burns (Robertson et al. 2005). Others have demonstrated fundoscopic proof of insult to the retinal pigment epithelium (Luttrull & Hallisey 1999). In our patient, the two hypofluorescent spots (Fig. 2) match the two episodes of exposure. Some may feel that our patient suffered from idiopathic central serous choroidopathy (ICSC) and that the laser injury was coincidental. We feel the sudden nature of symptoms in addition to the paracentral scotoma suffered by our patient makes ICSC unlikely. However, we do agree the fluorescein angiogram and OCT are characteristic of ICSC and we feel the effects of the laser pointer incident followed a pathological process similar to that of ICSC. This case illustrates the seriousness of retinal exposure to laser pointers. We urge others to use their laser pointers with care.