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Fariza and Castellote,
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The lesions probably represented hemorrhage caused by small areas of choroidal neovascularization emanating from breaks in Bruch's membrane (lacquer cracks) or within areas of chorioretinal atrophy. An exudative detachment within the macula can also occur when choroidal neovascularization is present, and would be consistent with the whitish changes seen in this patient1. These findings are common in patients with high myopia. The occurrence in both this patient's eyes may simply be coincidental.
Fluorescein angiography is the standard procedure for diagnosing chorioretinal disorders. Choroidal neovascularization and light toxicity both have characteristic features, and therefore this test would aid in determining whether this patient truly had light damage. Also, clarification of the exposure time of the macula is critical to the implication of light toxicity. Exposure to the indirect ophthalmoscope for more than 15 minutes is necessary to cause retinal lesions2. In general, examination of the macula by indirect ophthalmoscopy takes only several seconds, and most patients cannot stand longer exposures of the macula. It would seem highly unlikely that this patient's maculas were examined for more than a few minutes at most, thereby greatly reducing the possibility of light damage.
Finally, I think there are several errors in the letter: the strength of timolol is 0.5 percent, not 5 percent; and in Figure 1, the photographs of the left eye are labeled as being those of the right and vice versa, and the upper righthand photograph is reversed and inverted.
Elias Reichel, M.D.
New England Eye Center
Boston, MA 02111
References
To the Editor: Dr. Reichel suggests that the retinal lesion reported in the letter could have been myopic choroidal neovascularization. As he states, fluorescein angiography is the procedure of choice for assessing choroidal neovascularization, in which it shows neovascularization and leakage1. We performed fluorescein angiography during the patient's first visit. This test revealed leakage characteristic of myopic chorioretinal degeneration, but no leakage or neovascularization in the macular regions. We therefore concluded that the retinal pigment epithelium was probably intact. This finding largely excludes the possibility of myopic choroidal neovascularization. However, so-called occult subretinal new vessels (new vessels difficult to see with fluorescein angiography) have been described in age-related macular degeneration and could have been present in this patient. These vessels have characteristic angiographic features, however, and patients with such vessels usually have progressive deterioration of their vision1. To my knowledge, spontaneous recovery from myopic ocular neovascularization without residual scarring of the retina has not been described. Our patient had regression in both eyes. Spontaneous regression and recovery of vision are characteristic of low-to-moderate light damage in patients whose retinal pigment epithelium is undamaged2,3. Furthermore, the almost perfectly round shape of the lesions is characteristic of instrument-induced light damage4 but not choroidal neovascularization1.
Our patient was very cooperative, which may explain her tolerance of an unusually long examination of each macula. She estimated that the examination took 20 minutes per eye. I do not know why such a lengthy examination was performed.
Visual psychophysics (visual perception) also provides a clue favoring a diagnosis of light damage. The patient described her vision as having a green hue. Ophthalmoscopes use large quantities of blue and red light,3 and they bleach blue and red photoreceptors, causing a color shift to the green5.
Dr. Reichel's final comments are correct; the strength of timolol was 0.5 percent, not 5 percent, and the retinal photographs were misaligned.
Enrique Fariza, M.D., Ph.D.
Hospital Provincial de Castellon
12001 Castellon, Spain
References
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Related Letters:
Clinical Light Damage by Indirect Ophthalmoscopy
Fariza E., Castellote M.
Extract |
Full Text
N Engl J Med 1993;
329:1505-1507, Nov 11, 1993.
Correspondence
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