Photo injuries arising from the use of arc welding are quite rare, and the first case was described by Terrier in 1902. The main cause of the appearance of macular degeneration is due to the failure to use proper eye protection [7].
Electrical systems in place for welding emit electromagnetic waves at high temperature and frequency ranges; from ultraviolet to the blue spectrum, however, all radiation can damage the ocular structures.
Today the most commonly welding techniques that use the ionized plasma of noble gases can cause retinal damage.
These gases are brought to temperatures so high that single molecules are broken down into atoms and then into electrons and protons, which is the so-called fourth phase of matter or the plasma phase. The plasma results from a marked rise in temperature that can reach values between 10,000 and 30,000°C, emitting light radiation harmful to retinal structures.
Phototoxic retinal damage appears to be multifactorial and involves several mechanisms of action depending on the chromophore involved in the bright damage.
The visual pigments, rhodopsin in particular, are among the main chromophores responsible for such damage, and lead to the alteration of cellular function and cytotoxicity.
The mechanism of action of rhodopsin mainly occurs in two ways: the first due to a prolonged activation of rhodopsin as meta-rhodopsin, which leads to a reduction of the concentration of intracellular calcium, initiating apoptosis, and the second through the issuance of phototoxic substances such as retinal [8]. Histological examination immediately following light exposure reveals that photoreceptor cell damage begins at the apex of the photoreceptor outer segment and advances over time to include the entire outer segment [9–12].
However, given the large number of phagosomes detected in the RPE, the photodamaged outer segment discs are digested, leading to a general decrease in the length of the photoreceptor outer segment [13].
The cascade of photochemical reactions may also release free radicals, superoxide anions and hydrogen peroxide, which react with the tissue and cell membranes to form aldehydes. If these substances are not readily degraded, the damage to the photoreceptor can be permanent.
What makes the case interesting is that the patient was not a welder and had monocular symptoms having seen only once a plasma welding process. The FA was normal but with OCT we found changes in the reflectivity of ELM and mfERG showed a reduction in amplitude in the central 2° in both eyes.
The negative FA did not help to address our initial diagnosis, also because of frequent negative retinal angiography in cases of photo trauma [14]. Therefore, it was important to perform OCT [15–17] and mfERG [18].
In our case the spectral-domain OCT showed a hyperreflectivity area in the ELM. This particular aspect was not detected with previous time-domain OCT technique [7]. In cases of photo injury assessed with spectral-domain technique a normal ELM was found [19], together with frequent hyporeflective space between the outer and inner hyperreflective layers and RPE-choriocapillaris complex [17]. This last OCT finding is similar to cases of solar retinopathy [20] whereas phototoxic effect is associated with a direct thermal damage of the photoreceptor outer segment-RPE complex. The mfERG showed a reduction in the amplitude in the central 2° in both eyes; this reduction has been improving over time as confirmed by control mfERG made a month later, confirming the importance of this exam in the diagnosis and in the follow-up of retinal photo injury [18, 20].
As for the asymmetrical involvement, this was likely due to the patient's positioning with respect to the welding tool, rather than a difference in the ocular structures in terms of sensitivity to photo damage.
With regard to the treatment of this disease, the data seem to be discordant regarding the use of corticosteroids [21–23]. The use of vitamin A and aspirin appears to reduce the risk of phototoxic damage to the retina [24], similar to the use of antioxidants such as vitamins B, C and E and ginkgo biloba [25, 26].
In our case after treatment with antioxidants, we observed a resolution of visual symptoms with improvement of the mfERG values but the persistence of phototoxic damage charged to the external limiting membrane found with OCT.
