Metallic gold deposition in human tissue, chrysiasis, may occur during systemic administration of gold salts.1–3 Deposition of gold in ocular structures is generally known to be safe and inert.4
Exogenous deposition rarely occurs; however, if it does it can be life threatening. We describe a rare initial presentation of exogenous gold deposition and discuss the clinical management and outcomes.
A 27-year-old man whose occupation was goldsmith presented to the emergency room 2 hours after trauma with sudden onset of intense irritation, tearing, and severe photophobia in both eyes associated with reduced vision. He had a history of accidental injury to both eyes while converting gold bullion to gold salt that accidentally overheated, leading to a sudden gold–amine compound explosion. There was no history of any medication, episodes of ocular trauma, eye discomfort, or injury with chemical substances. Additionally, no family history of ocular or systemic disease was noted.
The corrected distance visual acuity (CDVA) was counting fingers in the right eye and light perception in the left eye. External examination revealed edematous lids that were lacerated to the lid margins superiorly in both eyes. On slitlamp examination, the cornea in the right eye had a partial-thickness laceration measuring 4.0 mm in length paracentrally extending to the nasal sclera and in the left eye, a corneal perforation with prolapsed iris at the 9 o'clock position near the limbus. In the left eye, the pupil was distorted and the anterior lens capsule was disrupted with prolapsed vitreous into the anterior chamber.
Golden-brown diffusely confluent metallic luster deposits similar to a galaxy were seen in the deep stromal layer near Descemet membrane in both eyes, as well as gold deposition on the limbus, conjunctiva, and sclera (Figure 1). Extraocular movement was normal in both eyes. Anterior and posterior chamber evaluation was impossible due to severe edema and gold deposition accompanied by severe irritation.
Systemic evaluation was unremarkable. On day 1 of admission, immediate and prolonged irrigation was performed with normal saline followed by foreign-body removal, corneal surface remodeling, and lid repair in the right eye; corneal repair followed by anterior vitrectomy, iris repositioning, and lid repair was done in the left eye. The patient was started on topical betamethasone twice hourly, tropicamide (Mydriacyl) 1.0% eyedrops 3 times a day, and topical erythromycin 3 times a day. On day 3 of admission, he was taken to the operating room because of severe irritation, photophobia, and foreign-body sensation. The corneas were irrigated, and visible foreign bodies were carefully removed under topical anesthesia. On day 7, the B-scan revealed a normal retina and vitreous cavity with clear media in both eyes. Two weeks later, a lensectomy and foldable intraocular lens implantation in the sulcus was done in the left eye.
Over the next 6 weeks, the topical betamethasone was tapered gradually and the symptoms resolved. Four months later, the remaining granular golden-brown shiny pigmented deposits caused a severe diffuse corneal opacity. Visual acuity was not improved and remained hand motion in the right eye. The LP in the left eye was due to macular scar formation secondary to severe traction on the macula causing macular detachment, which happened after the injury. At 8 months, penetrating keratoplasty was performed in the right eye.
After follow-up of 1 year, the patient was asymptomatic and the CDVA had improved to 5/10 in the right eye. No stromal inflammation was seen, but a small, shiny, flat foreign body with golden luster remained at the cornea, limbus, and conjunctiva. At that time, there was no sign or symptom of inflammatory reaction in the anterior chamber, conjunctiva, limbus, or cornea (Figure 2). In the right eye, the ocular media was clear and the fundus healthy.
Gold deposition in ocular structures is rare and normally considered to be inert, with no intraocular or extraocular inflammatory reactions.5 Deposition of gold occurs in the epithelium,6 Bowman layer,4 stroma,7,8 Descemet membrane,4 and, infrequently, the lens2 when cumulative doses exceed 1 gm during systemic administration.7,8 Exogenous deposition, however rare, may occur in some circumstances; eg, during ornament preparation by alloying pure gold with copper9,10 or amine.11
To our knowledge, only 2 cases with clinical findings of metallic, multicolored gold deposition in the cornea similar to our case have been reported.11,12 However, in neither of the studies was diffuse confluent gold deposition associated with severe irritation described.
In our case, 24-carat gold was used for gilding; however, reported semiquantitative analysis of a sample from the laboratory showed pure gold cation (75.71%), chlorine (8.19%), nitrogen (7.29%), calcium (4.21%), manganese (2.30%), silicon (1.70%), and sodium (1.49%).
Wardrop12 reported eye irritation following gold contamination with copper or zinc in the globe. Moreover, severe eye irritation was reported previously due to eye exposure to manganese and silicone.13–15
In the present study, semiquantitative analysis revealed contamination of gold with manganese and silicon. The stoichiometry ratio of nitro-hydrochloric acid and ammonium was reported as not properly arranged during the processing. Both factors could explain our finding. Furthermore, Raj et al.11 demonstrated localized ulcerative keratitis adjacent to deep-seated gold in the cornea but with no apparent long-term problem. Similarly, we did not find any problems in the cornea after 1 year of follow-up.
In conclusion, although gold is safe and inert, it can lead to sacrifice of eyesight and life-threatening complications when contaminated with other toxic elements. Immediate and prolonged irrigation followed by proper management is essential for patients who present after acute injury and early recognition of such injuries. Appropriate intervention may prevent permanent damage to the eye.
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