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A healthy 12-year-old boy had a subcutaneous triamcinolone acetonide steroid injection at the site of a keloid on his left earlobe in November, 2008, at a plastic surgery clinic. Within 5 min, he developed left-sided facial numbness, diaphoresis, dizziness, hypaesthesia of the left side of the mouth and tongue, left upper lid ptosis, and nearly complete vision loss in his left eye. Several hours later his systemic symptoms had resolved, he had regained partial vision in his left eye, and his right eye was asymptomatic. On examination by a retina specialist he was noted to have a visual acuity of 20/400 as well as multiple white steroid emboli in the retinal arteries of his left eye (fi gure). He also had diff use retinal whitening in the macula and other regions of the retina consistent with a central retinal artery occlusion (fi gure). 3 days later, his visual acuity improved to 20/150. This case represents a vision-threatening and potentially fatal complication of subcutaneous auricular steroid injection. Subcutaneous injections of dermal fi llers and corticosteroids are done in many specialties such as dermatology, otolaryngology, plastic surgery, and ophthalmology. Corticosteroid injections in the face, including the orbit, eyelids, nose, oral cavity, and maxilla, have been reported to cause ocular embolic events such as anterior segment ischaemia, branch and central retinal artery occlusions, and ophthalmic artery occlusions. Due to diff use anastomoses in the facial arterial system, facial injections can cause retrograde embolisation of the ophthalmic or central retinal arteries. This may cause severe, irreversible vision loss. For all injections within the face, good practice is to aspirate before injection and to inject as slowly as possible in order to limit forces that could propel emboli. Patients with visual problems after steroid injection should have immediate ophthal mological evaluation to allow intervention that might improve visual acuity. In embolic central retinal artery occlusion, ocular massage and reduction of intraocular pressure (by anterior chamber paracentesis and intraocular pressure lowering drugs) might help to mobilise emboli and restore ocular blood fl ow, although evidence that this could help is scarce.

A 56-year-old African-American man presented with 20/30 best-corrected visual acuity bilaterally. Fundoscopic examination, fundus photographs, and fl uorescein angiography showed signifi cant bilateral tortuosity of second and third order arterioles (fi gure). Other fi ndings in the left eye included an occluded superotemporal artery with arteriosclerosis and macular pigmentary changes. The tortuosity was believed to be most consistent with familial retinal arteriolar tortuosity (fRAT), a rare autosomal dominant disorder. However, the patient stated that he had no family history of ocular disease, and the only one of eight siblings accessible for examination did not demonstrate fRAT. Is olated tortuosity of the second and third order arterioles is pathognomonic for fRAT. Although a few associated systemic vascular abnormalities have been identifi ed, fRAT is considered to be an isolated retinal fi nding. Branch retinal artery occlusion has not been reported in fRAT, and this feature may be attributed to the patient’s other risk factors of cocaine use and signifi cant hypertension.