Ophthalmic Artery Occlusion and Subsequent Retinal Fibrosis From a Calcium Hydroxylapatite Filler Injection

Introduction

Facial fillers of various compositions used for cosmetic purposes in the periorbital region have been reported to have serious ophthalmic complications including anterior segment ischemia, oculomotor palsy, periorbital cutaneous infarctions, branch and central retinal artery occlusions, ophthalmic artery occlusions, and cerebral vascular infarction. ^1,2 While there have been multiple proposed mechanisms of action, the most commonly accepted mechanism is from the retrograde flow of the injected material through branches of the ophthalmic artery such as the supratrochlear or supraorbital arteries. It is thought that sufficiently high intraarterial injection pressure will cause retrograde flow and secondary embolic infarctions once the injection pressure is released. ³

Despite the increasing number of reported ocular complications in the literature, no effective treatments are available. Calcium hydroxylapatite is a semipermanent soft-tissue filler, lasting 1-2 years in the facial tissue. ⁴ Like autologous fat and hyaluronic acid filler injections, calcium hydroxylapatite has also been subject to ocular embolism leading to orbital and ocular complications. The objective of the case is to demonstrate the acute and serious sequelae of an ophthalmic artery occlusion from calcium hydroxylapatite microspheres (Radiesse, Merz North America, Inc).

Case Report

A 48-year-old healthy woman presented with a 4-day history of complete loss of vision in the right eye after injection of a soft-tissue filler in the glabellar region, the skin between the eyebrows and above the nose, with calcium hydroxylapatite microspheres. The patient noted she had immediate loss of vision after several injections around her upper, lower, and lateral lid areas at a local spa 4 days prior to presentation.

At initial presentation to the University of Illinois at Chicago, her visual acuity was no light perception (NLP) in the right eye (OD), and 20/20 in the left eye (OS). Her intraocular pressures by applanation were 11 mmHg OD and 18 mmHg OS. There was a relative afferent pupillary defect OD and the pupil was mid-dilated, and nonreactive at 6 mm. Extraocular movements were intact. Anterior segment examination was otherwise within normal limits. Funduscopic examination of the right eye revealed an ophthalmic artery occlusion with diffuse disc pallor, whitening of the retina, and marked attenuation of retinal vessels (Figure 1, A and B). The left eye examination was normal.

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Figure 1.

(A) Ophthalmic artery occlusion seen on fundus examination of the right eye at presentation. (B) A widefield fundus photograph of the right eye at presentation. (C) A late-frame image at 4 minutes of the fluorescein angiogram of the right eye showing patchy choroidal fluorescence and leakage in the superior periphery. (D) Spectral domain-optical coherence tomography of the right eye through the macula demonstrating diffuse retinal thickening and hyperreflective foci in the inner retinal layers.

Fluorescein angiogram of the right eye showed an almost complete absence of flow in the posterior pole with some patchy choroidal fluorescence and leakage in the superior periphery in the late frames (Figure 1C). Spectral-domain optical coherence tomography (SD-OCT) through the fovea demonstrated diffuse retinal thickening and several hyperreflective foci in the inner retinal layers (Figure 1D). Observation was recommended, as there was no feasible therapy available to restore visual function. The patient returned monthly for follow-up examinations, and by month 3, the examination demonstrated an increasing amount of macular fibrosis and scarring (Figure 2, A and B).

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Figure 2.

(A) Fundus photograph at month 4 demonstrating diffuse retinal ischemia and fibrosis of the right eye. (B) Widefield fundus photograph at month 4 demonstrating diffuse retinal ischemia and fibrosis of the right eye.

The patient was most recently seen at month 9 following her periocular injections. She remained NLP with an intraocular pressure of 15 mmHg. There was no sign of neovascularization despite significant ischemia and fibrosis on examination of the retina (Figure 3A). In contrast to her acute presentation, her SD-OCT now showed diffuse thinning attributed to retinal atrophy (Figure 3B). The patient was counseled once again regarding the possible risk of neovascular glaucoma and was given instructions regarding monocular precautions.

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Figure 3.

(A) Fundus photograph at month 9 demonstrating increasing fibrosis and retinal atrophy. (B) Spectral-domain optical coherence tomography at month 9 of the right eye through the macula demonstrating retinal thinning and scarring.

Discussion

Injectable cosmetic fillers have been reported to cause various ophthalmic and orbital complications. The various fillers include calcium hydroxylapatite, autologous fat, hyaluronic acid, and collagen. Common injection sites include the glabellar region, nasolabial folds, or both areas. ⁵ Of the fillers used, autologous fat is believed to most commonly cause visual deterioration from branch or central retinal artery occlusion, ophthalmic artery occlusion, and posterior ischemic optic neuropathy. ⁶

Hyaluronic acid fillers, eg, Restylane (Galderma) have also been reported to cause ocular complications including ophthalmic artery occlusions. ^2,7,8 Retinal branch artery occlusions have been observed in patients, with the presumed mechanism of action being retrograde arteriolar flow after intraarterial injection into a peripheral branch of the ophthalmic artery. ^7,8 One case series by Kim et al reviewing ophthalmic and/or retinal artery occlusions in 7 patients noted that 4 receiving hyaluronic acid and 3 receiving autologous fat in the glabella and/or nasal dorsum region showed symptoms of sudden vision loss occurring between 1 and 4 hours after administration. ² All patients received facial filler injection in the glabella and/or nasal dorsum region.

Calcium hydroxylapatite fillers have also been subject to similar complications including hypersensitivity, orbital ecchymosis, inflammation, and ocular necrosis. ^{1,4,9 -11} To date, only a few adverse case reports have been described with calcium hydroxylapatite fillers, leading to variable long-term consequences. ^{1,4,9 -11} Cohen and colleagues described a patient with initial fixation-sparing superotemporal central scotoma with otherwise 20/20 vision after calcium hydroxylapatite filler injection to the nose bridge. ⁴ After 18 months of follow-up, the patient’s vision declined to 20/60 with significant progressive visual field deterioration and pallor of the optic disc. ⁴ Such cases are highly variable in outcome. One case was reported that led to bilateral NLP vision following a filler injection also at the nasal bridge. ¹⁰ In addition, there was subsequent bilateral anterior segment ischemia, total ophthalmoplegia, and skin necrosis. ¹⁰ Another case described a young man who suddenly developed blepharoptosis and orbital pain that subsequently led to significant anterior segment ischemia. ¹ Ultimately, orbital computed tomography showed multiple emboli along the conjunctival vessels and a diagnosis of ocular ischemic and ischemic oculomotor nerve palsy was made. ¹ However, after 3 months his symptoms including visual acuity resolved completely. ¹ Orbital concerns have also been raised, showing that focal orbital inflammation and dysmotility were consequences of calcium hydroxyapatite filler injection. ¹¹

Only 1 other case report has described vision loss after calcium hydroxylapatite injection to the glabella region. ⁹ While the patient’s best-corrected visual acuity ultimately improved from hand motion at 15 cm to 0.1 over 3 months, in this case a shower of small emboli was observed as hyperreflective depositions in the retinal layer on OCT and fundus photographs. In our case, we noted that a glabellar injection with calcium hydroxylapatite led to complete ophthalmic artery occlusion. Thus a large embolus can result from synthetic microsphere suspensions, such as Radiesse. The complete ophthalmic artery occlusion was subsequently confirmed by diffuse macular fibrosis, ultimately leading to retinal atrophy.

Unfortunately, our patient never recovered any vision in the affected right eye. We report that the periocular injection of calcium hydroxylapatite microspheres in the glabellar region should be performed with caution. While inducement of a total ophthalmic artery occlusion is rare, it is a devastating complication for which there remains no viable or proven treatment option.