Ipsilateral Ophthalmic and Cerebral Infarctions After Cosmetic Polylactic Acid Injection Into the Forehead

A 55-year-old woman developed no light perception vision in her right eye 5 days after an injection of polylactic acid cosmetic filler into her right forehead. Diffuse corneal edema and anterior chamber inflammation prohibited any view to the posterior segment to identify the cause of her profound vision loss. MRI of the orbits with diffusion-weighted imaging showed hyperintensity of the right optic nerve with signal reduction on apparent diffusion coefficient mapping, consistent with ischemia. Our patient also was found to have acute infarctions in the distribution of the right anterior cerebral artery on MRI of the brain despite having no permanent focal neurologic deficits aside from vision loss.

Photo Essay Section Editor: Timothy J. McCulley, MD Ipsilateral Ophthalmic and Cerebral Infarctions After Cosmetic Polylactic Acid Injection Into the Forehead Ashwinee Ragam, MD, Steven A. Agemy, MD, Sarita B. Dave, MD, Azita S. Khorsandi, MD, Rudrani Banik, MD FIG. 1. A. At presentation, there are right forehead skin lesions in the area of polylactic acid injection. B. The right eye reveals conjunctival and scleral injection, corneal edema, and fibrin in the anterior chamber. C. The right fundus shows widespread, white intravascular thromboemboli within the arcades, intraretinal hemorrhages, and intraretinal whitening. The image clarity is limited by dense anterior chamber inflammation. The Department of Ophthalmology, New York Eye and Ear Infirmary of Mount Sinai, New York, New York. The authors report no conflicts of interest. Address correspondence to Rudrani Banik, MD, 310 E 14th Street, New York, NY 10003; E-mail: [e-mail] Ragam et al: J Neuro-Ophthalmol 2017; 37: 77-80 Abstract: A 55-year-old woman developed no light perception vision in her right eye 5 days after an injection of polylactic acid cosmetic filler into her right forehead. Diffuse corneal edema and anterior chamber inflammation prohibited any view to the posterior segment to identify the cause of her profound vision loss. MRI of the orbits with diffusion-weighted 77 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo Essay imaging showed hyperintensity of the right optic nerve with signal reduction on apparent diffusion coefficient mapping, consistent with ischemia. Our patient also was found to have acute infarctions in the distribution of the right anterior cerebral artery on MRI of the brain despite having no permanent focal neurologic deficits aside from vision loss. Journal of Neuro-Ophthalmology 2017;37:77–80 doi: 10.1097/WNO.0000000000000459 © 2016 by North American Neuro-Ophthalmology Society A 55-year-old woman received an injection into her right forehead of AestheFill (Esthemedica, Singapore, Singapore), a polylactic acid subcutaneous cosmetic filler, by a nonmedical cosmetologist. During the procedure, the patient experienced right eye pain, dizziness, and left upper and lower extremity weakness followed by loss of consciousness. She was evaluated in an emergency department where brain computed tomography was unremarkable. Visual acuity in the right eye was noted to be counting fingers. She was discharged without any further management. The following morning, the patient developed worsening right periorbital pain and complete loss of vision in the right eye. On our initial examination 5 days after the injection, she had violaceous, necrotic skin lesions of the right forehead (Fig. 1A). Vision was no light perception (NLP) in the right eye and 20/20 in the left eye. There was a right relative afferent pupillary defect. Extraocular motility revealed mild abduction and infraduction deficits in the right eye and full ductions in the left eye. Intraocular pressure was 17 mm Hg in each eye. Slit-lamp examination of the right eye revealed significant chemosis and injection of both the conjunctiva and sclera. There was no view to the right fundus on dilated examination due to diffuse corneal edema with Descemet folds and anterior segment inflammation with fibrin formation. B-scan ultrasonography of the posterior segment was unremarkable. Slit-lamp and dilated funduscopic examinations of the left eye were normal. No focal deficits were noted on neurologic testing. Emergent MRI of the brain and orbits revealed hyperintense signal within the right optic nerve on diffusionweighted imaging (DWI) with corresponding apparent FIG. 2. A. Signal changes (arrows) on diffusion-weighted imaging (DWI) (left) and apparent diffusion coefficient map (right) demonstrate restricted diffusion, indicative of acute ischemia of the right optic nerve. B. DWI of the brain shows acute ischemia (arrows) involving the right frontal lobe (left) and corpus callosum (right). 78 Ragam et al: J Neuro-Ophthalmol 2017; 37: 77-80 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo Essay FIG. 3. Fluorescein (A) and indocyanine green (B) angiography of the right eye reveals retinal and choroidal ischemia. diffusion coefficient reduction, consistent with acute ischemic optic neuropathy (Fig. 2A). There also were acute infarcts of the right frontal lobe and genu of the corpus callosum in the distribution of the right anterior cerebral artery (Fig. 2B). Magnetic resonance angiography of the head and neck was normal. The patient was admitted to hospital and given 125 mg IV methylprednisolone followed by 2 days of 60 mg of prednisone. Neurologic examination was unremarkable. Because the patient had no other identifiable stroke risk factors, anticoagulation was not initiated. One week later, the patient’s forehead skin lesions had improved and the corneal edema resolved, revealing fibrinous material in the anterior chamber (Fig. 1B). With topical corticosteroids, the fibrin began to clear, permitting visualization of the right fundus and revealing white intravascular thromboemboli within the arcades, intraretinal hemorrhages, and macular edema (Fig. 1C). The optic disc appeared normal. Fundus angiography was consistent with choroidal ischemia and central retinal artery occlusion (Fig. 3). Vision in the right eye remained NLP. Vision loss after cosmetic facial filler injection is a rare complication due to vascular occlusion with filler particles (1–3). The proposed mechanism is inadvertent injection of filler material into superficial facial arteries that anastomose with distal branches of the ophthalmic artery. In the case of forehead fillers, material can be injected into the supraorbital or supratrochlear arteries, which are direct branches of the ophthalmic artery. Depression of the syringe results in retrograde repulsion of filler material into or beyond the ophthalmic artery. On release of the plunger, arterial flow carries the emboli anterograde to block distal branches of retinal circulation including the central retinal artery. Emboli also can occlude the long posterior ciliary and anterior ciliary arteries, resulting in anterior segment ischemia (4–6). Filler emboli injected into the ophthalmic artery can continue to be pushed retrograde into the internal carotid artery and cerebral circulation, which likely occurred in our patient. Fundus examination coupled with fundus angiography can reliably demonstrate occlusion of the ophthalmic artery and its branches to the retina and choroid in patients who Ragam et al: J Neuro-Ophthalmol 2017; 37: 77-80 present with vision loss after cosmetic filler injections (1). Our patient presented with NLP vision, but there was no view of the fundus because of diffuse corneal edema and anterior chamber inflammation, likely from anterior segment ischemia. However, ocular ischemic syndrome was not sufficient to explain the severity of her vision loss. Signal change on DWI of the right optic nerve aided in the diagnosis of acute posterior ischemic optic neuropathy (7–13). Occlusion of ophthalmic and cerebral vasculature due to retrograde embolization should be recognized by practitioners as a rare but devastating complication after any cosmetic facial filler procedure. Any case of vision loss after a facial filler injection should be treated as an acute ischemic stroke, and MRI of the orbits with DWI sequences should be obtained promptly. This diagnostic tool is especially useful when visualization of the posterior pole is limited. In addition, we recommend obtaining MRI of the brain in such cases as it may detect concurrent cerebral infarctions. REFERENCES 1. Park KH, Yim YK, Woo SJ, Kang SW, Lee WK, Choi KS, Kwak HW, Yoon IH, Huh K, Kim JW. Iatrogenic occlusion of the ophthalmic artery after cosmetic facial filler injections. A national survey by the Korean Retina Society. JAMA Ophthalmol. 2014;132:714–723. 2. Carruthers JD, Fagien S, Rohrich RJ, Weinkle S, Carruthers A. Blindness caused by cosmetic filler injection: a review of cause and therapy. Plast Reconstr Surg. 2014;134:1197–1201. 3. Beleznay K, Carruthers JD, Humphrey S, Jones D. Avoiding and treating blindness from fillers: a review of the world literature. Dermatol Surg. 2015;41:1097–1117. 4. Sung MS, Kim HG, Woo KI, Kim YD. Ocular ischemia and ischemic oculomotor nerve palsy after vascular embolization of injectable calcium hydroxylapatite filler. Ophthal Plast Reconstr Surg. 2010;26:289–291. 5. Kim YG, Kim SS, Song WK, Lee SY, Yoon JS. Ocular ischemia with hypotony after injection of hyaluronic acid gel. Ophthal Plast Reconstr Surg. 2011;27:e152–e155. 6. Hsieh YH, Lin CW, Huang JS, Yeh PT. Severe ocular complications following facial hydroxylapatite injections: two case reports. Taiwan J Ophthalmol. 2015;5:36–39. 7. Purvin V, Kuzma B. Intraorbital optic nerve signal hyperintensity on magnetic resonance imaging sequences in perioperative hypotensive ischemic optic neuropathy. J Neuroophthalmol. 2005;25:202–204. 79 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo Essay 8. Al-Shafai LS, Mikulis DJ. Diffusion MR imaging in a case of acute ischemic optic neuropathy. AJNR Am J Neuroradiol. 2006;27:255–257. 9. Mathur S, Karimi A, Mafee MF. Acute optic nerve infarction demonstrated by diffusion-weighted imaging in a case of rhinocerebral mucormycosis. AJNR Am J Neuroradiol. 2007;28:489–490. 10. Park YJ, Lee IH, Song CJ, Hwang HY. Diffusion MR imaging of postoperative bilateral acute ischemic optic neuropathy. Korean J Radiol. 2012;13:237–239. 11. Cauquil C, Souillard-Scemama R, Labetoulle M, Adams D, Ducreux D, Denier C. Diffusion MRI and tensor tractography in ischemic optic neuropathy. Acta Neurol Belg. 2012;112:209–211. 12. Kilani R, Marshall L, Koch S, Fernandez M, Postel E. DWI findings of optic nerve ischemia in the setting of central retinal artery occlusion. J Neuroimaging. 2013;23:108– 110. 13. Lee YJ, Kim HJ, Choi KD, Choi HY. MRI restricted diffusion in optic nerve infarction after autologous fat transplantation. J Neuroophthalmol. 2010;30:216–218. Images in Neuro-Ophthalmology Clinical-neuroimaging-OCT correlation in multiple sclerosis. A 21 year-old man was found to have an incongruous right homonymous hemianopia (A). He was ultimately diagnosed with multiple sclerosis. During his evaluation, initial optical coherence tomography (OCT) was unremarkable (C). Magnetic resonance imaging revealed a lesion (arrow) involving the left optic tract (E) which was confirmed with diffusion tensor imaging tractography (F). Six months later, visual fields showed marked improvement (B), yet the OCT demonstrated retinal nerve fiber layer thinning and macular ganglion cell loss (D) corresponding to the homonymous visual field defect. (courtesy of Fraser CL, Tan I, Klistorner A. Sydney, Australia). 80 Ragam et al: J Neuro-Ophthalmol 2017; 37: 77-80 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.