A 24-year-old woman reported blindness in the left eye upon awakening from fat autotransplantation to her forehead for soft tissue augmentation in the face. Clinical findings on the third postoperative day suggested ipsilateral ophthalmic artery occlusion with infarction of the optic nerve and retina. There were also clinical manifestations of a mild right hemiparesis. MRI diffusion-weighted imaging (DWI) revealed restricted diffusion of the left optic nerve and left middle cerebral artery domain indicative of the cytotoxic edema of infarction. This is the second report of optic nerve infarction after fat autotransplantation to the forehead and the first report of DWI restricted diffusion in this setting.
Departments of Radiology (YJL, HJK), Neurology (K-DC), and Ophthalmology (H-YC), Pusan National University Hospital, Pusan National University School of Medicine and Medical Research Institute, Pusan, Republic of Korea.
Address correspondence to Hak Jin Kim, MD, PhD, Department of Radiology, Pusan National University Hospital, Pusan National University School of Medicine and Medical Research Institute, #1-10, Ami-Dong, Seo-gu, Pusan 602-739, Republic of Korea; E-mail: firstname.lastname@example.org
Apart from pain at the puncture sites, autologous fat injection for soft tissue augmentation in the face is reported to be a safe procedure (1). However, patients have rarely had acute visual loss and cerebral infarction (2-6). Fluorescein angiography, brain MRI, and cerebral angiography have been used in diagnosis of these events (2-4,6), but diffusion-weighted imaging (DWI) has not been described.
First described in 1986 (7), DWI is most commonly used to identify acutely infarcted cerebral tissue, which has an increased intracellular fraction of water. Owing to the availability of higher magnet strength MRI scanners and improvement in software, DWI can now be applied to smaller structures. Indeed, this MRI pulse sequence, which measures changes in water diffusion during acute stroke related to cytotoxic edema (8), is now being reported in optic nerve infarction (9-12).
We present a patient who developed acute optic nerve infarction and cerebral infarction after autologous fat transplantation documented by DWI restricted diffusion for the first time in this setting.
A 24-year-old woman presented with swelling and blindness in the left eye for 2 days. Three days earlier she had received an injection of autologous fat in her forehead under intravenous anesthesia.
On the day of the procedure she was unable to open both eyes due to the swelling of her eyelids. On the first postoperative day she became aware of visual loss in the left eye, decreased sensation on the forehead and scalp, and paresthesias of the right leg. She still could not open her left eye and dragged her right leg on walking.
On our examination on the third postoperative day, blood pressure was 110/70 mm Hg, pulse was 68/min, and temperature was 36.1°C. Blood count, erythrocyte sedimentation rate, C-reactive protein, and electrocardiogram were normal. She had no history of trauma, diabetes, or hypertension.
She was alert and mental status was intact. The left eye had no light perception, ptosis, and restricted extraocular motility in all directions. The left pupil did not constrict to direct light, and there was an afferent pupillary defect in the left eye. Ophthalmoscopy was normal in the right eye but showed pallid optic disc swelling and widespread retinal whitening in the left eye.
Pain, touch, and temperature senses were reduced in the left forehead and scalp. Motor function was intact in the upper and lower extremities. Deep tendon reflexes were increased in the right side. There was no Babinski sign.
Brain and orbit MRI at 5-mm slice thickness performed on the third postoperative day revealed hyperintensity in the left middle cerebral arterial territory and subtle hyperintensity in the left optic nerve on DWI and subtle hypointensity in corresponding regions on the apparent diffusion coefficient (ADC) map (Fig. 1). The ADC values were 2.75 × 104 in the affected optic nerve and 14.6 × 104 in the unaffected optic nerve, confirming markedly restricted diffusion in the affected optic nerve and normal diffusion in the unaffected optic nerve. T2 MRI did not show any signal abnormality in the affected optic nerve (Fig. 1C).
A follow-up DWI MRI at 3-mm slice thickness performed on the fourth postoperative day revealed an increase in the hyperintensity in the left middle cerebral arterial territory and the left optic nerve (Fig. 2A). The ADC map showed more prominent hypointensity of the corresponding regions (Fig. 2B). The ADC values were 2.37 × 104 in the affected optic nerve and 12.6 × 104 in the unaffected optic nerves.
The patient was treated with 1 g/day intravenous methylprednisone for 3 consecutive days. Five months later she still had no light perception in the left eye. Ophthalmoscopy disclosed severe retinal fibrosis in that eye. A relative afferent pupillary defect persisted in that eye, but ocular motility was normal except for a mild adduction deficit.
Our patient experienced complete visual loss in the left eye shortly after the injection of autologous fat into her forehead. Clinical findings on the third postoperative day suggested ipsilateral ophthalmic artery occlusion with infarction of the optic nerve and retina. There were also clinical manifestations of a mild right hemiparesis. DWI obtained on the third and fourth postoperative days revealed restricted diffusion of the left optic nerve and left middle cerebral artery domain indicative of the cytotoxic edema of infarction.
Ours is not the first report of acute visual loss and cerebral infarction after fat injection into the face (2-5). Mori et al (2) reported immediate onset of infarction of the ophthalmic artery during the time of injection of autologous fat in the glabellar area. Obstruction of the ophthalmic artery was irreversible. Feinendegen et al (3) described a patient with acute blindness in the left eye and right hemiplegia and global aphasia immediately after autologous fat injection into the periorbital areas. Ophthalmoscopic examination and carotid angiography revealed findings consistent with ipsilateral occlusion of the retinal and carotid arteries. It was assumed that intravasated fat reached the ophthalmic artery and the middle cerebral artery through the arteries on the forehead and led to immediate vessel occlusion. Egido et al (4) reported a case of sudden visual loss with hemiplegia immediately after autologous fat injection into the glabellar area. Brain CT showed embolic infarction in the right middle cerebral artery territory 8 days later. It was thought that fat material had been injected into a distal branch of the ophthalmic artery such as the supratrochlear artery. Dreizen and Framm (5) reported a similar patient showing permanent visual loss. Lee et al (6) reported a patient with central retinal arterial occlusion and unconsciousness. The patient recovered consciousness within a week but did not recover vision in the affected eye. The injection forces were postulated to have been strong enough to allow fat to reach the internal carotid artery, with embolism occurring to the ophthalmic artery and a branch of the middle cerebral artery (6).
Our contribution is to present DWI documentation of such an event for the first time. As in previous reports, we presume that the pressure of fat injection was high enough to reverse the flow through a branch of facial artery and force fat into the ophthalmic and distal internal carotid arteries (3,4). To avoid this problem, the physician must be careful to exert minimal force while injecting the fat into the facial tissue and to inject slowly (3).
There were 4 previous reports of restricted diffusion in DWI of acute ischemic optic neuropathy (9-12). The causes were rhinocerebral mucormycosis (9), nonarteritic posterior ischemic optic neuropathy (10), thrombotic arterial occlusion with underlying cavernous sinus thrombophlebitis (11), and thromboembolism with underlying arterial thrombosis (12). In these cases, restricted diffusion, which occurs promptly as in other ischemic strokes, is critical in demonstrating optic nerve infarction, especially when other MRI pulse sequences show no abnormalities (9,12) and in distinguishing infarction from inflammation (10).
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