Stroke and ischemic ocular syndrome following facial injection of autologous fat managed by tissue plasminogen activator

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The tendency toward nonsurgical cosmetic procedures is increasing worldwide.1 Autologous fat injection is a minimally invasive cosmetic procedure that is used to correct tissue loss and treat wrinkles and folds. While fat injection is generally considered safe when performed by a qualified and experienced practitioner, there are potential risks associated with this procedure. The complication rate associated with facial fat grafting is estimated to be approximately 4.8%. The actual complication rate of facial fat grafting is unknown due to underreporting and lack of consensus on defined side effects and diagnosis.2 The most catastrophic side effect of fat injection is vascular occlusion.3 Compared to other fillers, the risk of major vascular complications is higher in fat injection due to its large particle size, enabling it to occlude relatively large vessels, such as the ophthalmic artery.3 Although these complications are often temporary, the frequent and sometimes unauthorized injection of fat may lead to rare but serious and irreversible vascular complications caused by symptomatic arterial occlusion.4 The major vascular complications include skin necrosis, ophthalmoplegia, permanent unilateral or bilateral vision loss, and stroke. Ocular and cerebral embolism may occur as a result of the displacement of injected material from distal to proximal retinal and ophthalmic arteries, causing abrupt unbearable pain, loss of sight, and further tissue necrosis.1 Here we report a patient who suffered acute visual loss and stroke after autologous temporal fat injection to correct temporal hollowing by an unauthorized physician. Informed consent was obtained from this patient and the institutional board committee approved the report of this patient. A 42-year-old woman presented to the emergency room with sudden visual loss in her right eye, followed shortly by confusion, dysarthria, and left hemiplegia when she was undergoing autologous fat injection into the right temporal area. The patient arrived at our hospital 1.5 h after the onset of symptoms. She was immediately admitted to the stroke unit and after primary evaluation and meeting the criteria for receiving rTPA, she received 50 mg (0.9 mg/kg) intravenous recombinant tissue plasminogen activator. Physical examination revealed agitation, severe dysarthria, and complete left hemiplegia. The right eye visual acuity exam revealed no light perception and the left eye was normal. Her right pupil was dilated and nonresponsive to light. Proptosis, periorbital edema, conjunctival hyperemia, and corneal opacity in the right eye were noticeable. Skin examination revealed ecchymosis with a livedo reticularis pattern of the right frontotemporal area (Figure 1). She had no prior significant medical history. Routine laboratory tests and cardiac assessments were normal. TCD and MRA of the brain and cervical vessels did not show stenosis. The initial imaging with a CT scan revealed no significant findings; however, the follow-up imaging after the rTPA injection revealed extensive cerebral infarction of the right frontoparietal lobes after rTPA injection (Figure 2). MRI findings showed an acute stroke (Figure 3). Two weeks later, the patient was able to raise her left upper limb and walk with help. The left hand could perform simple grasping tasks. However, there was minimal visual acuity improvement in her left eye with only slight light perception. Eventually, the Modified Rankin Score (MRS) was about 3 during discharge. With the ongoing progress of techniques and the constant pursuit of beauty, the rate of facial fat grafting has dramatically increased. The incidence of related adverse events is about 4.8%, the majority of which are moderate and transient, such as scarring, fibrosis, and edema.5 Acute stroke and visual loss are rare but serious complications.3 Both vascular adverse events, especially the latter have no effective treatment options and have a poor prognosis.3 According to the current evidence, fat injection-induced blindness or stroke occurs if a sharp needle perforates the vessel wall or the operator applies excessive force and speed during the injection. The fat embolus can reach the ophthalmic artery and branches of the middle cerebral artery by reversed flow through anastomoses of the superficial temporal and the ophthalmic artery. Aesthetic injectors need to be properly trained and completely familiar with the anatomy of the injection sites and meticulous technique with blunt needles and appropriate pressure to avoid any serious vascular complications.4 In a previous systematic review and meta-analysis of patients with vascular complications occurring after aesthetic procedures, unilateral blindness was the most frequent vascular adverse event associated with cosmetic fillers for facial tissue augmentation.3 Among fillers, autologous fat was the most frequent culprit of permanent vascular damage. According to the literature, ophthalmic artery occlusion is routinely associated with irreversible blindness.3 Preventing stroke caused by fat injection requires particular attention to the technique used during the procedure. Fat injection should be performed by a qualified practitioner with a small, blunt cannula.1 Management of stroke in the setting of fat injection involves timely recognition of the symptoms and immediate supportive care including airway, breathing, and circulation as well as prompt discontinuation of the procedure. Currently, there is no consensus on the treatment of blindness or stroke induced by fat injection. We managed our patient by rTPA and the outcome was favorable. However, the role of thrombolytic therapy in the cases of stroke following fat injection is not yet clear but injection should be performed within the golden time of 4.5 h of stroke. Other treatments include decompressive craniotomy, hyperbaric oxygen therapy, and corticosteroids.6 Our case has several distinctive characteristics including a frozen eye due to complete ischemic ocular syndrome and improvement of the patient's motor deficiency and tissue sparing in the brain MRI after receiving rTPA. Parisa Azizjalali and Sahar Dadkhahfar performed the research. Shirin Zaresharifi, Bredsin Benyamin, and Fahimeh Alipour wrote the paper. Martin Kassir revised the manuscript and supervised it. All authors have read and approved the final manuscript. The data that support the findings of this study are available from the corresponding author, Dr.Sahar Dadkhahfar, upon reasonable request.

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