This Month’s Guideline: Visual Loss Secondary to Cosmetic Filler Injection

J Clin Aesthet Dermatol. 2018 May; 11(5): E53–E55.

By Lee Walker, MD and Martyn King, MD


Any impairment or loss of vision (temporary or permanent) secondary to central retinal or retinal branch artery occlusion occurring as a direct consequence of percutaneous injection for aesthetic treatment


Blindness after facial injection is extremely rare and was first reported by von Bahr over 50 years ago after scalp injection of a hydrocortisone suspension to treat alopecia. The first cases after aesthetic filler treatments were reported in the 1980s (four cases) and rose to at least 16 reported cases between 2000 and 2010, presumably related to the increase in the number of treatments being performed. Depending on which artery is occluded, vision loss can be classified into six subtypes:

  • Ophthalmic artery occlusion (OAO)

  • Generalized posterior ciliary artery occlusion with relative central retinal artery sparing (PCAO)

  • Central retinal artery occlusion (CRAO)

  • Branch retinal artery occlusion (BRAO)

  • Anterior ischaemic optic neuropathy (AION)

  • Posterior ischaemic optic neuropathy (PION).

There are also four subtypes of periocular complications associated with blindness following cosmetic filler injection:

  • Type I –Blindness without ophthalmoplegia (paralysis or weakness of ocular muscles) and ptosis

  • Type II – Blindness with ptosis but without ophthalmoplegia

  • Type III – Blindness with ophthalmoplegia but without ptosis

  • Type IV – Blindness with ophthalmoplegia and ptosis.

Based on previously reported case studies, improvement of visual acuity in patients with vascular occlusion after filler injection is extremely rare. By contrast, periocular symptoms such as ptosis and ophthalmoplegia recovered dramatically.


Terminal branches of the ophthalmic artery, namely the supraorbital and supratrochlear, supply the medial forehead, and anastomoses between these vessels and the terminal branches of the angular artery are well documented. Similarly, anastomoses with the superficial temporal arteries and the orbit have also been demonstrated. Injection of filler material into one of these vessels can lead to retrograde flow to beyond the point of the origin of the ophthalmic artery, and when pressure from the plunger is released, systolic pressure drives the product forward to enter the ophthalmic artery or central retinal artery, resulting in visual loss.

In order for blindness to occur, there must be retrograde and subsequent anterograde passage of material, injection pressure exceeding systolic pressure, and sufficient amount of material within the lumen of the vessel. Findings indicate that the average entire volume of the supratrochlear artery from the glabella to the orbital apex is 0.085mL (range 0.04–0.12mL), and injection volume should not exceed this volume in critical injection points.


Globally, at least 98 cases of vision loss after aesthetic facial injection have been reported prior to 2015.,,, A review of the world literature by Belezany identified 98 cases of vision change. Reported high risk areas include glabella (38.8%), nasal region (25.5%), nasolabial fold (13.3%), and forehead (12.2%). Autologous fat was responsible for most of the complications (47.9%) followed by hyaluronic acid (23.5%), and,in cases when autologous fat had been injected,, worse outcomes have been reported

In 2012, the United Kingdom reported its first case (after injection to the temple with Poly-L-Lactic Acid, the first report with this product). In 2013, the first two cases of bilateral blindness were reported (calcium hydroxyapatite to the nose and hyaluronic acid to the glabella, which also led to cerebral infarction). The exact incidence of this devastating adverse event remains to be determined due to the heterogeneity of data.

Due to the seriousness of this complication, as part of the consent process, significant visual loss should be explained to the patient as a possible rare complication.


  • Pain (ocular, facial, headache or a combination)

  • Nausea

  • Vision loss

  • Paralysis or weakness of ocular muscles

  • Ptosis

  • Posterior displacement of the eye • Strabismus (misalignment of the eyes when looking at an object)

  • Corneal oedema

  • Pupillary abnormality

  • Iris atrophy

  • Anterior chamber inflammation

  • Phthisis bulbi (shrunken, non-functional eye)

  • Livedo reticularis (a mottled, reticulated vascular pattern of the skin).

Visual loss following embolization of dermal filler typically occurs within seconds of injection, although visual loss has been reported seven hours post-treatment in the case of a posterior ciliary artery occlusion. Complete loss of vision is the normal presentation, although there might be visual field defects. Visual loss is often accompanied by sudden onset of severe pain (ocular, facial, and/or headache), although central retinal and retinal branch artery occlusions might present without ocular pain. Other symptoms include ophthalmoplegia (paralysis or weakness of ocular muscles), ptosis, enophthalmos (posterior displacement of the eye), and horizontal strabismus (abnormal alignment of the eyes). These symptoms accompany blindness due to disturbed flow to the superior and inferior branches, which supply the extraocular muscles.

Many cases with visual loss and periocular symptoms also subsequently develop enophthalmos, and surgery should be considered in patients demonstrating greater than 2mm descent within six weeks of the injury.

Other symptoms and signs include corneal edema, anterior chamber inflammation, nausea, headache, pupillary abnormality, iris atrophy, phthisis bulbi, and livedo reticularis.

Cerebral infarction can accompany retinal artery occlusion, and therefore signs and symptoms such as aphasia or even contralateral hemiparesis might also be present. Central nervous system complications were seen in 23.5 to 39 percent of cases where vision was affected.

An magnetic resonance imaging (MRI) scan should be performed in all patients who suffer visual loss or ocular pain as a result of filler injections.


Injections into the nose and glabella form the vast majority of reported cases of blindness, although moderate risk sites include the nasolabial folds, forehead, periocular region, temple, and cheek. Uncommon sites are the eyelid, lips, and chin. Due to its complex vascularity, any region of the face is at risk for this complication.


The key preventative strategies are as follows:

  1. Know the location and depth of facial vessels and the common variations. Injectors should understand the appropriate depth and plane of injection at different sites.

  2. Inject slowly and with minimal pressure.,,

  3. Inject in small increments, so that any filler injected into the artery can be flushed peripherally before the next incremental injection. This prevents a column of filler traveling retrograde and subsequently anterograde. No more than 0.1mL of filler should be injected with each increment.

  4. Move the needle tip while injecting so as not to deliver a large deposit in one location.

  5. Always aspirate before injection,,, though this recommendation is controversial as it might not be possible to get flashback into a syringe through fine needles with thick gels. In addition, the small size and collapsibility of facial vessels limit the efficacy.

  6. Use a small-diameter needle., A smaller needle necessitates slower injection and is less likely to occlude the vessel. If a sharp needle is being used, a perpendicular injection directly in contact with the bone is recommended; injecting into a deeper plane might avoid vessels.

  7. Smaller syringes are preferred to larger ones as a large syringe can make it more challenging to control the volume and increases the probability of injecting a larger bolus.

  8. Consider using a cannula (minimum size 25G), as it is less likely to pierce a blood vessel., Some authors recommend using the cannula in the medial cheek, tear trough, and nasolabial fold.

  9. Use extreme caution when injecting a patient who has undergone trauma or a previous surgical procedure in the area.

  10. Ensure that you are adequately trained, are using an appropriate product, are competent in treating the area you will be injecting, and are competent in the management of complications.

  11. A technique to possibly prevent embolism of filler is digital compression of the inferior-medial orbital rim and the side of the nose while injecting.

Sometimes the ophthalmic artery does not arise normally from the internal carotid artery, but from the middle meningeal artery, which originates from the external carotid artery. Furthermore, the zygomatic-orbital artery raised from the superficial temporal artery has an anastomosis with branches of the ophthalmic artery, and might be a retrograde arterial embolic route. Facial anatomy can be diverse; the facial artery originated from a single arterial trunk in 86 percent of specimens, and branching patterns were only symmetrical in 53 percent of cases. In conclusion, there is no absolute safe area of the face to inject.


Once the retinal artery has been occluded, there is a window of 60 to 90 minutes before blindness is irreversible. It is advisable to transfer the patient to the nearest hospital with an eye specialist via blue light ambulance as quickly as possible. Transfer to a non-specialist emergency department might lead to inordinate delay and worse outcome. Ensure that you know where the closest hospital witih an eye specialist team is, and contact the on-call team as soon as possible to inform them of the situation. Provide the medical staff as much information as possible about the product, where it was injected, and the volume of injection used.

Although there is no generally agreed-upon treatment regimen, there are actions that can help. Prado suggests a six-step therapy protocol with a “blindness safety kit” that can be used in a clinical setting and then continued into hospital. The protocol was adapted from Lazzeri et al.


Indications for treatment are sudden onset ocular pain and/or loss of vision. The goal is to quickly reduce the intraocular pressure to allow for the emboli to dislodge downstream and improve retinal perfusion. Treatment must start within 90 minutes.

  • Stop treatment immediately.

  • Place patient in supine position.

  • Call emergency medical service and prepare to transfer patient to hospital setting as soon as possible.


Reduce intraocular pressure. Administer Timolol, 0.5% 1 to 2 drops in the affected eye only. This beta-adrenergic antagonist will aim to reduce intraocular pressure by reducing aqueous humor production. The patient should be encouraged to “rebreathe” in a paper bag to increase CO2 levels within the blood, which will cause retinal arteries to vasodilate and could help dislodge blockage. An alternative to rebreathing through a paper bag is the inhalation of carbogen (95% O2, 5% CO2). Oral acetazolamide,, may be considered, although intravenous administration in a hospital is likely to be of greater benefit. Give the patient 300mg of aspirin to prevent blood clotting.

Dislodge the embolus to a more peripheral position. Massage the globe with repeated increasing pressure. Prolonged ocular massage can dislodge emboli by rapidly changing intraocular pressure, thereby changing the pressure and flow in the retinal arteries. Increasing the intraocular pressure also causes a reflexive dilation of the retinal arterioles, and dropping it suddenly increases the volume of flow significantly. Ocular massage is performed with the patient looking straight ahead with eyes closed. Gentle pressure is applied over the sclera with a finger, indenting the globe by a few millimetres and then releasing at a frequency of 2 to 3 times a second. This should be continued until advised otherwise by staff at the eye hospital. Commonly, firm ocular massage is advised for several seconds and repeated only a few times. The alternative advice originates from two case studies where embolised retinal arteries were directly visualised during the massage process. This showed that even when the emboli were dislodged, more would occlude the vessel when massage stopped. Prolonged high frequency massage (up to three hours) had a better clearing effect.

Administer hyaluronidase. If hyaluronic acid has been used, administer hyaluronidase to the treatment area according to ACE Group Guideline “The Use of Hyaluronidase in Aesthetic Practice.” Retrobulbar injection of hyaluronidase has been advocated by many plastic surgeons as emergency treatment; however, an evaluation by Zhu et al failed to show any improvement in visual loss following 1500 to 3000 units of hyaluronidase injected into the retrobulbar space in four patients. Consensus from ophthalmologists is that retrobulbar hyaluronidase injections are technically difficult procedures even to a competent ophthalmological surgeon, and the scope for causing more harm by an aesthetic dermatology not very skilled at the procedure means the risks outweigh any benefit. However, Chestnut recently reported in Dermatologic Surgery achieving full restoration of vision in a patient who received hyaluronic acid fillers in the midface. Vision was restored following three retrobulbar hyaluronidase injections and aspirin. A total of 750 units were administered, 450 units as retrobulbar injections and 300 units to surround the supraorbital and infraorbital foramina. Retrobulbar injections should only be considered by practitioners competent in this procedure in a specialist eye unit. Injection of hyaluronidase into the supratrochlear or supraorbital arteries to reach the embolus seems a more sensible approach. The use of hyaluronidase has been shown to be ineffective at recanalizing the retinal artery occlusion or improving the visual outcome after four hours after onset of blindness.


Once the patient has been transferred to the hospital setting, the aim is to further reduce intraocular pressure, remove/reverse central retinal ischaemia, and increase blood flow to the retina. The following treatment methods may be used:

  • Injection of 500mg IV acetazolamia, which should increase retinal blood flow and reduce intraocular pressure.

  • Use of enoxaparin subcutaneously or IV heparin for anticoagulation—If the patient is having signs or symptoms of cerebral infarction, defer this step until a neurologist has assessed the patient.

  • Intravenous infusion of mannitol 20% (100mLover 30 minutes).,

  • Injection of hyaluronidase via the transorbital approach into the more prominent and tortuous postseptal ophthalmic artery.


  • Anterior chamber paracentesis, to immediately lower intraocular pressure

  • Steroid administration, intravenous dexamethasone,

  • Judicious use of antibiotics for suspected infection

  • Hyperbaric oxygen may salvage vulnerable retinal damage.,, Practitioners should familiarise themselves with their nearest hyperbaric oxygen chamber.

  • Intravenous prostaglandin E14 to increase blood flow to the retina and decrease activation of thrombocytes and neutrophils.


The ACE Group have produced a series of evidence based and peer reviewed guidelines to help practitioners prevent and manage complications that can occur in aesthetic practice. These guidelines are not intended to replace clinical judgement and it is important the practitioner makes the correct diagnosis and works within their scope of competency. Some complications may require prescription medicines to help in their management and if the practitioner is not familiar with the medication, the patient should be appropriately referred. Informing the patient’s General Practitioner is considered good medical practice and patient consent should be sought. It may be appropriate to involve the General Practitioner or other Specialist for shared care management when the treating practitioner is not able or lacks experience to manage the complication themselves. Practitioners have a duty of care and are accountable to their professional bodies and must act honestly, ethically and professionally.

VISION LOSS EXPERT GROUP: Dr. Martyn King (Chair); Emma Davies, RN, NIP (Vice Chair); Sharon King, RN, NIP; Dr. Cormac Convery; Dr. Lee Walker

VISION LOSS CONSENSUS GROUP: Constance Campion, RN, NIP; Helena Collier, RN, NIP; Dr. Ben Coyle; Dr. Harryono Judodihardjo; Dr. Sam Robson; Mr Taimur Shoaib


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