Navigating Vision Risks in Facial Filler Applications

Source: 2 Rare, But Real, Side Effects Everyone Should Know Before Getting Fillers

Facial rejuvenation through dermal fillers has witnessed widespread acceptance as a seemingly uncomplicated and secure procedure. The diverse range of materials, such as hyaluronic acid, calcium hydroxyapatite, and poly-L-lactic acid (PLLA), utilized in over 30 FDA-approved dermal fillers adds a layer of complexity to the field. Among the various materials, hyaluronic acid gel fillers stand out as the most favored due to their commendable safety profile, reversibility, versatile formulations, and applications. However, even with these attributes, complications persist, albeit mostly mild and reversible. Notably, rare but serious complications, including tissue ischemia, skin necrosis, and permanent blindness, underscore the imperative need for a comprehensive approach to ensure global filler safety.

The evolving landscape of dermal filler usage has witnessed an uptick in reported cases of visual compromise, with Beleznay and colleagues documenting 146 reported instances of sudden vision loss secondary to filler injections. A striking revelation is the surge in cases, with 98 occurrences recorded between 1906 and 2015 and an additional 48 cases between 2015 and 2018. It is crucial to acknowledge the potential underreporting of such cases, emphasizing the need for heightened awareness among injectors, staff, and patients regarding this consequential complication. Heightened awareness of potential complications, especially filler-induced blindness, is paramount, necessitating ongoing research and a collective commitment to advancing safety in the field of aesthetic medicine. In this blog, we will discuss the complication management of vision loss in facial filler injection and the steps to mitigate them.

Source: External carotid artery to ophthalmic artery flow associated with internal carotid artery stenosis (2022)

Understanding the Types of Risks

Classification frameworks based on the occluded artery, symptom presentation, and onset characteristics offer a nuanced understanding of these complications. The occluded artery becomes a focal point for categorizing vision loss or blindness into six distinct subtypes.

Ophthalmic artery occlusion (OAO) represents a complete blockage of the ophthalmic artery, leading to potential visual loss, ptosis, and ophthalmoplegia. Generalized posterior ciliary artery occlusion with relative central retinal artery sparing (PCAO) introduces variations in visual outcomes. Isolated central retinal artery occlusion (CRAO) primarily entails visual loss alone, while branch retinal artery occlusion (BRAO) may result in partial visual impairment. Anterior ischaemic optic neuropathy (AION) and posterior ischaemic optic neuropathy (PION) represent additional patterns of ocular complications. Combinations of these occlusion types are conceivable, each carrying distinctive prognostic implications, with diffuse occlusions generally bearing a poorer prognosis.

Moreover, blindness or vision loss can be classified based on the presentation of symptoms. Four presentation subtypes of periocular complications associated with blindness following cosmetic filler injection are:

DESCRIPTION OF BLINDNESS	PRESENTATION
Type I	Blindness without ophthalmoplegia or 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 clinical patterns of filler-induced blindness, they are classified into:

DESCRIPTION OF BLINDNESS	TIME TO ONSET AFTER INJECTION	MECHANISM/THEORY
Type I (Acute Onset)	Immediate to minutes	Embolus of main trunk ophthalmic artery with associated choke spasm
Type II (Delayed Onset)	1–24 hours	Progressive migration of embolus further along ophthalmic circulation
Type III (Late Onset)	Days to weeks	Arteriovenous shunt of emboli via connections in glabella and orbit

Based on the degree of vision loss associated with the affected artery, they are classified into:

ARTERY OCCLUDED	DEGREE OF VISION LOSS
Ophthalmic Artery	Complete blindness/ NLP
Central Retinal Artery	Complete blindness/NLP
Branch Retinal Artery	Partial Blindness/DLP
Posterior Ciliary Artery	Blurred vision/DLP

Understanding the Potential Factors for Filler-Induced Blindness

The intricate dynamics underlying filler-induced blindness reveal a sophisticated interplay of arterial embolization pathways, with a primary mechanism arising from the direct intraarterial injection of fillers. This process leads to the embolization of filler material through vascular conduits, notably the ophthalmic artery. Understanding the nuanced details of this phenomenon is crucial for experts in the field, as it pertains to the advanced intricacies of facial anatomy and the vascular network.

Injectable Filler Application Pressure

Filler-induced blindness hinges on injecting fillers at pressures surpassing arterial pressure and overcoming friction forces due to viscous flow. This results in ophthalmic artery embolization, where filler material initially travels in a retrograde direction and subsequently, upon reduction of injection pressure, moves anterogradely with blood flow. The consequence is a dispersal of emboli anteriorly, including into the circulation of the ophthalmic artery.

Ophthalmic Artery Branches and "Danger Zones"

Understanding the arterial branches emanating from the ophthalmic artery is paramount. These branches include the supratrochlear, supraorbital, dorsal nasal, lacrimal, ethmoidal, palpebral, muscular, posterior ciliary, and central retinal arteries. Notably, the facial artery may anastomose with the ophthalmic artery via the angular artery. Anatomically, supratrochlear, supraorbital, and dorsal nasal arteries consistently connect directly to the ophthalmic artery, with the angular artery anastomosing in 54% of cases. This anatomical insight corresponds to recognized "danger zones" for visual compromise or blindness.

Filler Particle Size

The degree of visual compromise is intricately linked to the level of obstruction within the ophthalmic artery, with filler particle size playing a pivotal role. The ophthalmic artery, with an approximate diameter of 2 mm, and the central retinal artery, with a diameter of 160 mm, set the stage for potential ischemia downstream. Larger filler particles than the vessel's diameter pose a significant risk of arterial occlusion.

Filler Materials

All major filler types, including autologous fillers like fat and synthetic ones like hyaluronic acid, can result in visual compromise. Particle size variations contribute to the complexity of arterial occlusion. Hyaluronic acid fillers, such as Restylane and Perlane, exhibit different particle sizes, as do Juvederm products, which consist of "cohesive molecules" of cross-linked hyaluronic acid. Similarly, CaHA-based Radiesse and PLLA-based Sculptra display varying particle sizes, highlighting the diverse landscape of filler-induced complications.

Central Retinal Artery Occlusion

In cases of filler-induced blindness, ophthalmic artery occlusion is the most prevalent type of obstruction, often resulting in central retinal artery occlusion (CRAO) and branch retinal artery occlusion. Ophthalmic artery occlusion extends beyond the immediate effects, causing downstream vessel occlusion (ciliary arteries) and subsequent manifestations such as ptosis, ophthalmoplegia, and anterior segment ischemia. Understanding the multifaceted nature of filler embolization is imperative, as it may involve not only the ophthalmic artery but also other critical arteries, such as the supratrochlear, supraorbital, dorsal nasal, and angular arteries. The implications extend to clinical outcomes, as evidenced by findings of skin necrosis in patients experiencing filler-related vision loss.

Injection location

Source: Consensus Opinion for The Management of Soft Tissue Filler Induced Vision Loss (2021)

Certain facial regions exhibit a heightened susceptibility to vision loss following soft tissue filler injections. As shown in table below, the prevalence of blindness is correlated with the anatomical zone subjected to injection. Intriguingly, the nasal region has surpassed the glabella, emerging as the area with the most substantial incidence of vision loss in association with soft tissue filler injections. This shift in risk patterns underscores the dynamic nature of risks associated with various treatment indications, prompting a reevaluation of safety considerations in specific anatomical zones.

Rates of blindness relative to the anatomical zone injected:

ANATOMICAL AREA	INCIDENCE IN 2015	INCIDENCE IN 2019
Nose	25.5%	56.3%
Glabella	38.3%	27.1%
Forehead	12.2 %	18.8%
Nasolabial fold	13.3%	14.6%

Understanding The Symptoms and Prognoses

Source: Blindness After Filler Injection (2021)

The prognostication of filler-induced vision loss hinges significantly on the degree of vision impairment and its correlation with the embolus location. This factor assumes paramount importance, as evidenced by the fact that 80% of fat emboli instances manifest as complete vision loss, while 50% of hyaluronic acid (HA) emboli present with partial vision loss, contributing to its comparatively more favorable prognosis. Instances of complete vision loss or blindness, characterized by no light perception (NLP), are predominantly associated with ophthalmic artery occlusion (OAO) or central retinal artery occlusion (CRAO), and notably, most cases in this category do not exhibit recovery.

Contrastingly, cases presenting with partial vision loss (i.e., ranging from blurry vision to diminished light perception [DLP]) are less frequently linked to OAO/CRAO. Instead, they more commonly involve distal branches of both the posterior ciliary arteries and the central retinal artery, often attributed to the presence of smaller emboli. Notably, partial vision loss subsequent to HA filler administration tends to carry a more optimistic prognosis compared to instances of complete vision loss.

Among the various types of occlusions, branch retinal artery occlusion (BRAO) stands out with the most favorable prognosis. Existing literature underscores the importance of treatment, with all patients who either fully or partially recovered from vision loss having received some form of intervention. Distinctive features characterizing periocular embolism include immediate-onset and simultaneous blindness along with ocular pain. This stands in stark contrast to facial skin ischemia, which typically manifests as blanching followed by delayed pain.

Incidence of signs and symptoms of soft tissue filler induced vision loss:

SIGN/SYMPTOM	INCIDENCE
Complete Blindness	54.2%
Unilateral Blindness	45.8%
Ocular Pain	56.3%
Skin Changes	43.8%
Ophthalmoplegia	54.2%
Ptosis	52.1%
Nausea/Vomiting	16.7%
CNS symptoms	18.8%

In a recent comprehensive review encompassing 48 new cases of vision loss, 54.2% exhibited complete vision loss, while the rest experienced complete unilateral vision loss. Initial symptoms, reported in 56.3% of cases, included periorbital, ocular, periocular, orbital, eye pain, or headache. Additionally, 43.8% reported associated skin changes, commonly described as erythematous to violaceous mottling or skin necrosis.

Ophthalmoplegia (i.e., reduced extraocular muscle movement) was observed in 54.2% of cases, with ptosis in 52.1%. Notably, ophthalmoplegia and ptosis typically achieved complete recovery. Nausea and/or vomiting were noted as presenting symptoms in 16.7% of cases, and central nervous system (CNS) complications were evident in 18.8% of cases, encompassing stroke-like features such as unilateral weakness or evidence of brain infarction on imaging.

Understanding Preventive Methods

Prior to embarking on dermal filler injections, a fundamental comprehension of facial vascular anatomy and precise filler material placement is imperative. Despite the omnipresent risk of ophthalmic artery embolization across facial regions, specific "danger zones" prone to vascular compromise encompass the glabella, nasal area, nasolabial folds, forehead, and temple.

Initiating dialogue regarding potential vision loss associated with fillers is crucial during patient consultations preceding injection and before securing informed consent. Indicators of filler-induced visual compromise encompass vision loss, acute pain, ophthalmoplegia, ptosis, central nervous system (CNS) complications, and nausea/vomiting. Notably, pain may exhibit variable presence and might be concealed by lidocaine, a common component in filler products, or prior administration of topical anesthetics or nerve blocks.

Prompt cessation of filler injection is imperative upon detecting signs of filler-induced blindness, necessitating practitioners to be adept at managing ensuing complications. It is advisable for filler injectors to exercise caution, steering clear of high pressures and volumes during injection. A study utilizing a cadaver head perfusion model revealed that the average injection pressure leading to ophthalmic artery embolization via cannulation and hyaluronic acid filler injection in the supratrochlear artery was 166.7 mm Hg. Acknowledging the potential for injectors to surpass 200 mm Hg within a brief timeframe reinforces the clinical recommendation to avoid elevated injection pressures.

The administration of fillers should involve the use of small aliquots per pass, informed by a cadaver study revealing the entire volume of the supratrochlear artery from glabella to orbital apex to be 0.085 mL. Accordingly, pass volumes below 0.1 mL are recommended. The debate between cannulas and needles for filler injections persists; however, it is crucial to recognize that filler-induced blindness can result from both needle and cannula applications. Analyzing 48 cases of blindness following filler injections from 2015 to 2018, only 33% documented needle or cannula usage, with varying diameters.

The implementation of reflux in the filler syringe to assess intraarterial placement of the needle or cannula. However, such evaluations present challenges as larger bore needles resulted in positive aspirations in all filler materials, emphasizing the nuanced rheological properties of fillers compared to fluids. Recommended injection techniques include using small volumes per pass, maintaining continuous movement of the needle or cannula during injection, employing low injection pressure, and aspirating before injection. Nevertheless, caution is warranted as these techniques may yield false-negative results.

Forestall intraarterial embolization encompass the utilization of local vasoconstrictors (e.g., epinephrine) to constrict blood vessels, limiting filler volume, and applying occlusive pressure in the area of the supraorbital notch.

Understanding Migigation Methods

CURRENT TREATMENT STRATEGIES	MODE OF ACTION	MECHANISM OF ACTION
Ocular massage	Dislodge	Repeated compression of the eyeball to dislodge blockage: a sudden drop in intraocular pressure (IOP) with release increases the retinal perfusion.
Anterior chamber paracentesis	Reduce intraocular pressure	Extracting 0.1-0.2ml aqueous fluid via needle to reduce IOP and to allow an increase in perfusion pressure.
Hyperbaric oxygen	Increase perfusion	Increase oxygen tension and oxygen delivery to ischaemic retinal tissue—involves intermittent inhalation of 100% oxygen under a pressure greater than 1 atm.
CO2 rebreathing	Increase perfusion	Rebreathing into a bag produces both hypercapnia which is known to increase retinal blood flow and hypoxia which causes vasodilation. In addition, both hypercapnia and hypoxia can increase cardiac out-put and raise systemic arterial blood pressure, which in turn, increases ocular perfusion pressure.
Timolol drops	Reduce intraocular pressure	Suppress aqueous humour formation, reduce IOP and increases perfusion.
IV Mannitol, Acetazolamide	Reduce intraocular pressure	Medication used in glaucoma to reduce intraocular pressure.
Aspirin	Prevents clot formation	Prevents platelet aggregation, allowing body to breakdown embolus element of blockage.
Topical and systemic steroids	Reduce intraocular pressure	Reduction in vascular endothelial oedema.
Sublingual isosorbide mononitrate	Increase perfusion	Causes a mild decrease in intraocular pressure along with corresponding dilation of retinal vasculature and increased perfusion in the retinal artery.

Reference:

Consensus Opinion for The Management of Soft Tissue Filler Induced Vision Loss (2021)

Ocular Pain and Impending Blindness During Facial Cosmetic Injections: Is Your Office Prepared? (2016)

Blindness After Filler Injection Mechanism and Treatment (2021)

Visual loss following cosmetic facial filler injection (2019)

2 Rare, But Real, Side Effects Everyone Should Know Before Getting Fillers (2024)

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