Received: 31 May 2018 | Revised: 22 June 2018 | Accepted: 1 June 2018

DOI: 10.1111/jocd.12705

MASTER CASE PRESENTATION

Severe vision loss caused by cosmetic filler augmentation:

Case series with review of cause and therapy

Wilai Thanasarnaksorn MD1,2 | Sebastian Cotofana MD, PhD3 |

Christina Rudolph MD3 | Patcharahatai Kraisak MD2 | Nongsak Chanasumon MD1 |
Atchima Suwanchinda MD, MS1,4

1
Division of Dermatology, Department of
Medicine, Faculty of Medicine, Ramathibodi Summary
Hospital, Mahidol University, Bangkok, Hyaluronic acid (HA) injection is a popular nonsurgical, facial rejuvenating procedure.
Thailand
2 Due to the rapidly expanding use of HA injections, significant potential complica-
Samitivej Esthetics Institute, Samitivej
Sukhumvit Hospital, Bangkok, Thailand tions have also increased in frequency. Among these complications, the rare but
3
Department of Medical Education, Albany most devastating one is arterial occlusion, which can result in skin necrosis or blind-
Medical College, Albany, New York,
4
ness. To describe the mechanisms behind vision loss secondary to hyaluronic acid
School of Anti‐Aging and Regenerative
Medicine, Mae Fah Luang University, injection and the efficacy of treatments to restore vision and associated ocular func-
Bangkok, Thailand
tionality. We reviewed six cases of patients from October 2011 to December 2017
Correspondence: Atchima Suwanchinda, who experienced vision loss after receiving facial HA injections and the subsequent
Division of Dermatology, Department of
treatments undertaken to attempt to reverse the vision loss and additional eye com-
Medicine, Faculty of Medicine, Ramathibodi
Hospital, Mahidol University, 58/59 plications. Of the six patients, four received nose, one received forehead, and
Soi.Chinnakhet2, Tungsonghong, Laksi,
another one received temple injections. All six patients developed vision loss sec-
Bangkok, Thailand (dr.atchima@gmail.com).
ondary to hyaluronic acid embolization in retinal or ophthalmic arteries. Additional
complications included severe periorbital pain, ptosis, impairment of extraocular
muscle functionality. Recovery of vision was dependent on the type, frequency, and
duration of subsequent treatment. Vision loss is a rare but catastrophic complication
caused by hyaluronic injection that occurs secondary to hyaluronic acid embolization
in retinal or ophthalmic arteries due to retrograde flow from facial vascular anasto-
moses. We suggest the early supratrochlear/supraorbital hyaluronidase injection,
ocular massage, and re‐breathing into a plastic bag as safe, uncomplicated and effec-
tive methods to restore the retinal circulation and reverse vision loss.

KEYWORDS
augmentation, cosmetic filler, hyaluronic acid injection, vision loss

1 | INTRODUCTION
Hyaluronic acid (HA) injection is a popular nonsurgical, rejuvenating
procedure due to its effectiveness and reduced downtime compared
to the surgical technique. Hyaluronic acid acts as a soft tissue filler
due to its glycosaminoglycan structure, which allows it to retain
water, and in turn, volumize the overlying skin.1 Soft tissue fillers,
like hyaluronic acid, have become the second most frequently used
cosmetic minimally invasive procedure with about 2.1 million people
undergoing HA injection in 2017.2
As HA injection use has rapidly expanded from previous years,2
the number of reported adverse events has also increased. While
temporary, localized injection site reactions, including limited pain,
bruising, and redness continue to be the most common, more severe
complications are being identified.1 Among these complications, the

J Cosmet Dermatol. 2018;1–7. wileyonlinelibrary.com/journal/jocd © 2018 Wiley Periodicals, Inc. | 1

2 |
rare but most devastating one is arterial occlusion, which can result
in skin necrosis or blindness. Unless managed appropriately, this
vision loss can become irreversible. Despite the severity of this com-
plication, there currently is not one recognized gold standard for the
treatment of ocular blindness secondary to hyaluronic acid injection.
From October 2011 to December 2017, six cases of severe
vision loss from cosmetic filler injection with hyaluronic acid were
enrolled to this review. The objective of this case series is to
describe the potential mechanisms behind vision loss secondary to
hyaluronic acid injection and the efficacy of treatments to restore
vision and associated ocular functionality.
2 | CASE 1
A healthy 36‐year‐old woman underwent nasal augmentation with
1 mL of hyaluronic acid (Restylane, Galderma, Uppsala, Sweden)
injection using a blunt 27 G cannula under infraorbital nerve block
with 1% xylocaine on both sides. Immediately after completing the
injection, the patient developed sudden‐onset nausea and pain in the
left eye. Within 1 minute, the patient opened her eyes and experi-
enced decreasing vision in left eye with total ophthalmoplegia and
complete ptosis, as well as dizziness. She was referred to a hospital
nearby.
Initial physical examination yielded a visual acuity of 20/20 in the
right eye and only light perception in left eye. The left globe was
very soft. The left eye demonstrated a total ophthalmoplegia with
complete ptosis, a cloudy cornea, and a fixed, dilated pupil. The view
of the anterior chamber, lens, and posterior segment could not be
visualized due to cloudy cornea. Purplish discoloration was evident
over her left orbital area, forehead, and nasal bridge.
CT angiogram showed a left ophthalmic artery occlusion with an
anterior segment ischemia grade IV. An MRI of the brain and orbit
showed a multifocal restricted lesion at the cortical gray matter of
the bilateral frontal, left parietal and occipital lobes, caudate nucleus,
periventricular white matter of left frontal lobe, and external capsule,
which likely is representative of an acute infarction due to embolic
phenomenon. Left optic nerve edema was also noted.
Six hours later, she was referred to our center for complication
management and 3 mL (150 units/mL) of hyaluronidase was injected
at the nasal area. Hyperbaric oxygen therapy was administered and
low‐level laser therapy (LLLT) was given to reduce inflammation on
the lesion. Anterior chamber paracentesis was done on left eye.
Methylprednisolone and antiplatelet drugs were given in addition to
an oral antibiotic to prevent secondary infection. An antiepileptic
drug was started to prevent seizure. Topical steroid eye drop, and
topical antibiotic eye drop were provided.
A follow‐up ophthalmologic examination in the following days
showed a progression of the corneal edema with a gradual increase
in conjunctival chemosis. Anterior segment ischemia was suspected.
Visual acuity of left eye remained light perception.
Two months afterward, her vision in the left eye remained lim-
ited to light perception. The lid ptosis and ophthalmoplegia was
completely resolved. The left globe exhibited microphthalmia. The
THANASARNAKSORN ET AL.
left cornea became much clearer with mild posterior striae and the
left lens showed moderate cataract. Six months later she received a
left artificial eye.
3 | CASE 2
A healthy 36‐year‐old woman suddenly developed severe pain and
vision loss in her right eye after nasal augmentation with hyaluronic
acid (Restylane, Galderma) injected by blunt 27 G cannula. The
patient performed self‐ocular massage and breathed into a plastic
bag were performed while she was transferred to the hospital as the
recommendation of the ophthalmologist.
A right eye examination performed 60 minutes after the incident
found no evidence of light perception, a 2 mm ptosis, and limited
extraocular muscle movement (EOM; start from 12 o'clock: 60, 100,
50, 90). The right pupil was reactive to light; however, there was a
positive relative afferent papillary defect (RAPD).
The patient was diagnosed with a central retinal artery occlusion
in right eye. She was initially treated with carbogen for 30 minutes
every 2 hours, and right ocular massage for 10 seconds for three
cycles every hour for first 24 hours. The patient also received a
3 mL injection of hyaluronidase (150 units/mL) at nasal area. Hyper-
baric oxygen therapy was administered 5 hours after the incident.
She was also prescribed oral acetazolamide (1000 mg), an eye drop
consisting of dorzolamide combined with timolol, and an oral aspirin
(325 mg/d).
Extraocular movements of right eye slightly improved 7 days
after the incident (95, 100, 80, 85) but the patient still demonstrated
no light perception in the right eye. After 21 days following the inci-
dent, the ptosis completely resolved, and the patient had significant
improvements in EOM function (90, 100, 90, 90) until full recovery
30 days after the incident.
4 | CASE 3
A healthy 26‐year‐old woman who underwent a 0.4 mL nasal hya-
luronic acid injection (Modelis, Merz, Frankfurt, Germany) with a 25
G blunt cannula, suddenly developed periorbital pain, headache and
severe blurred vision of the right eye immediately after the proce-
dure. The patient then received 2 mL of a hyaluronidase (150 mg/
mL) injection on the augmented area and a nitroglycerin transdermal
pad on the chest 15 minutes after the incident. The patient per-
formed ocular massage and breathed into a plastic bag in the ambu-
lance during inter‐hospital transfer.
On initial physical examination, there was evidence of deep blue
petechiae and an erythematous patch on the nose and glabella area.
Eye examination shows visual field defect in right eye at temporal
side and their white yellowish triangular ischemia area, temporalnasal
angular ischemia at 3 and 8 o'clock. The patient was diagnosed with
right peripheral retinal ischemia and choroidal ischemia. She was
treated with pulse electromagnetic frequency while waiting for fur-
ther examination, which reduced her right eye pain from a score of
10/10 down to 5/10. Hyperbaric oxygen therapy was performed
THANASARNAKSORN ET AL.
4 hours after the incident. Patient had done self‐ocular massage for
6 hours.
Five days after the hyaluronic acid injection, an eye examination
showed normal extraocular muscle function testing of both sides,
confrontation visual field test showed temporal side equal to nasal
side.
5 | CASE 4
A healthy 23‐year‐old man, who received hyaluronic acid injection
on the nose (Hyacorp, Bioscience, Dümmer, Germany) with a blunt
cannula by a nonphysician (Figure 1A), suddenly developed vision
loss in right eye, severe right periorbital pain, headache, nausea, and
vomiting. The patient was referred to the hospital and prescribed
intravenous parecoxib, metoclopramide, acetazolamide, carbogen,
timolol drops, and aspirin. Hyaluronidase (2 mL) was injected into
the nose area.
A CT scan of the brain showed no detectable abnormality of the
brain or visual orbit, no evidence of acute infarction or intracranial
hemorrhage, and no detective abnormality on CTA or CTV.
The initial physical examination revealed right eye blindness, a
5 mm pupil that was not reactive to light, ptosis, limit EOM, skin dis-
coloration (Figure 1B), and tenderness of the nasal tip and surround-
ing area.
The patient was diagnosed as with a right eye central retinal
artery occlusion with a concomitant cranial nerve III palsy.
Twelve hours later, hyperbaric oxygen was administered. The
patient continued to report pain inside nasal cavity, in the right peri-
orbital area and nasal congestion, so hyaluronidase was injected into
the nose and paranasal area in multiple planes, which relieved the
pain inside the nasal cavity and nasal congestion symptoms. On the
next day, 2 mL of a retrobulbar hyaluronidase (500 units/mL) injec-
tion was performed on right eye and significantly decreased the pain
in the right periorbital area. Moreover, EOM function and ptosis on
the right eye were significantly improved on the same day. Two days
later, another 3 mL of retrobulbar hyaluronidase (500 units/mL) was
injected, which on the next day, further improved the EOM function
and ptosis of right eye. The patient's EOM function and ptosis con-
tinued to gradually improve until full recovery 6 days later (Fig-
ure 1C).
6 | CASE 5
A 61‐year‐old woman with a bone deformity on the left side of her
forehead underwent filler augmentation in the left side of her fore-
head on the periosteum with 1 mL of hyaluronic acid (Restylane with
lidocaine, Galderma) injection by a 25 G blunt cannula. The patient
developed a severe headache, skin blanching and blurred vision in
her left eye immediately after the injection.
Within 15 minutes after the incident, the patient received
9 mL of an intralesional hyaluronidase (150 units/mL) injection and
8 mL of a retrobulbar hyaluronidase (150 units/mL) injection by
the doctor who performed filler augmentation. A nitroglycerin
| 3
transdermal pad was applied on the chest then ocular massage
and rebreathing in a plastic bag were performed during the
patient referral.
Initial physical examination showed a well‐demarcated purplish
discoloration of the skin along the territory of the left supraorbital
and supratrochlear arteries and upper eyelid and mild swelling and
ptosis of the left upper eyelid. The right eye pupil was 2.5 mm and
was reactive to light, while the left eye pupil was 3 mm and slowly
reacts to light. On assessment of visual acuity, the left eye was lim-
ited to only light perception.
MRA and MRI of the brain showed a small subacute infarction at
left temporal lobe, suggestive of an acute left optic neuropathy at
the infraorbital segment with restricted diffusion, which was consid-
ered to be due to an ischemic cause. The origin of the ophthalmic
arteries was patent with limited evaluation of the distal part.
The patient was diagnosed with a left ophthalmic artery occlu-
sion and prescribed an intravenous antibiotic, systemic steroid and
hyperbaric oxygen therapy. Pulsed electromagnetic frequency was
applied to reduce the pain.
Ptosis and EOM function partially improved 20 days after initial
injury. Ophthalmoplegia was almost fully recovered at 30 days after
initial injury; however, the visual acuity of the left eye was still lim-
ited to light perception.
7 | CASE 6
A 31‐year‐old female patient received a hyaluronic acid (Belotero
Volume, Merz) injection with 23 Gauge needle at the left temporal
area. The physician injected 0.4 mL of filler at point A with no symp-
toms (Figure 2). Conversely, after injection of 0.1 mL of filler at point
B (Figure 2) which the physician used deep bolus injection technique
on this area. The filler was injected while the tip of the needle
touching the bone, the patient suddenly developed blurred vision of
left visual field and inability to elevate the left upper eyelid. Hyaluro-
nidase (600 units/mL × 7.5 mL) was immediately injected over the
left forehead and temporal area without improvement of visual
symptoms. Hyaluronidase was then injected into the supratrochlear
notch (1.5 mL × 600 units/mL) and around the supratrochlear notch
(1 mL × 600 units/mL; Figure 3), which brought immediate relief of
the visual symptoms with residual blurred vision in the left central
field only (Figure 4). The patient was referred to the ophthalmologist
and ocular massage was performed during the transfer. Additional
treatment of ocular massage (4.5 hours) and hyperbaric oxygen
(90 minutes) were done. The patient experienced full recovery of
her vision and a subsequent eye examination on the next day was
also normal.
8 | DISCUSSION
Vision loss from HA injection can occur when used to treat any loca-
tion on the face due to the rich supply of vascular anastomoses that
connect to the ophthalmic artery. The ophthalmic artery gives off a
branch called the central retinal artery, which travels through the
4 |
(A)
optic nerve and its branches supply the retina. High‐risk areas
include the glabella (supratrochlear and supraorbital arteries), nasal
region (lateral and dorsal nasal arteries), nasolabial fold (angular
artery), forehead (supratrochlear and supraorbital arteries) and tem-
ple area (superficial temporal artery).3–5 In this case series, vision loss
occurred when HA was used at nasal area in four out of six patients,
and at forehead and temple area in the other two patients. Nonethe-
less, there is no safe area; hence, the physician should be very cau-
tious and must perform the procedure with an awareness of facial
vascular anatomy and variation.
The proposed mechanism of blindness secondary to HA injec-
tion is the retrograde flow from the peripheral branches including
the supratrochlear, the supraorbital, dorsal nasal, superficial
THANASARNAKSORN ET AL.
F I G U R E 1 Case 4: A 23‐year‐old man,
who received hyaluronic acid injection with
a blunt cannula on the nose by a
nonphysician and suddenly developed
vision loss in right eye, severe right
periorbital pain, headache, nausea, and
vomiting. He developed limited EOM of his
right eye with ptosis and 5 mm fixed
dilated pupil and no perception of light on
visual acuity exam. A, Photograph indicates
(B) the location of the HA injection. B, The
patient developed significant bruising and
swelling after injection as noted by the red
dashed line in the left‐sided picture. In this
case, the HA likely was injected into the
dorsal nasal artery and underwent
retrograde flow (blue arrows) through the
dorsal nasal artery to the ophthalmic artery
and then underwent anterograde flow and
then blocking (yellow arrows) the central
retinal artery. The skin discoloration
occurred in the areas of vascular supply for
the supraorbital and supratrochlear
arteries, which were also affected by the
emboli (yellow arrows). C, These images
demonstrate the effect of the retrobulbar
hyaluronidase on the patient's ptosis.
Before injection (top left picture), the
patient had significant right eye ptosis,
which gradually continued to improve after
2 injections of retrobulbar hyaluronidase.
(C) He experienced full recovery of his EOM
and ptosis 6 d after the second retrobulbar
hyaluronidase injection
temporal, and angular arteries to the ophthalmic circulation, which
can ultimately reach the central retinal artery due to the high
injection pressure with sufficient amount of filler product.6 It has
been postulated that the average volume of filler necessary to
occupy the supratrochlear artery from the glabella to the bifurca-
tion of the ophthalmic and central retinal artery is 0.085 mL.7 In
case 4, the patient developed ptosis, vision loss and EOM limita-
tions after HA injection on the nose. In this case, the HA likely
was injected into the dorsal nasal artery and underwent retrograde
flow through the dorsal nasal artery to the ophthalmic artery and
ultimately blocking the central retinal artery. The skin discoloration
occurred in the areas of vascular supply for the supraorbital and
supratrochlear arteries, which were also affected by the emboli
THANASARNAKSORN ET AL. | 5

F I G U R E 2 Case 6: Left picture: A 31‐year‐old female patient was injected with 0.4 mL of HA first at point A without symptoms, then
received 0.1 mL of HA at point B, which the physician used deep bolus injection technique on this area. The filler was injected while the tip of
the needle touching the bone, the patient suddenly developed blurred vision of left visual field and inability to elevate the left upper eyelid.
Right picture: The second injection was likely placed into the frontal branch of the superficial temporal artery, which anastomoses with
branches from the supraorbital artery, causing a HA embolus to either the ophthalmic or central retinal artery, thereby yielding vision loss

F I G U R E 3 Case 6: Left picture: The red circle indicates the location of the supratrochlear notch, where hyaluronidase was injected (red
circle, 1.5 mL × 600 units/mL) after hyaluronidase injection into the temporal and over the left forehead area did not improve the 31‐year‐old
female's vision loss. This injection brought immediate relief of the visual symptoms. Right picture: Once the hyaluronidase is injected (blue
circle) it undergoes retrograde flow (blue arrows) from the supratrochlear artery to the ophthalmic artery and into the central retinal artery
(yellow arrow) to break up the HA embolus

F I G U R E 4 The right and left eye examination after the 31‐year‐old female with left eye visual loss received a supratrochlear hyaluronidase
injection, but before ocular massage

(Figure 1B). Similarly, in case 6, HA was likely injected directly Early diagnosis of visual compromise from HA injection can be
into the superficial temporal artery, whose terminal branches anas- made by recognizing the signs and symptoms of sudden onset of
tomose with the supraorbital artery (Figure 3). severe pain accompanied by complete or partial loss of vision,
6 |
blurred vision, visual field defect, nausea, vomiting, and headache.
Nevertheless, central retinal artery occlusion may present without
ocular pain and it is necessary to be cognizant of other red flag ocu-
lar signs which have been described, including ptosis, ophthalmople-
gia, exotropia, and pupillary defect.5, 6
Strategies to mitigate the vascular risk from HA injection include
a thorough knowledge of facial anatomy and plane of injection
(especially vascular anatomy and variation), the complete history of
the patients (previous cosmetic procedures, previous complications),
the use of blunt cannula/small needle/small syringe, the aspiration
before injection (slowly count 1–10 × 3 times), and the need for a
slow speed of injection with small amount of product. In addition,
the proper selection of patients and the monitoring during the pro-
4
cedure are also crucial.
The golden period to reverse retinal artery occlusion is 90 min-
utes.5 The patient should be transferred to the specialist as soon as
possible. Once retinal artery occlusion is suspected, several immedi-
ate actions should be taken to mitigate the adverse effects: termina-
tion of HA injection, administration of a hyaluronidase injection,
ocular massage, and re‐breathing in the plastic bag to increase CO2,
which causes subsequent vasodilatation, while transferring.
In case 1, the treatment was delayed and the ocular massage was
not done. The patient suffered from complete blindness and subse-
quent artificial eye replacement, which EOM function retuned after
2 months. Whereas, in case 2, 3, and 5, ocular massage and plastic bag
inhalation were performed during the transfer to the hospital, leading
to the improvement of EOM function in case 2, 3, and 5 within 30 days,
and complete recovery of visual defect in case 3 after additional ocular
massage for 6 hours. While in case 6, ocular massage was only done
after arriving the hospital for additional 4.5 hours which resulted in full
recovery of visual function. These improvements demonstrate the
strong benefit of performing ocular massage during transfer or even
after. Ocular massage aims to decrease intraocular pressure, increase
blood flow and dislodge the emboli, during the transfer. It is performed
with the patient closing his or her eyes and looking downward in order
to turn the globe upward exposing to the vascular tunnel. The patient
then places a finger over the eyeball and gently indents the globe while
counting from 1 to 10, followed by a sudden finger release. The cycle of
ocular massage should be for at least 5 minutes.8 Ocular massage has
been demonstrated to have an increased efficacy when performed with
high frequency for more than 3 hours.3, 9 We recommend to do ocular
massage immediately after the embolism and should be done long
enough until the emboli dislodged.
Hyaluronidase is an enzyme used to catalyze hyaluronic acid by
injection into the vessel to reverse ischemia. This enzyme will break
down the glucosaminidic bond between C1 of the glucosamine moi-
ety and C4 of the glucuronic acid.10 It has been reported that hya-
luronidase can diffuse across the arterial wall to degrade the
hyaluronic acid without the insertion into the affected artery. Thus,
it is recommended to inject high dose of hyaluronidase at the site of
filler injection and surrounding areas.
Regarding blindness, many techniques of hyaluronidase injection
have been reported with optimal outcomes; however, these
THANASARNAKSORN ET AL.
techniques remain debatable. Direct intraarterial hyaluronidase injec-
tion to ophthalmic artery via angiogram has been theoretically postu-
lated, which requires highly specialized skill and medical instruments.
Retrobulbar injection is another technique to recover blindness.
This procedure can be achieved by localized injection of local anes-
thetic at the lower eyelid. A 25‐gauge needle or cannula is then
inserted into the inferotemporal quadrant of the orbit at a depth of
at least 1 inch to target the intraconal space (inferolateral to optic
nerve). Then, 2–4 mL of hyaluronidase (300–600 units) is injected
into the retrobulbar space at the inferolateral orbit. The volume of
hyaluronidase should be limited, as the volume effect of retrobulbar
injection more than or equal to 7 mL may cause significant optic disc
edema, which can further complicate the patient's vision.11 This
technique contains the risk of injury to the eyes and therefore,
should be performed only by a trained ophthalmologist.12
In case 5, despite immediately injecting hyaluronidase into the
retrobulbar space, the visual defect was not reversed. This could be
due to the hyaluronic acid already embolizing in the central retinal
artery in the area of the optic sheath, which hyaluronidase cannot
pass through. Furthermore, too much volume of hyaluronidase injec-
tion (8 mL in this case) may have resulted in a magnification of pres-
sure effect, which could have forced the hyaluronic acid further into
the central retinal artery. Moreover, the time to treatment is always
crucial: Zhu et al13 performed a study of retrobulbar hyaluronidase
treatment and concluded that it is not possible to reverse visual acu-
ity in patients with more than 4‐hours blindness even with hyaluro-
nidase in the dosage of 1500–3000 units. In contrast, case 4
demonstrates that retrobulbar hyaluronidase injection can reverse
the symptoms of ophthalmoplegia and ptosis, which results in the
esthetic improvement of the eyes within 1 week.
According to the proposed mechanism of retrograde emboliza-
tion from a peripheral branch to the central retinal artery, we would
like to suggest another technique of hyaluronidase injection into the
supratrochlear and supraorbital notch to allow for retrograde flow of
the hyaluronidase to the HA material inside the retinal artery simi-
larly to the route taken by the filler embolus. This procedure is sim-
ple, safe, and easy to follow performing by the injection of 300–
1500 units of hyaluronidase into the supratrochlear and supraorbital
notch and surrounding areas. The landmark of supratrochlear and
supraorbital notch can be identified by palpating along the inferior
side of superior orbital rim until the depression notches can be felt.
From midline, the average distance to the supratrochlear and
supraorbital arteries are 16.4 ± 1.7 mm and 26.5 ± 2.6 mm, respec-
tively. The injection should be inserted into the notch from above to
the ophthalmic circulation. The effectiveness of this method was
mentioned by Goodman and Clague and confirmed by the successful
treatment in case 6.14
The supratrochlear artery and supraorbital artery are effective
locations for hyaluronidase injection due to their locations and con-
nections. These arteries are the branches of ophthalmic artery. The
supratrochlear artery passes through the supratrochlear notch, which
is located at the superomedial orbit 1.7–2.2 cm lateral to the midline.
It travels along within a 5 mm deviation to the medial vertical line.
THANASARNAKSORN ET AL.
This vessel is 1–2 mm deep in the muscle layer. It becomes subcuta-
neous 15–25 mm above the supraorbital rim as it runs superiorly.15
The supraorbital artery is the closest arterial branch to the oph-
thalmic circulation.16 It runs deep into the corrugator muscle at the
level of the supraorbital rim, corresponding to the vertical line of
medial limbus of the cornea. When it exits the supraorbital foramen,
which located within 1 mm of medial iris and 1–1.5 cm medial to
superior temporal line, it divides into a superficial branch and deep
branch. The vertical and brow branches arise from the superficial
branch, whereas the deep branch gives rise to medial, oblique, and
lateral rim branches. The superficial vertical branch anastomoses
with the supratrochlear and the frontal branch of superficial tempo-
ral artery.15, 17
The other treatment options also aim to lower intraocular pres-
sure (carbonic anhydrase inhibitors, ocular massage), increasing reti-
nal blood flow (ocular massage, breathing in plastic bag, carbogen
anhydrase inhibitor, topical and systemic steroids), and increasing
oxygen delivery (hyperbaric oxygen therapies).3
9 | CONCLUSIONS
In conclusion, vision loss is a rare but catastrophic complication
caused by hyaluronic injection. Prevention of this side effect requires
proper injection technique; however, when vision loss does occur,
with limited time of visual restoration, early recognition and prompt
treatment are the keys to hopefully reverse the vision. To the best
of our knowledge, there is no gold standard for the treatment of
retinal artery embolization. Nevertheless, every possible attempt
should be performed to dissolve the embolized filler and reverse the
tragic blindness. We suggest the early supratrochlear/supraorbital
hyaluronidase injection, ocular massage, and re‐breathing into a plas-
tic bag as safe, uncomplicated and effective methods to restore the
retinal circulation and reverse vision loss.
CONFLICT OF INTEREST
None of the authors listed have any commercial associations or
financial disclosures that might pose or create a conflict of interest
with the methods applied or results presented in this study.
ORCID
Atchima Suwanchinda http://orcid.org/0000-0002-3432-7090
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How to cite this article: Thanasarnaksorn W, Cotofana S,
Rudolph C, et al. Severe vision loss caused by cosmetic filler
augmentation: Case series with review of cause and therapy.
J Cosmet Dermatol. 2018;00:1–7. https://doi.org/10.1111/
jocd.12705