Blindness Following Cosmetic Injections of the Face

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SPECIAL TOPIC
Blindness following Cosmetic Injections of
the Face
Davide Lazzeri, M.D.
Tommaso Agostini, M.D.
Michele Figus, M.D., Ph.D.
Marco Nardi, M.D.
Marcello Pantaloni, M.D.
Stefano Lazzeri, M.D.
Pisa and Florence, Italy

Background: Complications following facial cosmetic injections have recently
heightened awareness of the possibility of iatrogenic blindness. The authors
conducted a systematic review of the available literature to provide the best
evidence for the prevention and treatment of this serious eye injury.
Methods: The authors included in the study only the cases in which blindness
was a direct consequence of a cosmetic injection procedure of the face.
Results: Twenty-nine articles describing 32 patients were identified. In 15 patients, blindness occurred after injections of adipose tissue; in the other 17, it
followed injections of various materials, including corticosteroids, paraffin, silicone oil, bovine collagen, polymethylmethacrylate, hyaluronic acid, and calcium hydroxyapatite.
Conclusions: Some precautions may minimize the risk of embolization of filler into
the ophthalmic artery following facial cosmetic injections. Intravascular placement
of the needle or cannula should be demonstrated by aspiration before injection and
should be further prevented by application of local vasoconstrictor. Needles, syringes, and cannulas of small size should be preferred to larger ones and be replaced
with blunt flexible needles and microcannulas when possible. Low-pressure injections with the release of the least amount of substance possible should be considered
safer than bolus injections. The total volume of filler injected during the entire
treatment session should be limited, and injections into pretraumatized tissues
should be avoided. Actually, no safe, feasible, and reliable treatment exists for
iatrogenic retinal embolism. Nonetheless, therapy should theoretically be directed
to lowering intraocular pressure to dislodge the embolus into more peripheral
vessels of the retinal circulation, increasing retinal perfusion and oxygen delivery
to hypoxic tissues. (Plast. Reconstr. Surg. 129: 995, 2012.)
CLINICAL QUESTION/LEVEL OF EVIDENCE: Risk, V.

F

acial soft-tissue augmentation and rejuvenation procedures using various injections of
filler materials are widely performed for cosmetic enhancement because of their highly predictable, convenient, and pleasing outcomes.1,2 In
recent years, complications following facial cosmetic injections have heightened awareness of the
possibility of iatrogenic visual loss.3–31 Nevertheless, transitory and permanent blindness has followed routine aesthetic injection of the face during which a serious injury is not expected.3–31
We reviewed and examined the influences of
injection pressures; material type; and needle,
From the Plastic and Reconstructive Surgery and Ophthalmology Units, University Hospital of Pisa, and the Maxillofacial Surgery Unit, University of Florence.
Received for publication September 12, 2011; accepted October 5, 2011.
Copyright ©2012 by the American Society of Plastic Surgeons
DOI: 10.1097/PRS.0b013e3182442363

cannula, and syringe size in causing retrograde
flow of the substance to understand the conditions
under which retrograde flow can lead to retinal
circulation embolism and blindness. We sought to
elucidate risk factors for retinal vascular occlusion in addition to the cause, prevention, and
treatment options following cosmetic injections
into the face that resulted in blindness or severe
visual disability, and we hope to provide a useful
guide for physicians who perform these cosmetic procedures.

PATIENTS AND METHODS
We reviewed the available literature regarding
the occurrence of blindness following injections

Disclosure: There are no financial conflicts or
interests to report in association with the content of
this article.

www.PRSJournal.com

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Plastic and Reconstructive Surgery • April 2012
of fillers of the face. Data were identified by
searches in MEDLINE, the Cochrane database,
Google and Google Scholar, Current Contents,
and PubMed. We used the search terms “blindness
after steroid injection,” “blindness after fat injection,” “blindness after facial injections,” “blindness after sclerotherapy,” “blindness after cosmetic
medicine,” “ischemic optic neuropathy after injection of the face,” “emboli facial filler,” “arterial occlusion after soft tissue filler,” “blindness after facial
filler,” and “arterial occlusion after facial filler.” All
cases of blindness or visual impairment that were not
a direct consequence of an injection procedure into
the facial skin were excluded, as were those in which
blindness was not produced by retinal or retinal
branch artery occlusion. Thus, cases of blindness
following intraturbinate steroid injections,32–36 anesthetic injections into the nasal septal mucosa,37– 40
oral and palatal mucosal injections,41 and tonsillar
injections42,43 were excluded. A single case of visual
impairment subsequent to the use of nasal decongestant was also excluded.44 All articles that described cases in which facial injection had no pure
cosmetic aim, such as sclerotherapy of vascular
lesions45–51 and corticosteroid injections for the treatment of chalazia,52,53 were excluded.

nose15). In the remaining two cases, fat tissue was
grafted to multiple regions of the face.9,12
Procedural details of the cannula, syringe, and
needle used were available in only three articles. A
10-ml syringe was used twice: once with a 20-gauge
(0.812-mm) needle and once with a 16-gauge (1.291mm) sharp needle.9 In one case, a 20-ml syringe was
used with a 2-mm-diameter cannula.7
In all cases described,3–15 the signs and symptoms
of visual adverse effects were evident immediately
following the injection, characterized by complaint
of excruciating pain and a sudden blackout of the
involved eye. Three cases5,7,10 presented with further
neurologic complications caused by cerebral vessel
embolus. Information such as history, family history,
and other physical findings was not available for any
cases in this group.3–15
In nine cases, no information about the treatment was available.3– 6,8 –10 In six cases, therapy (ocular massage,7 carbon dioxide rebreathing,7 hyperbaric oxygen therapy,7,12 oral and intravenous
corticosteroids,11–14 antiplatelet drugs,11 and fibrinolytic agents12,15; or mechanical thrombolysis15) was
administered without effects. Neither the treated
nor the untreated patients had any return of
vision.3–15

RESULTS

Other Injected Materials Group
Seventeen patients16 –31 (15 women and two
men; mean age, 38 ⫾ 11.5 years; range, 24 to 65
years) who suffered transitory (three cases)18,26,29 or
permanent (14 cases)16,17,19 –25,27,28,30,31 blindness following the injection of materials other than adipose
tissue were identified (Table 2). The injected substances included corticosteroids16,18,21 and filler materials such as paraffin,17 silicone oil,19,22,28 bovine
collagen,20,23,30 polymethylmethacrylate,24,25 hyaluronic acid,26,31 and calcium hydroxyapatite.29 The
nose (root,18,22,29 dorsum,21,22,25,29 and tip30,31) and the
scalp16,18 were the most frequently injected sites, with
seven and three cases, respectively; whereas the remaining seven cases involved the forehead,17,23
glabella,24,27 glabella and cheek20,26 (two cases for
each area), and temple area28 (one case). The syringe and needle used were described in only one
case (25-gauge needle,21 0.455 mm).
Several different individualized treatments
were attempted in this group of patients. Systemic
corticosteroids29,31 were administered in two patients,
diuretic agents (carbonic anhydrase inhibitors19,26,28)
were used in three cases, and vasodilators19 and antiaggregant drugs (antiplatelet agents,30 aspirin31) were
used in one case each. An alternative approach such as
ocular massage16,19,28 was attempted in only three

Using strict a priori criteria for our review, we
identified a total of 29 articles representing 32
cases.3–31 We divided patients into two groups: the
first group included patients (n ⫽ 15)3–15 diagnosed with blindness following fat injection of the
face for cosmetic reasons, and the second group
included patients (n ⫽ 17)16 –31 diagnosed with
transitory or permanent blindness after facial aesthetic injections of other materials. The results of
our review are summarized in Tables 1 and 2.
Fat Tissue Injection Group
A review of the literature revealed a total of 15
reports of blindness following cosmetic facial fat
tissue transfer3–31 (mean age, 40.0 ⫾ 8.0 years;
range, 24 to 49 years), including 11 women3–7,10 –15
and two men.7,8 In two cases, no demographic data
were available (Table 1).9 Three patients received
autologous fat injections into the lower third of
the face (nasolabial folds,6,13 lips, and chin).9 In
seven cases, the site of injection was the upper
third of the face, including the forehead,4,5,14
glabella,5,10,11 and nasal bridge,8 and in three cases,
fat tissue was transferred to the mid third of the
face (cheek,9 periorbita,7 and left side of the

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Volume 129, Number 4 • Blindness after Facial Cosmetic Injection
cases. Surgical treatment, specifically, anterior
chamber paracentesis, was attempted in just one
patient.28 Data on local and systemic treatments
were not available in nine patients.17,18,20,22–25,27
Only three patients recovered their sight.18,26,29
One patient recovered sight 5 minutes after injection of corticosteroids for alopecia areata, but
detailed information about the treatment was not
available.18 In another case,26 vision recovered
completely and the visual field defect improved
after prompt administration of acetazolamide
(500 mg). A healthy 25-year-old man had complete recovery of visual acuity, oculomotor nerve
palsy, and skin necrosis after treatment with oral
and topical corticosteroid tapers,29 although his
dilated pupil did not improve. Permanent visual
loss without light perception persisted in all the
remaining patients regardless of the type of treatment attempted.16,18,19,21–25,28,30,31 In three cases,
outcomes were not available.17,20,27

DISCUSSION
Pathophysiology
Central retinal artery embolization is related
to the retrograde arterial displacement of the injected products from peripheral vessels into the
ophthalmic arterial system proximal to the central
retinal artery and follows the subsequent anterior
movement of the injected substance (Fig. 1). This
may occur when the wall of a distal branch is
accidentally perforated by the injecting needle or
cannula. In this case, the force of the injection
used for the product delivery exerted on the
plunger of a syringe can significantly expand these
arterioles many times their normal caliber and can
cause retrograde flow. Once an injection pressure
higher than systolic arterial pressure is applied,33,54
the injected material displaces the arterial blood
and travels proximally past the origin of the retinal
artery. When the plunger is released, the arterial
systolic pressure then propels the resulting column of material into the ophthalmic artery and its
branches. Although larger particles can block
larger and more consequential vessels, ophthalmic artery and central retinal artery blockage can
follow wedging of a very small amount of material
in the retinal artery.
Just as the pressure exerted during injection
may push a column of filler into the ophthalmic
artery, a higher injection pressure may cause the
retrograde migration of the column in the internal carotid artery, permitting cerebrovascular embolization and stroke.30,50 Discoloration and necrosis of the facial skin and cerebral ischemia after

filler injection have the same pathophysiologic
mechanism.55– 64 Ocular circulation embolization
requires the concurrent coexistence of three factors, including the retrograde flow caused by high
injection pressure and a sufficient amount of material delivered into the vessel.54,65,66
The injection of the filler into an artery will cause
retrograde flow if the injection pressure is greater
than the sum of the systolic arterial pressure and the
frictional forces caused by viscous flow pressure
drops within the vessel. A mean pressure drop from
the eyelid to the apex of the orbit is calculated to be
approximately 23 mmHg at a mean flow rate of 4
ml/minute, assuming an axial distance to the medial
orbit of 4.5 cm and a lumen diameter of 0.05 cm for
an arteriole.54,65– 67 The calculated resistance to flow68
(8L␩/pr4) is less within a terminal artery than in
capillaries69,70; thus, the injected material will flow
predominantly in the direction of least resistance. As
the distance between the injection site and the retinal circulation increases, higher injection pressures
are required to generate retrograde flow until the
ophthalmic artery.
Retrograde flow caused by high injection pressure may lead to retinal embolism only when a sufficient amount of product is propelled into the vessel. The proximity of the injection site to the orbit
also modulates the probability of symptomatic obstruction: injections closer to the orbit increase the
probability that a meaningful volume of injected
filler will gain access to the ophthalmic artery proximal to the central retinal artery. Egbert et al. brilliantly demonstrated this concept.54 Occlusion of a
nourishing arteriole of the retina proximal to the
central retinal artery would theoretically require the
minimum amount of material to occlude the lumen
and, subsequently, the vessel’s blood flow. A volume
of 0.01 ml should occlude an arteriole 4.5 cm from
the medial orbit with a diameter of 0.05 cm.54,67
However, this estimation is not realistic because it
does not adequately address the complexity of the
orbital circulation web and the many nourishing
vessels branching from the ophthalmic artery67 or
the exact location of the injection site. These complex elements, particularly when combined with the
unpredictable dispersion of the product during
travel, preclude an accurate calculation of the exact
volume of injected material required to cause ocular
embolization.
The risk of retrograde flow caused by high injection pressure should not be avoided by adjusting
the size of the needle and the syringe. The plunger
of a 50-ml syringe has a greater cross-sectional area
than the plungers of smaller syringes and should
therefore theoretically allow lower pressure injec-

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Plastic and Reconstructive Surgery • April 2012
Table 1. Review of 15 Cases of Visual Loss after Facial Cosmetic Injection of Fat Tissue

Reference

Age
(yr)

Sex

Aesthetic
Procedure(s)

Injecting
Physician

Diameter/Size of
the Cannula/Needle
(Gauge or mm)

Complaint of Symptoms
Procedure/Symptoms
Interval

Teimourian, 19883

45

F

Fat grafts to improve glabellar
frown lines

Plastic surgeon

N/A

Dreizen and Framm,
19894

44

F

Several milliliters of
autologous fat injection into
the forehead to remove
facial wrinkles

Plastic surgeon

N/A

Egido et al., 19935

47

F

Autologous fat injection into
the forehead area

N/A

N/A

During the injection
a sudden, severe
periocular pain with
complete visual loss
in RE

Lee et al., 19966

42

F

0.5 ml of autologous fat
transplantation to her
nasolabial groove

Plastic surgeon

N/A

During the injection:
headache and dyspnea,
irritability, and felt in
an unconscious state

Feinendengen et al.,
19987

45

M

Autologous fat injection into
the nasolabial folds, lower
lip and chin

N/A

20-ml syringe and 2-mmdiameter cannula

7 hr later: global aphasia
and mild right
sensorimotor
hemiparesis
CT and MRI: infarction of
the temporoparietal
region of the left MCA

47

F

Autologous fat injection into
the periorbital areas to
correct crow’s feet

N/A

N/A

Immediately: LE pain and
violent headaches;
complete flaccid right
hemiplegia, global
aphasia and deviation
of the head and eyes
toward the left

43

M

Autologous fat injection on
the left side of the bridge of
the nose (0.5 ml), each
nasolabial fold (3 ml each)
and the upper and lower
lips (3 ml)

N/A

N/A

Within 10 minutes: eye
and head pain,
disorientation, and
aphasic with right
hemiparesis

N/A

N/A

Unspecified
operating
surgeon

10-ml syringe with a 20gauge Angiocath
needle

After recovering from
general anesthesia:
unilateral blindness

N/A

N/A

Injection of 3 ml of
autologous fat into the
cheek to fill a small
deficiency
Fat injection of 0.5 ml in each
oral commissure and lateral
canthal area, 0.25 ml in
each nasojugal trough, and
1.5 ml into a transverse scar
and wrinkle in the forehead

Unspecified
operating
surgeon

A 16-gauge sharp needle
from a 10-ml syringe
with the assistance of a
Dispos-a-ject
mechanical gun

During the injection of
the forehead: unilateral
blindness and
excruciating
hemicranial pain

Danesh-Meyer et al.,
20018

Coleman, 20029

998

Immediately: loss of vision
and excruciating pain
in the RE
Immediately: severe right
hemicranial pain and
total RE loss of vision

Volume 129, Number 4 • Blindness after Facial Cosmetic Injection
Table 1. (Continued)
Immediate
Ocular
Situation

Risk
Factors
N/A

N/A

N/A

N/A

No cardiovascular
risk factor

N/A

Concomitant
bilateral neck and
face rhytidectomy
and liposuction of
the cheeks; high
level of TG and
low level of HDL
Excision of a Baker’s
cyst, removal of
femoral varices,
cosmetic
correction of the
inframammary
folds, and
liposuction of the
thighs 4 days
prior; patent
foramen ovale
N/A

N/A

N/A

Pathogenesis/
Diagnosis
Retinal arterial occlusion
probably secondary to
fat particle embolism
Multiple fat emboli
occlusions of distal
branches of the
ophthalmic artery

Time When
Therapy
Started

Therapy

Outcomes

N/A

N/A

Totally and permanently
blind in RE

N/A

N/A

BCVA RE: no light perception
Choroidal and retinal
Pupil: nonreactive to light, but
infarction caused by fat
consensual reflex still present;
embolism and emboli
complete left hemiplegia
into the branches of the
involving the lower face
upper division of the
Fundus: pale ONH and several
MCA and ophthalmic
retinal arteries occluded
arteries
Left pupil: nonreactive to direct
CRAO caused by
autologous fat emboli
light stimulus and reactive to
indirect
Fundus: a cherry-red spot on the
macula, marked retinal
ischemia and multiple emboli
in retinal arterioles
FA: decreased caliber of the left
ophthalmic artery leading to
ophthalmic artery insufficiency
and disappearance of the
image of ocular blush
Fundus: multiple fat emboli in the Multiple branch occlusions
right retinal and choroidal
of the retinal and
arterioles
choroidal arterioles by
fat emboli

N/A

N/A

On day 75: BCVA RE: no
light perception
BCVA LE: 20/25
Fundus: pale ONH and
few scattered retinal
hemorrhages, no
cherry-red macular
spot
On day 21: no light
perception

Not specified

Ocular massage, carbon
dioxide, oxygen
therapy

After 1 wk: Recovery of
the mental status but
loss of VA
After 3 mo: No light
perception in LE with
a thick fibrous
membrane on the
posterior pole and
optic atrophy

Not specified

Not specified

Pupils: symmetrical
Left pupil: weakly reactive to
direct light stimulation
Few hours later, areactive and
mydriatic pupil
Fundus: papilledema and
ischemia of the retina

Not specified

Not specified

On day 3:
Fundus: no evidence of
multiple fat embolisms
in the retinal and
choroidal arterioles
10-mo follow-up: no
report about ocular
situation
On day 1, CT: large
hypodensities in the
left frontotemporal
area the next day
After several weeks: no
restoration of LE vision

BCVA LE: no light perception
Fat embolism to branches
Pupil: amaurotic
of the left MCA and the
Fundus: pale ONH and
ophthalmic artery
widespread retinal whitening
with visible emboli in several
retinal arterioles; preretinal
and intraretinal hemorrhages
Fundus: an embolus in the central CRAO
retinal artery

N/A

N/A

Over the ensuing 5 days,
the LE remained blind;
no longer follow-up
has been described

Not specified

Not specified

Follow-up not specified:
permanent unilateral
blindness

N/A

N/A

N/A

N/A

Multiple branch occlusions
of the retinal artery by
fat emboli
Selective angiography:
occlusion of left carotid
artery with cerebral
infarction

CRAO

(Continued)

999

Plastic and Reconstructive Surgery • April 2012
Table 1. (Continued)
Aesthetic
Procedure(s)

Injecting
Physician

Diameter/Size of
the Cannula/Needle
(Gauge or mm)

Complaint of Symptoms
Procedure/Symptoms
Interval

Reference

Age
(yr)

Sex

Yoon et al., 200310

39

F

5 ml of autologous fat
injection into the glabella to
correct frown lines

N/A

N/A

1 minute later: mental
change, aphasia, and
right hemiplegia

Allali et al., 200611

49

F

Autologous fat injection into
the glabellar area to treat
wrinkles

N/A

N/A

24 hr after the aesthetic
procedure: a sudden,
severe ocular pain with
complete visual loss
in RE

Mori et al., 200712

30

F

Cosmetic fat injection into
breasts, nose, and glabellar
area

N/A

N/A

Immediately: nausea,
pain, and visual loss
in RE

Park et al., 200813

27

F

Autologous fat injection into
the right nasolabial fold

Unspecified
surgeon
operating in
a plastic
surgery clinic

N/A

Within 10 minutes:
sudden visual loss

Lee et al., 201014

24

F

Autologous fat transplantation
to her forehead for softtissue augmentation in the
face

N/A

N/A

On the day of the
procedure: impossible
to open both eyes
because of the swelling
of her eyelids

Park et al., 201115

39

F

Autologous fat injection into
the left side of the nose
(dosage not specified)

Plastic surgeon

N/A

Immediately: sudden pain
and vision loss in her
LE

F, female; RE, right eye; N/A, not available; BCVA, best corrected visual acuity; ONH, optic nerve head; MCA, middle cerebral artery; LE, left eye; FA,
fluorescein angiography; CRAO, central retinal artery occlusion; VA, visual acuity; M, male; CT, computed tomography; MRI, magnetic resonance imaging;
TG, triglyceride; HDL, high-density lipoprotein; VEP, visual evoked potentials; OAO, ophthalmic artery occlusion; IOP, intraocular pressure.

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Volume 129, Number 4 • Blindness after Facial Cosmetic Injection
Table 1. (Continued)
Risk
Factors
None

None

N/A

None

None

None

Immediate
Ocular
Situation
30 minutes later:
LE: midline fixed
Pupil: dilated and unresponsive to
direct light stimulation
Corneal opacity
IOP: 0 mmHg
Pupil: fixed mid dilated
Fundus: retinal ischemic edema with
segmentary occlusions of multiple
branches of the central retinal
artery by yellow emboli, serous
macular detachment, absence of
cherry-red macular spot
ONH: pale and edematous
Ptosis. FA: choroidal and retinal
unilateral occlusion
BCVA RE: no light perception
Funduscopy: widespread retinal
whitening and obstruction of the
retinal vessels of the fundus with
remarkable edema of the entire
retina
FA: no filling of the retinal arterioles
BCVA RE: hand motion
Right upper eyelid: slight ptosis
Pupil: fixed and mid-dilated
FA: multiple whitish patchy lesions
with macular and ONH edema
and deterioration of choroidal
circulation with patchy choroidal
filling
Fundus: absence of a cherry-red spot
Flash VEP: no response
Swelling and redness of the
eyelids

Pathogenesis/
Diagnosis
Occlusion of the ocular
and facial vessels and
branches of the external
carotid arteries

Time When
Therapy
Started


Therapy

Outcomes

None

After 2 days: necrosis of
the LE
After 4 days: patient died

Multiple BRAOs by fat
emboli with posterior
ciliary arteries
involvement

After more
than 24 hr

Intravenous
corticosteroids and
antiplatelet therapy

No visual recovery

OAO

Not specified

No improvement

Choroidal infarctions
caused by multiple
occlusions of the short
posterior ciliary artery

On day 5

Drip infusion of
urokinase and
hyperbaric oxygen
therapy
Subsequent
administration of
corticosteroid
Methylprednisolone 1
g/day intravenously
for 3 days and dose
tapering with oral
administration

After 6 mo: no change in
vision

OAO with infarction of the Not specified 1 g/day intravenous
On the first postoperative
ONH and retina
(at least 24
methylprednisolone
day: visual loss in the LE,
hr later)
for 3 consecutive days
decreased sensation on
the forehead and scalp
3 days after BCVA: no light
perception; ptosis;
restricted extraocular
motility in all directions
LE: afferent pupillary defect
Fundus: LE ONH swelling
and widespread retinal
whitening
5 months later:
BCVA: no light perception
Fundus: severe retinal
fibrosis
BCVA LE: no light perception
OAO from the proximal
Some hours
Pharmacomechanical
6 days later:
Corneal edema
segment with thrombus
later
thrombolysis with a
BCVA: no light perception;
No pupillary reflex, total
and flow stagnation in
microwire and
no corneal edema and
ophthalmoplegia, and large-angle
the distal segment
500,000 IU of
improved choroidal and
(45 prism diopters) exotropia of
urokinase and 500 ␮g
retinal perfusion
the LE
of tirofiban
17 mo later BCVA: no light
Fundus: ischemic retina with multiple
perception
intraarterial yellowish emboli in
Fundus LE: fibrous
the LE
membrane on the
FA: minimal choroidal perfusion with
posterior pole with a
the absence of central retinal
large region of necrosis
arterial filling
in the nasal retina
After 1 day: Corneal edema
Complete recovery of ocular
FA: complete recanalization of the
movement
ophthalmic artery with
Nasal sectorial iris atrophy
visualization of the choroidal blush

1001

Plastic and Reconstructive Surgery • April 2012
Table 2. Review of 17 Cases of Visual Loss after Facial Cosmetic Injection of Various Substances
Complaint of Symptoms
Procedure/Symptoms
Interval

Reference

Sex

Aesthetic Procedure(s)

von Bahr, 196316

25

F

8-ml injection of a suspension of
hydrocortisone into the bare
spots on the scalp (left
anterior part of the crown, a
few centimeters within the
frontal limit of the hair)

Dermatologist

N/A

During the procedure:
pain in the head and
in the LE

Lee et al., 196917

50

F

Subcutaneous injection of
paraffin on the forehead

N/A

N/A

Immediately: loss of vision

Baran, 1964*

24

F

N/A

N/A

N/A

Baran, 1965*

31

F

N/A

N/A

Immediately: transitory
blindness

Shin et al., 198819

30

F

Injection of hydrocortisone
suspension for alopecia areata
Injection of methylprednisolone
acetate suspension for
alopecia areata
Injection of silicone oil
subcutaneously at the root of
her nose

N/A

N/A

Sudden loss of vision and
pain RE of 24-hr
duration

Castillo, 198920

34

F

N/A

N/A

Few minutes: sudden
amaurosis

Shafir et al., 199921

37

F

Injection of Zyderm collagen
implant into glabellar lines
and acne scars in the cheeks
Long-acting steroid to
subcutaneous scarring of the
dorsum of the nose

Unspecified
surgeon

25-gauge needle

Jee and Lee, 200222

44

F

Augmentation rhinoplasty using
liquid silicone

N/A

N/A

Within seconds of the last
injection: no light
perception; no
pupillary reflex could
be elicited
1 day after injection:
acute visual loss in LE
and RE hemiplegia

Apte et al., 200323

48

F

Intradermal injection of 0.5 ml
of Cymetra to improve the
contour of a depressed
forehead scar

N/A

N/A

10 minutes later: nausea,
diaphoresis, and left
side periocular pain
After 30 minutes: blurred
vision

Silva and Curi,
200424

52

F

Aesthetic PMMA injection into
the glabellar area

Plastic surgeon

N/A

Immediately after
injection: severe RE
pain and visual loss

1002

Injecting
Physician

Diameter/Size of the
Cannula/Needle (Gauge
or mm)

Age
(yr)

Volume 129, Number 4 • Blindness after Facial Cosmetic Injection
Table 2. (Continued)

Risk Factors
Three previous
treatments with the
same substance

Immediate Ocular Situation

Pathogenesis/
Diagnosis

Time When
Therapy
Started

Therapy

Outcomes

N/A

Immediately: no light perception;
direct pupillary reaction
abolished
Fundus: block of several arterial
branches of the retina and
choroid by small deposits of a
light substance
On day 1:
LE BCVA: “hand motions”
LE pupil: relatively wide and very
slightly reactive to direct light
ONH: normal; marked ischemic
turbidity on the macula and
interruption of the blood
column in some parts
Immediately: loss of vision

CRAO

Few minutes
later

Massage of the eye

On day 9, BCVA:
perception of “hand
movements” in the
temporal VF only
LE pupil: moderately
reactive
ONH: slightly pale
Retina: white and opaque
in the macular region
Fovea: brownish and
surrounded by a yellow
zone
4 mo later: unchanged

N/A

N/A

CRAO and thrombosis
of the ophthalmic
vein
N/A

N/A

N/A

N/A

N/A

N/A

Persistent impairment of
sight
After 5 minutes: return of
vision

N/A

N/A

N/A

N/A

N/A

N/A

BCVA RE: “counting fingers,” RE
afferent papillary defect
Fundus: pale, partially opacified,
edematous retina extending
from the ONH toward the
fovea; in the center of this
zone a white retinal vessel;
edema of RNFL in the inferior
nasal margin

CRAO and PCAOs

Immediately

Digital massage,
vasodilators, and
acetazolamide

N/A

N/A

N/A

N/A

N/A

N/A

N/A

Central retinal
embolus and
choroidal occlusion

Immediately

Routine treatment for
vascular occlusion
of the bulb

After 4 yr: no recovery of
vision

N/A

N/A

CRAO

N/A

N/A

Concomitant injection of
1.0 ml of Cymetra to
the bilateral nasolabial
regions and 0.5 ml of
Cymetra to the
bilateral oral
commissure regions
under a local
anesthetic without
incident

After several hours: BCVA of
“hand motions,” papillary
afferent defect, mild ptosis,
and exotropia

CRAO and PCAOs

N/A

N/A

None

BCVA RE: no light perception;
white opacity in the right
cornea and iris atrophy; total
ophthalmoplegia

CRAO and PCAOs

N/A

N/A

On day 30: development of
right carotid cavernous
fistula with right ocular
pain
2 mo later,
BCVA: light perception;
marked afferent pupillary
defect; mild left
hypertropia and
exotropia, without ptosis,
large areas of RPE
atrophy
FA: large areas of choroidal
nonperfusion in the
posterior pole and
temporal peripheral
retina
10 mo later,
BCVA: no light perception;
total right
ophthalmoplegia
(Continued)

On day 9, BCVA: no
improvement
Fundus: retinal hemorrhage
FA: no dye filling of the
white vessel, ONH dye
leakage, zones of retinal
ischemia
VF examination: inferior
altitudinal defect, central
scotoma, RNFL defect in
the superior temporal
region
N/A

1003

Plastic and Reconstructive Surgery • April 2012
Table 2. (Continued)
Complaint of Symptoms
Procedure/Symptoms
Interval

Sex

Kubota and Hirose,
200525

29

F

Injection of 0.7 ml of MetaCrill
into the dorsum of the nose
without local anesthetics

Cosmetic
surgeon

N/A

After 15 minutes: ocular
pain and a decrease of
vision in RE to “hand
motion”

Peter and Mennel,
200626

48

M

Injection of hyaluronic acid in
the glabellar area and in the
cheeks for wrinkles

N/A

N/A

1 minute after: partial
visual loss in the
inferior half of the VF
of his RE

Kang et al., 200727

65

F

N/A

N/A

Sudden visual loss

Tangsirichaipong,
200928

36

F

Injection of a filler into the
glabellar area
Silicone injection in the temple
area

N/A

N/A

Immediately: RE sudden
painful visual loss and
headache

Sung et al., 201029

25

M

Calcium hydroxyapatite filler
injection for nose
augmentation

Dermatologist

N/A

Immediately:
blepharoptosis and
orbital pain on the
right side
Some hours later: central
necrosis and
surrounding reddish
reticular pattern
affecting the right
eyelid

Kwon et al., 201030

39

F

Injection of collagenous filler
material into the left anterior
nasal septum for a nasal tipplasty

An acquaintance
performed
this
procedure
illegally at a
beauty salon

A self-manufactured
syringe

Immediately: complete
loss of vision in her left
eye and a headache

Kim et al., 201131

30

F

Injection of 0.8 ml of hyaluronic
acid in the nasal tip and
bridge as an augmentation
and contouring

N/A

N/A

Immediately: visual loss in
the LE

Reference

Aesthetic Procedure(s)

Injecting
Physician

Diameter/Size of the
Cannula/Needle (Gauge
or mm)

Age
(yr)

F, female; LE, left eye; N/A, not available; BCVA, best corrected visual acuity; ONH, optic nerve head; CRAO, central retinal artery occlusion;
VF, visual field; RE, right eye; RNFL, retinal nerve fiber layer; PCAO, posterior ciliary artery occlusion; FA, fluorescein angiography; RPE, retinal
pigment epithelium; PMMA, polymethylmethacrylate; AC, anterior chamber; MRI, magnetic resonance imaging; M, male; BRAO, branch
retinal artery occlusion.
*Selmanowitz VJ, Orentreich N. Cutaneous corticosteroid injection and amaurosis: Analysis for cause and prevention. Arch Dermatol. 1974;
110:729 –734.

1004

Volume 129, Number 4 • Blindness after Facial Cosmetic Injection
Table 2. (Continued)

Risk Factors
N/A

Tobacco abuse; no
previously systemic
embolic episodes

N/A
No medical problem

None

None

N/A

Immediate Ocular Situation
Pupil: dilated but still reactive
Ocular motility: restricted on
upward and leftward gaze with
temporary displacement of the
eyeball
Blepharoptosis; on day 1, BCVA
RE: light perception
Biomicroscopy: corneal edema and
2⫹ cells in the AC
MRI: orbital inflammation
BCVA RE: 6/7.5
After 24 hr, BCVA RE: 6/6
Funduscopy: evidence of an
embolus in the peripheral
retinal associated with retinal
edema
Necrosis of the glabellar area
BCVA RE: No light perception
Relative afferent pupillary defect
Diffuse retinal whitening, a
cherry-red spot in the macula,
vascular attenuation, and
boxcar flow in arteries and
veins
8 hr hours later:
BCVA RE: hand movement
Pupil: fully dilated without
reverse afferent pupillary
defect
Right exotropia
Severe AC reaction, including
hyphema, hypopyon, and
corneal edema

LE: no light perception, with
complete opacification of the
cornea and iris, complete
ophthalmoplegia, and ptosis of
the LE
Fundus photography: multiple
BRAOs
MRI: acute cerebral infarction of
the superior frontal subcortex
and subarachnoid hemorrhage
of another part of the distal
branch of the middle cerebral
artery
Immediately: strong pain in the left
upper face
BCVA LE: no light perception
Funduscopy: retina pale and
swollen with a cherry-red spot
On day 2, slit lamp examination:
severe chemosis, edematous
cornea, Descemet folds, and iris
atrophy
Ultrasonography: severe
chorioretinal swelling without
detachment
Left eyeball movement restricted at
all gazes

Pathogenesis/
Diagnosis

Time When
Therapy
Started

Therapy

Outcomes

Direct toxic effect
because of a
foreign body
reaction and
vasculitis secondary
to BRAO

N/A

N/A

4-mo follow-up,
BCVA RE: no light
perception; full ocular
motility and no
blepharoptosis; clear
cornea
Fundus: ONH atrophy

BRAO of the superior
temporal artery

Immediately

500 mg of
acetazolamide

BVCA: complete recovery;
visual field defect
improved

Retinal branch artery
occlusion
CRAO for silicone
embolism into the
central retinal
artery

N/A

N/A

N/A

After 2 hr

Ocular massage, AC
paracentesis, and
oral acetazolamide

On day 30: no light
perception

PCAOs, choroidal
ischemia limited in
the nasal area and
occlusion of the
branch to the
oculomotor nerve

After 8 hr

Topical and
intravenous
antibiotics and
topical steroids,
followed by low
dose of tapering
oral corticosteroids

After 3 mo
BCVA RE: 20/20 with
pinhole
No intraocular
inflammation or
oculomotor nerve palsy;
still fixed dilated pupil

Multiple BRAOs

On day 3

Low-dose antiplatelet
agent and a calcium
channel blocker

Blindness

CRAO

On day 2

Intravenous
methylprednisolone
at 1 g/day for 3
days and tapered
high-dose oral
prednisolone and
aspirin at 100 mg;
daily Comfeel
dressing

At 6 mo:
Complete recovery of the
eyeball movement
Progressive exudative and
tractional retinal
detachment at the
inferonasal retina caused
phthisis bulbi

1005

Plastic and Reconstructive Surgery • April 2012

Fig. 1. Schematic drawing that shows the anatomy, distribution, and connections
between the ophthalmic and the facial arterial systems. The supratrochlear artery
is the terminal branch of the ophthalmic artery and exits at the superior and medial
corner of the bony orbit by piercing the orbital septum with the supratrochlear
nerve. It runs superiorly into the forehead, where it supplies the integument, muscles, and pericranium and maintains numerous anastomoses with the supraorbital
artery and with the contralateral vessels. This is the vessel most likely to be involved
when intraarterial injection of fat and foreign material of the glabella and forehead
is responsible for embolization. The supraorbital artery may occasionally be the
route of embolization of injected material. It arises from the ophthalmic artery and
divides into superficial and deep branches that nourish the integument, muscles,
and pericranium of the forehead. Its terminal branches anastomose with the supratrochlear artery, the frontal branch of the superficial temporal artery, and the
contralateral supraorbital artery. The second terminal branch of the ophthalmic
artery, the dorsal nasal artery, may be responsible for transmission of emboli following injections low in the glabella or proximal to the nasal root. It anastomoses
with the angular artery, the dorsal nasal artery of the opposite side, and the lateral
nasal branch of the facial artery. The facial artery arises from the external carotid
artery that supplies the structures of the face. The facial artery passes forward and
upward across the cheek to the angle of the mouth, where it arborizes and gives rise
to the labial systems and, more distally, to the lateral nasal artery that supplies the
ala and dorsum of the nose. It further forms anastomoses with its contralateral
counterpart, with the septal and alar branches, with the dorsal nasal branch of the
ophthalmic artery, and with the infraorbital branch of the internal maxillary. The
facial artery then ascends along the side of the nose, ending at the medial canthus,
where it is named the angular artery. After supplying the lacrimal sac and orbicularis oculi, it ends by anastomosing with the dorsal nasal branch of the ophthalmic
artery. The angular artery on the cheek distributes branches that anastomose also
with the infraorbital artery. The facial artery should be considered for embolization
following injections of the cheek, nasolabial folds, and lips.

tions (Pascal’s law71). However, beyond the fact that
the surgeon’s control over the volume injected is
severely impaired by the use of a large syringe for
fine injection of filler materials and fat, injection

1006

with large syringes can result anyway in pressures
greater than the systolic blood pressure.54 Even the
use of a small-gauge needle does not seem to prevent
retrograde flow. The decreased pressure resulting

Volume 129, Number 4 • Blindness after Facial Cosmetic Injection
from the use of a small-gauge needle or cannula does
not decrease the injection pressure below the systemic arterial pressure.54 Furthermore, the initiation
of an injection requires an order of magnitude more
pressure than does maintenance of flow. Smaller
needle sizes require greater initial pressure to overcome resistance to flow and thus result in higher
initial pressures transmitted to surrounding tissues.54
Obviously, in daily clinical practice, the most commonly used devices for injecting cosmetic substances
into the face are 1-, 3-, and 10-ml syringes, in which
the plunger has a manyfold smaller cross-sectional
area than the plungers of a 50-ml syringe and should
therefore allow higher pressure injections to occur.
The use of a smaller syringe even with a small needle
will increase the risk for the physician to exceed the
systolic arterial pressure. Thus, the force with which
the product is delivered becomes a really important
variable to control.
Treatment
To optimize the possibility of fully or partially
regaining normal vision, early recognition and treatment are essential for treating ocular circulation
emboli. The goal of treatment is rapid restoration of
perfusion to the retina and optic nerve head.48,54,72,73
After 90 minutes, the damage caused by retinal ischemia becomes irreversible and retinal necrosis occurs. Thus, limiting the length of ischemia may allow
various degrees of recovery.54,74 –77 Although current
standard therapies have not been shown to alter the
natural course of the disease, it should be assumed that
shortening the ischemic period increases the probability of residual visual function.54,74 The recovery pattern after branch retinal artery occlusion should be
similar, but remaining visual function is more likely.
Nonsurgical Management
Current treatments may not satisfactorily treat
arterial retinal occlusions caused by fat graft emboli or foreign materials that are widely used as
facial cosmetic fillers or rejuvenating procedures.
The currently available recommendations for retinal
embolism54,78 attempt to rapidly reduce intraocular
pressure to dislodge the embolus to a downstream
location to improve retinal perfusion. Because our
review identified only two cases with improvement
following known treatments,26,29 we cannot recommend any treatments as safe or effective.
Anterior chamber decompression with a needle
or sharp cutting blade paracentesis results in an instantaneous decrease of intraocular pressure.79,80
However, this treatment failed in the case28 included
in the present review. Ocular massage may lower

intraocular pressure and increase arteriolar flow, potentially dislodging the embolus, but it has been
ineffective in all four of the cases included in this
study.6,16,19,28 Intravenous administration of diuretics
such as acetazolamide81 may both increase retinal
blood flow and immediately reduce intraocular pressure. This approach failed in two patients19,28 but was
successful in one case.26 Retinal arteriolar dilation
and oxygen delivery to ischemic tissues from ophthalmic vessels may be encouraged by carbogen (5
percent carbon dioxide and 95 percent oxygen)
inhalation.82 The only patient6 who underwent carbogen rebreathing had no substantial recovery of his
sight. Although hyperbaric oxygen therapy may theoretically be beneficial, transportation to the
nearest chamber may usurp precious time. Neither
patient6,12 treated with oxygen therapy improved.
Systemic and topical corticosteroids were successfully administrated in one case, with full recovery of
sight but with a persistently dilated pupil.29 Systemic
and local intraarterial fibrinolyses have failed to dissolve cholesterol or heterologous materials83 as reported in four cases.11,12,15,30
In the European Assessment Group for Lysis in
the Eye study,77 a significant improvement in best
corrected visual acuity in patients with an acute central retinal artery occlusion was obtained in 60 percent of patients at 1 month after a six-step therapy
administered within 20 hours after the ischemic
event. In the present review, improvement after therapy was achieved in only two cases (14 percent), both
of which suffered ocular embolism following injection of heterologous material (hyaluronic acid26 and
calcium hydroxyapatite,29 respectively). In the first
case, partial visual loss in the inferior visual field
improved to a best corrected visual acuity of 6/6
within 24 hours after immediate administration of
500 mg of acetazolamide,26 and in the second case,
a best corrected visual acuity of “hand movement”
improved to 20/20 at 3 months after topical antibiotics and steroids, including intravenous antibiotics,
were initiated 8 hours after the occlusive event and
followed by a low-dose oral corticosteroid taper.29 In
the first case,26 the recovery was attributable to both
the natural history of a branch retinal artery
occlusion82 and to the therapy that could have dislodged the embolus peripherally relative to the retinal edema. Both effects would have allowed resolution of the retinal edema and thus explained the
visual improvement. In the second case,29 the injury
was a posterior ciliary artery occlusion, and the choroidal ischemia was limited to the nasal area; thus,
the recovery was likely determined by resolution of
the corneal edema and the severe anterior chamber
reaction, which included hyphema and hypopyon,

1007

Plastic and Reconstructive Surgery • April 2012

Table 3. Tips and Techniques to Diminish the Risk of Intravascular Injection
1. Aspiration before injection. As mentioned previously, the small size and collapsibility of facial vessels limits the efficacy
of preinjection aspiration for avoiding arteriolar injection*. Some authors* consider this precaution useless because,
in several reported cases, aspiration did not identify intraarterial needle placement. It is our opinion, however, that
aspiration will at least occasionally demonstrate intravascular placement of the needle and should thus be used. The
needle should be withdrawn and repositioned if blood appears in the syringe during the aspiration. This precaution
may not be applied easily during fat injection procedures because of the high viscosity of the product and the
possible presence of residual blood within centrifuged fat.
2. Injections should be performed slowly and with the least amount of pressure possible. Thus, even if the tip of the
needle has perforated the arterial wall, the column of filler will not be propelled retrograde in the artery. This may be
the most important precaution for practitioners and has already been generally accepted by several authors†‡§.
3. The tip of the needle should be moved slightly to deliver the filler at different points along a line rather than as a
single deposit. This precaution minimizes the chance of depositing a critical amount of material into an artery even if
the needle has perforated the arterial wall by limiting the time during which the needle remains within the arteriole.
4. Incremental injections should be fractionated so that any filler injected into the artery can be flushed peripherally
before the next incremental injection is performed. The surgeon should limit therefore to 0.1 ml of filler regardless
of the filler type†‡§. This stepwise procedure minimizes the risk that a column of filler will extend proximally into the
ophthalmic arterial system.
5. Although high injection pressures cannot be controlled by the size of the syringe or needle used during injection,
small syringes should be preferred to larger ones. As already mentioned previously, a bolus injection technique is
more likely to transmit a column of filler to the ophthalmic artery or the internal carotid system. The use of a highvolume syringe (ⱖ10 ml) may increase the probability of this complication because the surgeon cannot easily control
the volume of the filler delivered.
6. Small needles should be preferred to larger ones. Although their initial pressure is higher and their drop pressure is
insufficient, smaller needles slow injection speed and are less likely to occlude the vessel or block peripheral flow.
7. Repeated treatments with smaller volumes may be preferred to single-stage high-volume injections. Pretreatment with
botulinum toxin type A may help reduce the volume of filler required for cosmesis.
8. When indicated, the use of recently introduced tools such as blunt, flexible microcannulas and nontraumatic flexible
blunt tip needles should be preferred for filler injection¶. Both the microcannula and the blunt tip needle are
inserted into the skin through a hole previously made with a sharp tip needle having the same diameter. These
techniques allow facial injection with a limited number of insertion points for the whole face, thus reducing the risk
of arterial entry.
9. Either the perforation of an arterial wall or the cannulation of an artery lumen will occur more frequently in a
vasodilated artery. Thus, procedural risks should be reduced by application of a topical vasoconstrictor prior to filler
delivery. Some authors†#** recommend local anesthesia with epinephrine to promote vasoconstriction. It can be
combined with topical anesthesia or regional nerve block before injection to avoid excessive tissue distortion.
10. When performing autologous fat tissue transfer, sharp cannulas and small cannulas are much more likely to perforate
the wall of an artery and cannulate the artery lumen than are larger, blunt cannulas†.
11. Extensive gentle pretunneling (e.g., moving of the cannula without applying vacuum or pressure) is usually
advocated because the delivery of small fat parcels into multiple soft-tissue tunnels allows better revascularization
and results in more predictable and more persistent results. This method may cause a hidden vascular lesion.
Thus, it becomes extremely important to allow a low-pressure microdroplet injection technique with blunt
cannulas to avoid a dramatically high injection pressure for a highly viscous substance such as fat tissue. The
injection should be accomplished by delivering very small, noncontinuous amounts of 0.1 ml per pass†. Some
authors emphasize the use of 0.025 to 0.05 ml per tunnel or even less for the periorbital region††.
12. When surgical procedures of the head and neck, such as face lifts and liposuction, are combined with local
autologous fat grafting, the risk of ocular arterial system embolism increases, because intravascular delivery of fat
tissue is easier in pretraumatized soft tissue.‡‡ This condition should be prevented.
*McCleve DE, Goldstein JC. Blindness secondary to injections in the nose, mouth, and face: Cause and prevention. Ear Nose Throat J.
1995;74:182–188.
†Coleman SR. Avoidance of arterial occlusion from injection of soft tissue fillers. Aesthet Surg J. 2002;22:555–557.
‡Matsuo T, Fujiwara H, Gobara H, Mimura H, Kanazawa S. Central retinal and posterior ciliary artery occlusion after intralesional injection
of sclerosant to glabellar subcutaneous hemangioma. Cardiovasc Intervent Radiol. 2009;32:341–346.
§Egbert JE, Paul S, Engel WK, Summers CG. High injection pressure during intralesional injection of corticosteroids into capillary hemangiomas. Arch Ophthalmol. 2001;119:677– 683.
Thomas EL, Laborde RP. Retinal and choroidal vascular occlusion following intralesional corticosteroid injection of a chalazion. Ophthalmology
1986;93:405– 407.
¶Niamtu J III. Filler injection with micro-cannula instead of needles. Dermatol Surg. 2009;35:2005–2008.
#Coleman SR. Structural fat grafting: More than a permanent filler. Plast Reconstr Surg. 2006;118(Suppl):108S–120S.
**Berlin A, Cohen JL, Goldberg DJ. Calcium hydroxylapatite for facial rejuvenation. Semin Cutan Med Surg. 2006;25:132–137.
††Tzikas TL. Facial fat injection. In: Thomas JR, ed. Advanced Therapy in Facial Plastic and Reconstructive Surgery. Shelton, Conn: People’s Medical
Publishing House; 2010:573–580.
‡‡Feinendegen DL, Baumgartner RW, Vuadens P, et al. Autologous fat injection for soft tissue augmentation in the face: A safe procedure?
Aesthetic Plast Surg. 1998;22:163–167.

1008

Volume 129, Number 4 • Blindness after Facial Cosmetic Injection

Fig. 2. A useful algorithm approach is presented to minimize the occurrence of ophthalmic arterial system embolization during
facial cosmetic injections.

rather than by the resolution of the choroidal ischemia. In the other 12 cases in which the therapy was
administered, no improvement was achieved regardless of the nature of the embolus (fat6,11–15 or heterologous material16,19,21,28,30,31). The time between the
occlusive event and the onset of the therapy could
have contributed to these failures, however. In the
European Assessment Group for Lysis in the Eye
study,77 the authors suggested that the visual prognosis in patients with acute central retinal artery
occlusion depends in part on the duration of symptoms, with a shorter duration associated with better
visual outcome. In five cases described in this review,
the therapy was administered after more than 20
hours11,13,14,30,31; in two cases,6,12 the timing was not
specified; and in five cases, it was administered
within 20 hours.15,16,19,21,28
Incomplete treatment could also have contributed to failure. In the European Assessment Group
for Lysis in the Eye study,77 the standard treatment
of central retinal artery occlusion included a six-step

therapy: topical (a single eye drop of timolol 0.5%)
and systemic (intravenous injection of 500 mg of
acetazolamide) lowering of intraocular pressure, isovolemic hemodilution in patients with a hematocrit
greater than 40 percent (500 ml of blood was withdrawn and 500 ml of 10% hydroxyethyl starch was
simultaneously infused within 15 to 30 minutes),
globe massage (repeated increased pressure was applied to the globe for 10 to 15 seconds, followed by
a sudden release with an in-and-out movement using
a three-mirror contact lens for 3 to 5 minutes), and
anticoagulation with heparin and acetylsalicylic
acid. In our review, all of the treated patients
underwent at most a three-step therapy, which
included other treatment options, such as carbon
dioxide,6 oxygen therapy,6,12 oral or intravenous
corticosteroids,11–14,31 pharmacologic or pharmacomechanical thrombolysis,12,15 vasodilators,19 anterior chamber paracentesis,28 and calcium channel blockers.30 Monotherapy was administered
in four cases,13–16 dual therapy was administered in

1009

Plastic and Reconstructive Surgery • April 2012
two cases,11,30 and triple therapy was administered
in five cases6,12,19,28,31; in one case, an unspecified
routine treatment for vascular occlusion of the
bulb was administered.21
Surgical Management
Contrasting opinions about the feasibility and
efficacy of reperfusion of the occluded retinal artery
through surgical removal of the emboli have been
expressed.84,85 No data support the assumption that
surgical embolectomy of the iatrogenically injected
materials within the retinal circulation is a safe
method for restoring ophthalmic system circulation
after embolization from cosmetic facial injections.
The same caution applies to transluminal neodymium:yttrium-aluminum-garnet laser embolysis.86 Surgical treatment has not been used or proposed by
any of the articles reviewed.
Tips and Techniques to Diminish the Risk of
Intravascular Injection
Although no rule can completely prevent the
occurrence of ocular circulation embolization, some
reasonable precautions that may decrease the risk of
vascular occlusion during facial cosmetic injections
are discussed in Table 3.2,7,9,51,52,54,78,87– 89 A useful algorithm approach is also presented in Figure 2.

CONCLUSIONS
Some steps may minimize the risk of embolization of filler into the ophthalmic artery following
facial cosmetic injections. Intravascular placement
of the needle or cannula should be demonstrated by
aspiration before injection and should be further
prevented by application of local vasoconstrictor.
Needles, syringes, and cannulas of small size should
be preferred to larger ones and be replaced with
blunt flexible needles and microcannulas when possible. Low-pressure injections with the release of the
least amount of substance possible should be considered safer than bolus injections. The total volume
of filler injected during the entire treatment session
should be limited, and injections into pretraumatized tissues should be avoided. Actually, no safe,
feasible, and reliable treatment exists for iatrogenic
retinal embolism. Nonetheless, therapy should theoretically be directed to lowering intraocular pressure to dislodge the embolus into more peripheral
vessels of the retinal circulation, increasing retinal
perfusion and oxygen delivery to hypoxic tissues.

1010

Davide Lazzeri, M.D.
Plastic and Reconstructive Surgery Unit
Hospital of Pisa
Via Paradisa 2
Cisanello, 56100 Pisa, Italy
[email protected]

ACKNOWLEDGMENTS

The authors thank Dr.ssa Ilaria Bondi (MEDICAL
ILLUSTRATOR, Via Carlo Lugli, Carpi, Modena,
Italy) for help with Figure 1.
REFERENCES
1. Eppley BL, Dadvand B. Injectable soft-tissue fillers: Clinical
overview. Plast Reconstr Surg. 2006;118:98e–106e.
2. Coleman SR. Structural fat grafting: More than a permanent
filler. Plast Reconstr Surg. 2006;118(Suppl):108S–120S.
3. Teimourian B. Blindness following fat injections. Plast Reconstr Surg. 1988;82:361.
4. Dreizen NG, Framm L. Sudden unilateral visual loss after
autologous fat injection into the glabellar area. Am J Ophthalmol. 1989;107:85–87.
5. Egido JA, Arroyo R, Marcos A, Jime´nez-Alfaro I. Middle cerebral artery embolism and unilateral visual loss after autologous fat injection into the glabellar area. Stroke 1993;24:
615–616.
6. Lee DH, Yang HN, Kim JC, Shyn KH. Sudden unilateral visual
loss and brain infarction after autologous fat injection into
nasolabial groove. Br J Ophthalmol. 1996;80:1026–1027.
7. Feinendegen DL, Baumgartner RW, Vuadens P, et al. Autologous fat injection for soft tissue augmentation in the face:
A safe procedure? Aesthetic Plast Surg. 1998;22:163–167.
8. Danesh-Meyer HV, Savino PJ, Sergott RC. Case reports and
small case series: Ocular and cerebral ischemia following
facial injection of autologous fat. Arch Ophthalmol. 2001;119:
777–778.
9. Coleman SR. Avoidance of arterial occlusion from injection
of soft tissue fillers. Aesthet Surg J. 2002;22:555–557.
10. Yoon SS, Chang DI, Chung KC. Acute fatal stroke immediately following autologous fat injection into the face.
Neurology 2003;61:1151–1152.
11. Allali J, Bernard A, Assaraf E, Bourges JL, Renard G. Multiple
embolizations of the branches of the ophthalmic artery: An
unknown serious complication of facial surgeries (in
French). J Fr Ophtalmol. 2006;29:51–57.
12. Mori K, Ohta K, Nagano S, Toshinori M, Yago T, Ichinose Y.
A case of ophthalmic artery obstruction following autologous
fat injection in the glabellar area (in Japanese). Nippon Ganka
Gakkai Zasshi 2007;111:22–25.
13. Park SH, Sun HJ, Choi KS. Sudden unilateral visual loss after
autologous fat injection into the nasolabial fold. Clin Ophthalmol. 2008;2:679–683.
14. Lee YJ, Kim HJ, Choi KD, Choi HY. MRI restricted diffusion
in optic nerve infarction after autologous fat transplantation.
J Neuroophthalmol. 2010;30:216–218.
15. Park SJ, Woo SJ, Park KH, et al. Partial recovery after intraarterial pharmacomechanical thrombolysis in ophthalmic
artery occlusion following nasal autologous fat injection.
J Vasc Interv Radiol. 2011;22:251–254.
16. von Bahr G. Multiple embolisms in the fundus of an eye after
an injection in the scalp. Acta Ophthalmol (Copenh.) 1963;41:
85–91.
17. Lee JH, Lee KH, Moon HJ. A case of unilateral blindness after
paraffin injection on the forehead. J Korean Ophthalmol Soc.
1969;10:49–51.

Volume 129, Number 4 • Blindness after Facial Cosmetic Injection
18. Selmanowitz VJ, Orentreich N. Cutaneous corticosteroid injection and amaurosis: Analysis for cause and prevention.
Arch Dermatol. 1974;110:729–734.
19. Shin H, Lemke BN, Stevens TS, Lim MJ. Posterior ciliaryartery occlusion after subcutaneous silicone-oil injection.
Ann Ophthalmol. 1988;20:342–344.
20. Castillo GD. Management of blindness in the practice of
cosmetic surgery. Otolaryngol Head Neck Surg. 1989;100:559–
562.
21. Shafir R, Cohen M, Gur E. Blindness as a complication of
subcutaneous nasal steroid injection. Plast Reconstr Surg.
1999;104:1180–1182; discussion 1183–1184.
22. Jee DH, Lee KI. A case of left ophthalmic artery occlusion
and right carotid cavernous fistula after illegal rhinoplasty.
J Korean Ophthalmol Soc. 2002;43:898–904.
23. Apte RS, Solomon SD, Gehlbach P. Acute choroidal infarction following subcutaneous injection of micronized dermal
matrix in the forehead region. Retina 2003;23:552–554.
24. Silva MT, Curi AL. Blindness and total ophthalmoplegia after
aesthetic polymethylmethacrylate injection: Case report. Arq
Neuropsiquiatr. 2004;62:873–874.
25. Kubota T, Hirose H. Permanent loss of vision following cosmetic rhinoplastic surgery. Jpn J Ophthalmol. 2005;49:535–
536.
26. Peter S, Mennel S. Retinal branch artery occlusion following
injection of hyaluronic acid (Restylane). Clin Experiment Ophthalmol. 2006;34:363–364.
27. Kang YS, Kim JW, Choi WS, Park HS, Jang SJ, Chio JC. A case
of sudden unilateral visual loss following injection of filler
into the glabella. Korean J Dermatol. 2007;45:381–383.
28. Tangsirichaipong A. Blindness after facial contour augmentation with injectable silicone. J Med Assoc Thai. 2009;
92(Suppl 3):S85–S87.
29. Sung MS, Kim HG, Woo KI, Kim YD. Ocular ischemia and
ischemic oculomotor nerve palsy after vascular embolization
of injectable calcium hydroxyapatite filler. Ophthal Plast Reconstr Surg. 2010;26:289–291.
30. Kwon DY, Park MH, Koh SB, et al. Multiple arterial embolism
after illicit intranasal injection of collagenous material. Dermatol Surg. 2010;36:1196–1199.
31. Kim YJ, Kim SS, Song WK, Lee SY, Yoon JS. Ocular ischemia
with hypotony after injection of hyaluronic acid gel. Ophthal
Plast Reconstr Surg. 2011;27:e152–e155.
32. Byers B. Blindness secondary to steroid injections into the
nasal turbinates. Arch Ophthalmol. 1979;97:79–80.
33. Mabry RL. Visual loss after intranasal corticosteroid injection: Incidence, causes, and prevention. Arch Otolaryngol.
1981;107:484–486.
34. Mabry RL. Intranasal corticosteroid injection: Indications,
technique, and complications. Otolaryngol Head Neck Surg.
1979;87:207–211.
35. Whiteman DW, Rosen DA, Pinkerton RM. Retinal and choroidal microvascular embolism after intranasal corticosteroid injection. Am J Ophthalmol. 1980;89:851–853.
36. Wilkinson WS, Morgan CM, Baruh E, Gitter KA. Retinal and
choroidal vascular occlusion secondary to corticosteroid embolisation. Br J Ophthalmol. 1989;73:32–34.
37. Savino PJ, Burde RM, Mills RP. Visual loss following intranasal anesthetic injection. J Clin Neuroophthalmol. 1990;10:
140–144.
38. Cheney ML, Blair PA. Blindness as a complication of rhinoplasty. Arch Otolaryngol Head Neck Surg. 1987;113:768–769.
39. Rettinger G, Christ P, Meythaler FH. Blindness caused by
central artery occlusion following nasal septum correction
(in German). HNO. 1990;38:105–109.

40. Meythaler FH, Naumann GO. Intraocular ischemic infarcts
in injections into the lid and parabulbar region (without
perforation of the eye) (in German). Klin Monbl Augenheilkd.
1987;190:474–477.
41. Rishiraj B, Epstein JB, Fine D, Nabi S, Wade NK. Permanent
vision loss in one eye following administration of local anesthesia for a dental extraction. Int J Oral Maxillofac Surg.
2005;34:220–223.
42. Ellis PP. Visual loss following tonsillectomy; possible association with injections in tonsillar fossae. Arch Otolaryngol. 1968;
87:436–438.
43. McGrew RN, Wilson RS, Havener WH. Sudden blindness
secondary to injections of common drugs in the head and
neck: I. Clinical experiences. Otolaryngology 1978;86:147–
151.
44. Fivgas GD, Newman NJ. Anterior ischemic optic neuropathy
following the use of a nasal decongestant. Am J Ophthalmol.
1999;127:104–106.
45. Chamot L, Zografos L, Micheli JL. Ocular and orbital complications after sclerosing injections in a case of a frontal
cutaneous angioma. Ophthalmologica 1981;182:193–198.
46. Shorr N, Seiff SR. Central retinal artery occlusion associated
with periocular corticosteroid injection for juvenile hemangioma. Ophthalmic Surg. 1986;17:229–231.
47. Ruttum MS, Abrams GW, Harris GJ, Ellis MK. Bilateral retinal
embolization associated with intralesional corticosteroid injection for capillary hemangioma of infancy. J Pediatr Ophthalmol Strabismus 1993;30:4–7.
48. Egbert JE, Schwartz GS, Walsh AW. Diagnosis and treatment
of an ophthalmic artery occlusion during an intralesional
injection of corticosteroid into an eyelid capillary hemangioma. Am J Ophthalmol. 1996;121:638–642.
49. Gupta V, Sharma SC, Gupta A, Dogra MR. Retinal and choroidal microvascular embolization with methylprednisolone.
Retina 2002;22:382–386.
50. Edwards AO. Central retinal artery occlusion following forehead injection with a corticosteroid suspension. Pediatr Dermatol. 2008;25:460–461.
51. Matsuo T, Fujiwara H, Gobara H, Mimura H, Kanazawa S.
Central retinal and posterior ciliary artery occlusion after intralesional injection of sclerosant to glabellar subcutaneous
hemangioma. Cardiovasc Intervent Radiol. 2009;32:341–346.
52. Thomas EL, Laborde RP. Retinal and choroidal vascular
occlusion following intralesional corticosteroid injection of
a chalazion. Ophthalmology 1986;93:405–407.
53. Yag˘ci A, Palamar M, Eg˘rilmez S, Sahbazov C, Ozbek SS.
Anterior segment ischemia and retinochoroidal vascular occlusion after intralesional steroid injection. Ophthal Plast Reconstr Surg. 2008;24:55–57.
54. Egbert JE, Paul S, Engel WK, Summers CG. High injection
pressure during intralesional injection of corticosteroids
into capillary hemangiomas. Arch Ophthalmol. 2001;119:
677–683.
55. Bachmann F, Erdmann R, Hartmann V, Wiest L, Rzany B.
The spectrum of adverse reactions after treatment with injectable fillers in the glabellar region: Results from the Injectable Filler Safety Study. Dermatol Surg. 2009;35(Suppl 2):
1629–1634.
56. Bellman B. Complication following suspected intra-arterial
injection of Restylane. Aesthet Surg J. 2006;26:304–305.
57. Georgescu D, Jones Y, McCann JD, Anderson RL. Skin necrosis after calcium hydroxyapatite injection into the glabellar and nasolabial folds. Ophthal Plast Reconstr Surg. 2009;25:
498–499.

1011

Plastic and Reconstructive Surgery • April 2012
58. Glaich AS, Cohen JL, Goldberg LH. Injection necrosis of the
glabella: Protocol for prevention and treatment after use of
dermal fillers. Dermatol Surg. 2006;32:276–281.
59. Hanke CW, Higley HR, Jolivette DM, Swanson NA, Stegman
SJ. Abscess formation and local necrosis after treatment with
Zyderm or Zyplast collagen implant. J Am Acad Dermatol.
1991;25:319–326.
60. Inoue K, Sato K, Matsumoto D, Gonda K, Yoshimura K.
Arterial embolization and skin necrosis of the nasal ala following injection of dermal fillers. Plast Reconstr Surg. 2008;
21:127e–128e.
61. Hirsch RJ, Lupo M, Cohen JL, Duffy D. Delayed presentation
of impending necrosis following soft tissue augmentation
with hyaluronic acid and successful management with hyaluronidase. J Drugs Dermatol. 2007;6:325–328.
62. Park TH, Seo SW, Kim JK, Chang CH. Clinical experience
with hyaluronic acid-filler complications. J Plast Reconstr Aesthet Surg. 2011;64:892–896.
63. Schanz S, Schippert W, Ulmer A, Rassner G, Fierlbeck G.
Arterial embolization caused by injection of hyaluronic acid
(Restylane). Br J Dermatol. 2002;146:928–929.
64. Lowe NJ. Arterial embolization caused by injection of hyaluronic acid (Restylane). Br J Dermatol. 2003;148:379; author
reply 379–380.
65. Paul S, Egbert JE, Walsh AW, Hoey MF. Pressure measurements during injection of corticosteroids. Med Biol Eng Comput. 1998;36:729–733.
66. Paul S, Hoey MF, Egbert JE. Pressure measurements during
injection of corticosteroids: In vivo studies. Med Biol Eng
Comput. 1999;37:645–651.
67. Dutton JJ. Arterial supply to the orbit. In: Clinical and Surgical
Orbital Anatomy. Philadelphia, Pa: Saunders; 1994:68–71.
68. Badeer H. Hemodynamics for medical students. Adv Physiol
Educ. 2001;25:44–52.
69. Zweifach BW. Quantitative studies of microcirculatory structure and function: I. Analysis of pressure distribution in the
terminal vascular bed in cat mesentery. Circ Res. 1974;34:
843–857.
70. Zweifach BW. Quantitative studies of microcirculatory structure and function: II. Direct measurement of capillary pressure in splanchnic mesenteric vessels. Circ Res. 1974;34:858–
866.
71. Bullock JD, Warwar RE, Green WR. Ocular explosion during
cataract surgery: A clinical, histopathological, experimental,
and biophysical study. Trans Am Ophthalmol Soc. 1998;96:243–
276; discussion 276–281.
72. Hayreh SS. Vascular disorders in neuro-ophthalmology. Curr
Opin Neurol. 2011;24:6–11.
73. Chen CS, Lee AW. Management of acute central retinal
artery occlusion. Nat Clin Pract Neurol. 2008;4:376–383.

1012

74. Hayreh SS, Weingeist TA. Experimental occlusion of the
central artery of the retina: IV. Retinal tolerance time to
acute ischaemia. Br J Ophthalmol. 1980;64:818–825.
75. Selle´s-Navarro I, Villegas-Pe´rez MP, Salvador-Silva M, RuizGo´mez JM, Vidal-Sanz M. Retinal ganglion cell death after
different transient periods of pressure-induced ischemia and
survival intervals: A quantitative in vivo study. Invest Ophthalmol Vis Sci. 1996;37:2002–2014.
76. Roth S, Li B, Rosenbaum PS, et al. Preconditioning provides
complete protection against retinal ischemic injury in rats.
Invest Ophthalmol Vis Sci. 1998;39:775–785.
77. Schumacher M, Schmidt D, Jurklies B, et al. Central retinal
artery occlusion: Local intra-arterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology 2010;117:1367–1375.e1.
78. McCleve DE, Goldstein JC. Blindness secondary to injections
in the nose, mouth, and face: Cause and prevention. Ear Nose
Throat J. 1995;74:182–188.
79. Ffytche TJ. A rationalization of treatment of central retinal
artery occlusion. Trans Ophthalmol Soc UK. 1974;94:468–
479.
80. Augsburger JJ, Magargal LE. Visual prognosis following treatment of acute central retinal artery obstruction. Br J Ophthalmol. 1980;64:913–917.
81. McGrew RN, Wilson RS, Havener WH. Sudden blindness
secondary to injections of common drugs in the head and
neck: II. Animal studies. Otolaryngology 1978;86:152–157.
82. Alm A, Bill A. Ocular circulation. In: Alder FH, Moses RA,
Hart WM, eds. Adler’s Physiology of the Eye. 8th ed. St. Louis:
Mosby; 1987:183–203.
83. Hayreh SS. Prevalent misconceptions about acute retinal
vascular occlusive disorders. Prog Retin Eye Res. 2005;24:493–
519.
84. Garcı´a-Arumı´ J, Martinez-Castillo V, Boixadera A, Fonollosa
A, Corcostegui B. Surgical embolus removal in retinal artery
occlusion. Br J Ophthalmol. 2006;90:1252–1255.
85. Hayreh SS. Surgical embolus removal in retinal artery occlusion. Br J Ophthalmol. 2007;91:1096–1097.
86. Opremcak EM, Benner JD. Translumenal Nd:YAG laser embolysis for branch retinal artery occlusion. Retina 2002;22:
213–216.
87. Tzikas TL. Facial fat injection. In: Thomas JR, ed. Advanced
Therapy in Facial Plastic and Reconstructive Surgery. Shelton,
Conn: People’s Medical Publishing House; 2010:573–580.
88. Niamtu J III. Filler injection with micro-cannula instead of
needles. Dermatol Surg. 2009;35:2005–2008.
89. Berlin A, Cohen JL, Goldberg DJ. Calcium hydroxylapatite for
facial rejuvenation. Semin Cutan Med Surg. 2006;25:132–137.

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