Blindness Following Cosmetic Injections of the Face

SPECIAL TOPIC Blindness following Cosmetic Injections of the Face Davide Lazzeri, M.D. Tommaso Agostini, M.D. Michele Miche le Figus 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. Someprecaution tionss may maymin minimi imize ze the theris risk k of embo emboliz lizatio ation n of fil filler lerinto into Conclusions: Someprecau the ophthalmic artery following facial cosmetic injections. Intravascular placement of theneed theneedle le or can cannul nulaa sho shouldbe uldbe dem demons onstra trate ted d by asp aspir irati ation on bef beforeinjec oreinjecti tion on and should be further prevented by application of local vasoconstrictor. Needles, syringe ri nges, s, andcannu andcannulasof lasof sm smal alll si size ze sho shouldbe uldbe pr pref eferr erred ed to lar largerones gerones andbe re repla place ced d with wit h blunt flexible flexible needles needles and microcann microcannulas ulas when when possible. possible. Low-press Low-pressure ure injecinjectionswith ti onswith therele thereleaseof aseof theleas theleastt am amoun ountt of sub substa stanceposs ncepossibl iblee sho shoul uld d be co consi nside dered red 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 iatrogenicc retinal embolism. Nonetheless, therapy should theoreti iatrogeni theoretically cally be directe directed d to lowering intraocular pressure to dislodge the embolus into more peripheral vessel ves selss of the ret retinal inal circula circulation tion,, incr increasi easing ng retinal perfusio perfusion n and oxygen oxygen del delive ivery ry to hy hypox poxic ic ti tissu ssues es.. (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 met ic inj inject ection ionss hav havee hei height ghtene ened d awa awaren reness ess of the 3–31 possibility of iatrogenic visual loss. 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 injec tion pres pressures sures;; materi material al type; and need needle, le, From the Plastic and Reconstructive Surgery and Ophthal- mology Units, University Hospital of Pisa, and the Maxil- lofacial lofac ial Surgery Unit, Unive University rsity of Floren Florence. ce. Received for publication September 12, 2011; accepted Oc- tober 5, 2011. Copyri Cop yright ght ©20 ©2012 12 by the Ame Americ rican an Soc Societ ietyy of Pla Plasti sticc Surg Surgeon eons s

cannula, and syringe size in causing retrograde flow flo w of the su subst bstanc ancee to und unders erstan tand d the con condit dition ionss under which retrograde flow can lead to retinal circul cir culati ation on emb emboli olism sm and bli blindn ndness ess.. We sou sought ght 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 visuall disabil visua di sability, ity, and we hope h ope to t o provide pro vide a useful us eful guide gui de for ph physi ysicia cians ns who pe perfo rform rm the these se cos cos-metic procedures.

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

There are no fi fina nanc ncial ial co conf nfli lict ctss or Disclosure: There interests to report in association with the content of this article.

DOI: 10.1097/PRS.0b013e3182442363

www.PRSJournal.com

995

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 andcorticosteroidinjections forthe 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)needleandonce 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 allcases described,3–15 the signs andsymptoms 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 andtip30,31)andthe 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 usedin one caseeach. 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

996

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 in jection 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 in jected 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 thefiller 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 calculatedresistance to flow 68 (8L/pr4) is less within a terminal artery than in capillaries69,70; thus, the injected material will flow predominantlyin 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 artery 67 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 in jection 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-

997


•

April 2012

Table 1. Review of 15 Cases of Visual Loss after Facial Cosmetic Injection of Fat Tissue Age (yr)

Reference 3

Sex

Aesthetic Procedure(s)

Injecting Physician

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

Complaint of Symptoms Procedure/Symptoms Interval

Teimourian, 1988

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

Aut ologous fat injection int o 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

Aut ologous fat injection int o 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

Aut ologous 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


•


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 light stimulus and reactive to autologous fat emboli 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 After 1 wk: Recovery of dioxide, oxygen the mental status but therapy 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 specif ied

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

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

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

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

CRAO

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

(Continued )

999


•

April 2012

Table 1. (Continued ) Injecting Physician

Complaint of Symptoms Procedure/Symptoms Interval

Sex

10

Yoon et al., 2003

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

Aut ologous fat injection int o 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

Aut ologous fat injection int o 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

Aut ologous fat injection int o the left side of the nose (dosage not specified)

Plastic surgeon

N/A

Immediately: sudden pain and vision loss in her LE

Reference



Age (yr)

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, centralretinal artery occlusion; VA, visualacuity;M, male; CT,computed tomography; MRI, magnetic resonanceimaging; TG, triglyceride; HDL, high-density lipoprotein; VEP, visual evoked potentials; OAO, ophthalmic artery occlusion; IOP, intraocular pressure.

1000


•


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


Occlusion of the ocular and facial vessels and branches of the external carotid arteries


—

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


•

April 2012

Table 2. Review of 17 Cases of Visual Loss after Facial Cosmetic Injection of Various Substances Complaint of Symptoms Procedure/Symptoms Interval

Sex


16

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 inject ion 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 Inject ion of sili cone 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

Inject ion 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

Aesthet ic PMMA i njection int o the glabellar area

Plastic surgeon

N/A

Immediately after injection: severe RE pain and visual loss

Reference

von Bahr, 1963

1002

Injecting Physician


Age (yr)


•


Table 2. (Continued )

Risk Factors

Three previous treatments with the same substance


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

N/A


CRAO


Few minutes later

Therapy

Outcomes

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

N/A

CRAO and thrombosis N/A of the ophthalmic vein N/A N/A

N/A

N/A

N/A

N/A

N/A

N/A

Persistent impairment of sight After 5 minutes: return of vision

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 After several hours: BCVA of 1.0 ml of Cymetra to “hand motions,” papillary the bilateral nasolabial afferent defect, mild ptosis, regions and 0.5 ml of and exotropia Cymetra to the bilateral oral commissure regions under a local anesthetic without incident

CRAO and PCAOs

N/A

N/A

None

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 )

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

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


•

April 2012

Table 2. (Continued ) Complaint of Symptoms Procedure/Symptoms Interval

Sex

Kubota and Hirose, 200525

29

F

Inject ion of 0.7 ml of Met aCrill 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

Inject ion of a filler int o 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

Aesth etic Procedure(s)

Injecting Physician


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


•


Table 2. (Continued )

Risk Factors

N/A

Tobacco abuse; no previously systemic embolic episodes

N/A No medical problem

None

None

N/A


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



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 f ield 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

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

On day 3

Low-dose antiplatelet agent and a calcium channel blocker

Blindness

On day 2

Intravenous At 6 mo: methylprednisolone Complete recovery of the at 1 g/day for 3 eyeball movement days and tapered Progressive exudative and high-dose oral tractional retinal prednisolone and detachment at the aspirin at 100 mg; inferonasal retina caused daily Comfeel phthisis bulbi dressing

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

LE: no light perception, with Multiple BRAOs 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 CRAO 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

1005


•

April 2012

Fig. 1. Schematic drawing thatshows the anatomy,distribution,and connections between the ophthalmic andthe facial arterial systems. The supratrochlear artery isthe terminalbranch of theophthalmicartery andexits atthe superiorand medial corner of the bony orbit by piercing the orbital septum with the supratrochlear nerve.It runs superiorly into theforehead, where it supplies theintegument,muscles,and pericranium andmaintainsnumerous anastomoses withthe supraorbital arteryandwiththecontralateralvessels.Thisisthevesselmostlikelytobeinvolved whenintraarterial injection of fat andforeign material of the glabella andforehead is responsible for embolization. The supraorbital artery may occasionally be the route of embolization of injected material.It arisesfrom theophthalmic arteryand 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, thedorsal nasal arteryof theopposite side, and thelateral nasal branch of the facial artery. The facial artery arises from the external carotid arterythat supplies the structures of the face. Thefacial artery passes forward and upwardacrossthecheektotheangleofthemouth,whereitarborizesandgivesrise to thelabial systems and, more distally,to thelateral nasal artery that supplies the ala and dorsum of the nose. It further forms anastomoses with its contralateral counterpart,with theseptal andalar branches,with thedorsal nasal branchof the ophthalmic artery, and with the infraorbital branch of the internal maxillary. The facialartery then ascends alongthe side of thenose, endingat themedial canthus, where it is named the angular artery. After supplying the lacrimal sac and orbicularis oculi,it ends by anastomosingwith thedorsal nasal branchof theophthalmic artery. Theangular arteryon the cheek distributes branches that anastomose also withthe infraorbital artery. Thefacial artery should be consideredfor embolization following injections of the cheek, nasolabial folds, and lips.

tions (Pascal’s law 71). 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


•


from theuse of a small-gauge needleor 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 initialpressurestransmitted to surroundingtissues.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 mayallow various degrees of recovery.54,74–77 Although current standard therapies have not been shown to alter the natural courseof thedisease, it should beassumedthat 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. Thecurrentlyavailablerecommendations 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 flowandimmediately reduceintraocular 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 patient 6 who underwent carbogen rebreathing hadno substantial recovery of his sight. Although hyperbaric oxygen therapy may theoretically be beneficial, transportation to the nearest chamber may usurp precious time. Neither patient 6,12 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 thepresent 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


•

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 high volume syringe (10 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


•


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 wasachieved regardless of the nature of the embolus (fat 6,11–15 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, iso volemic 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 suddenrelease 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 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 ocularcirculation 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 theneedle 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

•

April 2012

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 Re- constr Surg. 1988;82:361. 4. Dreizen NG, Framm L. Sudden unilateral visual loss after autologous fat injection into the glabellar area. Am J Oph- thalmol. 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. LeeDH, YangHN, Kim JC,Shyn KH.Suddenunilateral 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 tissueaugmentation in theface: 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, BernardA, 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 theglabellar 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 Oph- thalmol. 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 thefundus of an eye after an injection in the scalp. Acta Ophthalmol (Copenh.) 1963;41: 85–91. 17. Lee JH, Lee KH, MoonHJ. A case ofunilateral blindnessafter paraffin injection on the forehead. J Korean Ophthalmol Soc. 1969;10:49–51.


•


18. Selmanowitz VJ, Orentreich N. Cutaneous corticosteroid in jection 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.Blindnessand 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 Oph- thalmol. 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 Re- constr Surg. 2010;26:289–291. 30. Kwon DY, Park MH, Koh SB, et al. Multiple arterialembolism after illicit intranasal injection of collagenous material. Der- matol 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 injectionsin 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,AbramsGW, Harris GJ,Ellis MK.Bilateral retinal embolization associated with intralesional corticosteroid in jection for capillary hemangioma of infancy. J Pediatr Oph- thalmol 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 Der- matol. 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 Re- constr 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 in jectable fillers in the glabellar region: Results from the In jectable 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 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 Aes- thet Surg. 2011;64:892–896. 63. Schanz S, Schippert W, Ulmer A, Rassner G, Fierlbeck G. Arterial embolizati on 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 Com- put. 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

•

April 2012

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 Ophthal- mol 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. Ophthal- mology 2010;117:1367–1375.e1. 78. McCleve DE, Goldstein JC. Blindness secondary to injections in the nose, mouth, andface: Cause andprevention. Ear Nose Throat J. 1995;74:182–188. 79. Ffytche TJ. A rationaliza tion 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 Oph- thalmol. 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.

Blindness Following Cosmetic Injections of the Face

Recommend Documents