Visual Loss after Cosmetic Blepharoplasty Using Local Anaesthesia Containing Epinephrine - A Case Series : Annals of Maxillofacial Surgery

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Visual Loss after Cosmetic Blepharoplasty Using Local Anaesthesia Containing Epinephrine - A Case Series

Der Kelen, Louise Van; Mommaerts, Maurice Yves

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Annals of Maxillofacial Surgery 11(2):p 340-343, Jul–Dec 2021. | DOI: 10.4103/ams.ams_36_21
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Most surgeons perform blepharoplasties using a local anaesthetic containing a vasoconstrictor agent (e.g., epinephrine). The incidence of permanent vision loss after blepharoplasty is 0.04%.[1] The exact pathophysiology has not been established. However, retrobulbar haemorrhage is a frequent cause.[2] This occurs in 0.055% and leads in 0.005% to permanent vision loss. In this case series, we present some literature cases of acute angle-closure glaucoma (ACG) and perioperative posterior ischaemic optic neuropathy (PION) [Table 1]. We discuss possible pathophysiological mechanisms with an emphasis on the role of epinephrine.

Table 1:
Epidemiology, local anaesthesia, medication and diagnosis[3 4 5 6]


Case 1

Patient concerns: Fuzzy vision and redness of the left eye. She also developed a headache and nausea. Diagnostic aids: Visual acuity (VA) and intraocular pressure (IOP) were 20/40 and 56 mmHg, respectively. Slit lamp examination revealed corneal oedema and a mid-dilated pupil. Appositional angle closure was seen on dynamic gonioscopy. Treatment: Medically (IV mannitol and topical antiglaucoma medication) and surgically (bilateral YAG laser peripheral iridotomy). Outcome and follow-up: Full recovery.[3]

Case 2

Patient concerns: Continuous ocular pain and decreased vision in the left eye, 1–2 days postoperative. Diagnostic aids: VA was 20/200 and IOP was 50 mmHg. Slit lamp examination revealed a hazy cornea, a shallow anterior chamber, and a mid-dilated pupil. Treatment: Pilocarpine gtt 4%, oral acetazolamide, IV mannitol, and a peripheral YAG laser iridotomy. Because the IOP remained above normal limits, a combined phacotrabeculectomy was performed. Outcome and follow-up: Full recovery.[4]

Case 3

Patient concerns: Subtotal vision loss in the right eye. Diagnostic aids: Bilateral eyelid haematomas and subconjunctival bleeding. VA was light perception, no Ishihara plates could be identified and a relative afferent pupil defect (RAPD) was seen. All other examinations were normal. Perioperative PION was a diagnosis of exclusion based on the RAPD. Treatment: IV methylprednisolone. Outcome: After 3 weeks VA was 20/25 and one out of 15 Ishihara plates was identified. Fundoscopy revealed a slightly pale optic disc and the Goldmann visual field test showed an optic nerve-related visual field defect [Figure 1]. Follow-up: Three months later, an optic disk atrophy was indicated by a pale optic disk. VA was 20/25 and six out of 15 Ishihara plates could be identified.[5]

Figure 1:
Goldmann visual field: A superior altitudinal visual field defect combined with loss of the inferior temporal visual field and additional generalized constriction of the remaining inferior nasal visual field. Reproduced in high quality after the original

Case 4

Patient concerns: Left-sided headache and vision loss. Diagnostic aids: VA of no light perception and an IOP of 35 mmHg. Computed tomography was normal and a blood test revealed a normal erythrocyte sedimentation rate (ESR) and a slightly elevated C-reactive protein (CRP) level. Treatment: Left lateral canthotomy and cantholysis improved the IOP. She received IV methylprednisolone for 2 days and was then placed on 60 mg/day prednisone. Outcome: VA was unchanged with a RAPD in the left eye. There was mild left lower lid ecchymosis and subconjunctival haemorrhage. Diffusion-weighted imaging showed an infarction of the orbital segment of the left optic nerve [Figure 2a and b]. Follow-up: Given the elevated CRP levels, a temporal artery biopsy was performed; the result was negative and prednisone was tapered off.[6]

Figure 2:
Diffusion-weighted imaging (a) with apparent diffusion coefficient map (b). Restricted diffusion of the left optic nerve consistent with ischaemic infarction6


Complications of cosmetic blepharoplasty are rare, but can be severe.[1] Surgeons should be aware of these complications and intervene quickly to minimize the chance of permanent vision loss.

Retrobulbar haemorrhage occurs when orbital bleeding persists after wound closure. Because it takes place in an enclosed space, the IOP increases which can lead to central retinal artery occlusion and decreased perfusion pressures with ischaemic optic neuropathy that manifests as loss of vision.[7] Retinal ischaemia is also a possible, but less likely, consequence of retrobulbar haemorrhage.[8] In the absence of intraorbital bleeding, the onset of ischaemia can be explained by vasospasms. This can be caused either by pulling on the fat pedicles, by the use of vasopressor agents, or by action of vasoactive agents released from extravasated blood.[9] Robbe's study indicated that anoxaemia (caused by increased tissue metabolism and acidosis), not ischaemia, is the primary mechanism of optic nerve dysfunction following blepharoplasty. Epinephrine can cause both conditions, but anoxaemia does not occur when ornipressin is used instead. Slower dissipation of the effects of ornipressin also reduces the likelihood of rebound vasodilation.[10]

ACG is characterized with an increase in IOP which results in the following signs and symptoms: (peri-) ocular pain, nausea and/or vomiting and intermittent blurry vision with haloes and conjunctival injection, corneal oedema, a mid-dilated fixed pupil and a narrow/closed anterior chamber respectively[311] The mechanism of ACG after blepharoplasty is unknown. However, hypotheses suggest that ACG is triggered in patients with risk factors that cause development of a narrowed anterior chamber angle. These include advanced age, Inuit/Asian ethnicity, family history of ACG, increased lens thickness (cataract), an anteriorly positioned lens, plateau iris, hyperopia, and pupillary dilation. Surgical factors such as stress, postoperative coverage of the eyes and pharmacologically-induced mydriasis can cause pupil dilatation, which is considered the most important risk factor after periorbital facial procedures[13] ACG during the immediate postoperative period (within two days) is likely due to the use of local anaesthesia. A later-onset presentation is usually attributable to other surgical factors.[3] Epinephrine, used in local anaesthesia, causes pupil dilation.[4] In addition, lidocaine produces mydriasis and transient internal ophthalmoplegia.[12] Because a higher pH improves corneal penetration of local anaesthetic agents, these effects can be increased when lidocaine is buffered with sodium bicarbonate.[1]

Most patients who undergo blepharoplasty have some risk factors. It is therefore important to perform a preoperative history-taking and eye examination. The decision to use prophylactic laser iridotomy, epinephrine, or sodium bicarbonate should be based on the total number of risk factors and clinical judgement. More frequent follow-ups should be used in high risk patients.[3] Finally, it is important to keep ACG in mind as differential diagnosis of postoperative pain, especially when patients have visual symptoms.[1] Late diagnoses or misdiagnoses can be explained by the fact that all the symptoms and signs are, to different degrees, similar to normal postoperative symptoms and signs.[3] Perioperative analgesics or local anaesthesia might attenuate the symptoms and result in a milder presentation. ACG should be excluded in each patient with postoperative complaints by checking pupillary responses. If a fixed mid-wide pupil is present, an ophthalmologic referral is needed.[1]

PION is another possible cause of vision loss after blepharoplasty. It can be classified as perioperative, arteric or nonarteric PION and presents as acute vision loss without optic disc oedema[1314] Etiologies include direct mechanical compression of the arteries that perfuse the optic disc caused by retrobulbar injection and vasoconstrictive activity of the local anaesthetic, vasospasms induced by use of vasoconstrictor agents, enhancement of vasoconstriction by vasoconstrictive agents released from retrobulbar blood,[5] and increased IOP and compromise of the vasculature caused by marked oedema or congestion of the intraorbital fat. Because of differences in vascular supply demands, the posterior/retrobulbar segment of the optic nerve is more vulnerable to damage than the anterior segment.[15] PION is a diagnosis of exclusion. A case of acute vision loss, an optic nerve-related visual field defect (e.g., an altitudinal visual field defect as in case 3), a RAPD, a normal optic disc and fundus at presentation with development of optic disc pallor at six to eight weeks, and no other abnormalities to explain the vision loss are suggestive of PION. Finally, laboratory studies (mainly ESR and CRP) should be used to differentiate between arteric and non-arteric PION. These should be normal in patients with nonarteric PION.[16]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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Acute angle-closure glaucoma; blepharoplasty; blindness; epinephrine; posterior ischaemic optic neuropathy; postoperative complications

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