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Posterior Ischemic Optic Neuropathy After Blepharoplasty

Distefano, Alberto, G., MD; Pasol, Joshua, MD

Journal of Neuro-Ophthalmology: June 2018 - Volume 38 - Issue 2 - p 200–201
doi: 10.1097/WNO.0000000000000636
Clinical Correspondence

Department of Ophthalmology, Bascom Palmer Eye Institute, School of Medicine, University of Miami Miller, Miami, Florida.

Address correspondence to Alberto G. Distefano, MD, Department of Ophthalmology, Yale School of Medicine, 40 Temple Street, Suite 3A, New Haven, CT 06510; E-mail:

The authors report no conflicts of interest.

Vision loss, a rare complication of blepharoplasty, usually is due to retrobulbar hemorrhage leading to compression of the optic nerve and retinal vasculature (1). We present a case of severe vision loss after blepharoplasty due to posterior ischemic optic neuropathy.

A 62-year-old woman with a history of hypertension, breast cancer, and obstructive sleep apnea underwent bilateral upper and lower eyelid blepharoplasties under local anesthesia and intravenous sedation. Local anesthesia was established using 10 mL of lidocaine 2% with epinephrine 1:100,000 infiltrated into both upper lids and transconjunctivally into the medial, central, and lateral fat pads of the lower lids. She became aware of vision loss in the left eye 2 days later but could not determine the exact timing because of eyelid swelling. She also experienced left-sided headache since the time of surgery.

The patient was seen urgently by her surgeon who found visual acuity of 20/25, right eye and no light perception (NLP), left eye. The intraocular pressure on the left was elevated at 35 mm Hg, and the patient underwent immediate left lateral canthotomy and cantholysis with improvement in intraocular pressure. She was sent to an emergency department. Her sedimentation rate was 6 mm/hour, C-reactive protein (CRP) was 1.2 mg/dL (normal: <1.0 mg/dL), and orbital computed tomography was unremarkable. The patient was treated with intravenous methylprednisolone over 2 days (total dose: 750 mg) and then placed on 60 mg/day of prednisone.

The patient was referred to our institution 5 days after her surgery. Examination showed unchanged visual acuities with a left relative afferent pupillary defect. There was mild left lower lid ecchymosis and subconjunctival hemorrhage. Dilated fundus examination was normal bilaterally. Magnetic resonance imaging (MRI) revealed no evidence of orbital hemorrhage, soft tissue edema, or optic nerve enhancement. Diffusion-weighted imaging was consistent with infarction of the orbital segment of the left optic nerve (Fig. 1).

FIG. 1

FIG. 1

Although the patient denied symptoms of giant cell arteritis, given the slightly elevated CRP, a temporal artery biopsy was performed and was negative for arteritis. She was tapered off prednisone over 4 weeks.

Vision loss after blepharoplasty is rare, occurring in 1:50,000 cases and is persistent in 1:30,000 cases (2). Most commonly, this is due to retrobulbar hemorrhage, causing increased orbital pressure with compression of the optic nerve and vessels perfusing the optic nerve and retina.

Only 2 cases of posterior ischemic optic neuropathy (PION) after blepharoplasty have been reported. Good et al (3) described a 68-year-old woman with vision loss to NLP in the right eye after blepharoplasty associated with marked eyelid swelling and ecchymosis. Magnetic resonance imaging revealed 2 pockets of orbital hemorrhage with diffuse edema of the retrobulbar fat. In addition, there was increased signal of the posterior right optic nerve on T2 sequences. The authors speculated that the edema and elevated orbital pressure compromised blood flow to the posterior optic nerve through compression of the centripetal pial plexus. The anterior and intracanalicular optic nerves were spared because of blood flow from centrifugal vessels and separate branches of the ophthalmic artery, respectively. Kordic et al (4) reported a 47-year-old man with right vision loss to light perception, a right relative afferent pupillary defect, subconjunctival hemorrhage but a normal MRI. This patient was diagnosed with PION based on these findings, although infarction of the nerve was not demonstrated on neuroimaging.

In our patient, there were likely multiple factors leading to PION. Anterior soft tissue edema and ecchymosis may have led to increased orbital pressure. Small amounts of fluid not identifiable on neuroimaging may have spread to the orbital apex disrupting perfusion of the pial plexus to the posterior optic nerve. The use of lidocaine with epinephrine also may have contributed to decreased blood flow to the optic nerve. At one point, our patient's intraocular pressure in the left eye was 35 mm Hg, necessitating a lateral canthotomy and cantholysis. In addition, her history of hypertension and obstructive sleep apnea also may have been contributing factors.


Category 1: a. Conception and design: Alberto Distefano and Joshua Pasol; b. Acquisition of data: Alberto Distefano and Joshua Pasol; c. Analysis and interpretation of data: Alberto Distefano and Joshua Pasol; Category 2: a. Drafting the manuscript: Alberto Distefano and Joshua Pasol; b. Revising it for intellectual content: Alberto Distefano and Joshua Pasol; Category 3: a. Final approval of the completed manuscript: Alberto Distefano and Joshua Pasol.

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1. Leatherbarrow B, Saha K. Complications of blepharoplasty. Facial Plast Surg. 2013;29:281–288.
2. Mejia JD, Ergo FM, Nehai F. Visual loss after blepharoplasty: incidence, management, and preventive measures. Aesthet Surg J. 2011;31:21–29.
3. Good CD, Cassidy LM, Moseley IF, Sanders MD. Posterior optic nerve infarction after lower lid blepharoplasty. J Neuroophthalmol. 1999;19:176–179.
4. Kordic H, Flammer J, Mironow A, Killer HE. Perioperative posterior ischemic optic neuropathy as a rare complication of blepharoplasty. Ophthalmologica. 2005;219:185–188.
© 2018 by North American Neuro-Ophthalmology Society