NAION is the most common acute optic neuropathy in patients older than 50 years. It presents with painless vision loss that typically remains static after the initial course of events. Patients often have altitudinal visual field defects and diffuse or segmental hyperemic disc edema.
Optic nerves with small or absent physiologic cups are considered at risk for NAION, in theory because of anatomical crowding that can compromise circulation to the optic nerve. Other risk factors for NAION include hypertension, diabetes mellitus, hyperlipidemia, smoking, and other vasculopathic predispositions.
Traditionally, NAION causes monocular vision loss. However, bilateral and simultaneous NAION can occur in such settings as anemia or systemic hypotension, causing compromised flow to each eye. Several studies have found patients with shock-induced nonarteritic ischemic optic neuropathy after hemorrhage (most commonly of gastrointestinal origin) or after surgical procedures, such as spine surgery or coronary artery bypass graft.[2,3,4,5,6,7] Visual deficits occurred within 48 hours after the onset of hemorrhage in 50% of patients, whereas 40% experienced deficits 3-10 days later.[2,5]
The clinical findings of NAION include diffuse or segmental disc hyperemia with delayed optic disc filling on fluorescein angiography. Perimetry typically shows arcuate or altitudinal defects. Neuroimaging typically shows no acute abnormalities involving the optic nerves. Optic disc edema generally resolves after 6-10 weeks, and the nerve becomes atrophic.
Currently, there are no treatments or known preventive measures for NAION or shock-induced nonarteritic ischemic optic neuropathy. Surgery, including optic nerve surgery, offers no benefit for NAION.[9,10] Although vision loss after NAION usually remains stable, the Ischemic Optic Neuropathy Decompression trial reported visual recovery of 3 Snellen lines in 31% of patients after 2 years.
Medscape Ophthalmology © 2014
Cite this: A Case of Shock-Induced Vision Loss - Medscape - Aug 15, 2014.