It is the first day of your first neuroanesthesia rotation and you’re all set to start a major spinal reconstruction. You’re about to wheel your patient back to the operating room when the patient’s spouse (an attorney) tells you that she’s recently read about blindness after spine surgery and wants to know what you think and, specifically, what you are going to do to prevent blindness?

Postoperative visual loss (POVL) is a devastating injury that fortunately remains rare, with an occurrence rate of between 1/1,000 to 3/10,000 spine surgeries. The time of presentation is variable—patients may present with painless loss of vision immediately post surgery or up to 3 to 4 days postoperatively. The deficit can vary from a mild field cut to complete loss of light perception. Historically, POVL was most closely associated with cardiac surgery and cardiopulmonary bypass. However, with the advent of increasingly complex spine surgeries, the incidence of POVL may also be increasing. This is somewhat surprising because the eye has a dual blood supply: (a) the central retinal artery (CRA), and (b) a series of posterior ciliary arteries. The anterior optic nerve (Fig. 138.1) (anterior to the lamina cribrosa) is supplied by branches of posterior ciliary arteries. These are end arteries and therefore may produce watershed regions, placing the retina at risk for ischemia. The posterior optic nerve is supplied by pial vessels and, occasionally, branches of the CRA. Notably, up to 20% of normal individuals have minimal or absent autoregulation of the optic nerve blood supply.

Unfortunately, the mechanisms of POVL are poorly understood, but they may be categorized into at least two general subgroups. The first of these is central retinal artery occlusion (CRAO). CRAO is the predominant mechanism of POVL following cardiac surgery and is almost certainly embolic following cardiopulmonary bypass. CRAO following spine surgery may not only be embolic, but it may also result from reduced perfusion pressure to the retina by other mechanisms, such as direct pressure on the orbit while in the prone position (“head rest syndrome”). CRAO is generally unilateral and may present with periorbital edema suggesting decreased venous outflow from the orbit, thus reducing retinal perfusion
pressure. Funduscopic exam classically reveals a cherry red spot. The prognosis with CRAO is poor, and there is rarely significant improvement in vision.