Perioperative ischemic optic neuropathy: a comprehensive review of anesthetic implications, hemodynamic pathophysiology, and risk stratification.

introductionPerioperative visual loss (POVL) is a rare but catastrophic complication of non-ocular surgery, most commonly attributable to ischemic optic neuropathy (ION). Spine and cardiac surgeries account for the majority of cases, with posterior ION (PION) predominating after prone spine procedures and anterior ION (AION) more frequently observed following cardiac surgery. Despite its low incidence, the permanent nature of vision loss necessitates a clear understanding of underlying mechanisms and modifiable perioperative risk factors.

methodsThis narrative review synthesizes evidence from epidemiologic studies, the American Society of Anesthesiologists (ASA) POVL Registry, large administrative databases, and physiologic investigations. Particular emphasis is placed on optic nerve anatomy and vascular supply, ocular perfusion pressure dynamics, intraocular pressure changes during prone positioning, and multivariate risk factors identified in registry-based analyses.

resultsThe optic nerve's limited collateral circulation and confinement within rigid anatomic boundaries render it uniquely vulnerable to ischemia. Registry and physiologic data support a perfusion-failure model in which reductions in mean arterial pressure, anemia, and sustained elevations in intraocular and venous pressures converge to critically reduce ocular perfusion pressure. In spine surgery, PION is strongly associated with prolonged operative duration, prone positioning, venous congestion, obesity, blood loss, and fluid strategies that promote interstitial edema. In contrast, cardiac surgery-associated AION more often reflects preexisting vascular disease and perioperative hypotension. Embolic mechanisms account for a minority of cases.

conclusionsPerioperative ION most commonly results from global failure of optic nerve perfusion rather than focal vascular occlusion. Recognition of distinct pathophysiologic mechanisms across surgical contexts underscores the importance of prevention. Strategies that preserve ocular perfusion pressure, minimize venous congestion, limit interstitial edema, and avoid prolonged hypotension during high-risk procedures may reduce the incidence of this devastating complication.