Visual deterioration after endonasal endoscopic skull base surgery: causes, treatments, and outcomes

OBJECTIVE Visual deterioration after endoscopic endonasal transsphenoidal surgery (EETS) for sellar and parasellar masses is a rare but serious complication caused by either compressive or ischemic mechanisms. Timely diagnosis and intervention may restore vision if instituted appropriately. The associated risk factors and their relation to the success of intervention are not well understood. METHODS The authors examined a series of 1200 consecutive EETS cases performed by the senior author at Weill Cornell/NewYork-Presbyterian Hospital from 2010 to 2020. Cases with postoperative visual deterioration were identified. Pre- and postoperative clinical data, mechanism of visual decline, latency to intervention, and long-term visual outcome were retrospectively collected and analyzed with appropriate statistical methods. RESULTS Twenty-one patients (1.75%) complained of early postoperative visual deterioration. The most common pathology associated with postoperative visual loss was craniopharyngioma (7.69%), followed by meningioma (5.43%) and then pituitary adenoma (1.94%). Timely intervention restored vision in 81% of patients for a 0.33% rate of permanent visual deterioration. Average time to visual deterioration was 28.8 hours, and over 70% of patients experienced vision loss within the first 13 hours. Compressive etiology (n = 11), consisting of either hematoma (n = 8) or graft displacement (n = 3), occurred 7.3 hours and 70.3 hours after surgery, respectively, and was more common in adenomas. Acute postoperative visual deterioration was more common in firm closures (4.78%) compared with soft closures (1.03%; p = 0.0006). Ischemic etiology (n = 10) occurred 10.3 hours after surgery and was more common with craniopharyngiomas and meningiomas (p = 0.08). Sixteen patients (76.2%) underwent early reoperation to explore and decompress the optic apparatus. Vision was restored to baseline after reoperation in all 11 compressive cases, whereas 6/10 ischemic cases improved with supplemental oxygen and hypervolemic hypertensive therapy (p = 0.02). Fluid expansion from 8 to 16 hours (p = 0.034) and systolic blood pressure elevation from 32 to 48 hours (p = 0.05) after surgery were significantly higher in those ischemic patients who recovered some vision compared with those with persistent visual deficits. CONCLUSIONS Visual deterioration after EETS is a rare event but can be effectively treated if acted upon appropriately and in a timely fashion. Compressive etiology is reversible with early reoperation. Ischemic etiology can be successfully treated in roughly half of cases with supplemental oxygen and hypertensive hypervolemic therapy but may result in permanent visual deterioration if not instituted appropriately or if delayed with unnecessary exploratory surgery.