causes of these problems, several patient risk factors have been suggested. These include chronic hypertension, diabetes mellitus, smoking, vascular disease, and other disorders that result in increased blood viscosity.7,10,11 Because evidence for the role of these risk factors in the pathogenesis of visual loss has been determined from studies in diverse clinical settings, their exact influence on patients who undergo spinal surgery remains unknown. CRAO is a disease entity that occurs after trauma or embolic, thrombotic, or spasmodic episodes in both children and adults.12 However, postoperative CRAO has rarely been reported as a consequence of direct pressure on the eye during surgery. Slocum et al13 first observed this problem in a patient who underwent a neurosurgical procedure in the prone position using a Bailey headrest. He emphasized that CRAO was caused by the extraocular pressure due to the headrest, or because of anesthetic mask malposition in the presence of hypotension. Givner and Jaffe14 reported four cases of CRAO occurring during abdominal operations in the supine position under mask anesthesia. They suggested that CRAO in these cases was due to a combination of pressure on the eye from the mask under hypotension and prolonged anesthesia. Gillan15 reported two cases in which CRAO developed after general mask anesthesia with vascular hypotension in the supine position. The cause was believed to be similar to that in Givner and Jaffe's report.14 Hollenhorst et al3 put forth the possibility that CRAO followed neurosurgical procedures which took place in the prone position and that used a padded headrest. He reported eight cases of CRAO in his clinical setting that resulted from the inadvertent application of pressure to the orbital contents by the headrest. Bradish and Flowers16 reported the first case of CRAO in the prone position after an orthopedic procedure. They believed that CRAO was due to a combination of hypotensive anesthesia and extrinsic pressure on the inherently susceptible eye of a patient with osteogensis imperfecta. The mechanism of visual loss after surgery is retinal ischemia secondary to external ocular pressure. The potential causes of this ischemia are venous congestion and arterial occlusion.3,17 Hollenhorst et al3 reproduced visual loss and ophthalmoplegia experimentally in seven rhesus monkeys using orbital compression for 60 minutes in the presence of hypovolemia and hypotension. They proved them by suggesting a mechanism of partial or complete collapse of the arterial and venous channels of the orbit, which were produced by a temponade action of the ocular contents. When the external pressure is released, orbital edema, proptosis, paresis of ocular movement, and massive edema of the retina result from dilation of the ischemic vascular channels and from a transudation of fluid through the permeable walls into the tissue spaces.3 Halfon et al5 suggested that the reversi- bility of ophthalmoplegia probably depends on the degree of ischemia suffered by both the extraocular muscles and the Ⅲ, Ⅳ, and Ⅵ cranial nerves. In our case, postoperative signs of MS Chung, et al. VISUAL LOSS AFTER SPINAL SURGERY orbital swelling in the affected eye were appreciable evidence of external orbital compression. Our patinet's brain MRI and MRA showed no evidence of cavernous sinus thrombosis and revealed only mild periorbital swelling and enlargement with hyperintensity of the extraocular muscles in the right eye while sparing the tendons. Thus our case is believed to be similar to those reported by Halfon et al.5 CRAO with ophthalmoplegia has been more infrequently reported.2-5 Hollenhorst et al3 noted that the five most severe cases out of eight cases who had proptosis, ptosis, and paralysis of the extraocular muscles improved, even though there was no visual recovery. Halfon et al5 reported two cases of palpebral edema, ocular pain, and total ophthalmoplegia which recovered partial or full ocular motility without the return of vision. Our patient, who exhibited vision loss of the right eye with swelling, ocular pain, and ophthalmoplegia recovered nearly full ocular movement without any improve- ment of vision, and is therefore believed to be identical to those in the two aforementioned reports. A prolonged prone position during spinal surgery and excessive pressure on the eye, especially as a result of patient malposition, can cause injury to the orbital structures and can lead to serious ocular complications. Although postoperative vision loss can occur in the absence of globe compression, avoidance of mechanical injury to the globe is very important for the surgeon and anesthetist to be aware of. The surgeon and anesthetist must pay particular attention to avoid the consequences of possible intraoperative movement without adequate eye protection during surgery. Special attention must be given to bradyarrhythmia or other heart conduction illnesses during the operation, as these may be signals of vagal stimulation caused by increased intraorbital pressure.2 We believe this to be the first case report of CRAO with ophthalmoplegia after spinal surgery in the prone position in Korea. If patients show postoperative signs of orbital swelling, especially following surgery in the prone position, the condition must be evaluated and treated immediately. Ophthalmologists must be aware of the possibility of this complication, and always pay attention to avoid this devastating complication. References 1. Brown GC, Magargal LE, Shields JA, et al. Retinal arterial obstruction in children and young adults. Ophthalmology 1981;88:18-25. 2. Wolfe SW, Lospinuso MF, Burke SW. Unilateral blindness as a complication of patient positioning for spinal surgery. A case report. Spine 1992;17:600-5. 3. Hollenhorst RW, Svien HJ, Benoit CF. Unilateral blindness occurring during anesthesia for neurosurgical operations. Arch Ophthalmol 1954;52:819-30. 4. West J, Askin G, Clarke M, Vernon SA. Loss of vision in one eye following scoliosis surgery. Br J Ophthalmol 1990; 74:243-4. 5. Halfon MJ, Bonardo P, Valiensi S, et al. Central retinal artery occlusion and ophthalmoplegia following spinal 141