A 43-year-old man reported visual loss in his right eye after awakening from general anesthesia for endoscopic sinus surgery (ESS). Routine intranasal injection of epinephrine mixed with lidocaine was used to reduce bleeding and no associated cardiovascular side effects were reported during the procedure. During ESS, lamina papyracea was breached with direct injury to the right medial rectus and the procedure was stopped immediately. Five hours later, visual acuity was light perception, right eye, and 20/20, left eye. Intraocular pressure was 12 mmHg in the right eye. There was mild periorbital swelling and ecchymoses of the right upper and lower eyelids, and a large right exotropia with complete loss of adduction of the right eye (Fig. 1A). Subconjunctival hemorrhage was noted in the right eye on slit-lamp examination and the right pupil was dilated and nonreactive to light. The right fundus revealed a cherry red spot in the macula, pale and with extensive retinal edema, and diffuse retinal arterial narrowing (Fig. 1B). Yellow-colored fat emboli were seen within the retinal artery (Fig. 1C). Examination of the left eye was unremarkable. Neurological, physical, and laboratory findings were all within normal limits.
Fluorescein angiography (FA) of the right eye revealed a filling defect, due to emboli noted in the proximal retinal artery (Fig. 1D). In addition, there were marked filling delays in the retinal arteries combined with flow interruption of several arterial branches. Optical coherence tomography revealed diffuse thickening of the inner retinal layers and a central foveal thickness of 388 μm in the right eye, compared with 294 μm in the left eye. Kinetic visual field examination showed a diffuse visual field loss in the right eye, with vision preserved only in an inferonasal island.
Computed tomography demonstrated a right medial orbital wall fracture with a small amount of retrobulbar hemorrhage (Fig. 1E), while magnetic resonance imaging revealed disruption of the right medial rectus muscle (Fig. 1F). The right optic nerve was normal in appearance and no intracranial abnormalities were detected.
After 6 months, vision in the right eye remained light perception and the right exotropia was unchanged with complete loss of adduction. The fat emboli were no longer visible on fundus examination and FA showed normal retinal arterial perfusion.
While the frequency of ophthalmic complications following ESS is low (1,2), when they occur, they may have devastating consequences. Rene et al (3) reported a case of unilateral blindness following ESS in which direct optic nerve damage occurred in combination with central retinal arterial occlusion (CRAO). This was presumed to have occurred because of ophthalmic arterial spasm. A recognized cause of CRAO following ESS is the orbital compartment syndrome resulting from orbital hemorrhage (2–6). Patients generally present with pain, proptosis, tense eyelids, periorbital edema, subconjunctival hemorrhage, and external ophthalmoplegia.
We assume that the fat emboli from adjacent damaged bones or retrobulbar fat were released into the circulation leading to occlusion of the central retinal artery. Although pharmacomechanical thrombolysis was not performed in this case, it may be considered as a therapeutic option (7).
We thank Dr. Jae Hyoung Kim for his effort in selecting the best magnetic resonance imaging and computed tomography images.
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