Dolman P J, Glazer L C, Harris G J, Beatty R L, Massaro B M
Department of Ophthalmology, Medical College of Wisconsin, Milwaukee 53226.
Ophthalmic Plast Reconstr Surg. 1991;7(4):256-60. doi: 10.1097/00002341-199112000-00004.
Vision loss in orbital hypertension secondary to sudden space-occupying lesions is usually attributed to one of three causes: central retinal artery occlusion, direct compressive optic neuropathy, or compression of optic nerve vasculature. Accepted modes of decompressive therapy include lateral canthotomy and cantholysis; drainage of localized orbital air, hematoma, or abscess; and bony wall decompression. Five cases are presented in which orbital hypertension caused severe proptosis with traction on the optic nerve and tenting of the posterior globe. Another mechanism contributing to visual loss is proposed in these cases: ischemic optic neuropathy due to stretching of nutrient vessels. In these cases, rapid posterior decompression should theoretically be favored to reduce orbital pressure and relieve traction on the optic nerve vasculature.
