title: Blindness after reduction of facial fractures.
abstract: Blindness in patients suffering maxillofacial trauma is usually caused by optic nerve or optic canal injuries. It is, however, an uncommon complication of facial trauma, with a reported incidence of only 2 to 5 percent. Blindness may also follow surgical repair of facial fractures. Many mechanisms, such as intraoperative direct nerve injury, retinal arteriolar occlusion associated with orbital edema, or delayed presentation of indirect optic nerve injury sustained at the time of the initial trauma, have been implicated in causing this blindness. In this article, four cases of visual loss after surgical repair of facial trauma are reported. In a review of the University of Maryland Shock Trauma experience with facial trauma over 11 years, we discovered that 2987 of the 29,474 admitted patients (10.1 percent) sustained facial fractures, and that 1338 of these fractures (44.8 percent) involved one or both of the orbits. One thousand two hundred forty of these patients underwent operative repair of their facial fractures. Three patients experienced postoperative complications that resulted in blindness, a total incidence of only 0.242 percent. Postoperative ophthalmic complications seem to be primarily mediated by indirect injury to the optic nerve and its surrounding structures. The most frequent cause of postoperative visual loss is an increase in intraorbital pressure in the optic canal. When our data were added to the summarized cases, blindness was attributable to intraorbital hemorrhage in 13 of 27 cases (48 percent). In addition, 5 cases in our review attribute the visual loss to unspecified mechanisms of increased intraorbital pressure, bringing the total cases of visual loss caused by intraorbital pressure or hemorrhage to 18 of 27 cases, or 67 percent. Within the restricted confines of the optic canal, even small changes in pressure potentially may cause ischemic optic nerve injury.
authors.affiliation: Department of Surgery, Johns Hopkins School of Medicine, Baltimore, MD 21287-0980, USA.
authors.forename: J A
authors.initials: JA
authors.lastname: Girotto
authors.forename: W B
authors.initials: WB
authors.lastname: Gamble
authors.forename: B
authors.initials: B
authors.lastname: Robertson
authors.forename: R
authors.initials: R
authors.lastname: Redett
authors.forename: T
authors.initials: T
authors.lastname: Muehlberger
authors.forename: M
authors.initials: M
authors.lastname: Mayer
authors.forename: J
authors.initials: J
authors.lastname: Zinreich
authors.forename: N
authors.initials: N
authors.lastname: Iliff
authors.forename: N
authors.initials: N
authors.lastname: Miller
authors.forename: P N
authors.initials: PN
authors.lastname: Manson
mesh_terms: D000063:Accidents, Traffic; D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D001766:Blindness / Q000209:etiology*; D019299:Decompression, Surgical; D005147:Facial Bones / Q000293:injuries*; D005260:Female; D006470:Hemorrhage / Q000150:complications; D006801:Humans; D008297:Male; D008875:Middle Aged; D009900:Optic Nerve; D009916:Orbital Diseases / Q000150:complications; D011183:Postoperative Complications; D011312:Pressure; D012887:Skull Fractures / Q000150:complications* / Q000628:therapy; D013997:Time Factors
chemical_list: D000305:Adrenal Cortex Hormones