Girotto J A, Gamble W B, Robertson B, Redett R, Muehlberger T, Mayer M, Zinreich J, Iliff N, Miller N, Manson P N
Department of Surgery, Johns Hopkins School of Medicine, Baltimore, MD 21287-0980, USA.
Plast Reconstr Surg. 1998 Nov;102(6):1821-34. doi: 10.1097/00006534-199811000-00003.
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.
颌面创伤患者失明通常由视神经或视神经管损伤引起。然而,它是面部创伤的一种罕见并发症,报道的发生率仅为2%至5%。失明也可能发生在面部骨折的手术修复之后。许多机制,如术中直接神经损伤、与眶周水肿相关的视网膜小动脉阻塞,或初始创伤时所遭受的间接视神经损伤的延迟表现,都被认为与这种失明的发生有关。本文报告了4例面部创伤手术修复后视力丧失的病例。在回顾马里兰大学休克创伤中心11年来面部创伤的诊治经验时,我们发现,在29474例入院患者中,有2987例(10.1%)发生了面部骨折,其中1338例(44.8%)累及一侧或双侧眼眶。这些患者中有1240例接受了面部骨折的手术修复。3例患者出现了导致失明的术后并发症,总发生率仅为0.242%。术后眼部并发症似乎主要是由视神经及其周围结构的间接损伤介导的。术后视力丧失最常见的原因是视神经管内眶内压力升高。当我们的数据加入汇总病例后,27例中有13例(48%)失明归因于眶内出血。此外,我们回顾中的5例将视力丧失归因于眶内压力升高的未明确机制,使因眶内压力或出血导致视力丧失的病例总数达到27例中的18例,即67%。在视神经管的狭窄范围内,即使压力的微小变化也可能导致缺血性视神经损伤。