Direct fractures of the orbital floor can extend from fractures of the inferior orbital rim, whereas indirect fractures of the orbital floor are not associated with fractures of the rim. Indications for repair of both fracture types are similar.
It is thought that orbital floor fractures are caused by 1 of 2 mechanisms or a combination of the 2. According to the hydraulic mechanism theory, blunt trauma rapidly occludes the orbital aperture, resulting in increased intraorbital pressure. This pressure causes the orbital bones to break or “blow out” at their weakest point along the posterior medial part of the floor, which comprises the maxillary bone. By contrast, according to the buckling mechanism theory, a striking object causes deformation of the inferior rim, resulting in forces that are transmitted and focused on the orbital floor, resulting in a blowout. Regardless of the mechanism, orbital contents may prolapse through the fracture into the maxillary sinus and sometimes become entrapped.
The diagnosis of a blowout fracture of the orbital floor is suggested by the patient’s history, physical examination, and orbital imaging studies. There is often a history of the orbital aperture being struck by an object that is larger than its diameter (eg, a ball, an automobile dashboard, or a fist). An orbital blowout fracture should be suspected in any patient who has received a periorbital blow forceful enough to cause ecchymosis. Physical examination typically reveals the following:
In patients with orbital floor fractures, vision loss can result from globe trauma, injury to the optic nerve, or increased orbital pressure causing a compartment syndrome (discussed later in this chapter, in the section Orbital Compartment Syndrome). An orbital hemorrhage should be suspected if loss of vision is associated with proptosis and increased IOP. Injuries to the globe and ocular adnexa may also be present.
Management
Orbital CT with coronal, axial, and sagittal views enables evaluation of the fracture size and extraocular muscle relationships, providing information that may help predict enophthalmos and muscle entrapment. However, despite the publication of multiple studies suggesting neuroimaging criteria for extraocular muscle entrapment, restrictive strabismus related to blowout fracture remains a clinical diagnosis.
Most orbital floor fractures do not require surgical intervention. Patients may be observed from weeks to months to allow edema and orbital hemorrhage to subside. Oral steroids (1 mg/kg per day for the first 7 days) decrease edema and may help hasten the decision of whether surgery for diplopia is necessary.
An exception to observation is in pediatric patients (Fig 6-5) in which the inferior rectus muscle is more likely to become tightly ensnared within a trapdoor fracture. In these patients, vertical globe excursion is significantly limited, and CT reveals the inferior rectus muscle within the fracture site along the maxillary sinus. Eye movement may stimulate the oculocardiac reflex (Video 6-1), causing pain, nausea, and bradycardia. Urgent repair should be undertaken in these cases. Immediate release of the entrapped muscle may improve the final ocular motility by limiting fibrosis.
VIDEO 6-1 Orbital fracture associated with oculocardiac reflex.
Courtesy of David Kuo, MD and Bobby S. Korn, MD PhD. Access all Section 7 videos at
www.aao.org/bcscvideo_section07.
Otherwise, the indications and timing for surgery remain controversial. Presently, there are no prospective, randomized clinical trials to guide decision making, and recommendations are based on noncomparative, retrospective reports or case series. The following 3 criteria are suggested to define when surgery may be indicated:
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Diplopia with limitation of upgaze and/or downgaze within 30° of the primary position; positive forced duction test; and radiologic confirmation of an orbital floor fracture. These findings may indicate functional entrapment of tissues affecting the inferior rectus muscle. Diplopia will improve significantly over the course of the first several weeks to months as orbital edema and/or hemorrhage resolve and the entrapped tissues stretch. If the findings are still present after 2 weeks, some surgeons prefer to repair the fracture whereas others prefer to continue observing until findings are no longer improving. As mentioned earlier, tight entrapment of the inferior rectus muscle with possible muscle ischemia is an indication for immediate repair.
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Enophthalmos that exceeds 2 mm and is cosmetically unacceptable to the patient. Enophthalmos can be masked by orbital edema immediately after the injury and may delay recognition of the enophthalmos for weeks to months. Exophthalmometry measurements are taken at the initial evaluation and at subsequent visits to monitor for enophthalmos. Some surgeons believe that when significant enophthalmos is present within the first 2 weeks of a large orbital floor fracture, greater enophthalmos may ensue, and thus intervention is indicated. Others believe that late enophthalmos is rare, even in the case of large fractures, and thus longer observation is appropriate, with the patient ultimately deciding whether the degree of enophthalmos is aesthetically unacceptable.
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Large fractures involving at least half of the orbital floor, particularly when associated with large medial wall fractures as determined by CT. Orbital fractures of this size may have a higher incidence of subsequent significant enophthalmos, and early repair may be sought. However, studies have shown that it can be difficult to predict who will proceed to develop significant enophthalmos based on imaging alone.
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Burnstine MA. Clinical recommendations for repair of isolated orbital floor fractures: an evidence-based analysis. Ophthalmology. 2002;109(7):1207–1210.
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Kersten RC, Vagefi MR, Bartley GB. Orbital “blowout” fractures: time for a new paradigm. Ophthalmology. 2018;125(6):796–798.
Surgical management of orbital fractures
Some surgeons prefer to proceed with the repair within 2 weeks of the initial trauma, believing that scar tissue formation and contracture of the prolapsed tissue make later correction of diplopia and/or enophthalmos difficult. Other surgeons prefer to observe the fracture to allow complete resolution of the orbital edema and/or hemorrhage with a determination of whether residual diplopia and/or aesthetically significant enophthalmos merits repair. Satisfactory correction of diplopia and enophthalmos is obtainable even if surgery is delayed.
The surgical approach to blowout fractures of the orbital floor is ideally performed through an inferior transconjunctival incision either with or without a lateral canthotomy and inferior cantholysis. The approaches through the lower eyelid have the following steps in common: elevation of the periorbita from the orbital floor, release of the prolapsed tissues from the fracture, and, usually, placement of an implant over the fracture to prevent recurrent adhesions and prolapse of the orbital tissues.
Orbital implants can be alloplastic (porous polyethylene, nylon foil, polytetrafluoroethylene, silicone sheet, or titanium mesh) or autogenous (split cranial bone, iliac crest bone, or fascia). Alloplastic implants combined with both synthetic and metallic components enable microplating and are an option for the management of large orbital floor and/or combined medial wall fractures. The harvesting of autologous grafts requires an additional operative site, and bone grafts are rarely indicated.
Delayed treatment of blowout fractures to correct persistent restrictive diplopia or cosmetically unacceptable enophthalmos may include exploration of the orbital floor to free prolapsed tissue and reposition it in the orbit. In late surgery for enophthalmos, placement of an implant to reposition the globe anteriorly and/or superiorly may be necessary. Other treatment options include strabismus surgery and procedures to camouflage the narrowed palpebral fissure and deep superior sulcus associated with enophthalmos.
Complications of blowout fracture surgery include decreased vision or blindness, persistent or new diplopia, undercorrection or overcorrection of enophthalmos, retraction of the lower eyelid, hypoesthesia of the infraorbital nerve, infection, early or late extrusion of the implant, lymphedema, delayed orbital hemorrhage around the implant, and damage to the lacrimal drainage system.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.