Direct fractures of the orbital floor can extend from fractures of the inferior orbital rim. Indications for repair of the orbital floor in these cases are the same as those for indirect (blowout) fractures. Indirect fractures of the orbital floor are not associated with fracture of the inferior orbital rim.
Past theory held that blowout fractures were caused by increased intraorbital pressure when the impact of a blunt object rapidly occluded the orbital aperture. According to this theory, the contents of the orbit are compressed posteriorly toward the apex of the orbit, and the orbital bones break at their weakest point, usually the posterior medial part of the floor in the maxillary bone. The orbital contents prolapse through the fracture into the maxillary sinus and may be entrapped. More recently, however, it has been suggested that an impacting object may compress the inferior rim, directly buckling the orbital floor. In this case, the degree of increased orbital pressure determines whether orbital tissues are pushed down through the fracture into the maxillary antrum.
The diagnosis of a blowout fracture of the orbital floor is suggested by the patient’s history, physical examination, and radiographs. There is a history of the orbital entrance being struck by an object, usually one larger than the diameter of the orbital opening (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:
Eyelid signs. Ecchymosis and edema of the eyelids may be present, but other external signs of injury can be absent (white-eyed blowout).
Diplopia with limitation of upgaze, downgaze, or both. Limited vertical movement of the globe, vertical diplopia, and pain in the inferior orbit on attempted vertical movement of the globe are consistent with entrapment of the inferior rectus muscle or its adjacent septa in the fracture. Orbital edema and hemorrhage or damage to the extraocular muscles or their innervation can also limit movement of the globe. A significant limitation of both horizontal and vertical eye movements may indicate nerve damage or generalized soft-tissue injury. Limitations of globe movements caused by hemorrhage or edema generally improve during the first 1–2 weeks after injury. If entrapment is present, a forced duction test (traction test) shows restriction of passive movement of the eye; however, restriction can also result from edema and hemorrhage. This test is performed most easily with the instillation of anesthetic eyedrops followed by a cotton pledget of topical anesthetic in the inferior cul-de-sac for several minutes. Using a toothed forceps, the examiner grasps the insertion of the inferior rectus muscle through the conjunctiva and attempts to rotate the globe gently up and down. Comparing the intraocular pressure (IOP) as measured in primary position and in upgaze usually shows a significant increase in upgaze if the inferior rectus is entrapped.
Enophthalmos and ptosis of the globe. These findings occur with large fractures in which the orbital soft tissues prolapse into the maxillary sinus. A medial wall fracture, if associated with the orbital floor fracture, may significantly contribute to enophthalmos because of prolapse of the orbital tissues into both the ethmoidal and the maxillary sinuses. Enophthalmos may be masked by orbital edema immediately following the injury, but it becomes more apparent as the orbital edema subsides. Globe ptosis is often a sign of a sizable fracture.
Hypoesthesia in the distribution of the infraorbital nerve.
Emphysema of the orbit and eyelids. Any fracture that extends into a sinus may allow air to escape into the subcutaneous tissues. This occurs most commonly with medial wall fractures.
In patients with orbital floor fractures, visual loss can result from globe trauma, injury to the optic nerve, or increased orbital pressure causing a compartment syndrome (discussed in the section Traumatic Visual Loss With Clear Media). 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.
CT scans with coronal or sagittal views help guide treatment. They allow evaluation of fracture size and extraocular muscle relationships, providing information that can be used to help predict enophthalmos and muscle entrapment. Despite the publication of multiple studies suggesting neuroimaging criteria for associated extraocular muscle entrapment, restrictive strabismus related to blowout fracture remains a clinical diagnosis.
The majority of blowout or other orbital floor fractures do not require surgical intervention. Orbital blowout fractures are usually observed for 5–10 days to allow swelling and orbital hemorrhage to subside. Oral steroids (1 mg/kg per day for the first 7 days) decrease edema and may limit the risk of diplopia from inferior rectus contracture and fibrosis.
An exception to initial observation occurs in pediatric patients, in whom the inferior rectus muscle may become tightly trapped beneath a trapdoor fracture (Fig 6-5). In these patients, vertical globe excursion is significantly limited, and CT reveals the inferior rectus muscle within the maxillary sinus. Eye movement may stimulate the oculocardiac reflex, causing pain, nausea, and bradycardia. Urgent repair should be undertaken in these cases. Release of the entrapped muscle without delay may improve the final ocular motility result by limiting fibrosis.
Although the indications for surgery are controversial, certain guidelines are helpful in determining when surgery is advisable:
Diplopia with limitation of upgaze and/or downgaze within 30° of the primary position with a positive forced duction test result 7–10 days after injury and with radiologic confirmation of a fracture of the orbital floor. These findings indicate functional entrapment of tissues affecting the inferior rectus muscle. Diplopia may improve significantly over the course of the first 2 weeks as orbital edema, hemorrhage, or both resolve and as some of the entrapped tissues stretch. However, if the findings are still present after 2 weeks and if the entrapped tissues are not freed, vertical diplopia is likely to persist. As mentioned previously, tight entrapment of the inferior rectus muscle with a frozen globe is an indication for immediate repair.
Enophthalmos that exceeds 2 mm and is cosmetically unacceptable to the patient. Enophthalmos is usually masked by orbital edema immediately after the trauma, and several weeks may pass before the extent of this problem is fully appreciated. Appropriate measurements must be taken at the initial evaluation and at subsequent visits. If significant enophthalmos is present within the first 2 weeks in association with a large orbital floor fracture, even greater enophthalmos can be anticipated in the future.
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Large fractures involving at least half of the orbital floor, particularly when associated with large medial wall fractures (determined by CT). Orbital fractures of this size have a high incidence of subsequent significant enophthalmos.