Diagnosis

The orbit is a bony cone made of the frontal, zygomatic, ethmoid, lacrimal, sphenoid, palatine, and maxillary bones. When the orbit is subjected to direct, high-velocity blunt force, the bony struts supporting the eye crack. The weakest point in this structure is the orbital floor, which makes it the most common fracture location. In 1957, Smith and Regan first described an orbital floor fracture with inferior rectus entrapment and subsequent restricted ocular motility as an orbital “blow-out fracture.” (Am J Emerg Med 2001;19[2]:147.) Orbital fractures most commonly involve the inferior, medial, lateral, and superior walls in that order. (J Trauma 1989;29:388.) In most countries, traffic accidents are the leading cause of orbital fractures, followed by falls, assault, and sports injuries. (Curr Opinion Ophth 2004;15[5]:416.)FigureFigurePatients with orbital fractures can present with a range of signs and symptoms depending on the size and location of the fracture. Patients may describe minimal pain, nausea, vomiting, ptosis, diplopia (especially with attempted upward gaze), decreased vision, or ipsilateral hypesthesia in the distribution of the infraorbital nerve. Any change in vision could signal a serious ocular injury. Initial evaluation of the trauma patient is to identify serious and life threatening injuries with adherence to standard trauma evaluation and resuscitation principles. Examination of the face typically reveals periorbital ecchymosis and swelling. If the fracture is significant, the eye may appear sunken (enophthalmos). Palpation of the orbital rim may illicit point-tenderness and a bony defect. If the fracture involves the medial orbital wall and violates the maxillary sinus, pathoneumonic orbital emphysema may be present or may develop. Subcutaneous emphysema is a common and usually benign complication of medial wall fractures. In rare cases, it can lead to optic neuropathy or pneumomediastinum. (Curr Opinion Ophth 2004;15[5]:416.) Blow-out fractures can create a “trap door” effect with entrapment of periorbital fat and at times the inferior rectus muscle. Direct entrapment of the muscle in the fracture, or resultant edema and hemorrhage of the periorbital fat, can restrict conjugate movement upward or downward. (See photo.) Ultimately, these direct and indirect pressure forces on the optic nerve can result in optic nerve ischemia and vision loss, also known as orbital compartment syndrome. The incidence of ocular injury associated with orbital floor fractures is 35 percent. (Canadian Ophthalmlogical Society: www.eyesite.ca/7mod-ules/Module3/html/Mod3Sec5.html; accessed Nov. 7, 2006.) Meticulous evaluation of the globe, including visual acuity, intraocular pressure, and eye motility, should be performed to rule out other underlying traumatic ocular injuries. Injuries associated with orbital wall fractures include retinal hemorrhage, viteous hemorrhage, retinal detachment, corneal abrasion, globe rupture, hyphema, lens dislocation, and retrobulbar hematoma. Computerized tomography scanning with axial and coronal sections remains the gold standard for assessing orbital fractures. Breach of the maxillary sinus will create air fluid levels in the affected sinus. Protrusion of orbital contents into the maxillary sinus can create the classic “teardrop sign.” (See photo.) Recent studies have evaluated the use of ultrasonography as a screening tool to rule out fractures in trauma cases, but are not considered a definitive diagnostic modality at this time. (Curr Opinion Ophth 2004;15[5]:411.) The majority of blow-out fractures do not require surgical intervention. Patients with orbital blow-out fractures who have minimal displacement, no diplopia, and no entrapment can be safely discharged home. All patients should be evaluated by an ophthalmologist within one week of the event. Cold packs applied to the affected eye for the first 48 hours and elevating the head of the bed may help decrease swelling. If violation of the sinus occurs, the patient should be placed on prophylactic antibiotics and instructed not to blow his nose. Nausea and vomiting are common with eye injuries, and should be treated with standard antiemetics. Surgical management of orbital blow-out fractures has been controversial. In general, surgical treatment is recommended for patients with diplopia, enopthalmos, or entrapment. In the emergency department, consultation with an ophthalmologist or facial surgeon is appropriate. Surgery, if indicated, is generally performed within two weeks of the inciting injury. This ensures time for adequate hemorrhage and edema resolution before scar tissue formation prohibits adequate correction. The use of corticosteroids to manage orbital blow-out fractures also is controversial. A few small trials have found that oral corticosteroids in patients with clinical entrapment reduced tissue edema (CurrSurg 2004;61:25; Adv Opth Maxillofac Surg 1999;37:312) and may limit the risk of long-term diplopia. At this time, consultation with an ophthalmologist may be prudent before initiating this therapy. Blow-out fractures can result in numerous complications including decreased visual acuity, enopthalmos, infraorbital hypesthesia, lymphedema, and damage to the lacrimal pump.