Saturday, December 18, 2010

Blow-out Fracture

Patients manifesting orbital blow-out fracture always present with a history of blunt ocular trauma. Blow-out fracture is usually caused by a large, low-velocity object, such as a fist or a ball. Sports-related injuries are common. If the trauma is recent, the patient may present with symptoms of pain, local tenderness and double vision. Complaints of an intense pressure feeling or swelling of the eye associated with nose blowing may also be reported.

Critical signs of recent blow-out fracture include:

edema and ecchymosis of the lid tissues
restriction of ocular motility, especially with vertical movements
orbital crepitus (subcutaneous emphysema)
hypoesthesia of the ipsilateral cheek, due to entrapment of the infraorbital nerve.

There may also be an associated nosebleed due to communication between the orbit and maxillary sinus. Orbital edema initially surrounds and displaces the globe, in some cases causing the eye to appear proptotic. However, as the swelling subsides, the eye is likely to drop down and back, becoming enophthalmic. Associated traumatic uveitis and/or hyphema may be noted as well.

In some cases, patients suffering orbital blow-out fracture initially ignore treatment, and may present long after the initial inflammatory manifestations of trauma have subsided. In these patients, evaluation reveals only relative enophthalmos and motility restriction, usually in upgaze, and possible infraorbital hypoesthesia.

Blow-out fracture may result in cases of abrupt trauma to the eye by any object >5cm in diameter. Because the orbital rim is very strong, the forces of blunt trauma are reflected back, compressing the eye and creating a tremendous increase in pressure within the orbit.

Since the larger bones which comprise the orbit contain sinuses, the orbital walls are at great risk for fracture; should the trauma be of sufficient force, these walls can literally "blow out." The medial wall (ethmoid bone) is occasionally affected. But most commonly, the orbital floor (the superior aspect of the maxillary bone) sustains the damage. In cases of floor fractures, the eye may partially drop down into the maxillary sinus, causing enophthalmos and entrapment of the inferior rectus or inferior oblique muscle.

This entrapment leads to a tethering effect, resulting in a limited downgaze ability and, more notably, an inability toward upgaze in the affected eye. While this situation can be surgically corrected in the early stages, prolonged entrapment leads to fibrosis of the muscle(s) and permanent motility impairment. Associated medial wall fractures may induce damage to the medial rectus muscle and/or the lacrimal apparatus, but this is uncommon.

In most cases, these fractures result in orbital emphysema, creating a direct communication between the ethmoid sinus and the orbit. This produces the feeling of pressure within the orbit when the patient attempts to blow his/her nose. The greatest risk to consider with medial wall fractures is orbital cellulitis, secondary to sinus infection, should pathogenic organisms within the sinus invade the post-tarsal eyelid.

All cases of blunt ocular trauma with resultant crepitus or motility restriction warrant orbital imaging studies. Computed tomography (CT scan) is the procedure of choice. CT is better at imaging the bony structures of the orbit than either plain skull films (X-ray) or MRI. Obtain both axial and coronal scans.

Should you discover a floor fracture with associated herniation of the orbital contents, consider surgical intervention. Generally, surgery is only for patients with recent trauma who manifest significant diplopia in primary gaze or downgaze, or in cases of cosmetically unacceptable enophthalmos. Most oculoplastic specialists will wait 10 to 14 days following the trauma to allow for resolution of the associated edema and hemorrhage. The treatment consists of surgical resection of the periosteum and repair of the fracture, utilizing a bone graft or synthetic material such as silicon or Teflon.

Long-standing entrapment of the extraocular muscles leads to fibrosis and irreversible scarring; intervention to improve motility after four weeks is typically unsuccessful. Initiate prophylactic antibiotic therapy immediately in the event of associated medial wall fractures with orbital emphysema, or if there is any suspicion of ethmoid damage. A broad spectrum oral preparation such as cephalexin or erythromycin (250-500mg QID) may be used for 10 to 14 days. Surgical repair of the medial wall is unnecessary in uncomplicated ethmoid fractures, since the condition resolves spontaneously in three to four weeks.


Cases of orbital blow-out fracture do not constitute an emergency, however, accurate diagnosis and management of the associated ocular manifestations is paramount.
One test that is very helpful in differentiating muscle entrapment in orbital fracture from other muscle or nerve complications is the forced duction test. Entrapped muscles will resist forced movements with a forceps or even a cotton-tipped applicator. Again, this test should ideally be performed after resolution of the orbital swelling.
Check for crepitus by palpating the bony rim of the orbit or lid-small bubbles of air will "pop" when compressed.
For long-standing fractures in which the patient experiences diplopia in downgaze, but is not a surgical candidate, consider incorporating unilateral pr

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