An orbital blowout fracture is a traumatic deformity of the orbital floor or medial wall, typically resulting from impact of a blunt object larger than the orbital aperture, or eye socket. Most commonly the inferior orbital wall i.e. the floor is likely to collapse, because the bones of the roof and lateral walls are robust. Although the bone forming the medial wall is thinnest, it is buttressed by the bone separating the ethmoidal air cells. The comparatively thin bone of the floor of the orbit and roof of the maxillary sinus has no support and therefore it is the inferior wall that collapses mostly. So the medial wall blowout fractures are second most common, whereas superior wall i.e. the roof and lateral wall blowout fractures are uncommon & rare respectively. There are two broad categories of blowout fractures: open door, which are large, displaced and comminuted, and trapdoor, which are linear, hinged, and minimally displaced. They are characterized by double vision, sunken ocular globes, and loss of sensation of the cheek and upper gums due to infraorbital nerve injury. In pure orbital blowout fractures, the orbital rim is preserved, while with impure fractures, the orbital rim is also injured. With the trapdoor variant, there is a high frequency of extra-ocular muscle entrapment, despite minimal signs of external trauma, a phenomenon referred to as a 'white-eyed' orbital blowout fracture. They can occur with other injuries such as transfacial Le Fort fractures or zygomaticomaxillary complex fractures. The most common causes are assault and motor vehicle accidents. In children, the trapdoor subtype are more common. Surgical intervention may be required to prevent diplopia and enophthalmos. Patients that are not experiencing enophthalmos or diplopia, and that have good extraocular mobility can be closely followed by ophthalmology without surgery.
The force of a blow to the orbit is dissipated by a fracture of the surrounding bone, usually the orbital floor and/or the medial orbital wall. In blowout fractures, the medial wall is fractured indirectly. When an external force is applied to the orbital cavity from an object whose diameter is larger than that of the orbit, the orbital contents are retropulsed and compressed. The consequent sudden rise in intraorbital pressure is transmitted to the walls of the orbit, which ultimately leads to fractures of the thin medial wall and/or orbital floor. Theoretically, this mechanism should lead to more fractures of the medial wall than the floor, since the medial wall is slightly thinner. However, it is known that pure blowout fractures most frequently involve the orbital floor. This may be attributed to the honeycomb structure of the numerous bony septa of the ethmoid sinuses, which support the lamina papyracea, thus allowing it to withstand the sudden rise in intraorbital hydraulic pressure better than the orbital floor. In children, the flexibility of the actively developing floor of the orbit fractures in a linear pattern that snaps backward. This is commonly referred to as a trapdoor fracture. The trapdoor can entrap soft-tissue contents, thus causing permanent structural change that requires surgical intervention.
Diagnosis
Diagnosis is based on clinical and radiographic evidence. Periorbital bruising and subconjunctival hemorrhage are indirect signs of a possible fracture.
Imaging
Thin cut CT scan with axial and coronal view is the optimal study of choice for orbital fractures. Plain radiographs, on the other hand, do not have the sensitively capture blowout fractures. On Water's viewradiograph, polypoid mass can be observed hanging from the floor into the maxillary antrum, classically known as teardrop sign, as it usually is in shape of a teardrop. This polypoid mass consists of herniated orbital contents, periorbital fat and inferior rectus muscle. The affected sinus is partially opacified on radiograph. Air-fluid level in maxillary sinus may sometimes be seen due to presence of blood. Lucency in orbits usually indicate orbital emphysema.
Treatment
Initial management
All patients should follow-up with an ophthalmologist within 1 week of the fracture. To prevent orbital emphysema, patients are advised to avoid blowing of the nose. Nasal decongestants are commonly used. It is also common practice to administer prophylactic antibiotics when the fracture enters a sinus, although this practice is largely anecdotal. Amoxicillin-clavulanate and azithromycin are most commonly used. Oral corticosteroids are used to decrease swelling.
Surgery
Surgery is indicated if there is enophthalmos greater than 2 mm on imaging, Double vision on primary or inferior gaze, entrapment of extraocular muscles, or the fracture involves greater than 50% of the orbital floor. When not surgically repaired, most blowout fractures heal spontaneously without significant consequence. Surgical repair of a "blowout" is rarely undertaken immediately; it can be safely postponed for up to two weeks, if necessary, to let the swelling subside. Surgery to treat the fracture generally leaves little or no scarring and the recovery period is usually brief. Ideally, the surgery will provide a permanent cure, but sometimes it provides only partial relief from double vision or a sunken eye. Reconstruction is usually performed with a titanium mesh or porous polyethylene through a transconjunctival or subciliary incision. More recently, there has been success with endoscopic, or minimally invasive, approaches.
Epidemiology
Orbital fractures, in general, are more prevalent in men than women. In one study in children, 81% of cases were boys. In another study in adults, men accounted for 72% of orbital fractures.
History
Orbital floor fractures were investigated and described by MacKenzie in Paris in 1844 and the term blow out fracture was coined in 1957 by Smith & Regan, who were investigating injuries to the orbit and resultant inferior rectus entrapment, by placing a hurling ball on cadaverous orbits and striking it with a mallet.
