An orbital blowout fracture is a traumatic deformity of the orbital floor or medial wall that typically results from the impact of a blunt object larger than the orbital aperture, or eye socket. Most commonly this results in a herniation of orbital contents through the orbital fractures. The proximity of maxillary and ethmoidal sinus increases the susceptibility of the floor and medial wall for the orbital blowout fracture in these anatomical sites. Most commonly, the inferior orbital wall, or 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 the 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 so the inferior wall collapses mostly. Therefore, medial wall blowout fractures are the second-most common, and superior wall, or roof and lateral wall, blowout fractures are uncommon and rare, respectively. They are characterized by double vision, sunken ocular globes, and loss of sensation of the cheek and upper gums from infraorbital nerve injury. The two broad categories of blowout fractures are open door and trapdoor fractures. Open door fractures are large, displaced and comminuted, and trapdoor fractures are linear, hinged, and minimally displaced. The hinged orbital blowout fracture is a fracture with an edge of the fractured bone attached on either side. In pure orbital blowout fractures, the orbital rim (the most anterior bony margin of the orbit) is preserved, but 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 that is referred to as a "white-eyed" orbital blowout fracture. The fractures can occur of pure floor, pure medial wall or combined floor and medial wall. 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. Smaller fractures are associated with a higher risk of entrapment of the nerve and therefore often smaller fracture are more serious injuries. Large orbital floor fractures have less chance of restrictive strabismus due to nerve entrapment but a greater chance of enopthalmus. There are a lot of controversies in the management of orbital fractures. the controversies debate on the topics of timing of surgery, indications for surgery, and surgical approach used. Surgical intervention may be required to prevent diplopia and enophthalmos. Patients not experiencing enophthalmos or diplopia and having good extraocular mobility may be closely followed by ophthalmology without surgery.
Signs and symptoms Some clinically observed signs and symptoms include:
Orbital pain Eyes displaced posteriorly into sockets (enophthalmos) Limitation of eye movement (restrictive strabismus) Loss of sensation (hypoesthesia) along the trigeminal (V2) nerve distribution Seeing-double when looking up or down (vertical diplopia) Orbital and lid subcutaneous emphysema, especially when blowing the nose or sneezing Nausea and bradycardia due to oculocardiac reflex Inability to elevate eyeball, and move eyeball downward due to inferior rectus entrapment Bruising/ecchymosis Decreased movement of eyes Cranial nerve palsies (III, IV, VI) subconjunctival hemorrhage
Causes Common medical causes of blowout fracture may include:
Direct orbital blunt injury Sports injury (squash ball, tennis ball etc.) Motor vehicle accidents Falls Assault sports work-related injuries Any source of direct force
Mechanism There are two prevailing theories to how orbital fractures occur. The first theory is the hydraulic theory. The hydraulic theory states that a force is applied to the globe which results in equatorial expansion of the globe due to increasing hydrostatic pressure. The pressure is eventually released at the weaker point in the orbit (the medial and inferior walls). Theoretically, this mechanism should lead to more fractures of the medial wall than the floor, since the medial wall is slightly thinner (0.25 mm vs 0.50 mm). 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. The second prevailing theory is known as the buckling theory. The buckling theory states that a force is transmitted directly to the facial skeleton and then a ripple effect is transmitted to the orbit and causes buckling at the weakest points as described above. 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.
Anatomy The bony orbital anatomy is composed of 7 bones: the maxillary, zygomatic, frontal, lacrimal, sphenoid, palatine, and ethmoidal. The floor of the orbit is the roof of the maxillary sinus. The medial wall of the orbit is the lateral wall of the ethmoid sinus. The medial wall is also known as the lamina papyrcea which means "paper layer." This demonstrates the thinness which is associated with increased fractures. The clinically important structures surrounding the orbit include the optic nerve at the apex of the orbit as well as the superior orbital fissure which contains cranial nerves 3, 4, and 6 therefore controlling ocular muscles of eye movement. Inferior to the orbit is the infraorbital nerve which is purely sensory. Five cranial nerves (optic, oculomotor, trochlear, trigeminal, and abducens), and several vascular bundles, pass through the orbital socket.
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