Etiology
Orbital fractures are generally caused by either assault, accidents (falls or road traffic accidents), or sports injuries.[6][11] In women, intimate partner violence is the third leading cause of orbital fractures.[12][13] In one study, alleged assault accounted for 63.6% of injuries among children and young adults; 18% were caused by sports injuries and accidents during play accounted for 13.6%.[11]
Pathophysiology
The term "blowout fracture" is often misused to refer to all orbital fractures. It refers to the phenomenon of orbital floor and/or medial wall fracturing with blunt trauma to the globe. The orbital rim (frontal, maxillary, and zygomatic bones) protects the globe from direct trauma. However, smaller objects such as squash balls or knuckles can pass between margins of the orbital rim and contact the globe itself. The globe is liquid-filled, and this liquid is not compressible. Instead, the globe distorts in all directions away from the area of depression to maintain volume. The weakest part of the orbit is the medial wall and orbital floor, the "lamina papyracea" (i.e., paper-thin layer). This fractures first, and the orbital soft tissues can pass through the hole created, causing the globe level to drop (hypoglobus) and sink back (enophthalmos). This is called a pure orbital blowout fracture. In an impure orbital blowout fracture, a direct blow to the inferior orbital rim causes a buckling of the orbital margin and results in a blowout pattern of fracture with a concomitant rim fracture.
In adults, the orbital floor/medial wall bone is quite brittle and a hole of varying size may be created. However, in children the bone is more elastic, and so a trapdoor type of fracture may result, which is pushed down but springs back like a trapdoor, trapping the inferior rectus muscle, or at least some orbital fat, and preventing the eye from looking up.[14] Such injuries, although less common, do occur in adult patients.[15] Without release of the entrapped muscle within 24 to 48 hours, an irreversible ischemia of the muscle may occur, leading to a Volkmann ischemic contracture and irreversible visual mobility derangement if not treated.[16] Tension on the inferior rectus may cause oculovagal syndrome (the oculocardiac or Ashner-Dagini response). In this, the afferent trigeminal ophthalmic sensory fibers communicate via the ascending reticular formation with vagal efferents. This induces bradycardia, hypotension, headache, nausea, vomiting, and malaise, and may be life-threatening.[14][17] However, the main features of presentation may be only nausea and vomiting with a history of facial trauma.[11][18] The effects of the syndrome may only stop when the trapped soft tissues are released.[19] Up to one third of children with this complaint may be admitted for head injury observation. It is often misdiagnosed due to computed tomography brain scanning not covering the fractured orbital floor.[11]
Superior orbital fissure syndrome and the more severe orbital apex syndrome may occur in fractures of the posterior orbit. When the superior orbital fissure is involved in a fracture, a combination of cranial nerve injuries occurs. These may include: lid ptosis, globe proptosis, ocular movement disorder, and sensory loss of the forehead, upper lid, conjunctiva, and globe surface. The more severe orbital apex syndrome includes all of these features plus blindness. The etiology is damage to cranial nerves III, IV, and VI, plus the optic nerve involved in the orbital apex. These are typically seen in craniofacial trauma where medium-velocity blunt trauma to the cranium or face creates force focused at the posterior orbit and a buckling-type fracture pattern.
Classification
Anatomic classification
This may best be achieved according to anatomic location and whether the fractures are isolated to the orbit or part of more complex fracture patterns.
Isolated: medial wall/floor "blowout"
The most common intraorbital fracture pattern.
Pure: does not involve the infraorbital rim, just the orbital floor and/or medial wall.
Impure: includes the infraorbital rim.
Complex
Lateral: zygomatic complex.
Roof/posterior orbit: "blow in" fracture (orbital apex syndrome).
Severe craniomaxillofacial fractures (e.g., naso-ethmoid-orbital fractures). As well as correction of the functional and cosmetic aspects of all orbital fractures, the importance of reconstruction of the medial canthal ligamentary support of the globe must be attended to in these fractures.
Naso-ethmoid-orbital fractures[2][3][4]
Several classifications exist for naso-ethmoid-orbital fractures:
Markowitz & Manson[2]
Single segment central fragment
Comminuted central fragment with fractures remaining external to the medial canthal tendon insertion
Comminuted central fragment with fractures extending into bone bearing the canthal insertion.
Ayliffe[3]
En bloc minimal displaced fracture of the entire naso-ethmoid complex
En bloc displaced fracture, usually associated with large pneumatized sinus and minimal fragmentation
Comminuted fracture but canthal ligaments firmly attached with bone fragments that are big enough to plate
Comminuted fracture with free canthal ligaments not large enough to capture by bone plating
Gross comminution needing bone grafting.
Gruss[4]
Severe naso-ethmoid-orbital injuries are classified into 5 types:
Isolated injury to bony naso-orbital region
Associated fractures of central maxilla
Associated le Fort II/III fractures
Naso-orbital fractures with orbital dystopia
Naso-orbital fractures with bone loss.
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