The orbital floor is composed of thin maxillary and zygomatic bone. Anteriorly, just behind the orbital rim, the floor is concave and becomes convex, posterior to the axis of the globe. It is bordered laterally by the lateral orbital wall, which is relatively thick, and consists of the frontal process of the zygoma, and greater and lesser wings of the sphenoid. Medially, the floor slopes upward toward the medial orbital wall, which is also a thin bony structure, made of the frontal bone superiorly, lacrimal bone anteriorly, and lamina papyracea of the ethmoid and lesser wing of the sphenoid posteriorly. The lamina papyracea, as its name implies, is thin and fragile.

The inferior orbital fissure is located between the orbital floor and lateral orbital wall. Structures present in the fissure include the maxillary division of the trigeminal nerve, infraorbital artery, zygomatic nerve, branches of the sphenopalatine ganglion, and branches of the ophthalmic vein. The inferior orbital fissure is also known as the sphenomaxillary fissure (FIG 1).

The orbital plate of the maxilla and a portion of the zygoma represent the orbital floor. The zygoma makes up the anterior portion of the orbital floor, anterior to the inferior orbital fissure. The infraorbital nerve runs through the orbital floor in the infraorbital groove posteriorly and in the infraorbital canal anteriorly. The nerve often provides a landmark and a good plane of dissection.

The infraorbital rim is made of zygomatic bone and maxilla. The frontal zygomatic suture is exposed during dissection. Just inferior to the inferior orbital rim, the infraorbital foramen is located about 1 cm below the rim, generally in line with the midaxis of the pupil.

Both the orbital floor and medial orbital wall are vulnerable to injury because they are relatively thin compared to the surrounding structures.

Knowledge of anatomy is essential to perform safe dissection and optimal exposure of the orbital floor defect.

Orbital blow-out fracture is often the result of blunt injury to the globe and/or orbital rim, sustained during altercations, falls, sports-related injury, or motor vehicle accidents. These injuries transmit an external force to the orbital contents and orbital bones. The weakest portion of the orbit then fractures, resulting in herniation of orbital contents through the bony defect. The anterior and posterior portions of the orbital floor are thicker. The middle portion of the orbital floor is thinner, which accounts for the majority of fractures into the maxillary sinus. The medial orbital wall also commonly fractures into the ethmoid sinus air cells.

The globe typically moves posteriorly, inferiorly, and medially if there is significant prolapse or herniation of the orbital content into the orbital floor defect.

Untreated fractures generally result in enophthalmos. Depending on the volume increase associated with orbital fracture, it will range from minimally to significantly noticeable. Enophthalmos can be identified clinically with 2 mm of posterior displacement of the globe.² A 5% increase in orbital volume is sufficient for a clinical diagnosis of enophthalmos.² An important part of informed surgical consent is to discuss the anticipated natural history of untreated defects. Hypoesthesia in the distribution of a second branch
of the trigeminal nerve generally resolves over several months. Diplopia may improve if it is secondary to muscle contusion.

If an entrapped muscle is not treated promptly, permanent ischemic injury to the extraocular muscle will result in diplopia. It is the only emergency associated with orbital floor fractures. Our experience, as previously reported, is that it is more common in children than in adults.

Retrobulbar hematoma that results in optic nerve compression is an emergency; however, in a blow-out fracture, there is typically an expanded volume that alleviates the pressure on the orbital apex.

Patients with large orbital floor defects are generally treated acutely secondary to obvious enophthalmos. Patients with more subtle findings may be observed initially and surgically treated when/if they develop enophthalmos. These are generally patients with smaller defects on computed tomography (CT) scans.³

The decision of whether or not to operate can generally be made within the first 6 weeks following injury. Longer follow-up may be recommended in patients managed nonoperatively.

Specific trauma-related history helps elucidate the amount of force transmitted to the globe and orbit.

Previous eye surgery, eye injury, or pathology should be documented as well as the use of prescription glasses or contact lenses.

Physical examination often reveals

Visual acuity, extraocular movements, and pupil examination need to be assessed

Preoperative consultation with ophthalmology may be beneficial, especially in patients with decreased visual acuity or retrobulbar hemorrhage.

Orbital or maxillofacial CT scan with 1 to 2 mm axial cuts and coronal and sagittal cuts will help understand the size and location of the defect, as well as soft tissue herniation. It will help determine the length and width of the bone graft or implant required for adequate repair⁴ (Video 1).

A three-dimensional (3D) reconstruction is often beneficial in patients with multiple associated facial fractures. It is not essential for isolated orbital floor fractures.

Small defects without herniation of orbital contents and without entrapment may be managed conservatively with close follow-up.

The primary objective of surgical intervention is to recreate normal anatomy with restoration of the orbital floor integrity and reduction of herniated soft tissue into normal position. Restoration of orbital shape and volume should help rebalance extraocular muscles and correct diplopia.

Indications to correct orbital floor fractures include the following: