Orbital Floor Fractures (Blowout)

According to Ng et al, orbital floor fractures were first described by MacKenzie in Paris in 1844. ^[2] In 1957, Smith and Regan described inferior rectus entrapment with decreased ocular motility in the setting of an orbital floor fracture and used the term blowout fracture. ^[3]

Over the past decade, rigid internal fixation has become the most frequently used technique in repair of floor fractures. According to Patel and Hoffmann, materials employed for fixation reach back to the introduction of stainless steel wires by Dr Buck in the 19th century. ^[4]

Plating has gained widespread acceptance, eclipsing stainless steel wiring in the repair of facial fractures. Refinement of plating for the repair of long bones, microplating systems, and biocompatible implants offer the surgeon several choices for restoration of normal bony architecture.

Orbital floor fractures can increase volume of the orbit with resultant hypoglobus and enophthalmos.

The inferior rectus muscle or orbital tissue can become entrapped within the fracture, resulting in tethering and restriction of gaze and diplopia.

Significant orbital emphysema from a communication with the maxillary sinus can occur. Orbital hemorrhage is possible with risk of a compressive optic neuropathy.

The globe can be ruptured or suffer less severe forms of trauma, resulting in hyphema, retinal edema, and profound visual loss. A study by Gaier et al indicated that the visual and ocular prognosis is worse in patients in whom open globe injury is concomitant with orbital fracture than in those with isolated open globe injury. The investigators reported, for example, that the presence of an orbital fracture is an independent risk factor for subsequent evisceration/enucleation, with an odds ratio of 4.6. Orbital floor fractures were the most common orbital fractures in the study. ^[5]

Frequency

Orbital floor fractures alone or in conjunction with other facial skeletal fractures are the most commonly encountered midfacial fractures, second only to nasal fractures.

The frequency of orbital floor fractures depends on demographics and socioeconomic conditions. Trauma centers and urban facilities encounter a higher prevalence of this injury type.

A retrospective, cross-sectional study by Iftikhar et al found that between 2001 and 2014, of an estimated 671,324 US inpatient admissions for ophthalmic disorders, orbital floor fractures were among the three most prevalent diagnoses (9.6%), together with orbital cellulitis (14.5%) and eyelid abscesses (6.0%). ^[6]

Pure orbital floor fractures, referred to as isolated floor fractures, result from impact injury to the globe and upper eyelid. The object is usually large enough not to perforate the globe and small enough not to result in fracture of the orbital rim.

Orbital floor fractures are secondary to a sudden increase in intraorbital hydraulic pressure. A high-velocity object that impacts the globe and upper eyelid transmits kinetic energy to the periocular structures. This energy results in pressure with a downward and medial vector usually targeting the infraorbital groove. Most fractures occur in the posterior medial region that is comprised of the thinnest bones. ^[7]

Another proposed mechanism that is less favored describes buckling of the orbital floor without displacement of orbital contents following high-velocity trauma.

Although most pure orbital fractures affect the region medial to the infraorbital groove, any fracture type, size, or geometry is possible.

After facial trauma, patients may describe decreased visual acuity, blepharoptosis, binocular vertical or oblique diplopia (especially in upgaze), and ipsilateral hypesthesia, dysesthesia, or hyperalgesia (in the distribution of the infraorbital nerve). In addition, patients may complain of epistaxis and eyelid swelling, following nose blowing.

Periorbital ecchymosis and edema accompanied by pain are obvious external signs and symptoms, respectively. Enophthalmos is possible but initially can be obscured by surrounding tissue swelling. This swelling can restrict ocular motility, giving the impression of soft tissue or inferior rectus entrapment. Retrobulbar or peribulbar hemorrhage may be heralded by proptosis. A bony step-off of the orbital rim and point tenderness are possible during palpation.

Examination of the globe is essential, albeit difficult because of soft tissue edema. Desmarres retractors may be helpful to spread edematous eyelids

Pupillary dysfunction coupled with decreased visual acuity should alert one to the possibility of a traumatic or compressive optic neuropathy.

Ocular misalignment, hypotropia or hypertropia, and limitation of elevation ipsilateral to the fracture are possible. Forced duction testing can differentiate entrapment versus neuromyogenic etiologies of muscle underaction.

There may be a deepening of the supratarsal crease, along with narrowing of the palpebral fissure stemming from enophthalmos or fibrous tissue contraction. Although the palpebral fissure may in fact narrow, the geometric shape is preserved, since dehiscence or disruption of the canthal tendons is uncommon.

A retrospective study by Bartoli et al of 301 orbital floor fractures found the most common symptom to be hypesthesia extending through the region of the maxillary nerve (32.9% of patients). Diplopia was also common, being found in 20.2% of patients, while enophthalmos and reduction of extraocular movement occurred in 2.3% and 1.7% of patients, respectively. ^[8]

A study by Firriolo et al indicated that in pediatric patients with orbital floor fracture, the presence of nausea and/or vomiting is indicative of tissue entrapment, with a sensitivity of 83.3% and a negative predictive value of 98.1%. ^[9]

Wilkins and Havins reported a 30% incidence of a ruptured globe in conjunction with orbital fractures, supporting the notion that a thorough and complete ophthalmic examination is needed. ^[10]

A study by Boffano et al of patients with blow-out fractures indicated that the characteristics of diplopia vary according to the position of the fracture. In the report, in which just over 50% of 447 patients with pure blow-out fractures presented with evidence of diplopia, statistically significant associations were found between orbital floor fractures and diplopia on eye elevation, and between medial wall fractures and horizontal diplopia. The investigators suggested, therefore, that the form of diplopia that a patient presents with may offer clues to the type of orbital fracture sustained. ^[11]

The timing and requirements for surgical repair of pure orbital floor fractures has been long debated. Most literature supports a 2-week window for repair to prevent fibrosis, resulting tissue contracture and entrapment. The authors often wait several days to allow dissipation of edema and hemorrhage in order to better assess enophthalmos and extraocular muscle function. In the event of tense inferior rectus incarceration, more immediate action is taken.

Pediatric patients with an orbital floor fracture, nausea, vomiting, and extraocular muscle dysfunction experienced rapid improvement of these signs and symptoms and less risk of residual extraocular muscle dysfunction when the fracture was repaired within 7 days. ^{[12, 13]}

A pure orbital floor fracture involving more than 50% of the floor, with orbital tissue prolapse, usually results in significant enophthalmos (>2 mm). These 2 findings indicate the need for timely repair.

Diplopia within 30° of primary gaze, positive forced-duction testing, and CT scan confirmation of a fracture warrant an early repair. Trapdoor or anteroposterior fractures can have clinical findings that are out of proportion to radiologic studies.

Although diplopia within 30° of primary gaze, extraocular muscle entrapment, and enophthalmos greater than 2 mm are discussed in the context of large floor fractures, each on its own can be an indication for repair.

Infraorbital nerve dysfunction occurs and is often the only complaint following pure orbital floor fracture. This sensory disturbance traditionally has not been an indication for repair. Some authors have reported improvement of this neuropathy following repair and nerve decompression. ^[14]

The adult orbital floor is composed of the maxillary, zygomatic, and palatine bones (see image below). The orbital floor is the shortest of all the walls; it does not reach the orbital apex, measures 35-40 mm, and terminates at the posterior edge of the maxillary sinus.

The bones that contribute to the structure of the orbit.

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The infraorbital groove, canal, and foramen are contiguous and tunnel through the maxilla, encasing the maxillary branch of the trigeminal nerve. The maxillary branch of cranial nerve V exits as the infraorbital nerve, providing sensory innervations to the ipsilateral orbital floor, mid face, and posterior upper gingival. The infraorbital artery, a branch of the maxillary artery, and the infraorbital vein also are found within the infraorbital groove, flanking the infraorbital nerve and exiting the infraorbital canal.

Surgical correction is contraindicated in patients who are medically unstable and unable to tolerate anesthesia.