eMedicine Specialties > Plastic Surgery > Facial Fractures

Facial Trauma, Orbital Floor Fractures (Blowout)

Author: Adam J Cohen, MD, Eyelid and Facial Aesthetic and Reconstructive Surgery, Diseases and Surgery of the Orbit and Lacrimal System, Cosmetic Laser Surgery
Coauthor(s): Michael Mercandetti, MD, MBA, FACS, Consulting Staff, Department of Surgery, Doctors Hospital of Sarasota
Contributor Information and Disclosures

Updated: Oct 21, 2009

Introduction

Facial skeleton fractures can result from low-, medium-, or high-velocity trauma. Floor fractures may occur in combination with zygomatic arch fractures, Le Fort type II or III midface fractures, or fractures of other orbital bones.

The goal of treatment is to maintain or restore the best possible physiologic function and aesthetic appearance to the area of injury. A conservative approach may be warranted in some instances, whereas more invasive intervention may be necessary in other situations.

For excellent patient education resources, see eMedicine's patient education articles Facial Fracture and Black Eye.

History of the Procedure

According to Ng et al, orbital floor fractures were first described by MacKenzie in Paris in 1844.¹ 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 "blow-out fracture."²

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.³

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.

Problem

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.

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.

Etiology

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.

Pathophysiology

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.

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.

Presentation

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.

The supratarsal crease may deepen, 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.

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.⁴

Indications

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.^5,6

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.⁷

Relevant Anatomy

The adult orbital floor is composed of the maxillary, zygomatic, and palatine bones. The orbital floor 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.

Contraindications

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

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