Orbital Blowout Fractures

 Updated 3/2017 -- photos and all links removed as many no longer active and it was easier than checking each one.

Orbital fractures are challenging injuries. They frequently are a component of a more global facial injury. With this post, I'm going to try to concentrate on the orbital fracture, not the broader picture.

In 1957, Smith and Regan (in one article--5th reference) and Smith and Converse (6th reference) coined the term "blow-out fracture" when describing inferior rectus entrapment with decreased ocular motility in the setting of an orbital floor fracture. Pure orbital floor fractures are also referred to as isolated floor fractures.

ANATOMY

Seven bones make up the orbit: the frontal bone, maxilla, zygoma, ethmoid, lacrimal bone, greater and lesser wings of the sphenoid, and palatine bone.The orbital process of the frontal bone and the lesser wing of the sphenoid form the orbital roof. The orbital plate of the maxilla joins the orbital plate of the zygoma and the orbital plate of the palatine bones to form the floor. The medial wall of the orbit consists of the frontal process of the maxilla, the lacrimal bone, the sphenoid, and the thin lamina papyracea of the ethmoid. The lateral wall is formed by the lesser and greater wings of the sphenoid and the zygoma.

The major nerves and vessels to the orbit and globe enter through 3 openings: 1)the superior orbital fissure, 2) the infraorbital fissure, and 3) the optic canal. These three "fissures" create weak points.

For a complete discussion of the anatomy of the orbit, including the vessels, nerves, and ocular muscles, go to this eMedicine article: Orbit Anatomy by Guy J Petruzzelli MD (December 15, 2005).

The article by Manson (9th reference) gives an excellent description of the anatomy of the ligamentous support of the globe. Lockwood's suspensory ligament is a fascial hammock that extends from the medial to the lateral wall of the orbit, cradling the eyeball and helping maintain the vertical level of the globe. When intact, it can support the globe even when the bony orbital floor may be compromised.

MECHANISM OF INJURY

Fractures of the orbit usually result from an 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. Examples include a fist, tennis ball, baseball, snowball or door knob. These fractures are more common in males, between the ages of 21 to 30 years.

The mechanism of a blow out fracture is controversial. There are two main theories that are likely: 1) The fracture results from a sudden increase in intraorbital pressure when the globe is being pushed posteriorly. 2) The fracture is the result of "buckling" forces which are transmitted to the orbital bones by transient deformity of the orbital rim.

Fractures of the inferior orbital wall are most common because of a combination of factors, namely the thinness of the maxillary roof, presence of the infraorbital canal, and the curvature of the floor. Immediately posterior to the rim, the orbital floor is concave and farther back it becomes convex. This configuration predisposes it to buckling and plays a major role in posttraumatic enophthalmos. Isolated fractures of the orbital roof are uncommonly seen in the absence of a fracture of the superior orbital rim. Isolated roof fractures are more common in the presence of a well-pneumatized orbital roof, and have a better prognosis when the orbital rim is spared.

Significant ocular injuries occur in 22-29 % of cases. A careful eye examination is critical. The profound swelling in the periocular region may somewhat limit the eye exam, as may the associated head injury. Globes with a history of cataract removal or other surgery are at much greater risk for perforation following trauma. Any history of previous visual problems or the use of contact lenses or glasses should be documented.

CLINICAL SIGNS AND SYMPTOMS
The main signs of orbital blowout fracture are
I. Diplopia is usually caused by restricted ocular movement, particularly in the upward gaze.

• It is primary when in the central visual field. Under normal circumstances the eyes seldom deviate more than 20 degrees from the central axis, so diplopia in the the central visual field is very significant.
• It is secondary when present only on extreme peripheral gaze. This may only be an issue when the patient looks out of the "corner of the eye".

Non-mechanical causes are less common and include injury to one or more of the extraocular muscles (EOM), damage to one of the nerves to an EOM, hematoma, and edema.

The Forced Duction Test is unreliable during the first week after injury because of non-mechanical causes of restriction very often give spurious results. For more on Diplopia see this article by Dr Jeff Mann.

• 6th nerve palsy => diplopia is greatest when looking to the affected side (abduction)
• 3rd nerve palsy => diplopia is greatest when looking up and to the opposite side (adduction)
• 4th nerve palsy => diplopia is greatest when looking down and to the opposite side (adduction)

II. Enophthalmos
Posttraumatic enophthalmos results from

• Escape of orbital fat
• Enlargement of the bony orbital volume
• Muscle entrapment causing backward pull on the globe with secondary contracture
• Orbital fat necrosis

III. Hypesthesia (or anesthesia) of the infraorbital nerve is common. It manifests as numbness of the gingiva and of the skin of the midface. If there is anesthesia of the gums--think posterior blowout fracture.

IMAGINING

Accurate characterization of all orbital fractures requires a CT scan. It is critical that coronal views be obtained. This may be problematic for patients with suspected cervical spine injuries, as coronal imaging requires hyperextension of the neck. In these patients, the axial images should be reformatted to provide coronal information. Sagittal reconstructions may also be helpful, particularly for those less experienced with orbital trauma. These provide a graphic representation of the superior incline of the orbital floor as one approaches the apex, something often not fully appreciated on the coronal images. Unlike the other facial fractures, evaluation of the soft-tissue windows is helpful with orbital injuries. The soft-tissue details help to show entrapment and/or displacement of the periorbital tissues including the extraocular muscles.

MEDICAL MANAGEMENT

Patients without significant enophthalmos (2 mm or more), a lack of marked hypo-ophthalmus, absence of an entrapped muscle or tissue, a fracture less than 50% of the floor, or a lack of diplopia can be treated conservatively. They will need to be followed closely to make sure nothing changes over the first few weeks/months.

• The patient should be treated with oral or IV antibiotics (due to the disruption of the integrity of the orbit in communication with the maxillary sinus).
• A short course of oral prednisone also may benefit the patient by reducing edema of the orbit and muscle. This also may allow for a more thorough assessment of the relative contribution to enophthalmos or entrapment from the fracture versus that from edema.
• Discourage nose blowing to avoid creating or worsening orbital emphysema. Nasal decongestants can be used if not contraindicated.

SURGICAL MANAGMENT
Timing remains a controversial issue, though it is rarely ever considered emergent. Exceptions to this include situations when muscle is entrapped and possibly ischemic.

• The classic example of this is the pediatric trap door injury, in which a defect opens in the floor and, because of the greenstick nature of the fracture, subsequently closes again.
• Findings of entrapment include not just diplopia but often a vagal response, including nausea and syncope secondary to trapped parasympathetic nerve fibers that travel with the muscle.

So with the exception of entrapment, delaying the operation is feasible. This delay is beneficial in allowing the orbital swelling to resolve which improves exposure for the procedure. It takes 1-2 weeks for the swelling to resolve.

Prolonged delay may lead to suboptimal results. Up to 38% of patients who had surgery 2 months or longer after injury may be found to have diplopia compared to only 7% in those who had surgery within 2 months. It has been shown that 72% of patients who had operative repair after 6 month had enophthalmos compared to only 20% who had surgery within 2 weeks of injury.

Indications for surgery

• Enophthalmos greater than 2 mm during the first 6 weeks
• Significant hypoglobus
• Diplopia, especially in the primary field of gaze that fails to resolve after 2 weeks
• Large floor defect--defined by most as greater than 1 sq cm.

Significant advancements have been made in the evaluation and treatment of internal orbital fractures. Early operative intervention combined with wide exposure, meticulous reduction, and rigid fixation has significantly enhanced the treatment of internal orbital fractures.

BLINDNESS following blunt facial trauma is a rare but devastating injury caused by optic nerve compression. In 1982, Anderson reported on 7 cases of monocular blindness following frontal head trauma treated with megadose steroids or optic nerve decompression. Half had good response to steroids, while 1/4 had minor return of function after decompression. At Baylor, the following protocol is recommended:

1. Steroid therapy initially for all patients with optic nerve injury.
2. Decompression for all patients with subtotal or delayed vision loss and significant bony impingement or canalicular hematoma by CT.
3. Decompression for patient without CT findings that fail to respond to steroids within 12 hours
4. Decompression is not recommended for immediate blindness.

Dexamethasone Steroid Protocol ( from Anderson et al):

• loading dose 0.75mg/kg
• 0.33 mg/kg q 6h x 24h
• 1 mg/kg q day x 1 - 2 days
• If no response in 48 h, steroids stopped
• If response, slow taper for 5 - 7 days, then quick taper off

COMPLICATIONS
Lid Retraction

• This can be minimized with avoidance of the subciliary incision.
• If retraction is appreciable in the early postoperative period, aggressive lower eyelid massage and forced eye closure exercises are instituted. This resolves the majority of cases.
• Early operative intervention should be avoided unless significant corneal exposure and irritation are encountered. This is rarely seen with ectropion but is common in entropion, as the eyelashes are a source of constant irritation.
• After 4 to 6 months of conservative therapy, unresponsive retractions may be better managed operatively. Regardless of initial incision, operative correction of lower lid retraction should be approached by means of a transconjunctival incision. Release of the middle lamella, the most common cause of significant postoperative retraction, should be followed by filling the defect with a graft of hard palate mucosa and a lateral canthoplasty.

Ocular Motility Deficits

• Deficits in extraocular movements may be manifest as diplopia in the postoperative period. Although there is always concern regarding entrapment of these muscles, a normal forced duction test at the end of the procedure should effectively rule this out.
• Frequently, periorbital swelling or muscular contusion and edema may be the underlying cause. Many patients with diplopia only at the extremes of gaze are not sufficiently bothered to seek intervention.
• Diplopia is more problematic when in the primary field or in downgaze, which may interfere with walking.
• When the deficit appears first following surgery, a computed tomographic scan should be performed to determine whether the implant is causing interference with the extraocular muscles. If the implant is well positioned, the patient should be followed conservatively along with the ophthalmologist. The need for future surgery and its timing is determined in large part by whether or not any improvement is noted and how distressing these symptoms are to the patient. The majority of these cases will resolve without intervention.

Enophthalmos is perhaps one of the most distressing and common problems seen in orbital fracture management.

• The majority of cases are the result of persistent orbital volume enlargement secondary to nonanatomical restoration of the orbital cone.
• On occasion, the implant may have been unintentionally placed in a horizontal orientation into the maxillary sinus.
• The initial evaluation of postoperative enophthalmos should include a computed tomographic scan to determine implant location and to characterize intraorbital volume.
• In some cases, the existing implant may be repositioned. This maybe difficult, however, as scarring of the periorbita can impede removal of the implant. In these cases, the implant should be elevated with the periorbita and a second implant placed. If this does not result in an appropriate globe position, additional volume should be added to the orbit. This can be done by placing a carved wedge of high-density porous polyethylene in a posterolateral location within the orbital cone. This allows the globe to project further without altering the vertical position. Just as with primary cases, the position of the globe should be overcorrected.

REFERENCES
Comprehensive Management of Orbital Fractures; Plastic & Reconstructive Surgery. Craniofacial Trauma. 120(7) Supplement 2:57S-63S, December 2007; Cole, Patrick M.D.; Boyd, Vincent M.D.; Banerji, Soumo B.S.; Hollier, Larry H. Jr M.D.
Mechanisms of Extraocular Muscle Injury in Orbital Fractures; Plastic & Reconstructive Surgery. 103(3):787-799, March 1999; Iliff, Nicholas M.D.; Manson, Paul N. M.D.; Katz, Joel M.S., M.D.; Rever, Linda M.D.; Yaremchuk, Michael M.D.
Facial Trauma, Orbital Floor Fractures (Blowout) by Adam Cohen MD and Michael Mercandetti MD --eMedicine Article, December 18, 2006
Evaluation and Management of Acute Orbital Trauma by Philip A. Matorin, M.D.; Grand Rounds --Baylor College of Medicine; April 20, 1995
Blow-out fracture of the orbit; mechanism and correction of internal orbital fracture. Am J Ophthalmol 1957 Dec; 44(6): 733-9; Smith B, Regan WF Jr: [Medline]
Enophthalmos and Diplopia in Fractures of the Orbital Floor; Br J Plast Surg 9:265, 1957; Converse JM and Smith B
Superior Blowout Fracture of the Orbit: The Blowup Fracture; AJNR Am J Neuroradiol 19:1448–1449, September 1998; Rothman MI, Simon EM, Zoarski GH, and Zagardo MT
What are the origins, insertions, attachments, actions and blood supply of the Extraocular Muscles? by Ben Glasgow MD; MedRounds, March 2, 2006
Mechanisms of Global Support and Posttraumatic Enophthalmos: I. The Anatomy of the Ligament Sling and Its Relation to Intramuscular Cone Orbital Fat; Plastic & Reconstructive Surgery. 77(2):193-202, February 1986; Manson, Paul N. M.D.; Clifford, Carmella M. M.A., B.S.; Su, C. T. M.D.; Iliff, Nicholas T. M.D.; Morgan, Raymond M.D.