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