A 40-year-old Asian male presented with pain, photophobia and tearing in his left eye following blunt trauma caused by a fist. Additionally, he reported diplopia that was worse on left gaze. His systemic and ocular histories were noncontributory. He reported using no medications.

Diagnostic Data
His best-corrected visual acuity measured 20/20 O.U. at distance and near. The external examination was remarkable for extraocular muscle restriction in upgaze and left gaze in his left eye. There was no afferent pupillary defect. Other pertinent anterior segment findings included subconjunctival hemorrhage and mild iritis in his left eye as well as a small laceration on his left cheek. His intraocular pressure measured 14mm Hg O.U. The dilated fundoscopy was within normal limits in both eyes.

After being punched in the face, this patient presented with a subconjunctival hemorrhage in his left eye and a small laceration on his left cheek. What is the correct diagnosis?

Your Diagnosis
How would you approach this case? Does this patient require any additional tests? What is your diagnosis? How would you manage this patient? What’s the likely prognosis?

Discussion
Additional testing should include an expanded history to guide imaging selection and a CT scan to rule out the presence of fracture with extraocular muscle entrapment. Particular attention should be directed toward evaluation for crepitus and preorbital or orbital cellulitis. Additionally, forced duction testing would allow the clinician to rule out traumatic cranial nerve VI palsy, and exophthalmometry could help determine globe placement. In this case, however, the emergency department had already completed the appropriate imaging and had a positive diagnosis.

The diagnosis in this case is extraocular muscle entrapment secondary to an isolated orbital blowout fracture. These injuries often occur when the orbit is struck at low velocity by objects that have a greater diameter than that of the orbital aperture (e.g., baseballs or fists). The relatively thin bone of the orbital floor becomes displaced into the maxillary sinus due to a lack of resistance from the air-filled space. Blowout fractures frequently cause a net increase in intraorbital volume, which could lead to enophthalmos. Disruption of the orbital fibroadipose connective tissue system contributes to the formation of post-traumatic enophthalmos.

During the last 50 years, clinicians' opinions about the treatment of blowout fractures have varied dramatically. Some have argued that all orbital blowout fractures should be repaired, while others have suggested that repair in asymptomatic cases is completely unnecessary.

Nevertheless, in cases of blowout fracture with obvious evidence of frank muscle entrapment, promptly refer the patient to a maxillofacial specialist to assess the need for repair. Ultimately, when repairs are made, they serve to minimize muscle injury and fibrosis. In most cases, prophylactic oral antibiotics are prescribed to protect against infection from the external environment as well as topical and oral agents for pain and inflammation.

 A “blowout fracture” is defined as isolated orbital floor or medial wall fracture in the setting of an intact orbital rim.^1-3 Generally, patients present with a history of blunt-force trauma.⁵ Common symptoms of a blowout fracture include pain, photophobia and lacremation associated with posttraumatic uveal inflammation (iritis or iridocyclitis), variable facial swelling secondary to fluid or air (orbital emphysema), crepitous (a crackling noise heard when air-infiltrated tissue is palpated), gaze-evoked diplopia, and increased pain upon eye movement.⁶ Other associated collateral injuries include subconjunctival hemorrhage, ruptured globe, corneal abrasion, conjunctival laceration, hyphema, iridodialysis, lenticular subluxation, retinal detachment, vitreous hemorrhage, choroidal rupture and optic nerve evulsion. If the eye settles inferiorly or medially into the exposed sinus, enophthalmos with restricted ocular motility will be present, either with or without loss of facial sensation.

There is some debate about the mechanism of blowout fracture. When a blunt force impacts the face, it may produce a combination of various effects:

1. The force may strike the bone, producing a shockwave that results in “bone buckling.”
2. The force may be transmitted to the eyeball, which causes the globe to strike one of the orbital walls, resulting in fracture.
3. The force may be transmitted by the globe via the principle of fluid incompressibility (hydraulic effect), causing generalized, increased orbital content pressure that results in fracture.^9-12

While all three mechanisms are mentioned in the literature, the “buckling” and the hydraulic mechanisms have increased support.^10-12 The orbital floor has been found to have a lower threshold for fracture than the medial wall and other orbital bones. So, when it gives way, the globe and its attached components become unsupported, slipping down into the vacant sinus below, producing visible enophthalmos and gaze-evoked, symptomatic diplopia as well as various degrees of extraocular muscle dysfunction and infraorbital nerve hypoesthesia.^10,12,13

If the patient exhibits a compressive threat to the optic nerve via swelling and retrobulbar hemorrhage, you must refer him or her for an emergent lateral canthotomy and orbital decompression. Typically, unless large amounts of soft tissues are incarcerated in the bony ruture, surgical intervention is postponed until orbital health is consistent with a good surgical environment.¹⁴

Traditionally, management of orbital floor fractures has been accomplished through transconjunctival and subciliary incision.¹⁵ However, postoperative lid malposition is a common complication.¹⁵  Some surgeons have begun to evaluate an endoscopic approach to orbital floor fractures. The endoscopic approach offers a hidden incision and improved fracture visualization.¹⁵ When the orbital floor requires replacement or reconstruction, ultrathin, porous polyethylene implants serve as durable substitutes that mimic the pertinent anatomy and avoid the morbidity of rejection.¹⁶     

In our patient, we confirmed the absence of collateral injury and confirmed that there was no hyphema on four-mirror gonioscopy. We then referred him to the maxillofacial specialist for evaluation to rule out the need for surgery. He required endoscopic repair to release the entrapped extraocular muscle and made a full recovery.

In the short-term, we prescribed atropine 1% to provide pain-relieving cycloplegia, topical prednisolone acetate q.i.d. O.S. to mitigate the ocular inflammation, and 600mg Motrin (ibuprofen, Pfizer) t.i.d. p.o. with food, as necessary, for pain and discomfort. We made arrangements to follow him in two-week intervals until the local ocular issues were resolved as well as to rule out complications, such as steroid-induced IOP elevation.

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