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August 09, 2024
5 min read
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Young man presents with acute limitation of left lateral gaze after boxing injury

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A 20-year-old man presented to the Tufts Medical Center emergency department with left eye pain, lightheadedness, nausea and vomiting after blunt trauma to the left lateral periorbital region.

The patient was not wearing a boxing helmet while sparring with a friend and was struck in the head. He denied loss of consciousness. He complained of left eye pain exacerbated with right gaze along with difficulty moving his left eye laterally. He also noted new horizontal double vision exacerbated with horizontal eye movement and left or right head tilt. His medical, surgical and family histories were unremarkable. His ocular history was noteworthy for strabismus. His last dilated exam was unknown.

CT head coronal view with soft tissue window
Figure 1. CT head coronal view with soft tissue window showing left medial rectus entrapment (left) and CT maxillofacial axial view with bone window showing left lamina papyracea fracture (right).

Source: Varsha Pramil, MD, and Victoria North, MD

Examination

Ophthalmologic exam revealed visual acuities of 20/20 in each eye. The pupils were round and reactive with no afferent pupillary defect. Confrontation visual fields were full in both eyes. Ishihara color testing was normal in both eyes. Extraocular motility was full in the right eye and showed significant limitation of lateral gaze in the left eye. IOPs were normal. External examination showed mild left-sided periorbital erythema and edema. The bilateral globes were white and quiet without signs of trauma. On dilated fundus exam at bedside, bilateral optic nerves were pink and sharp with no swelling or pallor, and bilateral retina and retinal vasculature were normal.

In the emergency department, the patient was normotensive (117/47 mm Hg) but bradycardic with initial heart rates in the 50s. All other vital signs were within normal limits. CT of the head without contrast showed no acute findings. Maxillofacial CT showed a small lamina papyracea fracture with entrapment of the medial rectus muscle (Figure 1). Forced duction testing showed restriction of abduction of the left eye. An oculocardiac reflex was not elicited with forced duction testing or with sustained lateral gaze of the left eye.

What is your diagnosis?

See answer below.

Medial orbital wall fracture with medial rectus entrapment

In cases of acute limitation of lateral gaze in the setting of trauma, the differential diagnosis can include neurologic or mechanical causes. For example, sixth cranial nerve palsy is one of the most common nerve palsies due to its long and tortuous course from the pons to the orbit. It can be injured with trauma and result in abduction deficits. Abduction can also be affected by soft tissue swelling and hemorrhage in addition to medial rectus entrapment, direct lateral rectus injury such as contusion, detachment or tear, or bony spur impingement on the lateral rectus.

Jonathan T. Caranfa
Jonathan T. Caranfa
Angell Shi
Angell Shi

For our patient, as confirmed by imaging and forced duction testing, the cause of the limitation in left eye abduction was a medial orbital wall trapdoor fracture with medial rectus entrapment.

Clinical course

In summary, a patient presented with nausea, bradycardia and significant restriction in lateral gaze and was found to have a mildly displaced left lamina papyracea fracture with medial rectus entrapment. He was urgently taken to the operating room for exploration and release of the incarcerated medial rectus under general anesthesia.

Forced duction testing during surgery confirmed severe restriction of left abduction with modest restriction of left adduction. A left transcaruncular medial orbitotomy was performed. The medial wall was exposed. A trapdoor fracture was identified and found to extend posteriorly for 2 cm with orbital tissue herniated through the fracture site. The herniated tissue was freed from the fracture, and repeat forced ductions were found to be full. After release of the tissue, the medial wall was assessed and found to be essentially intact. Therefore, no plating was necessary.

The patient tolerated surgery without complication. A postoperative exam 1 hour after surgery was notable for stable visual acuity and IOP, and extraocular movements were full. His diplopia had resolved along with nausea and vomiting. On postoperative day 3, the patient continued to recover appropriately with no limitation in extraocular movements or any ocular complaints.

Discussion

Orbital trauma necessitates prompt evaluation with a comprehensive eye exam. Concomitant ocular injuries are found in 29% of patients with orbital fractures. In these cases, a dilated fundus exam can help avoid permanent vision loss by identifying treatable injuries such as retinal detachments.

Although the medial orbital wall is relatively weak, orbital floor fractures with or without concomitant medial wall fractures are more common. This is because the orbital floor has no central support, whereas the medial wall is supported by the bony septa of the ethmoid sinus.

Isolated medial wall fractures are rare — they make up approximately 10% of orbital fractures — and isolated medial orbital wall fractures with medial rectus entrapment are even rarer. The most likely mechanism is described by the hydraulic theory wherein a blow to the orbit displaces soft tissue and results in the fracture. Certain anatomic characteristics predispose patients to medial wall fractures. For example, children have thicker, more elastic bone structure. With trauma, these bones may crack and be transiently displaced. With discontinuation of the trauma, they may “snap” back into their original location, potentially entrapping muscle or fat in the process.

The most common signs of muscle entrapment include diplopia, pain with extraocular motility, nausea or vomiting, and a heart rate below 60 beats per minute. Trapdoor-type fractures with muscle entrapment often present without any external signs of injury. Diplopia, pain and limitation of abduction and/or adduction may be the only clinical signs. In these cases, imaging, careful extraocular motility examination and forced duction testing are important for correctly identifying the diagnosis.

In orbital floor fractures with muscle incarceration, restriction of globe elevation due to an entrapped inferior rectus muscle is the most common finding. However, patients with medial rectus entrapment are more likely to present with adduction limitation due to medial rectus paresis. Dysmotility may occur after an interval of several days following the initial trauma as ischemia of the entrapped muscle leading to functional issues occurs with time.

Restricted abduction is still common with medial rectus entrapment but depends on the location of the trapdoor fracture and entrapment. Abduction deficits can be caused by decreased laxity of the medial rectus due to the posterior nature of an entrapment whereas a more anterior entrapment leads to a surplus of free medial rectus muscle tissue resulting in preserved abduction. In the present case, abduction limitation was much more pronounced than the adduction deficit. This is likely because there was a small surplus of medial rectus length present anterior to the entrapment site as the fracture extended posteriorly.

Opinions differ regarding the optimal timing of orbital fracture repairs. Urgent surgical intervention is recommended in patients with muscle entrapment with a positive oculocardiac reflex and/or extreme extraocular dysmotility. It has also been long advised that blowout fractures in which more than 50% of the orbital floor is displaced or those with significant hypoglobus, enophthalmos or diplopia should be repaired within 2 weeks of the injury. However, whereas most surgeons agree that trapdoor fractures with muscle entrapment should be repaired urgently to avoid muscle ischemia and permanent extraocular dysmotility, there is less consensus regarding non-entrapped orbital fracture repair. Recent studies have shown that delayed repair (up to 6 months after initial injury) carries no increased risk for surgical complication or decreased motility. Many surgeons now recommend a prolonged period of observation before deciding whether surgical intervention is needed in non-entrapped orbital fractures.

This case highlights a rare clinical scenario and emphasizes the importance of a thorough ocular examination in patients with orbital trauma regardless of external appearance. It also demonstrates that urgent surgical exploration is necessary in trapdoor fractures at risk for extraocular muscle incarceration and subsequent necrosis, whereas observation is preferred in non-entrapped orbital fractures.