Orbital Fracture Resulting in Contralateral Optic Canal Fracture with Traumatic Optic Neuropathy: A Case Report

Traumatic optic neuropathy (TON) is a well-recognized cause of acute vision loss after head trauma, often affecting the intracanalicular optic nerve. The clinical presentation includes acute loss of visual acuity (VA), color perception, and/or visual field, an ipsilateral relative afferent pupillary defect, and an initially normal or swollen optic nerve with subsequent optic atrophy over time. TON usually occurs as a result of indirect shearing forces transmitted to the optic nerve but can also result from direct injury to the optic nerve, i.e., from a sheath hematoma or bony fragment from optic canal fracture (OCF) [1]. In these cases of direct TON, many authors recommend surgical decompression, which likely improves VA by reducing compressive ischemia of optic nerve fibers and vasculature from edema or hemorrhage [2]. The reported incidence of OCF in patients with TON ranges widely from 5 to 92% [3, 4], which may be attributable to lower sensitivity for OCF on radiographic studies compared to direct endoscopic visualization [3, 4]. Finally, OCF alone is not a clear predictor of visual recovery in patients with TON [3‒6]. We present a rare case of direct TON from an isolated OCF in association with a contralateral injury and orbital floor fracture. The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000545040).

A previously healthy 19-year-old male presented to an outside emergency room with sudden and total vision loss in the right eye (OD) after a direct cranio-orbital injury to the left side of the face. The patient had an election campaign lawn sign thrown at him; the metallic legs of the sign struck his left cheek. He experienced immediate loss of total vision OD without loss of consciousness or headache. Vision was no light perception (NLP) OD and a superficial abrasion on the left cheek and mild epistaxis were noted. Initial computed tomography (CT) of the head showed an acute fracture of the anterior and medial walls of the left maxillary sinus, hemorrhage within the left maxillary sinus, and a left orbital floor fracture without herniation of extraocular muscles.

He was transferred to a second outside emergency room for higher level ophthalmic care. The eye examination confirmed VA of NLP OD and 20/20 in the left eye (OS). Pupils were 5 mm in the dark and minimally reactive to light with grade 4 relative afferent pupillary defect OD and normally reactive OS. Motility exam showed a mild elevation and abduction deficit with a 10 prism diopter exotropia OS. External exam showed a superficial cutaneous abrasion on the left cheek overlying the zygomatic bone without penetrating injury or foreign body. Intraocular pressures measured 19 mm Hg OD and 16 mm Hg OS. Slit-lamp biomicroscopy and fundus examinations were normal bilaterally (OU). The patient was diagnosed with indirect TON and discharged home.

The patient was referred to the neuro-ophthalmology service at Houston Methodist Hospital for a second opinion and presented 2 days after the initial injury, where vision remained NLP OD. Magnetic resonance imaging (MRI) of the brain and orbit with and without contrast showed abnormal enhancement of the intracranial and intracanalicular segments of the right optic nerve (Fig. 1a). MRI of the cervical and thoracic spine with and without contrast showed no demyelinating lesions. The patient was empirically treated with 1,000 mg intravenous methylprednisolone for 5 days for a presumed inflammatory or traumatic optic neuropathy while the remaining diagnostic studies were pending. Lumbar puncture showed an opening pressure of 20 cm H2O. Cerebrospinal fluid analysis showed mild elevations in cerebrospinal fluid protein, myelin basic protein, IgG synthesis rate, Q-albumin ratio, and IgG but was negative for oligoclonal bands. Serum testing was negative for infectious, inflammatory, and demyelinating etiologies for optic neuropathy. After 3 days, the patient’s vision improved to light perception (LP), and the neurology service recommended plasma exchange therapy after completion of a 5-day course of intravenous steroids.

Repeat CT of the orbits with contrast obtained alongside the initial MRI was reviewed at a neuroradiology conference on day 7, redemonstrating the previously known fracture of the left maxillary sinus and inferior orbital rim, but review of the CT in the area of the optic nerve enhancement showed a depressed bony fragment suggesting fracture of the right inferomedial optic canal and roof of the right sphenoid sinus. The bony fragment projected superiorly with impingement of the intracanalicular right optic nerve (Fig. 1b), leading to a diagnosis of direct TON from bony impingement. The plasma exchange was discontinued after one session.

On day 8, otolaryngology and oculoplastics performed an endoscopic optic nerve decompression OD. A 4 × 5 mm bone fragment abutting the optic nerve was removed (Fig. 2). The patient tolerated the procedure well without complications and was discharged on hospital day 10 with an oral steroid taper. At 1-month follow-up, the patient’s vision was improved to hand motion OD.

TON has an incidence of 2–6% of patients with facial trauma [2, 5, 7] and up to 10.8% of patients with overt facial fracture [8]. Up to 82% of patients with TON have ipsilateral zygomaticomaxillary fractures, particularly orbital floor fractures and comminuted zygoma fractures [8‒11]. Finite element modeling studies demonstrate that OCFs are most likely to result from impact to the ipsilateral upper medial orbit [12, 13]; these injuries display a fracture pattern originating at the frontal bone, progressing through the upper orbital wall – presumably the superomedial orbital plate of the frontal bone with or without involvement of the ethmoid bone – and eventually reaching the optic canal [14]. Our patient experienced TON and OCF as a result of a contralateral injury and orbital floor fracture, solely possessing an isolated OCF without other continuous orbital fractures on the side of TON. Table 1 lists reported cases of orbital fractures contralateral to TON; these cases also demonstrated concurrent ipsilateral fractures, unlike our case. However, the under-reporting of ocular injuries in the setting of facial fractures remains a barrier to understanding the relationship between injury patterns and TON.

A potential mechanism for this fracture may be similar to the “buckling” theory for orbital floor fractures, in which posteriorly directed forces causing bony compression eventually cause “buckling” and fracture in the relatively thin bones of the orbital floor compared to the orbital rim and surrounding bones. The traumatic force in our patient may have been directed in a way that propagated the forces toward the thin bones of the contralateral optic canal. Further, Huempfner-Hierl et al.'s [13] use of finite element modeling revealed multiple oscillatory peaks of pressure in orbital trauma as the force is transmitted from the orbital rim posteriorly. Thus, oscillatory waves in our patient peaking at the ipsilateral orbital floor and contralateral optic canal may have caused fractures in these areas only and not in between.

Fracture pattern also determines the prognosis of OCF causing TON. Overall, 58.3% of patients with nondisplaced OCF experience some improvement in VA, compared to 28.6% of patients with displaced fractures optic nerve compression, as in our patient, and 8.3% of patients with displaced fractures penetrating the optic nerve [3]. Further, patients with a single fracture of the medial wall of the optic canal have the best visual prognosis, compared to lateral wall or multiple fractures [3]. Notably, 21–88% of patients with OCF confirmed at the time of endoscopic surgery lack preoperative radiographic evidence of OCF, even with high-resolution CT. Higher rates of missed OCF occurred in nondisplaced linear fractures or minimally displaced fractures [4]. Therefore, in assessing patients with TON, the absence of radiographic evidence of fracture does not preclude the possibility of OCF. In particular, CT head without dedicated imaging of the orbits may under-report the true rate of OCF.

Most clinicians will consider optic canal decompression in TON if imaging suggests mass effect on the optic nerve, i.e., from OCF. Surgical decompression results in VA improvement in 42–78% of patients with TON and OCF [3, 4], but post-surgical prognosis also depends on several other factors. Initial VA is worse in TON patients with OCF compared to those without OCF, but OCF alone is not an absolute predictor of poor visual recovery [3‒6]. Earlier surgical decompression, younger age, initial VA of LP or better, and optic nerve sheath edema or hematoma are associated with greater VA improvement [5, 15]. Initial NLP vision has a worse prognosis [3, 6, 15].

We report a rare case of direct TON due to isolated OCF with contralateral injury and orbital floor fracture; providers should be aware of typical and atypical fracture and injury patterns resulting in OCF. Initial CT of the head and orbits may fail to detect OCF, especially nondisplaced OCF. OCF causing TON may require prompt surgical decompression; earlier intervention, VA of LP or better, and certain fracture patterns result in better visual recovery. Therefore, providers should always consider the possibility of OCF even in the absence of visible fractures on imaging in order to prevent delayed surgical intervention. Though corticosteroid therapy in TON remains controversial, nerve enhancement in the setting of OCF may be an indication for preoperative high-dose corticosteroid therapy.

Ethics approval was not required for this case report. This retrospective review of patient data did not require ethical approval in accordance with local/national guidelines. Written informed consent was obtained from the patient for publication of the details of their medical case and any accompanying images.

Amina Malik is a speaker for Amgen. Masayoshi Takashima is a consultant for Neurent ENT and Medtronic ENT. Andrew Lee is a speaker for Amgen and Alexion and a consultant for Astrazeneca, Bristol Myers Squibb, Viridian, and Stoke. Paulina Truong, Saif Aldeen Alryalat, and Osama Al Deyabat do not have any conflicts of interest to disclose.

The authors report no funding received for this work.

All authors attest that they meet the current ICMJE criteria for authorship. P.T.: conceptualization, investigation, methodology, and writing – original draft, review, and editing. S.A.A. writing – original draft. O.A.D.: writing – original draft. A.M.: writing – review and editing. M.T.: writing – original draft, review, and editing. A.G.L.: supervision, conceptualization, investigation, methodology, and writing – review and editing.

All data analyzed during this study are included in this case report. Further inquiries can be directed to the corresponding author.