Optic Canal Decompression for Delayed Vision Loss in Posttraumatic Optic Neuropathy

Traumatic injuries to the skull base can be associated with optic canal trauma and resultant compressive optic neuropathy leading to severe visual loss. This is distinct from indirect optic nerve trauma associated with blunt force trauma without optic canal fracture. Treatment for both is somewhat controversial and typically involves high-dose corticosteroids and/or surgical optic canal decompression. We present a case of traumatic optic neuropathy with subacute worsening of vision who underwent remarkable improvement after optic canal decompression. A 46-year-old female presented to the emergency room with a blunt craniofacial trauma. She was walking on the sidewalk when a bicyclist traveling at 30 miles per hour collided into her. On examination, her visual acuity was 20/70 in the right eye and 20/30 in the left eye. A trace relative afferent pupillary defect (rAPD) was noted on the right, and color vision was 3/12 on the right and 12/12 on the left on testing with Ishihara plates. Fundus examination did not reveal optic disc edema or pallor. The rest of the examination was unremarkable.

A CT scan performed at the time demonstrated a comminuted right nasoorbitoethmoid complex fracture, along with other sphenoid fractures including an optic canal fracture with a displaced osseous fragment in the canal ([Fig. 1A and B]). On MRI, there was no abnormal signal intensity nor enhancement of the optic nerves. A trial of three doses of oral methylprednisolone was completed but did not result in any improvement in vision.

Three days after the trauma, her vision declined in the right eye to no light perception and a 3+ rAPD was noted. A new MR of the orbits depicted a focal T2 hyperintensity within the proximal canalicular segment of the right optic nerve, possibly representing optic nerve injury in the area of the dislodged bone spicule.

Right endoscopic optic nerve decompression was performed with removal of a bone fragment from the optic canal ([Fig. 1C]). The optic nerve sheath was notably frayed with associated hematoma at surgery. A pedicled nasal septal flap based on the sphenopalatine artery was rotated to cover the defect.

The patient's vision started to improve 2 weeks later and reached 20/25 at 3-month follow-up.

This case highlights remarkable visual recovery of a patient with traumatic optic neuropathy treated with surgical canal decompression and removal of bone fragment ([Fig. 2]). There is variability in the presentation and development of vision loss due to traumatic optic neuropathy. In some cases, where a defined anatomic anomaly can be identified may benefit from surgical intervention.

Fig. 1

Fig. 2

No conflict of interest has been declared by the author(s).

Publication History

Article published online:
12 February 2021