A 76-year-old patient presented to the emergency department with loss of consciousness due to a casual fall at home.
The patient reported loss of vision through the right eye (OD) when she regained consciousness.
Among the antecedents, type 2 diabetes mellitus stood out in treatment with oral antidiabetics and arthrosis.
She did not report any other relevant personal or family history.
On examination, an item-contussive wound was identified, as well as a diffuse right fronto-orbital hematoma.
Visual acuity (VA) was no light perception with a relative afferent pupillary defect (PARD) in the RE and 0.6 in the left eye.
The anterior pole was within normal limits, as well as intraocular pressure and eye fundus.
Cranial computed tomography (CT) with orbital sections was normal and magnetic resonance imaging (MRI) showed an increase in perineural fluid in the right NO sheath.
persistence of CO.Sagittal reconstruction of the optic canal of CT with lateral diameter was performed, observing linear fracture of the roof of the right orbita extending to the lesser wing of the right sphenoid region
Evoked visual potentials were performed using monocular stimulus (Medelec® Synergy.
Oxford.
Instruments, England) with Googles at 2 cycles per second, observing a strong stimulus morphology in the responses to the stimulation of both eyes, suggesting the absence of conduction of the visual stimulus in the right NO.
The patient was diagnosed with traumatic optic neuropathy (TON) of mixed production mechanism when it was a closed frontal trauma that was indirectly transmitted to the OC and a direct lesion of the NO when the lesser wing of the sphenoid was displaced.
Treatment was established with megadoses of corticosteroids (1 g of methylprednisolone followed by 250 mg every 6 hours for 48 hours), with no improvement.
