Sinusitis-induced optic neuropathy
Although it was once a common presentation of blindness, sinusitis-induced optic neuropathy has largely been forgotten about by clinicians in the present day due to widespread broad-spectrum antibiotic usage.
Sinusitis-induced optic neuropathy
Prior to the discovery of modern antibiotics, sphenoethmoid sinusitis (SES) was described as a “leading cause of optic neuropathy and vision loss” over a century ago. Infection of Onodi cells, which are posterior ethmoidal air cells that are superolateral to the sphenoid sinus extending into the anterior clinoid processes, may spread to the optic canal and lead to blindness. Contact with and invasion of the adjacent optic nerve associated with the affected sphenoid sinus by bacteria or fungi may occur through congenital pre-existing bony defect (6% of the normal population) or via acquired traumatic or surgical bony defects. Due to extensive antibiotic utilization in the modern era, SES is often no longer considered by clinicians when evaluating cause for presentations of optic neuropathy and typical versus atypical neuritis.
Sinusitis-induced optic neuropathy should be considered in patients with sinus, ear (otalgia) or eye pain, and ipsilateral vision loss due to optic nerve dysfunction (e.g., visual acuity and or visual field loss, and relative afferent pupillary defect (RAPD)).
Patients with SES and visual loss should undergo a comprehensive eye examination including visual acuity, formal perimetry, pupillary assessment (including RAPD), intraocular pressure measurement, slit lamp biomicroscopy, and dilated fundus examination. Optical coherence tomography (OCT) of the retinal nerve fiber layer (RNFL) may also be indicated.
Patients presenting with SES may have eye, face, sinus, or ear pain. The presence of examination evidence for optic nerve dysfunction should prompt further evaluation for sinusitis-induced optic neuropathy.
Radiographic imaging such as computed tomography (CT) scans of the head, orbit, and sinus can be used to diagnose SES and assess for possible bony deficiency in the sphenoid sinus wall. Magnetic resonance imaging (MRI) of the brain and orbit can help visualize the optic nerve for enhancement or contiguous spread of inflammatory disease to the optic nerve.
Early and aggressive treatment of the SES with medical (e.g., antibiotics and corticosteroids) or surgical decompression may be indicated as severe and acute permanent vision loss may occur from untreated SES.
The prognosis of SES associated optic neuropathy is variable. Sometimes the visual outcome is poor despite antibiotic therapy and surgery. Delay in treatment of SES optic neuropathy can lead to permanent and irreversible visual loss. Severe (especially fungal) SES can lead to secondary occlusive vasculitis and vaso-occlusive ischemic optic neuropathy. Intracranial spread can also occur and may be life threatening.
Clinicians should be aware of the possibility of visual loss due to optic neuropathy in patients with SES. Involvement of a posterior ethmoidal air cell (Onodi cell) can lead to direct contiguous involvement of the optic nerve in the orbital apex and optic canal. Delay in sino-orbital imaging and recognition of SES can lead to a worse visual prognosis. Aggressive medical and surgical therapy may be needed in acute and severe cases and can be vision saving.
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