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An Onodi cell, also known as a sphenoethmoidal air cell, is a posterior ethmoidal air cell that has pneumatized laterally and rarely superiorly to the sphenoid sinus and is in close approximation to the optic nerve.
When drainage of the cell is obstructed, visual disturbances can occur by physical compression, inflammation, or a combination of the 2. Nonetheless, optic neuropathy secondary to an isolated opacified Onodi cell is rare.
Herein, we report a case of episodes of unilateral, transient, and painless vision loss caused by an opacified Onodi cell secondary to a focal sinusitis.
Case
A 26-year-old male presented to the emergency department with rapid onset of painless progressive vision loss of the right eye first noted upon awakening. He denied any associated symptoms such as headache, sinus congestion, or eye pain. He had experienced a similar episode several weeks prior, which resolved spontaneously after a few hours.
On examination, his visual acuity was 20/CF at 4 feet OD and 20/20 OS. There was a relative afferent pupillary defect in the right eye. The intraocular pressure was normal. Extraocular movements were full without pain or diplopia. Funduscopic examination revealed an engorged, hyperemic right optic nerve with nasal edema and mild retinal vascular tortuosity. No vitritis or chorioretinitis was present. Dilated fundoscopic examination of the left eye was unremarkable.
Given that our patient had optic disc edema and vision loss, neuroimaging and laboratory studies were obtained to rule out a compressive, inflammatory, or infectious optic neuropathy. Findings of laboratory studies, including ESR, CRP, CBC, ACE, lysozyme, VDRL, FTA-TBS, Quantiferon TB, and Lyme panel antibodies, were negative. Magnetic resonance imaging (MRI) of the brain and orbit with and without contrast was obtained and was significant for an opacified Onodi cell on the right side in close proximity to the optic nerve (Fig. 1) and for sinus disease and mucosal thickening in the maxillary sinus. The otolaryngology service was consulted. A computed tomography (CT) scan with contrast was obtained and again was significant for similar findings, notably the absence of bony erosion (Fig. 2). The otolaryngology service attempted to perform sinus endoscopy but was unable to advance the scope on the right side secondary to a deviated septum. The patient’s vision spontaneously improved without treatment during his emergency department visit, and given that there was no bony erosion noted on neuroimaging, the otolaryngology service deferred further surgical management. The patient was started on a trial of oral antibiotics (amoxicillin/clavulanate) to treat sinus disease. Because the patient denied any symptoms of sinus congestion, a nasal decongestant was not prescribed.
Fig. 1Right opacified Onodi cell (yellow) on T2 coronal magnetic resonance imaging.
On his follow-up visit 1 day later, visual acuity had returned to 20/30 OD, and the patient noted significantly improved symptoms with only trace residual afferent pupillary defect present in the right eye. Optical coherence tomography of the nerve fibre layer showed relative thickening of the average retinal nerve fibre layer of the right eye at 117 µm in comparison to the 89 µm found in the left eye (Fig. 3). A Humphrey visual field was obtained, which was normal in both eyes with the exception of a slightly decreased foveal threshold in the right eye (35 dB OD and 41 dB OS). Unfortunately, the patient did not attend any of his subsequent follow-up visits. No further follow-up imaging was obtained.
Fig. 3Optical coherence tomography demonstrating thickening of the right nerve fibre layer. (Image taken at follow-up visit 2 days after initial presentation.)
Many case reports describe the development of an opacified Onodi cell resulting in compressive optic neuropathy secondary to an orbital apex syndrome. The literature also describes iatrogenic damage to the optic nerve during sinus surgery in a patient with an undiagnosed Onodi cell that was subsequently violated. However, a literature review reveals no reported cases of a single opacified Onodi cell causing transient vision loss.
The Onodi cell or sphenoethmoidal air cell was first described in 1904 by Adolf Onodi.
It is an anatomical variant of a posterior ethmoidal air cell present in approximately 7%–14% of the population. The optic nerve and, less commonly, the internal carotid artery are in close proximity to the Onodi cell with as little as 0.03 mm (median 0.08 mm) of bone separating them. Optic neuropathy can then develop by either physical compression from the enlarging Onodi cell or an inflammatory response to infection in the Onodi cell, or a combination of the 2. One theory suggests that bone erosion does not necessarily have to be present because inflammatory agents can diffuse through the bone resorption sites of the thin bony wall separating the sinuses and the optic nerve.
CT and MRI are excellent modalities for visualizing an opacified Onodi cell and can provide insight into the pathophysiology of a patient’s visual loss. CT reveals opacification of the Onodi cell. Hyperintensity on T2-weighted and hypointensity on T1-weighted MRI help differentiate an enlarging Onodi cell from other masses, such as a tumour. There may be variations in intensity depending on the percentage of mucus, protein, and water. Imaging may also show breakdown or displacement of the bony wall, although the mechanism by which this occurs remains unclear.
Because of our patient’s spontaneous improvement of vision and imaging showing no damage to the bony wall, medical management with oral antibiotics was the chosen course of treatment.
In conclusion, an opacified Onodi cell is rarely associated with optic nerve pathology but can present with vision loss by either a compressive or inflammatory mechanism. Accurate diagnosis can be obtained with detailed radiographic imaging and allows precise treatment of the condition, depending on its severity. Early treatment proves favourable in restoring visual acuity to the patient; thus, although rare, this diagnosis should remain on the differential of transient vision loss.
Disclosure
The authors have no proprietary or commercial interest in any materials discussed in this article.
References
Stammberger H.R.
Kennedy D.W.
Paranasal sinuses: anatomic terminology and nomenclature.
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