Hemorrhage in Onodi Cell Leading to Traumatic Optic Neuropathy

Abstract

Traumatic optic neuropathy (TON) is an important cause of vision loss in the setting of cranial and/or facial trauma. Both direct and indirect variants exist, with the latter being more common. We describe the case of a young male presenting with loss of vision following trauma with an intact globe, an intraorbital foreign body, and Onodi cell hemorrhage. The challenges in diagnoses of type of TON, exact pathology, and management are discussed. We also highlight the role of thin section digital computed tomography imaging which is paramount for timely detection of subtle injuries and their management.

Introduction

Traumatic optic neuropathy (TON) can lead to vision loss in the setting of cranial and/ or facial trauma, even in the absence of injury to the ocular structures. Two main types have been described—indirect (more common) and direct.[1] We describe a case of penetrating orbital foreign body (FB) with an intact globe presenting with total vision loss due to a seemingly indirect TON.

Case Description

An adolescent male presented to the eye emergency of a referral tertiary care center with complete loss of vision in the left eye following a history of fall from bicycle and penetrating injury with a wooden stick in the medial aspect of the left orbit about 18 hours prior. On slit lamp examination, the left globe was intact however the left pupil was not reacting to light. An urgent imaging was ordered and the patient was taken up for FB removal. The initial computed tomography (CT) scans revealed a radiolucent oblong FB in the superonasal left orbit not reaching up to the optic nerve. The globe and medial wall of the orbit were noted to be intact in the 3 mm sections of the CT scan. In view of these findings and visual acuity of no light perception in the left eye, an initial working diagnosis of indirect TON was made (Figure 1). Foreign body removal was uneventful and the patient was given intravenous methylprednisolone for management of TON. A visual evoked potential response was equivocal at 72 hours. Counselling was done for endonasal endoscopic optic nerve decompression, and a repeat CT scan with 0.75 mm cuts with digital reconstruction was requested. The second scan revealed the presence of hemorrhage in the Onodi cell, the posterior ethmoid cell, which lies in close proximity to the intracanalicular optic along with a fracture of the optic canal (Figure 2). The patient was taken up for endoscopic endonasal optic nerve decompression under general anesthesia. The standard technique was followed. Uncinectomy was done, maxillary antrum identified and opened, bulla ethmoidalis uncapped, basal lamellae breached, and the posterior ethmoids were opened. Medial orbital wall was exposed completely and the sphenoid sinus opened wide. The partition between the Onodi cell and sphenoid sinus was taken down and a single cavity was created. The orbital apex was identified and the optic canal drilled using a coarse diamond burr with adequate irrigation to prevent any thermal damage. After eggshell thinning of the canal, the bone was gently taken off with a curette and decompression performed. Intraoperative findings during the second surgery confirmed the Onodi cell hemorrhage. In addition, there was a fracture of the optic canal wall with underlying optic nerve bruising (Figure 3, Figure 4, Figure 5 and Figure 6). These unusual findings changed our diagnosis to a mixed (direct + indirect) variant of TON. Despite the second surgery, the patient did not gain vision in the left eye. At the 6-month follow-up, he had minimal scarring at the site of entry of FB. The optic disc showed atrophy and the patient had a left sensory exotropia.

Discussion

Guidelines for surgical decompression in cases of TON are vague and various studies have reported equivocal outcomes. The role of chemical decompression with high dose intravenous steroids has been extrapolated from the National Acute Spinal Cord Injury Study.[2]

Vision assessment and documentation at presentation is vital. Perception of light at presentation has been linked to a better prognosis with intervention for TON. The International Optic Nerve Trauma Study did not demonstrate a clear-cut benefit with high-dose corticosteroids or surgical optic nerve decompression. The study concluded that decision to treat with intravenous steroids and/or surgical decompression should be individualized from case to case.[3] Surgical decompression has also shown to have equivo-cal results. A large Cochrane systematic review by Yu-Wai-Man and Griffiths concluded that the decision to proceed with surgery in TON is controversial and should be individualized for each case.[4] Emanuelli et al studied 27 patients with TON and found an improvement in visual acuity in 65% of the cases in their study. They recommended a treatment protocol of intravenous steroid therapy within 8 hours of injury and endonasal endoscopic optic nerve decompression within 12 to 24 hours after beginning of medical therapy to maximize the risk–benefit ratio.[5]

Computed tomography imaging is the modality of choice in acute settings of orbital trauma especially when a metallic FB may be suspected. While 3 mm slice sections are adequate for orbital imaging, 1 mm cuts or less are essential for assessing the optic canal. Multiplanar image reconstruction and digital console views may help detect subtle fractures and adequately delineate pathologies at the orbital apex.[6]

In our case, there was no perception of light in the left eye at time of presentation. The orbital FB did not reach up to the optic nerve. In addition, there was no direct trauma to the eyeball. The initial CT scan sections were 3 mm and did not demonstrate the Onodi cell or fracture of the optic canal. Thinner sections (0.75 mm) and digital image reconstruction on the radiology console helped in identifying the fracture, Onodi cell, and associated hemorrhage. This is an interesting finding as the Onodi cell is an anatomic variation of pneumatization of posterior ethmoidal cells and is known to occur in only 8% to 20% of the population[7,8] It is not uncommon for the optic nerve to be dehiscent in the Onodi cell. Sinusitis affecting this cell has been shown to cause visual symptoms as a result of its proximity to the optic nerve. In addition, a mucocele in this cell can directly compress the optic nerve leading to retrobulbar optic neuropathy, optic neuritis, and visual loss. Yanagisawa et al have reported that the presence of an Onodi cell increases the risk of injury to both, the optic nerve and the internal carotid artery, because of their close anatomic relationship.[9]

Intraoperative findings of the Onodi cell hemorrhage could possibly indicate an additional underlying canal wall fracture, both of which may cause compression on the intracanalicular optic nerve and predispose the patient to TON, as seen in our case. Despite the prompt removal of FB, institution of systemic high dose steroids and subsequent optic nerve decompression, the patient did not regain vision. However, this case highlights the need for high index of suspicion in patients presenting with vision loss after trauma without any damage to the eyeball. The role of imaging with appropriate thin sections of CT scan as well as digital image reconstruction is paramount in detecting subtle injuries like in our case. The intraoperative findings of fracture of optic canal wall and hemorrhage in the Onodi cell with resultant optic nerve bruising were suggestive of an element of direct TON in our case, which is seen less frequently than the indirect variant. The finding of hemorrhage in the Onodi cell on imaging can be a possible diagnostic indicator which should alert the clinician to look for an associated optic canal fracture.

Conclusion

We would like to highlight the role of thin cut highresolution CT imaging in diagnosing and allowing timely appropriate intervention in cases of TON. Viewing the CT scans with reconstruction is invaluable in such acute presentations as it is easier to pick up anatomical anomalies as well as small fractures on the console.