Optic nerve decompression - role in preventing traumatic ischaemic optic neuropathy: case report

INTRODUCTION

Traumatic optic neuropathy (TON) is a devastating potential complication of closed head injury. The hallmark of an optic neuropathy, traumatic or otherwise, is a loss of visual function, which can manifest by subnormal visual acuity, visual field loss, or color vision dysfunction,

Vision loss associated with TON can be partial or complete and temporary or permanent.¹

Historically, the 3 treatment paradigms advocated for TON are observation, medical corticosteroid therapy, or optic canal decompression.²

Recent advances in endoscopic nasal surgery and availability of advanced instruments have redefined endoscopic surgical approaches for TON. Currently, endoscopic optic nerve decompression via an intranasal transethmoidal or transsphenoidal approach has gained popular support.

We report a case of 24 year old male with one sided visual loss who presented in the ENT emergency with maxillofacial trauma following high velocity road traffic accident.

CASE REPORT

24 year old male patient presented to the casualty department after 6 hours with complex maxillofacial trauma following high impact road traffic accident. Patient complained of blurring in vision of the left side. at the time of examination patient had perception of fingers at 1 metre distance. Radiological investigations were ordered and within 1 hour the vision deteriorated to light perception on left side. Computed tomography scan of orbit with paranasal sinus showed multiple comminuted fractures and fracture of the medial and lateral orbital walls causing impingement of the fracture fragments on the optic nerve (Figure 1).

Patient was immediately shifted to the operating room. Urgent surgical intervention was undertaken under general anaesthesia. Intraoperatively (Figure 2 and 3). The shattered septae of anterior and posterior ethmoid cells were extracted. Clotted blood was cleared. Medial orbital wall, the lamina papyracea was lifted off the orbital periosteum with a blunt elevator. The optic tubercle bone elevated with a currette followed by exposure of the sphenoid segment of the optic nerve. The annulus of Zinn was cut, thus exposing the oedemous and engorged portion of the intra canalicular and intracranial regions. Haemostasis attained by adrenaline soaked atraumatic cotton patties. Postoperative period was uneventful and patient attained ability to count fingers in the evening. Anti-inflammatory intravenous medications were continued for a week, followed by oral medications.

DISCUSSION

Length of optic nerve varies 35-55 mm from the eyeball to the chiasma (intraocular part 1 mm, intraorbital part 25 mm, intracanalicular part 4-10 mm and intracranial part 10 mm.³ TON occurs due to injury to optic nerve following complex maxillofacial trauma. Mode of injury may be direct i.e. penetrating trauma resulting in physical disruption of optic nerve, or indirect i.e. when traumatic /compressive forces are transmitted to the optic nerve with minimal disruption of the physical continuity of the nerve. TON can also be classified depending on the location of the injury for e.g. head of optic nerve, intraorbital segment, intracanalicular segment or intracranial segments.

The most common sites of indirect TON are the intracanalicular segment (optic nerve sheath is adherent to the periosteum) and intracranial segment (in close proximity to the dural rings).⁴

Medical research council corticosteroid randomisation after significant head injury study has shown potentially harmful effects of steroids in craniofacial trauma patient. Thereby the use of steroids for TON has become more limited, since the majority of patients with TON have some form of concomitant intracranial injury.⁵

A Cochrane review by Yu-Wai-Man et al compared 31 eligible double-blinded placebo controlled, randomised trials of high-dose intravenous steroids in patients with indirect TON. The study concluded that there is a high rate of spontaneous visual recovery and that there is no convincing suggesting any added benefit of steroids over observation alone. Nevertheless, many practitioners still use steroids as conservative management of the TON, but the decision must made on a case-by-case basis.⁶

Optic nerve decompression should be considered as a primary treatment modality when the pathology of injury is due to compression and amenable to surgical correction. Various approaches have been described for surgical optic nerve decompression for example, transfacial approaches using a microscope, neurosurgical craniotomy approaches, and the transnasal endoscopic approach. visual loss can be restored if the endoscopic optic nerve decompression is performed before the start of irreversible optic neuropathy.⁷

TON decompression the surgical management of choice with minimal morbidity as compared to external approaches to optic nerve.⁸

CONCLUSION

Endoscopic optic nerve decompression is a safe and effective treatment in selected cases of TON provided it is done before irreversible loss of vision occurs. In selected cases where the bony fragment is impinging on the optic nerve without causing transaction of the nerve fibres, surgical decompression should be considered as early as possible to prevent optic neuropathy. Steroids have limited role and should be given patient to patient basis.

Funding: No funding sources

Conflict of interest: None declared

Ethical approval: Not required

REFERENCES

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