Optic Nerve Contusion
Also referred to as traumatic optic neuropathy, the injury can occur at any segment of the optic nerve, from the retrobulbar portion to the intracranial portion. It is categorized into direct and indirect injuries, with common causes including traffic accidents, falls, and boxing injuries.
Direct injuries arise from tears in the optic nerve itself, or from lacerations caused by bone fragments or foreign objects. There can also be compressive injury due to fractures of the optic canal or hemorrhage within the orbit or the optic nerve sheath. Indirect injuries are the most prevalent type and are generally associated with head trauma, particularly trauma to the forehead, most commonly lateral to the supraorbital ridge. This is presumed to be related to the shearing forces acting on the optic nerve or the attachment points of the nourishing vessels within the optic canal.
Typical manifestations include an immediate and severe loss of vision, with 24% to 86% of patients reporting no light perception upon examination. External injuries are often minimal, but relative afferent pupillary defects are consistently present. At the onset of the condition, the optic disc usually appears normal, but optic nerve atrophy may develop within 4 to 8 weeks. Imaging studies aid in determining the extent of the injury and in identifying associated intracranial or facial injuries, intraorbital bone fragments, or hematomas. Early ophthalmologic examination is important in patients with concurrent head trauma who are in a coma, facilitating timely detection and management of optic nerve injuries.
Treatment
The visual prognosis for optic nerve contusion is generally poor; however, some recent reports indicate partial spontaneous recovery of visual function in certain cases. There is still no consensus on the management of indirect optic nerve contusion. Treatment options include conservative management, corticosteroids, and optic canal decompression surgery, while neuroprotection strategies remain under investigation. Different studies report varying approaches to treatment and inconsistent clinical outcomes, but early initiation of treatment is widely regarded as critical for improved effectiveness. General principles include starting high-dose intravenous methylprednisolone therapy as soon as possible in acute cases, with a recommended dosage of 500 mg per dose, twice daily. If visual function improves after treatment, oral tapering can continue after 48 hours of intravenous administration, generally lasting up to two weeks. When there is no response to medical therapy within 12 to 48 hours, or if vision deteriorates during the tapering process, transcranial or transethmoidal optic canal decompression surgery may be considered. However, some researchers believe that early steroid pulse therapy for indirect optic nerve contusion is unlikely to yield results if surgery is unsuccessful. Patients with progressive vision loss in the early stages of the injury, coupled with retrobulbar hematomas, optic sheath hematomas, deformity or narrowing of the optic canal due to fractures, or fractures impinging on the optic nerve, may benefit from optic canal decompression surgery to relieve compression or remove impinging fragments. When corticosteroids are used to treat optic nerve contusion, adjunctive therapy may include dehydrating agents, microcirculation-enhancing drugs, and neurotrophic agents, while also monitoring the risks of complications associated with high-dose corticosteroid therapy.
Optic Nerve Avulsion
Optic nerve avulsion can result from severe rotational forces on the globe, forward dislocation of the eye, sudden increases in intraocular pressure causing lamina cribrosa rupture, or backward traction on the optic nerve following penetrating orbital injuries. These mechanisms cause the optic nerve to be forcibly pulled away from the scleral canal and dislocated posteriorly, leading to optic nerve avulsion. The optic disc may appear as a cupped depression, with posterior hemorrhages and contusion-like necrosis. Vision is typically completely lost, and no effective treatments are currently available.