Reversible visual loss due to impacted lateral orbital wall fractures

Funk, Gerry F.; Stanley, Robert B.; Becker, Terry S.

doi:10.1002/hed.2880110403

Cited by 18 publications

(7 citation statements)

References 18 publications

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“…The tight adherence of the periosteum to the dural sheath of the nerve and a decreased vascularity compounded by a lack of a connective tissue cushion within the canal, all make the intracanalicular nerve susceptible to injury. 16 In contrast, the intra-orbital and intracranial parts of the nerve possess generous protective soft tissue cushions.…”

Section: Discussionmentioning

confidence: 99%

Trans-ethmoidal optic nerve decompression

et al. 1994

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Blunt head injury frequently results in visual impairment, the optimal treatment of which is still debated. Over a 5-year-period (1987-1991) 111 patients with indirect optic nerve injury resulting from closed head trauma have been treated. In each case loss of vision was the only neurological deficit. In group A, 66 patients were initially treated with large doses of prednisolone (80 mg/day) for 3 weeks. Twenty-seven patients improved on steroids alone. In the remaining 39 patients in whom either unsatisfactory or no improvement occurred a transethmoidal optic nerve decompression was performed. Twenty-two patients in the latter group improved, thus yielding an overall improvement rate of 74.2% in group A. Group B (control), in which 45 patients were treated with prednisolone only (80 mg/day for 3 weeks), had an overall improvement rate of 51% (23 patients). The study reveals that while nearly half of such patients can improve on steroids alone, optic nerve decompression significantly improves recovery rates in patients where conservative treatment is unsatisfactory (P < 0.05). Total loss of vision not responding to steroids, absence of waveform on visual evoked response, and presence of an optic canal fracture indicate a poor prognosis.

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Section: Discussionmentioning

confidence: 99%

Trans-ethmoidal optic nerve decompression

et al. 1994

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“…Surgery may also be necessary to relieve a relative constriction resulting from an increased volume in the canal or the nerve sheath due to edema or hematoma. Discussions regarding surgical treatment for traumatic optic nerve damage deal with the extent (cutting of the annulus of Zinn, additional sheath slitting), 80,81 the surgical approach, 82,83 and the time point for surgery. 84,85 Slitting of the optic nerve sheath cannot be considered as a standard procedure for the treatment of traumatic optic nerve damage.…”

Section: Therapeutic Options For Traumatic Optic Neuropathymentioning

confidence: 99%

Diagnosis and Treatment of Optic Nerve Trauma

et al. 2014

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Decreasing visual acuity secondary to orbital trauma or orbital and anterior skull base surgery may be caused by either sudden space-occupying intraorbital lesions, including retrobulbar hemorrhage (RBH), or direct damage to the prechiasmatic pathway. Contrary to traumatic optic neuropathy, RBH must be diagnosed and treated immediately to prevent permanent damage to the visual system. Therefore, monitoring and handling of visual pathway damage are mandatory. Flash visual evoked potentials and electroretinograms can provide evidence of the status of conductivity of the visual pathway when clinical assessment is not feasible. Both are thus essential diagnostic procedures not only for primary diagnosis but also for intraoperative evaluation. In case of RBH surgical decompression is compulsory. However, traumatic optic neuropathy does not respond to either corticosteroids or optic canal surgery. Modern craniomaxillofacial surgery requires detailed consideration of the diagnosis and treatment of traumatic visual pathway damage with the ultimate goal of preserving visual acuity.

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“…Surgery may also be necessary to relieve a relative constriction resulting from increased volume in the canal or the nerve sheath due to edema or hematoma. Discussions regarding surgical treatment for traumatic optic nerve damage deal with the extent (cutting of the annulus of Zinn, additional sheath slitting), 70,71 the surgical approach, 72,73 and the time point for surgery. 74,75 Slitting of the optic nerve sheath cannot be considered a standard procedure for the treatment of traumatic optic nerve damage.…”

Section: Therapy For Traumatic Optic Nerve Damagementioning

confidence: 99%

Optic Nerve Monitoring

Schumann

Kokemüller

Tavassol

et al. 2013

Craniomaxillofacial Trauma & Reconstruction

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Orbital and anterior skull base surgery is generally performed close to the prechiasmatic visual pathway, and clear strategies for detecting and handling visual pathway damage are essential. To overcome the common problem of a missed clinical examination because of an uncooperative or unresponsive patient, flash visual evoked potentials and electroretinograms should be used. These electrophysiologic examination techniques can provide evidence of intact, pathologic, or absent conductivity of the visual pathway when clinical assessment is not feasible. Visual evoked potentials and electroretinograms are thus essential diagnostic procedures not only for primary diagnosis but also for intraoperative evaluation. A decision for or against treatment of a visual pathway injury has to be made as fast as possible due to the enormous importance of the time elapsed with such injuries; this can be achieved additionally using multislice spiral computed tomography. The first-line conservative treatment of choice for such injuries is megadose methylprednisolone therapy. Surgery is used to decompress the orbital compartment by exposure of the intracanalicular part of the optic nerve in the case of optic canal compression. Modern craniomaxillofacial surgery requires detailed consideration of the diagnosis and treatment of traumatic visual pathway damage with the ultimate goal of preserving visual acuity.

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Reversible visual loss due to impacted lateral orbital wall fractures

Cited by 18 publications

References 18 publications

Trans-ethmoidal optic nerve decompression

Trans-ethmoidal optic nerve decompression

Diagnosis and Treatment of Optic Nerve Trauma

Optic Nerve Monitoring

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