Posttraumatic Venous Obstructive Retinopathy Associated With Enlarged Optic Nerve Sheath

Hupp, Saunders L.; Buckley, Edward G.; Byrne, Sandra Frazier; Tenzel, Richard R.; Glaser, Joel S.; Schatz, Norman S.

doi:10.1001/archopht.1984.01040030204027

Cited by 47 publications

(20 citation statements)

References 19 publications

(1 reference statement)

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“…In our patients glaucoma and arterial hypertension were often found, but we observed that not infrequently the development of the CRVO followed an acute event like a considerable hemorrhage or a head trauma. Head trauma can cause hemorrhage within the optic nerve sheath and compression of the retinal vein in its intraneural tract [13,14]. If acute disorders like these can produce CRVO, it can be explained in part why the risk of developing a late CRVO in the fellow eye is rare in young persons [7].…”

Section: Discussionsupporting

confidence: 40%

Central retinal vein occlusion in young people

1992

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In a study performed on 20 subjects with central retinal vein occlusion (CRVO) aged 40 years or less we found the ischemic form in 20%. Disc edema was a common finding at the onset, while macular edema was less frequently seen. Systemic or ocular disorders that could be related with the development of the CRVO were often found; a patient was affected with myasthenia gravis and another with Sturge-Weber syndrome: these two diseases were not previously reported in association with CRVO. In only two of the 11 patients followed-up the visual acuity improved. The visual prognosis in CRVO of young people is often poor; the more frequent cause of the reduced visual acuity is chronic cystoid macular edema.

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Section: Discussionsupporting

confidence: 40%

Central retinal vein occlusion in young people

1992

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“…In chronic meningitis, spinal block, and papilloedema associated with Guillain-Barre syndrome, raised CSF protein is strongly associated with limited efficacy of any CSF diversion procedure. 26,27 Transconjunctival medial orbitotomy approach to biopsy the optic nerve sheath obtain local CSF specimens, and sometimes the optic nerve parenchyma in blind eyes with suspected malignant infiltrative processes may be a useful low morbidity approach to diagnosis in selected patients 28 (Table 1).…”

Section: Csf Diversion Surgery By Shuntingmentioning

confidence: 99%

Optic nerve disorders: role of canal and nerve sheath decompression surgery

Acheson

2004

Eye

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Optic nerve sheath decompression (ONSD) maintains a role in the management of visual loss complicating papilloedema in selected patients primarily with idiopathic intracranial hypertension. The evidence base for this intervention is reviewed and audit data on visual outcomes for patients with acute, chronic, and atrophic forms of papilloedema are contrasted. Optic canal decompression has a role in the management of compressive optic neuropathies complicating mass lesions arising from paranasal sinuses and intracranially and can be achieved by transethmoidal, transbasal, and open craniotomy routes. The evidence base supporting this intervention in traumatic optic neuropathy and in primary bone disease causing canal stenosis (in particular fibrous dysplasia) is reviewed where the indications are more controversial.

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“…Surgical evacuation of nonresorbing nerve sheath hematoma should be considered when initial treatment with steroids fails to improve vision. [22][23][24][25] Timely surgical optic nerve sheath decompression is initiated in order to avoid irreversible damage to the axons of the optic nerve compressed by the subarachnoid blood within the swollen nerve sheath. In the case of iatrogenic traumatic neuropathy, it is general consensus that prevention is better than cure.…”

Section: Discussion and Management Protocolsmentioning

confidence: 45%

Traumatic Optic Neuropathy

Rode¹,

Hathiram²,

Khattar³

2011

An International Journal of Otorhinolaryngology Clinics

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Introduction: Traumatic optic nerve damage after craniofacial injury was first described by Hippocrates.1 Although the natural history of traumatic optic neuropathy is unknown, recent studies suggest that high dose steroids and, even surgical decompression of the optic canal or the nerve sheath (in cases of nerve sheath hematoma) may restore vision in selected patients.2-8 The commonest cause of optic nerve trauma is road-traffic accidents, when the patient has poly-trauma with head injury and the visual loss is noticed only after the general condition of the patient improves. Isolated trauma of the optic nerve is usually associated with blunt skull trauma involving fractures of both skull and optical canal, but may also occur from blunt ocular trauma.9 Iatrogenic trauma to the optic nerve is not unknown. Pathophysiology: The part of the optic nerve most vulnerable to blunt trauma of the head is the intracanalicular segment, which by virtue of its bony course is vulnerable to the fractures and compressive-elastic forces of its surrounding bone, which also being unyielding, allows for no space for inflammatory expansion or hemorrhage.10 Optic neuropathy following accidental trauma usually results from two distinct mechanisms: A primary injury as a result of a direct contusive force on the optic canal and nerve, which if untreated results in a secondary ischemia with further damage to the nerve. Investigations: Clinical assessment should include testing of visual acuity, extraocular muscle motility and papillary reactivity, visual field assessment and direct/indirect ophthalmoscopy. Visual evoked potentials (VEPs) to flash stimulation and the electroretinogram (ERG) might be supportive in unresponsive patients in the immediate aftermath of the traumatic event.11,12 The role of neuroimaging remains controversial, and practice varies between institutions. Recently, ultrasonography has been advocated to screen and detect abnormalities in optic nerve diameter. Management: Currently, there is no validated approach to the management of traumatic optic neuropathy. Thus, with numerous conflicting reports on the management of traumatic optic neuropathy, there is little world consensus on the optimal management of this condition. Keeping in mind the above, we have devised a management protocol for the same, simultaneously discussing the role of conservative/medical management as well as the surgical protocols followed by us. Discussion and conclusion: In summary, optic nerve decompression alone or combined with decompression of the nerve sheath may be indicated in selected patients who fail to respond to high-dose intravenous steroids. The definitive role of surgery in the management of traumatic optic neuropathy remains unclear. There is a need for a large, prospective, randomized controlled trial to assess the different therapeutic approaches in traumatic optic neuropathy, but such a trial may be challenging given the low frequency of the condition and the difficulties inherent in randomizing patients.

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Posttraumatic Venous Obstructive Retinopathy Associated With Enlarged Optic Nerve Sheath

Cited by 47 publications

References 19 publications

Central retinal vein occlusion in young people

Central retinal vein occlusion in young people

Optic nerve disorders: role of canal and nerve sheath decompression surgery

Traumatic Optic Neuropathy

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