- •Contents
- •Contributors
- •Preface
- •Glossary
- •2. Synthesising the evidence
- •3. Evidence in practice
- •4. Allergic conjunctivitis
- •6. Viral conjunctivitis
- •7. Screening older people for impaired vision
- •8. Congenital and infantile cataract
- •9. Congenital glaucoma
- •13. Infantile esotropia
- •14. Accommodative esotropia
- •15. Childhood exotropia
- •17. Entropion and ectropion
- •18. Thyroid eye disease
- •19. Lacrimal obstruction
- •20. Trachoma
- •21. Corneal abrasion and recurrent erosion
- •22. Herpes simplex keratitis
- •23. Suppurative keratitis
- •24. Ocular toxoplasmosis
- •25. Onchocerciasis
- •27. Cytomegalovirus retinitis in patients with AIDS
- •28. Anterior uveitis
- •29. Primary open angle glaucoma and ocular hypertension
- •30. Acute and chronic angle closure glaucoma
- •31. Modification of wound healing in glaucoma drainage surgery
- •32. Cataract surgical techniques
- •33. Intraocular lens implant biocompatibility
- •34. Multifocal and monofocal intraocular lenses
- •35. Perioperative management of cataract surgery
- •36. Age-related macular degeneration
- •37. Treatment of lattice degeneration and asymptomatic retinal breaks to prevent rhegmatogenous retinal detachment
- •38. Surgery for proliferative vitreoretinopathy
- •39. Rhegmatogenous retinal detachment
- •40. Surgical management of full-thickness macular hole
- •41. Retinal vein occlusion
- •42. Medical interventions for diabetic retinopathy
- •43. Photocoagulation for sight threatening diabetic retinopathy
- •44. Vitrectomy for diabetic retinopathy
- •45. Optic neuritis
- •47. Idiopathic intracranial hypertension
- •48. Toxic and nutritional optic neuropathies
- •49. Traumatic optic neuropathy
- •50. Ocular adnexal and orbital tumours
- •51. Uveal melanoma
- •52. Retinoblastoma
- •Index
49 Traumatic optic neuropathy
Andrew S Jacks
Background
Definition
Traumatic optic neuropathy is an injury to the optic nerve following an episode of trauma, which may be direct or indirect.1,2 Traumatic optic neuropathy is a clinical diagnosis based on reduced vision (not explicable by other ophthalmic problems), presence of a relative afferent pupil defect (RAPD),3 reduced colour vision, and an associated visual field defect.4–6 The clinical examination can be complicated by the level of the patient’s consciousness and other problems associated with the trauma.
Incidence
The incidence of traumatic optic neuropathy is estimated to be between 0·7% and 2% of all cases with head trauma,4,7,8 and the population affected is young and predominantly male. The international optic nerve trauma study showed an average age of 34 ± 18 years, of whom 85% were male.9 Similar results have been seen in other studies.10–12 These studies used patients who presented to the emergency department with head trauma who were subsequently identified to have an ophthalmic injury.
Aetiology
Motor vehicle or bicycle accidents are the most common cause of trauma.9–12 Direct optic nerve trauma results from a penetration of the orbit that involves the optic nerve, such as a stab to the orbit. These produce severe and immediate visual loss.2,13 Indirect optic nerve trauma is caused by forces transmitted from a distant injury to the optic nerve.1,14 These may be associated with visual recovery and delayed visual loss. The degree of visual loss can be severe or mild.14
Prognosis
Visual improvement in untreated cases of indirect traumatic optic neuropathy has been reported in 25% to 45% of patients.9,10,12,15 The prognosis is less good if the injury is direct and if the initial visual loss is more severe.10 This leaves a large percentage of indirect traumatic
optic neuropathy patients who make no post-trauma improvement and who have visual loss.
Treatment options
The treatment options are no treatment, medical treatment with the use of systemic steroids in high or very high doses, and surgical treatment with decompression of the optic canal.
Question
What is the best form of treatment for visual loss from indirect traumatic optic neuropathy that does not improve spontaneously?
The evidence
No randomised controlled trials were found.
Comment
Only one prospective study of indirect traumatic optic neuropathy has been performed.9 The study was a nonrandomised, non-masked comparative interventional study with concurrent treatment groups. The aim of this study was to compare corticosteroids, optic canal decompression, and no treatment. The study was performed over a three-year period on 206 patients by 76 investigators in 16 countries. The patients were treated as deemed appropriate by the individual investigators according to their customary practice. The results are summarised in Table 49.1. The results show that there is no significant difference in the improvement of vision between the three groups. The confounding features that might have influenced the results were that the surgical group included more severe cases and cases that did not respond to steroid treatment. The study was underpowered because of the relative rarity of the cases.
All other reports are those of retrospective studies,10,11,12,15 and these have not been randomised, controlled or masked studies. They all produced similar results showing no difference between the three treatment options.
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Evidence-based Ophthalmology
Table 49.1 Results of prospective, non-randomised study9
|
|
At least one month follow up |
|
At least three months follow up |
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|
No treatment |
Steroids |
Surgery |
No treatment |
Steroids |
Surgery |
||||
|
|
|
|
|
|
|
|
|
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Overall 3 or more lines improvement |
n = 7 |
n = 64 |
n = 25 |
n = 4 |
n = 54 |
n = 21 |
||||
|
4 (57%) |
33 (52%) |
8 |
(32%) |
2 (50%) |
29 (54%) |
8 |
(38%) |
||
Baseline NLP, LP, HM 3 or more |
n = 3 |
n = 34 |
n = 23 |
n = 2 |
n = 26 |
n = 19 |
||||
lines improvement |
1(33%) |
15 (44%) |
6 |
(26%) |
1 (50%) |
12 (46%) |
6 |
(32%) |
||
Baseline CF or better 3 or more |
n = 4 |
n = 30 |
n = 2 |
n = 2 |
n = 28 |
n = 2 |
||||
lines improvement |
3 (75%) |
18 (60%) |
2 |
(100%) |
1 (50%) |
17 (61%) |
2 |
(100%) |
||
Unadjusted (adjusted) P for |
– |
1·0 (1·0) |
0·38 (1·0) |
– |
1·0 (1·0) |
1·0 (1·0) |
||||
comparison with untreated group* |
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|
|
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|
|
|
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|
|
Unadjusted (adjusted) P for |
1·0 (1·0) |
– |
0·11 (0·52) |
1·0 (1·0) |
– |
0·31 (0·83) |
||||
comparison with steroid group* |
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*Fisher's exact test used for unadjusted comparison of proportion 3 lines improvement; exact test for common odds ratio used for adjusted comparison
NLP, no light perception; LP, light perception; HM, hand motion vision; CF, count fingers visual acuity
Implications for research |
4 |
Turner JWA. Indirect injury to the optic |
nerves. Brain |
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1943;66:140–50. |
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The study of traumatic optic neuropathy cases is difficult |
5 |
Edmund J, Godtfredson E. Unilateral optic atrophy following head |
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injury. Journal? 1963;41:693–7. Check on medline. |
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due to the uncommon nature of the problem, the wide |
6 |
Kennerdell JS, Amsbaugh GA, Myers EN. Transantral ethmoidal |
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variety of exact injury to the nerve and thus natural history |
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decompression of optic canal fracture. Arch Ophthalmol 1976;94: |
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1040–3. |
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outcome and how this will affect results. |
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7 |
Brandle K. Die posttraumatischen opticusschadigungen. Confina |
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Neurolog 1955;15:169–208. |
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8 |
Matsuzaki H, Kunita M, Kawai K. Optic nerve damage in head |
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Implications for practice |
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trauma: clinical and experimental studies. Jpn J Ophthalmol 1982; |
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26:447–61. |
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9 |
Levin LA, Beck RW, Joseph MP et al. The treatment of traumatic |
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The individual clinical situation is of course complex, and |
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optic neuropathy: the international optic nerve trauma study. |
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Ophthalmology 1999;106:1268–77. |
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faced with a patient with severe visual loss and no clear |
10 |
Wang BH, Robertson BC, Girotto JA et al. Traumatic optic |
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guidance from the above studies as to which treatment is |
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neuropathy: a review of 61 patients. Plast Reconstr Surg 2001;107: |
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1655–64. |
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better, the clinician will have to decide how to proceed on |
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11 |
Agarwal A, Mahapatra AK. Visual outcome in optic nerve injury |
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the merits of each case. |
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patients without initial light perception. Ind |
J Ophthalmol |
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1999;47:233–6. |
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12 |
Seiff SR. High dose corticosteroids for treatment of vision loss due to |
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indirect injury to the optic nerve. Ophthalmic Surg 1990;21:389–95. |
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References |
13 |
Elisevich KV, Ford RM, Anderson DP et al. Visual abnormalities with |
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multiple trauma. Surg Neurol 1984;22:565–75. |
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1 Kline LB, Morawtz RB, Swaid SN. Indirect injury to the optic nerve. |
14 |
Steinsapir KD, Goldberg RA. Traumatic optic neuropathies. In: Miller |
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NR, Newman NJ, eds. Walsh and Hoyt’s Clinical Neuro- |
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Neurosurgery 1984;14:756–64. |
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ophthalmology 5th edn. Baltimore: Williams and Wilkins, 1998. |
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2 Steinsapir KD, Goldberg RA. Traumatic optic neuropathy. Surv |
15 |
Lessell S. Indirect optic nerve trauma. Arch Ophthalmol 1989;107: |
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Ophthalmol 1994;38:487–518. |
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382–6. |
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3 Bilyk JR, Joseph MP. Traumatic optic neuropathy. Semin Ophthalmol |
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1994;9:200–11. |
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372
Section XII
Ophthalmic oncology
Arun D Singh, Editor
373
Ophthalmic oncology: mission statement
Ocular oncology is a small ophthalmic sub-specialty dealing with diagnosis and treatment of patients with ocular tumours and related disorders. Such specialist services are limited to a few large ophthalmic centres that can offer multi-specialty care involving oncologists, radiation oncologists, paediatricians, paediatric oncologists and genetic counsellors. As ocular tumours are rare, only few studies involving large numbers of patients have been conducted. Nevertheless, issues in ocular oncology are
important as they not only impact visual outcome but also ocular salvage and life prognosis.
The aims of this section are to describe the available evidence from large case series, retrospective studies as well as even small case series to highlight important questions that have yet to be addressed. The section comprises three chapters delaing with common ocular tumours such as eyelid tymours, uveal melanoma and retinoblastoma.
374
