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| CASE REPORT |
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| Year : 1991 | Volume
: 37
| Issue : 3 | Page : 179-80 |
Traumatic ischaemic optic neuropathy (a case report).
Gadkari SS, Ladi DS, Gupta S, Gandhi VH, Patel MV
Department of Ophthalmology, R. N. Cooper Hospital, Juhu, Bombay, Maharashtra.
Correspondence Address:
Department of Ophthalmology, R. N. Cooper Hospital, Juhu, Bombay, Maharashtra.
A 22-year-old patient presented with a clinical picture of unilateral optic neuropathy following blunt trauma to the orbit. Clinical findings, fundus fluorescein angiography and neurophysiological studies were suggestive of an ischaemia, a rare etiology.
How to cite this article:
Gadkari S S, Ladi D S, Gupta S, Gandhi V H, Patel M V. Traumatic ischaemic optic neuropathy (a case report). J Postgrad Med 1991;37:179 |
Traumatic optic neuropathy is known to occur following blunt trauma to the eye and the orbit. This may occur due to compression of the nerve by bony fragments or soft tissue swelling, concussion of the nerve, haemorrhage in or around the optic nerve sheaths and interference with the neural blood supply[4]. The latter is one of the least documented causes of traumatic optic neuropathy. In most of the cases, associated ocular injury, severe visual loss, and opaque media interfere with establishment of the exact etiopathology. We present here a case of traumatic optic neuropathy, diagnosed to be ischaemic in origin.
On 26 August 1989, a 22-year-old male presented with history of blunt trauma over the left lateral orbital margin, sustained in a vehicular accident five days ago. He complained of blurring of vision in the left eye since then, which was accompanied by the subjective perception of a field defect on the same side. On examination, the right eye was normal. The best corrected visual acuity in the left eye was 6/24 for distance and J 3 for near. Minimal lid ecchymosis was present. The conjunctiva, cornea, anterior chamber and extra-ocular movements and intra-ocular tension was normal. An afferent papillary defect was present. On direct ophthalmoscopy, the optic disc was pale as compared to the fellow eye. Macular oedema was present. There were no abnormalities of retinal vasculature, no haemorrhages or cherry red spot at the macula. The peripheral retina was normal on indirect ophthalmoscopy. Kinetic projection perimetry and scotometry revealed an altitudinal field defect involving the inferior hemifield and splitting the macula. Colour vision testing with Ishihara's pseudo isochromatic charts showed a red-green loss of colour vision in the affected eye. X-rays of the optic foramina and M' Scan of the orbit-brain were normal. Fundus flourescein angiography (FFA) performed a few days later showed decreased filling of the peripapillary capillaries in the early phase. The photopic and scotopic electro-retinography was normal. Visual evoked responses were obtained using 2/sec checker board pattern reversal and a monocular recording was obtained [Table - 1] The affected side showed a definite reduction in the amplitude with normal latency.
The patient was treated with oral prednisolone 20 mg daily and pentoxyphyline daily for 4 weeks. The patient was monitored over a period of 12 weeks. The vision improved to 6/6 and J 1 with resolution of the macular oedema. The afferent papillary defect and field changes persisted. The colour vision was restored to normal. The optic disc pallor became more obvious, as the patient developed a primary optic atrophy. There developed an area of peripapillary choroidal sclerosis around the disc.
The patient was thought to have had traumatic ischaemic optic neuropathy on basis of clinical features and investigations. While there is little doubt about the presence of traumatic optic neuropathy, the ischaemic etiology is supported on the basis of the following. The pallor of the disc was evident within 5 days of sustaining the injury. Disc oedema need not be present in all cases of ischaemic damage to the optic nerve, especially if the lesion is proximal to the exit of the central retinal vessels [3]. An altitudinal field defect was present which was involving the inferior hemifield, typically seen in ischaemic lesions of the optic nerve[2]. The patient had acquired colour blindness in spite of good visual acuity. This is common in ischaemic optic nerve pathologies[2]. The FFA showed decreased filling of the peripapillary capillaries. [3] Decreased amplitude of the visual evoked response in presence of normal latency is in favour of ischaemic lesions of the pathway[1]. The development of choroidal sclerosis (associated pathologically with drop out of the smaller choroidal vessels) with time around the disc, favours the diagnosis of an ischaemic pathology. There was no radiological or tomographic evidence of fracture or soft tissue compression.
While the manner of ischaemic damage is largely speculative, it may be due to direct occlusion or thrombosis in the posterior ciliary arteries or may result from vascular embarrassment due to compression by fragments or haematomas. Ischaemic etiology of traumatic optic neuropathy may be borne in mind in select cases.
Authors thank Dr. (Mrs) PN Wadia for electro-physiological studies.
| 1. |
Halliday AM, McDonald W, Mushin L. Delayed Visual evoked response in optic neuritis, Lancet 1972; 1:982-985.  |
| 2. | Miller NR. In: "Walsh and Hoyt's clinical neuro-ophthalmology". 4th edition. Baltimore: William and Wilkins; 1985, pp 213-214. |
| 3. | Peyman GA, Sanders DR, Goldberg MF. In: 'Principles and practice of Ophthalmology". 1st edition, Philadelphia: WB Saunders Co; 1987, pp 2121-2122. |
| 4. | Wyllic AM, Mcleod D, Cullen JF. Traumatic ischaemic optic neuropathy. Brit J Opthalmol 1972; 56:851-852.
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