|Year : 2002 | Volume
| Issue : 4 | Page : 324-325
Anterior ischaemic optic neuropathy at high atitude
S Bandyopadhyay, R Singh, V Gupta, A Gupta
Department of Ophthalmology, Postgraduate Institute of Medical Education & Research, Chandigarh-160 012, India
Department of Ophthalmology, Postgraduate Institute of Medical Education & Research, Chandigarh-160 012
Source of Support: None, Conflict of Interest: None
High altitude retinopathy with various manifestations is common after exposure to high altitude. Inadequate autoregulatory response of the retinal vascular system is thought to be responsible for this. We report a case of anterior ischaemic optic neuropathy following
exposure to high altitude.
Keywords: Anterior ischaemic optic neuropathy, high altitude, retinopathy
|How to cite this article:|
Bandyopadhyay S, Singh R, Gupta V, Gupta A. Anterior ischaemic optic neuropathy at high atitude. Indian J Ophthalmol 2002;50:324-5
|How to cite this URL:|
Bandyopadhyay S, Singh R, Gupta V, Gupta A. Anterior ischaemic optic neuropathy at high atitude. Indian J Ophthalmol [serial online] 2002 [cited 2020 May 29];50:324-5. Available from: http://www.ijo.in/text.asp?2002/50/4/324/14756
High altitude retinopathy is a recognised entity that occurs following exposure to heights of more than 4,500 meters above mean sea level. The various ocular changes reported are retinal haemorrhage,, retinal vascular tortuosity, disc oedema, cotton wool spots and central retinal vein occlusion. We report a case of unilateral anterior ischaemic optic neuropathy that occurred at an altitude of 5472 meters above mean sea level.
| Case report|| |
A 33-year-old male presented complaining of loss of vision in the lower half of the right eye of three weeks' duration. When he became symptomatic he had been staying at the Siachen glacier (5472 meters above mean sea level) for three months. Ten days after onset of symptoms he came down to the plains and presented to us. He had no associated systemic disease and was a non-smoker.
Ocular examination showed best corrected visual acuity of 6/6 in both eyes. There was relative afferent pupillary defect in the right eye. The anterior segment of both eyes was normal with intraocular pressure (IOP) of 14mm Hg in both eyes. Fundoscopy of the right eye showed pale disc oedema in the superior half of the optic disc [Figure - 1]a, while the left eye was normal. Fundus fluorescein angiography of the right eye showed initial hypofluorescence [Figure - 1]b with late optic disc staining in the superior half [Figure - 1]c, consistent with the diagnosis of anterior ischaemic optic neuropathy. Visual field examination (30-2 threshold list) on Humphrey's perimeter showed inferior altitudinal defect in the right eye with normal visual field in the left eye [Figure - 2]a.
The investigative work up including total blood counts, erythrocyte sedimentation rate, lipid profile and blood sugar were noncontributory and the hematocrit value was normal (44%). At three months' follow-up, he maintained 6/6 vision in the both eyes, but field loss persisted [Figure:2b].
| Discussion|| |
High altitude retinopathy is a well known distinct entity. Ischaemic optic neuropathy, however, has not been described after high altitude exposure. Autoregulation of retinal vessels may play a major role in maintaining normal circulation in eyes that are exposed to chronic hypoxia as may occur at high altitude. Measurement of retinal blood flow in mountaineers of the first Vienna Himalayan expedition showed a marked increase in retinal blood flow (up to 96%) in 5 of 7 eyes, of which two had retinal haemorrhage. The remaining two patients who had a 21-30% decrease in retinal blood flow due to spasm of retinal vessels, did not show any signs of high altitude retinopathy. This study showed that high altitude retinopathy is essentially seen in climbers with ocular vascular dysregulation. Another possible mechanism is an increased hematocrit value with increased blood viscosity that could be responsible for the occurrence of various manifestations of altitude-related retinal diseases. The patient described here had a normal hematocrit value. We speculate that an inadequate autoregulatory response, under conditions of chronic hypoxia, may have led to sustained vasospasm, which could in turn have reduced the blood supply to the optic nerve head, leading to anterior ischaemic optic neuropathy.
| References|| |
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[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5]
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