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Optic disc oedema in first degree relatives with different macrovascular risk factors (type 1 diabetes and hypertension)

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Case reports

CASE 1

A 43 year old man with type 1 (insulin dependent) diabetes for 16 years presented to the ophthalmology clinic with sudden onset of painless loss of vision in the right eye. On examination, visual acuity in the right eye was reduced to counting fingers. An afferent pupillary defect was noted and fundoscopy revealed a pale oedematous disc with surface flame  

haemorrhages (fig 1B). Visual acuity and examination of the left eye were normal. He had no microvascular or macrovascular complications of diabetes and had maintained good glycaemic control with glycated haemoglobin concentrations consistently below 8% (local non-diabetic range 5.0%–6.5%). He smoked 20 cigarettes per day, was normotensive, and his total plasma cholesterol was normal (4.6 mmol/l). Fluorescein angiography was consistent with oedema of the optic disc. Investigations including a computed tomography of the brain, full blood count, erythrocyte sedimentation rate, plasma biochemistry, serum vitamin B12 concentration, thrombophilia screen, and an autoantibody screen were all normal, and clinical examination by a neurologist detected no additional abnormalities. No improvement in vision occurred during the following 12 months and the right optic disc revealed optic atrophy.

Figure 1

Case 1: (A) right optic fundus before the development of acute ischaemia; (B) acute ischaemic phase in the right optic fundus; (C) optic fundi six months after the acute episode. The pale disc on the right is suggestive of optic atrophy.  

CASE 2

Two months after case 1 had presented with visual loss, his 73 year old mother presented to the same ophthalmology clinic complaining that she was experiencing “a curtain of blackness” in her left eye. In the left eye the visual acuity was 1/60 and less than N48 and in the right eye 6/12+2 and N6. Fundal examination revealed swelling of the left optic disc and an afferent pupillary defect. A lower left altitudinal field defect was demonstrated and investigations similar to those in case 1, did not show any abnormal findings. The patient had established hypertension treated with amlodipine and doxazosin. She was a non-smoker and her total plasma cholesterol was 6.0 mmol/l. An oral glucose tolerance test was normal. Her vision did not improve over the following eight months, but her left optic fundus showed features of optic atrophy (fig 2).

Figure 2

Case 2: optic fundi four months after the acute episode. The left disc is paler consistent with optic atrophy.

Questions

(1)
What are the diagnostic possibilities and what is the most likely diagnosis?
(2)
What are the risk factors for non-arteritic anterior ischaemic optic neuropathy?
(3)
What are the therapeutic options available for this condition?

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