Case 3: Sudden Loss of Vision in a 54 year old Man

A 54 year old man presented urgently to his local practice with sudden loss of vision in his R eye. He gave a history of loss of vision that occurred at 8am in the morning with no pain, photophobia or redness in his eye. He denies any previous trauma to the eye, gradual visual loss or any other problems with his vision until this morning.

He has a background of poorly controlled type II diabetes, mild angina and had previous episodes of recurrent transient ischaemic attacks. His HbA1C was elevated at 12 and he has a poor compliance with his hypoglycaemic medications. A carotid Doppler was arranged after his last TIA showing up to 50% stenosis of both carotid arteries. He is an ex-smoker, having quitted smoking 5 years ago before which he smoked 20 a day.

On examination, the gentleman has reduced visual acuity to counting fingers in his R eye, and normal vision in the L eye. His right pupil responded sluggishly to light and he has a relative afferent pupillary defect in his R eye. Fundoscopic examination revealed the following.



What is the likely diagnosis?



http://www.bnretina.com/CommonConditions/occlusion.jsp


The patient gives a history of sudden painless loss of vision suggesting a few possible diagnoses:

-proliferative diabetic retinopathy is possible in somebody who is a poorly controlled diabetic.
-central retinal vein occlusion
-central retinal artery occlusion

The fundoscopic examination points to the diagnosis of central retinal artery occlusion, with its characteristic appearance of a pale retina with cherry red spot.

Central retinal artery occlusion is a cause of sudden visual loss and should be suspected in those with vascular problems. The patient normally presents with a history of acute and painless visual loss with a relative afferent pupillary defect. The latter is demonstrated by the swinging flashlight test and the sign is also known as a Marcus Gunn pupil. It is important to distinguish this from other causes of sudden blindness such as central retinal vein occlusion because the management can be completely different.

On fundoscopic examination, the characteristic pattern is that of a pale retina with a cherry red spot in the middle due to relative ischaemia of the choroid, however this pattern only accounts for the initial 48 hours. Neovascularisation changes may occur, especially in the long term, possibly due to build up of angiogenic factors as a result of the ischaemia.

The cause of central retinal artery occlusion may include atheroembolic fragments, such as that arising from mural thrombus in the heart or carotid stenosis. Other causes include vasculitides such as giant cell arteritis and sudden increases in intraocular pressure. It should be noted that giant cell arteritis causes visual loss usually via anterior ischaemic optic neuropathy, rather than central retinal artery occlusion. Since this is a treatable cause, it is important to exclude the other signs such as jaw claudication, scalp tenderness and muscle pains and aches.

The majority of cases of central retinal artery occlusion is probably due to carotid artery embolism. This should be suspected in patients with cardiovascular risk factors, such as previous myocardial infarcts, strokes or transient ischaemic attacks. Amaurosis fugax is a transient form of visual loss that may predict the occurence of a cerebrovascular event.

Central retinal artery occlusion is a recognised emergency because it can cause irreversible sight loss if left untreated. Measures such as digital massage may help to dislodge the embolus from the eye. Lowering of the intraocular pressure may be attempted using acetazolamide or beta blockers. Use of other agents such as vasodilators of fibrinolytic agents are still being researched. Laser therapy may help to treat neovascularisation and its complications.