Story of a 58 year old obese man’s retina Extra Case 5

A 58 year old obese man presents distressed, after experiencing a loss of vision in the right eye approximately 2 hours previously. He describes the sensation of a black curtain suddenly dropping in front of that eye, lasting just under five minutes. There were no associated ocular symptoms, such as eye pain, and his vision is now normal. He is feeling physically fit, and he denies any other additional complaints in a review of symptoms. PMHx: HTN for 5 years – variable compliance with medication and follow up Meds: Atenolol 50mg daily SHx: Smoker

Q1 What condition is the patient describing? What are the possible aetiologies?

The obese man is describing a condition called amaurosis fugax. It is a sudden transient loss of vision in one eye. Only about a quarter of patients with transient monocular vision loss (TMVL) actually experience the classic ‘dark curtain’ descending over their field of vision: the rest experience blindness, dimming, fogging, or blurring of their vision. Duration of visual loss ranges from only a few seconds to a few hours depending on the aetiology of the vision loss. Eg. Obscured vision due to papilledema may last only seconds, while a severely atherosclerotic carotid artery may be associated with duration of one to ten minutes. There are 5 main categories of aetiology; embolic, hemodynamic, ocular, neurologic, and idiopathic.

Q1 What condition is the patient describing? What are the possible aetiologies? Embolic and hemodynamic causes Atherosclerotic carotid artery: presents as type of TIA  unilateral embolic obstruction of retinal or ophthalmic artery  ischemic retina. BUT can also be caused by hypoperfusion. "Unilateral visual loss in bright light may indicate ipsilateral carotid artery occlusive disease and may reflect the inability of borderline circulation to sustain the increased retinal metabolic activity associated with exposure to bright light." Cardiac emboli obstructing either retinal, ophthalmic and/ or ciliary arteries secondary to AF, valvular disease etc Temporary vasospasm – related to exercise and systemic hemodynamic challenge Giant cell arteritis – granulomatous inflammation within the central retinal and posterior ciliary arteries of eye.

Q1 What condition is the patient describing? What are the possible aetiologies? Ocular causes Close-angle glaucoma Transiently elevated ICP Neurological causes Optic neuritis Papilloedema – usually accompanied by headache. Optic disc swelling renders the small, low-pressure vessels that supply the optic nerve head vulnerable to compromise Multiple Sclerosis - unilateral conduction block secondary to demyelination and optic neuritis Migraine

On examination: BP 150/95 mm Hg. Visualisation of the retina with a direct opthalmoscope reveals the finding below.

Q2 What is demonstrated in this fundus photograph?

The opacity is called a Hollenhorst plaque – either a cholesterol emboli which usually dislodges from the carotid arteries, or calcific/ platelet-fibrin fragments from a stenosed aortic valve. The embolus normally lodges at a bifurcation point. The pathology caused by the Hollenhorst plaque is called Retinal Artery Occlusion (Can be CRAO or BRAO) where the affected retina (with the exception of the fovea) becomes pale and swollen and opaque while the central fovea still appears reddish.

Q3 What additional physical examination would you perform as part of your initial assessment?

Cardiovascular examination – especially looking for atherosclerotic plaques in the carotid arteries and valvular disease in the heart. Neuro examination – PEARLA, visual fields and acuity again etc Slit lamp examination Also need to find any evidence of coagulopathies!

A carotid Doppler ultrasonography indicates a severe 80% stenosis of the right internal carotid artery. There is also mild stenosis (50%) in the region of bifurcation of the left common carotid artery.

Q4. What additional investigations would you order at the same time?

Unless symptoms are very typical for migraine, some diagnostic testing is required. Erythrocyte sedimentation rate and C-reactive protein should be performed in all individuals over age 50 years with transient monocular or binocular visual loss to exclude giant cell arteritis (GCA) Other tests are ordered according to symptoms and clinical setting and may include cardiac workup (ECG, Holter monitoring and echocardiography) Coagulation profile Fasting Lipids (chol and TG) Somehow test Intraocular pressure magnetic resonance imaging (MRI) electroencephalogram (EEG) FBC (to screen for conditions such as polycythemia vera and essential thrombocythemia)

After evaluating the results of all investigations, you discuss possible treatment with the patient. The patient tells you that on the evening prior to the review appointment, while he was sitting watching television, his left arm became weak and he was unable to pick up his coffee cup. On trying to stand, he found his left leg was dragging, and he was forced to sit down. The episode lasted approximately 10 minutes.

Q5 Presented with this new history, what treatment would you recommend for the patient? Why?

Re-current TIA’s? ie: One TMVL (amaurosis fugax) and one transient cerebral ischemic episode. TMVL carries a lower risk for stroke in the setting of high-grade carotid disease, compared with cerebral ischemia. Ie. at higher risk for stroke now…. Since has had TIA in past now might consider follow-up investigations like CT/ MRI and standard treatment of post TIA – hinges on stroke prophylaxis

As an aside… Treatment options for uncomplicated (Central) Retinal artery occlusion are as follows… Immediate lowering of IOP to a target pressure of 15 mm Hg using medical management, ocular massage, and anterior chamber paracentesis. This hopefully dislodges the embolus to a point further down arterial circulation and improves retinal perfustion. Start timolol early in the treatment of RAO. Acetazolamide and mannitol should also be used when CRAO is suspected because there are few downsides to starting these medications early. CO 2 therapy (give patient a bag to rebreath in) carbon dioxide dilates retinal arterioles, and oxygen increases oxygen delivery to ischemic tissues. Thrombolytics may be useful if initiated within 4-6 hours of visual loss, but they may not be much help if the embolus is cholesterol, talc, or calcific. Thrombolytics are introduced via the proximal ophthalmic artery, delivering increased concentrations directly to the retinal artery and minimizing systemic complications. Results of noncontrolled retrospective studies have been mixed. As of 2007, a European controlled study is underway. Treatment with IV thrombolytics as with cerebral infarction has been discussed but currently is not the standard of care.

Q6 Discuss the various treatment options for TIAs.

MEDICATION: Noncardioembolic attacks In presumed or angiographically verified atherosclerotic changes in the extracranial or intracranial cerebrovascular circulation, antithrombotic medication is prescribed (Aspirin, clopidogrel, dipyridamole etc) Treatment with aspirin, (over 100mg) once daily orally, significantly reduces the frequency of TIA and stroke Anticoagulant drugs are not recommended; there is no benefit over antiplatelet therapy and risk of serious hemorrhagic adverse effects is greater (NOTE: is recommended in cardioembolic events) SURGERY Carotid thromboendarterectomy – Reduces the risk of ipsilateral carotid stroke, especially when TIAs are of recent onset (< 1 month) – Indicated when there is a surgically accessible high-grade stenosis (70–99% in luminal diameter) on the side appropriate to carotid ischemic attacks and there is relatively little atherosclerosis elsewhere in the cerebrovascular system OTHER THERAPEUTIC PROCEDURES Cigarette smoking should be stopped Treat any cardiac sources of embolization, hypertension, diabetes mellitus, hyperlipidemia, arteritis, or hematologic disorders appropriately Weight reduction and regular physical activity should be encouraged when appropriate

And that’s our story The end