Associated major artery disease

Ophthalmic artery

Ophthalmic artery occlusion mimics a CRAO clinically and produces opacification of the infarcted retina. The typical cherry-red spot may be absent or extremely indistinct due to coexisting infarction of the choroid.26-28 Visual loss is typically severe and permanent, with most eyes having no light perception or only bare perception of light.29 There may be associated eye pain and pupillary dilatation from concurrent ischaemia to the ciliary ganglion or iris sphincter. The eye may be hypotonic. The retinal vessels are markedly constricted and the optic disc may or may not be swollen. Over time, most patients develop a characteristic fundus appearance characterised by optic atrophy, arterial attenuation, and diffuse pigmentary changes.

The pathogenesis of ophthalmic artery occlusion is much the same as that of ICA occlusion. The artery may be occluded: firstly, by a thrombus originating in the artery itself; secondly, by a thrombus propagated from an occluded ICA; thirdly, by an embolus from a distant site, most often the heart,29 the common carotid artery, or the extracranial portion of the ICA; or, fourthly, by an extrinsic process that compresses the vessel, for example tumour or aneurysm. When only the proximal portion of the ophthalmic artery is occluded, there may be no ocular symptoms or signs because collateral channels from branches of the external carotid artery usually provide sufficient blood supply to the orbital and ocular vessels normally supplied by the ophthalmic artery. When the occlusion is more extensive, visual loss and typical ophthalmoscopic signs are present. Rarely, in isolated cases of ophthalmic artery occlusion, vision recovers from light perception vision to 20/30 or from an acuity of counting fingers at 6 inches (15 cm) to 20/50 with the restoration of normal retinal and choroidal blood flow.28

Diagnosis Fundus fluorescein angiography is diagnostic in CRAO or ophthalmic artery occlusion provided that:

• a timed transit is obtained within hours or days of the event

• a wide angle lens is used on the fundus camera

• the optic disc is photographed in the centre of the picture.

In isolated acute CRAO the choroidal circulation of the eye is normal and the delay is in the filling of the branches of the central retinal artery. In acute occlusion of the ophthalmic artery there is delayed filling in both the choroidal and retinal circulation.

Orbital colour Doppler imaging is, however, the diagnostic procedure of choice for establishing embolism as the cause of CRAO when no emboli are visible in the retinal circulation. This non-invasive technology enables prompt differentiation of embolic disease from arterial occlusion caused by intrinsic atherosclerosis, vasospasm, or vasculitis from giant cell arteritis. Clearly, recognition of emboli has important management implications for these patients.30

Emergency treatment The emergency treatment of ophthalmic artery occlusion is the same as for an acute CRAO.

Temporal artery

Occlusion of the central retinal artery occurs in 5-10% of elderly patients over the age of 60 with giant cell arteritis in the absence of classic cranial and systemic arteritic symptoms. Risk of blindness in the fellow eye is extremely high and all cases warrant an immediate Westergren ESR (<50 years of age: males 0-15 mm/h, females 0-20 mm/h; >50 years of age: males 0-20 mm/h, females 0-30 mm/h) and fibrinogen level (200-400 mg/dl) which, if elevated, indicate the need for high dose corticosteroid therapy and a temporal artery biopsy. Prednisone (60-80 mg per day) is the drug of choice. The dose should be regulated by the symptoms and the ESR and tapered slowly to a maintenance dose of 7 5-10 mg per day. Immediate corticosteroid therapy is advisable even when a clinical index of suspicion for giant cell arteritis is high in spite of a normal ESR and pending a temporal artery biopsy.

Diagnosis The diagnosis of giant cell arteritis is confirmed by biopsy of the temporal artery. Involvement of the vessel may be segmental and the diagnosis missed unless serial sections of a long biopsy specimen are performed. Dramatic response of headache, when present, to a trial of corticosteroids can confirm the diagnosis. There is usually no improvement in vision.

Internal carotid artery

The presence of ICA disease has varied among different series.25,31 Clinical features of value in predicting a potentially operable carotid lesion on angiography have included increasing age, a localised carotid bruit, and cholesterol emboli in retinal branches. No operable lesions have been found in patients under 50 who did not have either a carotid bruit or cholesterol emboli. Twenty years ago, Wilson and colleagues found 12 of 18 patients had carotid irregularities or stenosis on angiography.23 Ten years later, Merchut and associates,31 grouping CRAO and BRAO together, found 29 of 34 (85%) patients had an abnormal ICA on arteriography, of which 12 had occlusion or severe stenosis and 17 had plaques, ulcers, or stenosis of less than 60%. In five of 34 patients (15%) the angiograms were normal.

Diagnosis Auscultation of the neck, eyes, and head for a bruit is very important, the higher the pitch the tighter the carotid stenosis. High pitched bruits that fade into diastole are diagnostic of a haemodynamically significant (70%) stenosis. The most widely used tests to evaluate the carotid artery are carotid non-invasive studies which combine carotid duplex Doppler with colour flow imaging at the bifurcation of the common carotid artery, with anterior transcranial Doppler insonation of flow in the intracranial (siphon portion) of the internal carotid artery, the ophthalmic artery, and through the transtemporal window the middle, anterior, and posterior cerebral artery stems. When the stenotic lesion at the origin of the internal carotid artery is narrow enough to produce a pressure drop across it (haemodynamically significant is > 70% stenosis), it can be identified by these methods with highly significant specificity and confirmed by magnetic resonance angiography or CT angiography. It is not certain, however, if CRAO is more common in these haemodynamically significant stenoses as opposed to those that are not. What is certain is that the rate of stroke is higher significantly in patients with such haemodynamically significant lesions.32

Ipsilateral headache or neck pain with tinnitus preceding CRAO is highly suggestive of ICA dissection and early diagnosis is imperative to reduce the risk of hemispheric stroke by artery to artery embolism.33

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