To analyse previous literature and to formulate a management strategy for iris microhaemangiomas (IMH).A review of the literature in English language articles on IMH.Thirty five English language articles fulfilled the criteria for inclusion to the study and based on the contents on these articles a management strategy was formulated. Age at presentation ranged from 42 to 80 years with no sex or racial predisposition. Most patients with IMH have no systemic disease but a higher incidence had been reported in patients with diabetes mellitus, myotonic dystrophy, chronic obstructive pulmonary disease (COPD) and several other systemic and ophthalmic co-morbidities. Most patients remained asymptomatic until they experienced a sudden blurring of vision due to a hyphaema. Some patients only develop a self-limiting single episode of hyphaema and therefore the laser or surgical photocoagulation of iris should be reserved for the cases complicated with recurrent hyphaema. In some patients, several laser photocoagulation sessions may be needed and the recurrent iris vascular tufts may require more aggressive treatment. Iris fluorescein angiography (IFA) is useful in identifying the true extent of the disease and helps to improve the precision of the laser treatment. Surgical excision (iridectomy) should only be considered in patients who fail to respond to repeated laser treatment. In some cases IMHs has been initially misdiagnosed as amaurosis fugax, iritis and Posner-Schlossman syndrome.Owing to its scarcity, there is no good quality scientific evidence to support the management of IMH. The authors discuss the various treatment options and present a management strategy based on the previous literature for the management for this rare condition and its complications.

PURPOSE:

: To investigate systematically the prevalence of amaurosis fugax (AF) in various ocular vascular occlusive disorders individually and to discuss the pathogeneses of each.

METHODS::

The study comprised patients with central retinal artery occlusion (271 eyes), branch retinal artery occlusion (169 eyes), ocular ischemic syndrome (39 eyes), central retinal vein occlusion (864 eyes), hemi-central retinal vein occlusion (67 eyes), branch retinal vein occlusion (285 eyes), nonarteritic anterior ischemic optic neuropathy (946 eyes), and giant cell arteritis with visual loss (147 eyes). At first visit, all patients had a detailed ophthalmic and medical history and comprehensive ophthalmic evaluation and systemic evaluation.

RESULTS::

Prevalence of AF was 12.18% in central retinal artery occlusion, 14.20% in branch retinal artery occlusion, 15.38% in ocular ischemic syndrome, 4.86% in central retinal vein occlusion, 37.84% in central retinal vein occlusion with cilioretinal artery occlusion, 13.43% in hemi-central retinal vein occlusion, 0.35% in branch retinal vein occlusion, and 2.54% in nonarteritic anterior ischemic optic neuropathy. In giant cell arteritis, 32.4% of patients with ocular involvement had a history of AF or 26.5% of the involved eyes. Amaurosis fugax in central retinal artery occlusion, branch retinal artery occlusion, and nonarteritic anterior ischemic optic neuropathy is mostly because of transient embolism. The pathogenesis of AF in each ocular vascular occlusive disorder is discussed.

CONCLUSION:

: Prevalence and pathogenesis of AF in various ocular vascular occlusive disorders varies widely. Amaurosis fugax may be the presenting symptom in these disorders and that always requires urgent evaluation.

A 68-year-old man presented with right cervical carotid artery stenosis manifesting as ipsilateral amaurosis fugax. Angiography showed non-bifurcating cervical carotid artery with atherosclerotic stenosis near the branching of the superior thyroid artery. Carotid artery stenting (CAS) was carried out using two balloons for embolic protection of the internal carotid artery and middle meningeal artery because the ophthalmic artery was supplied by the middle meningeal artery. No procedure-related complications or restenosis occurred after stenting. Non-bifurcating cervical carotid artery is a very rare anomaly, in which the branches of the external carotid artery directly arise from the common trunk of the carotid artery without forming a bifurcation. The present patient was successfully treated with CAS for atherosclerotic stenosis associated with non-bifurcating cervical carotid artery.

A 36-year-old female with systemic lupus erythematosus and antiphospholipid syndrome was referred to our department because of mild weakness of left arm and an episode of right amaurosis fugax for twenty days. Brain MRI showed right ACA/MCA/PCA border zone infarction on DWI/T2WI/FLAIR and MR angiography (MRA) showed multiple segmental stenosis in right internal carotid artery, right and left middle cerebral artery, and bilateral posterior cerebral arteries. Treatment with oral aspirin (100 mg/day) and continuous infusion of heparin kept her neurological symptoms and signs stable. MRA on 28 days revealed complete recovery of multiple stenotic lesions, thus, diagnosis of reversible cerebral vasoconstriction (RCVS) was made. RCVS should be considered as a cause of neurological deficit in patients with SLE regardless of thunderclap headache.

A 69-year-old man was admitted to our hospital for persistent fever, myalgias, articular pain, headache, and hypoaesthesia of the scalp. The clinical scenario was typical for giant-cell arteritis. During hospital stay, patient developed fugax amaurosis, stroke, and acute coronary syndrome. The definitive diagnosis of infective endocarditis, supported by transesophageal echocardiography, was confirmed only by culturing the material obtained during angiography and coronary thromboaspiration.

Permanent visual loss (PVL) is the most dreaded complication of giant cell arteritis (GCA). It results from anterior ischemic optic neuropathy or, less commonly, retinal artery occlusion. This complication still occurs in 14 to 20% of patients and is typically devastating and permanent, although it is highly preventable by an early diagnosis of giant cell arteritis and appropriate glucocorticoid treatment. Transient ischemic symptoms such as amaurosis fugax, episodes of blurred vision or diplopia may occur, either heralding visual loss or remaining isolated. In studies, the main predictors of PVL are jaw claudication, amaurosis fugax, lack of systemic "B" symptoms, a modestly increased ESR and a higher haemoglobin level. The evaluation of a GCA patient with PVL includes emergency fundoscopy completed by fluorescein angiography, immediate erythrocyte sedimentation rate, C-reactive protein, and complete blood count. Treatment is extremely urgent mainly because, if left untreated, GCA is associated with visual loss in the fellow eye within days in up to 50% of individuals. Treatment may begin with high-dose intravenous methylprednisolone, followed by oral prednisone administered at 1 mg/kg per day. Daily adjunctive aspirin orally may be added since it has been shown, in retrospective studies, to protect against stroke and visual loss. Although treatment duration of complicated GCA is not codified, an initial PVL deserves close monitoring of patient's systemic symptoms, ESR and CRP to avoid relapses due to a significant risk of late recurrence of visual loss during steroid tapering.

TIA is a brief and transient ictal symptom due to a local disturbance of cerebral or ocular arterial circulation. Transitory blindness or blurred vision in one eye (amaurosis fugax) is a sudden TIA symptom lasting a few minutes, usually underlied by thromboembolism originating from an atherosclerotic plaque of the internal carotid artery, less frequently an embolus from the aorta or the heart, or localized thrombosis of vessels of the optic nerve or the retina. We describe two amaurosis fugax patients.