Uveal vascular bed in health and disease: lesions produced by occlusion of the uveal vascular bed and acute uveal ischaemic lesions seen clinically. Paper 2 of 2.

From studies on postmortem anatomical descriptions of the uveal vascular bed, it was generally concluded that occlusion of PCA or its branches should not produce an ischemic lesion. However, in vivo studies have recorded that the PCAs and their branches, right down to the terminal choroidal arterioles, and the choriocapillaris, have a segmental distribution in the choroid, and that PCAs and choroidal arteries function as end-arteries. This explains the basis of the occurrence of isolated inflammatory, ischemic, metastatic, and degenerative choroidal lesions, which are usually localized. Thus, in vivo studies have completely revolutionized our concept of the uveal vascular bed in disease.

Uveal vascular bed in health and disease: uveal vascular bed anatomy. Paper 1 of 2.

The uveal vascular bed is the largest vascular system in the eye and has a role in supplying almost every tissue in the eyeball. This makes it the most important ocular vascular system. This is an up-to-date review of the literature of the entire uveal vascular bed in health based on detailed anatomy of the posterior ciliary arteries (PCAs), anterior ciliary arteries, cilioretinal arteries, and vortex veins. Although postmortem injection cast preparations gave us useful information on the morphology of the choroidal vascular bed; in vivo studies showed that they misled us for centuries about the in vivo situation. According to the postmortem cast studies, the uveal vascular bed has no segmental distribution, the uveal vessels anastomose freely with one another, there are inter-arterial and arteriovenous anastomoses in the choroid, and the choriocapillaris form a freely communicating and an uninterrupted vascular bed in the entire choroid.

Familial giant cell arteritis.

This is a case report of 'familial giant cell arteritis' in three siblings from northwest India. This is the first case report of 'familial giant cell arteritis' in a non-Caucasian family.

Photocoagulation for retinal vein occlusion.

The role of photocoagulation in retinal vein occlusion (RVO) has been studied since 1974. The most serious complications of central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO) are: (i) visual deterioration, most commonly due to macular edema, and (ii) the development of ocular neovascularization (NV), particularly neovascular glaucoma (NVG), with hazardous consequences for vision and even the eye itself. Before discussing the role of photocoagulation in the management of NV and macular edema in RVO, it is crucial to gain a basic scientific understanding of the following relevant issues: classification of RVO, ocular NV in RVO, and the natural history of macular edema and visual outcome of RVO. These topics are discussed. In CRVO, ocular NV is a complication of ischemic CRVO but not of nonischemic CRVO. Photocoagulation has been advocated to prevent and/or treat the development of ocular NV and NVG. Since NVG is the most dreaded, intractable and blinding complication of ischemic CRVO, the role of photocoagulation and its management are discussed. Findings of three randomized, prospective clinical trials dealing with photocoagulation in ischemic CRVO are discussed. The role of photocoagulation in the management of ocular NV and macular edema in BRVO, and three randomized, prospective clinical trials dealing with those are discussed. Recent advent of intravitreal anti-VEGF and corticosteroid therapies has drastically changed the role of photocoagulation in the management of macular edema and NV in CRVO and BRVO. This is discussed in detail.

Giant cell arteritis: Its ophthalmic manifestations.

Giant cell arteritis (GCA) is the most important medical emergency in ophthalmology, because its most dreaded complication is visual loss, which is preventable if these patients are diagnosed early and treated immediately and aggressively. This is a brief review of GCA, its ophthalmic manifestations, and how to diagnose and manage them.

Controversies on neuroprotection therapy in non-arteritic anterior ischaemic optic neuropathy.

OBJECTIVE: There has long been a great interest in neuroprotection therapy for ischaemic stroke and various types of optic neuropathies. In view of that, I reviewed the literature on the role of neuroprotection for non-arteritic anterior ischaemic optic neuropathy (NA-AION). METHODS: The review is based on a PubMed search of literature about the use of neuroprotectors in stroke and optic neuropathies and about current clinical trials of RPh201 and QPI-1007 in NA-AION. RESULTS: Several neuroprotection agents for ischaemic stroke and various types of optic neuropathies have been evaluated extensively in experimental studies in animals and benefits claimed. However, translation of therapeutic strategies for neuroprotection from experimental research to humans has invariably been fraught with failure. Two currently ongoing studies dealing with neuroprotection by RPh201 and QPI-1007 in NA-AION may have limitations in their rationale and study designs. CONCLUSIONS: Unfortunately, in spite of all the experimental and clinical research on neuroprotection agents in NA-AION so far, we have no scientifically proven evidence of neuroprotection agents showing any benefit in the human clinical studies so far.

Adventure in three worlds.

The author relates an unlikely journey from his rural village in India, through medical school, a prestigious fellowship with Sir Stewart Duke-Elder, and a colorful career in the United Kingdom and the USA, as a clinician and researcher, particularly in the area of vascular disease of the eye and optic nerve.

Central retinal artery occlusion.

The pathogeneses, clinical features, and management of central retinal artery occlusion (CRAO) are discussed. CRAO consists of the following four distinct clinical entities: non-arteritic CRAO (NA-CRAO), transient NA-CRAO, NA-CRAO with cilioretinal artery sparing, and arteritic CRAO. Clinical characteristics, visual outcome, and management very much depend upon the type of CRAO. Contrary to the prevalent belief, spontaneous improvement in both visual acuity and visual fields does occur, mainly during the first 7 days. The incidence of spontaneous visual acuity improvement during the first 7 days differs significantly (P < 0.001) among the four types of CRAO; among them, in eyes with initial visual acuity of counting finger or worse, visual acuity improved, remained stable, or deteriorated in NA-CRAO in 22%, 66%, and 12%, respectively; in NA-CRAO with cilioretinal artery sparing in 67%, 33%, and none, respectively; and in transient NA-CRAO in 82%, 18%, and none, respectively. Arteritic CRAO shows no change. Recent studies have shown that administration of local intra-arterial thrombolytic agent not only has no beneficial effect but also can be harmful. Investigations to find the cause and to prevent or reduce the risk of any further visual problems are discussed. Prevalent multiple misconceptions on CRAO are discussed.

Do Patients With Retinal Artery Occlusion Need Urgent Neurologic Evaluation?

PURPOSE: To describe a framework for logical, immediate action to manage patients with retinal artery occlusion. DESIGN: Literature review and perspective. METHODS: Review of the literature and the author's experience. RESULTS: Since embolism is the most common factor causing retinal artery occlusion, to manage these patients, immediate evaluation and management of the source of embolism is critical to prevent further episodes. CONCLUSIONS: The logical, immediate action to manage patients with retinal artery occlusion is evaluation of the carotid artery and heart for embolism, fasting lipid levels and a complete blood count, rather than neurological evaluation, unless, of course, there are neurological symptoms.

Posterior Ciliary Artery Occlusion.

OBJECTIVE: To compare the severity of ischemic damage following posterior ciliary artery (PCA) occlusion in old, atherosclerotic, hypertensive monkeys to that in young monkeys. DESIGN: Experimental study. SUBJECTS: Seven eyes of normal, healthy rhesus monkeys and 8 of old, atherosclerotic, hypertensive monkeys. METHODS: By lateral orbitotomy, all PCAs were cut behind the eyeball in both groups of animals. The fundus and the optic disc were evaluated by repeated ophthalmoscopy, color fundus photography and fluorescein fundus angiography, before and immediately after cutting the PCAs and serially thereafter during the follow-up period. MAIN OUTCOME MEASURES: Severity of acute ischemic damage to the choroidal, outer retinal and optic nerve head. RESULTS: Cutting all the PCAs resulted in the development of ischemic infarction of the choroid, retinal pigment epithelium, outer part of the retina and the optic nerve head within 24-hours, in both groups of animals. The severity of the various ischemic fundus and retinal lesions and of the optic disc during the acute phase showed no statistically significant differences between the two groups of animals. Fluorescein fundus angiography soon after cutting the PCAs showed no filling of the entire choroid and the optic disc in both groups of animals. On follow-up for up to about 3 months, in both groups, the white opacity of the infract in the fundus seen during the acute phase gradually resolved in about 2-3 weeks, leaving greyish, granular, depigmented fundus, unmasking of the large choroidal vessels and optic atrophy; fluorescein angiography revealed gradual restoration of the choroidal blood flow and unmasking of the big choroidal vessels. CONCLUSIONS: The study showed that the severity of ischemic damage following occlusion of all the PCAs was similar in both the young healthy and the old, atherosclerotic, hypertensive monkeys. This is in contrast to the findings of our similar study dealing with central retinal artery occlusion, where the young suffered much severe ischemic damage than the old.