Central retinal artery occlusion--etiology, clinical picture, therapeutic possibilities

Abstract

An occlusion of the central retinal artery (CRAO) leads to a unilateral acute painless loss of vision. The individual etiology remains unclear in many cases. Potential pathomechanisms are embolism, vasoobliteration and vascular compression. Emboli (calcified, thrombotic, myxomatous, bacterial or cholesterol) are of carotid or cardiac origin. Atherosclerotic plaques, giant-cell arteritis and other types of vasculitis may cause vasoobliteration. A retrobulbar mass (hematoma, neoplasms, retrobulbar injections) may lead to an optic nerve and central retinal artery compression. Funduscopic signs of CRAO are described. Late development of iris neovascularization and neovascular secondary glaucoma may occur in up to 15 percent of cases. The prognosis of CRAO has been poor. A spontaneous remission and recovery of visual function is rare. It has been shown experimentally that the retinal damage is irreversible after 100 minutes of non-perfusion. The initial treatment should include an immediate paracentesis of the anterior chamber, digital massage of the globe, and i.v. administration of 500 mg azetazolamide in order to stimulate retinal reperfusion by lowering the intraocular pressure. This procedure is recommended for the first 6 (up to 24) hours after onset of CRAO. More promising success rates have recently be reported by a selective intra-arterial fibrinolysis with Urokinase (100,000-1,000,000 IU) or recombinant plasminogen activator (rtPA). In a personal series of 18 cases, intra-arterial fibrinolysis with Urokinase was performed. A final visual acuity of 6/10 to 6/6 was achieved in 30 percent of the cases.