The intraocular changes of anterior segment necrosis.
Anterior segment necrosis is an acute or chronic process occasioned by embarrassment of the blood supply of the anterior segment of the eye. In the acute form this vascular obstruction leads to severe corneal oedema, necrosis of anterior uvea, hypotony and cataract formation. Depression of aqueous humour formation accounts for severe reduction of glucose levels in corneal stroma and aqueous humour lasting for two days after cautery of the long posterior ciliary arteries (LPCA) in rabbits. Lactate levels are initially significantly elevated but return to normal after one week. Stromal hydration was elevated for one week but then returned to normal. Corneal epithelial glycogen was diminished at one and two days after surgery but then returned to normal. Although unproven, oxygen deprivation probably plays a major role in endothelial ischaemia and therefore corneal oedema. It is concluded that the abnormalities seen in anterior segment necrosis stem from changes in aqueous metabolic components resulting from severely reduced aqueous turnover. Hyperbaric oxygen and intracameral metabolite substitution are unproven treatments but merit further experimental study.
Pfister
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Research Laboratories, Brookwood Medical Center, Birmingham, Alabama 35209.
D000818:Animals; D000869:Anterior Eye Segment / Q000098:blood supply / Q000473:pathology*; D001082:Aqueous Humor / Q000378:metabolism; D002924:Ciliary Body / Q000473:pathology; D003315:Cornea / Q000378:metabolism; D004728:Endothelium, Corneal / Q000473:pathology; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007429:Intraocular Pressure; D007773:Lactates / Q000378:metabolism; D009336:Necrosis; D010101:Oxygen Consumption; D011817:Rabbits
D007773:Lactates; D005947:Glucose