Aphakic cystoid macular edema. The pharmacology of ocular trauma.
Ocular tissues, like those of other organs, exhibit limited morphologic reactions to trauma, i.e., hyperemia, abrupt vasodilation, increased blood flow; increased permeability of blood vessels, edema and increased tissue pressure (disrupted blood-ocular barrier); and later, a cellular inflammatory response. The cystoid macular edema (CME) that occurs after surgery for cataract has a considerably higher incidence in more severely traumatized eyes. It is characterized by increased perifoveal capillary permeability that may be related either to prior vasoconstriction or to vasodilation, and it may be accompanied by a cellular inflammatory response either in the (uvea) ciliary body, vitreous, or retina, or in combination thereof. Virtually all the physiologic, metabolic, and morphologic responses to trauma can be assigned to liberation of endogenous mediators. The lesions that occur after ocular trauma may be related to the synthesis and release of prostaglandins. There is moderate support for this hypothesis, but other or additional endogenous mediators must also be considered as contributing to the production of retinal edema as a nociceptive response to trauma. The various factors that may contribute to development of CME, and their mechanisms of action, are discussed. The speculations and hypotheses contained in this review need to be confirmed or denied by applications to the eye of techniques that have been used successfully in other organ systems. Adequate prophylaxis may be provided by cyclooxygenase inhibitors, but it is more likely accomplished with corticosteroids. However, definitive clinical tests have not been done, and it should be noted that excellent surgery with minimal disruption of the blood-ocular barrier is the best prophylaxis for this iatrogenic disease. When the lesion is established and does not respond to large doses of corticosteroids, a careful study is needed to decide whether vitreous inflammation and/or strand formation accounts for the irreversibility.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001095:Arachidonic Acids / Q000378:metabolism; D001775:Blood Circulation; D002199:Capillary Permeability; D002387:Cataract Extraction; D002634:Chemotaxis, Leukocyte; D011464:Epoprostenol / Q000502:physiology; D006801:Humans; D007431:Intraoperative Complications; D008269:Macular Edema / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D010105:Oxygenases / Q000378:metabolism; D010974:Platelet Aggregation; D011448:Prostaglandin Antagonists / Q000627:therapeutic use; D011453:Prostaglandins / Q000502:physiology*; D011817:Rabbits; D012160:Retina / Q000293:injuries; D012171:Retinal Vessels; D013189:SRS-A / Q000502:physiology; D014664:Vasodilation
D000893:Anti-Inflammatory Agents; D001095:Arachidonic Acids; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D013189:SRS-A; D011464:Epoprostenol; D010105:Oxygenases