Literature DB >> 6379950

Aphakic cystoid macular edema. The pharmacology of ocular trauma.

M L Sears.   

Abstract

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.

Entities:  

Mesh:

Substances:

Year:  1984        PMID: 6379950     DOI: 10.1016/0039-6257(84)90236-4

Source DB:  PubMed          Journal:  Surv Ophthalmol        ISSN: 0039-6257            Impact factor:   6.048


  7 in total

Review 1.  The incidence, pathogenesis and treatment of cystoid macular edema following cataract surgery.

Authors:  A J Flach
Journal:  Trans Am Ophthalmol Soc       Date:  1998

2.  Immunohistochemical localization of blood-retinal barrier breakdown sites associated with post-surgical macular oedema.

Authors:  S A Vinores; A Amin; N L Derevjanik; W R Green; P A Campochiaro
Journal:  Histochem J       Date:  1994-08

3.  Longitudinal analysis of the structural pattern of pseudophakic cystoid macular edema using multimodal imaging.

Authors:  Eric J Sigler; John C Randolph; Daniel F Kiernan
Journal:  Graefes Arch Clin Exp Ophthalmol       Date:  2015-04-12       Impact factor: 3.117

Review 4.  Cellular mechanisms of blood-retinal barrier dysfunction in macular edema.

Authors:  S A Vinores; N L Derevjanik; H Ozaki; N Okamoto; P A Campochiaro
Journal:  Doc Ophthalmol       Date:  1999       Impact factor: 2.379

5.  Anti-angiogenic Therapy for Retinal Disease.

Authors:  Yannis M Paulus; Akrit Sodhi
Journal:  Handb Exp Pharmacol       Date:  2017

6.  Light-evoked arachidonic acid release in the retina: illuminance/duration dependence and the effects of quinacrine, mellitin and lithium. Light-evoked arachidonic acid release.

Authors:  H Jung; C Remé
Journal:  Graefes Arch Clin Exp Ophthalmol       Date:  1994-03       Impact factor: 3.117

7.  Inflammation-mediated retinal edema in the rabbit is inhibited by topical nepafenac.

Authors:  M A Kapin; J M Yanni; M T Brady; T J McDonough; J G Flanagan; M H Rawji; D C Dahlin; M E Sanders; D A Gamache
Journal:  Inflammation       Date:  2003-10       Impact factor: 4.092

  7 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.