gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

Glaucoma and episcleral venous pressure: an evidence-based survey

Meeting Abstract

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  • corresponding author J. M. Selbach - Zentrum für Augenheilkunde, Universitätsklinikum Essen, Essen
  • S. Kremmer - Zentrum für Augenheilkunde, Universitätsklinikum Essen, Essen
  • K. P. Steuhl - Zentrum für Augenheilkunde, Universitätsklinikum Essen, Essen

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogDO.14.03

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Veröffentlicht: 22. September 2004

© 2004 Selbach et al.
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The role of the episcleral vascular system for regulation of intraocular pressure is still not known. Aqueous ouflow via the conventional outflow pathway is dependent on the pressure gradient between intraocular pressure (IOP) and episcleral venous pressure (EVP). According to the Goldmann equation IOP = F/C +EVP (F aqueous humor inflow, C outflow facility). This implies that aqueous outflow may also be influenced by changes of EVP. The definite relation between EVP and IOP, however, is difficult to predict.

The episcleral vasculature shows morphological specialities that distinguish it from other vessels. There are only few capillaries, but numerous arteriovenous anastomoses and an extended network of venules with a wall containing circularly arranged muscle cells. Furthermore there is a strikingly dense vasoconstrictive and vasodilative innervation of the veins. In summary there are a lot of morphological "requisites" that may allow a regulation of this vascular network. In animal studies changes of the vascular diameter as obtained by vasoactive substances such as epinephrine or sodium nitroprusside lead to a change in IOP. Vice versa, an increase in IOP leads to significant changes of the flow in the episcleral vasculature.

An artificial elevation of EVP in human volunteers (e.g. by inverted posture) was shown to induce an elevation of IOP. However, IOP increase was only 80% of that of EVP. Vice versa, an experimental elevation of IOP in monkeys lead to a smaller but significant increase in EVP. In human eyes, an increase of EVP and parallel of IOP was described after topical application of epinephrine. EVP was also measured in patients with high tension glaucoma, but results of these studies differed significantly. In a larger study of our group in patients with normal tension and open-angle glaucoma we found a highly significant difference of EVP (as well as the ratio EVP/IOD and the difference IOD-EVP) in glaucomatous eyes as compared to healthy control eyes. These studies give further hints that regulation at the level of the episcleral vasculature is possible.

Chronic increase of IOP caused by high EVP is known to be a cause of glaucomatous optic neuropathy, e.g. in association with carotid cavernous fistula, cavernous thrombosis, Graves disease, Sturge-Weber syndrome, scleritis, etc.

However, the role of the episcleral vasculature and its specialities for regulation of IOP as well as possible therapeutic aspects are still not fully understood and require further investigation.