Senile Retina Detachment

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It is not easy to define retinal detachment as senile. There are chorioretinal and vitreal alterations that are typically geriatric and may cause detachment of the retina:

1. Cystic degeneration of the periphery of the retina. On one hand, cystic degeneration causes a thinning and weakening of the retina, and on the other, it favors the formation of pathological adherence with the vitreo and therefore creates a predisposition to retinal rupture at the margin or at the operculum. Furthermore, the walls of the cysts may break and therefore retinal holes may form (Foulds, 1980).

2. Paved, cobblestone, or pavement degeneration as proposed by Straatsma et al. (1980) or Gonin's foci of atrophic choroidosis. From a histological point of view these lesions show the disappearance of the choriocapillaries and the pigment epithelium, atrophy of the inner layers of the retina—that is, those which depend on the trophism of the choriocapillaries for nutrition. The retina is strongly held to the choroid in these degenerative foci. They almost never form holes or ruptures of the retina. This type of degeneration does not favor the detachment of the retina per se, but shows that there is wear and choroidal and retinal degeneration at the periphery that may favor the onset of retinal detachment. In fact, O'Malley and Allen (1967) observed that numerous patients who show cobblestone degeneration also have, near to these lesions, cystic degeneration of the retina, fence degeneration, retinoschisis, retinal holes and ruptures, and cysts of the pars plana.

3. Senile degeneration of the vitreous. After 50 years of age, in emmetropic eyes, a fibrillar and lacunar degeneration of the vitreous begins, slowly progressing, and may result in the posterior detachment of the vitreous with its collapse. This is a typical senile disease that is found in 65% of individuals over 65 years old and more or less 100% of individuals over 77 years. The posterior detachment of the vitreous may cause, where there is an adherence between the vitreous and the retina, rupture of the retina by traction. The retinal rupture may be secondary to a choroidal exudation of congestive or allergic inflammatory origin, which passes the pigment epithelium, applying pressure to the retina toward the inside of the eye bulb, causing its rupture at a weak point. On contact with the choroidal exudation liquid, the vitreous then coagulates. Senile retinal detachment seems to be essentially caused by cystic degeneration of the retina and posterior detachment of the vitreous with collapse, due to the fact that in cases of senile detachment, posterior detachment of the vitreous with collapse is nearly always found. If we consider, however, the rarity of retinal detachment with respect to posterior detachment of the vitreous and cystic degeneration of the retina in senility, we must admit that many other factors must be relevant in retinal detachment such as genetic predisposition, vascular-retinal-choroidal factors, and abiotrophic factors.

The changes that lead to retinal detachment in senile eyes are very similar to those in myopic eyes. A study performed on 829 patients affected by retinal detachment and surveyed over three years found that about 34% were myopic and 66% were not. Of these, around 63% were individuals more than 40 years old. This shows therefore that senility plays an important role in the initiation of retinal detachment. Without doubt, retinal detachment results from degenerative lesions of the retina and the choroid, lesions which normally do not have characteristics appreciably different from degenerative myopic lesions. In the case of senility, the lesions are related to obstructions of the retinal and sometimes choroidal capillaries. The study of the cases in which the retinal detachment occurred in nonmyopic individuals in senile age confirms that normally in these degenerative lesions there is evidence of vascular obstruction in the form of thin obliterated blood vessels that prevail in the superior temporal quadrant. In the eyes of nonmyopic senile age subjects, it is possible to see, more frequently than in young subjects, small pigmented equatorial spots that are often hexagonal in appearance. These are often the starting point of horseshoe ruptures, on the borders of which pigment deposits are found. Finally, there can be interruptions in the continuity of the macula deriving from senile alterations. In senile degeneration of the macula, pits may form in the macular lamella, which, although not very frequent, become perforations with consequent retinal detachment. Senility, as well as favoring the arrival of regmatogenous retinal alterations, is also responsible for the degenerative vitreal changes that can produce traction, rupture, and therefore detachment of the retina (Marshall, 1987).

The influence of vascular alterations in the pathogen-esis of senile retinal detachment is without doubt to be taken into consideration. As aging causes a reduction in cardiac and lung performance, so it may cause a decrease of the retinal integrity. A parallel can be seen between the atherosclerotic lesions of the retinal blood vessels, and those of the other organs. We should remember, finally, that aphakia, not often seen these days as a result of good cataract operations, has a tight correlation with retinal detachment. It originates from small ruptures or holes in the ora serrata. In senile aphakic eyes, retinal degeneration very often is seen at the periphery and particularly at the ora serrata, with small holes generally located in the meridional folds of the retina.

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