Retinochoroidal lesions in concussion injuries of the eyes--an experimental study
Yamana, T.
Nippon Ganka Gakkai Zasshi 90(8): 1049-1066
1986
ISSN/ISBN: 0029-0203 PMID: 3766332 Document Number: 284046
Concussional injuries of the eyes experimentally produced by a blunt trauma using a toy gun were studied in twelve rabbits with particular attention to the correlation between clinical and histopathological changes of commotio retinae, concussional necrosis and retinochoroidal rupture. Soon after the trauma, the posterior fundus showed lesion of a milky white opacity. These retinal changes were divided into commotio retinae and concussional necrosis by fluorescein fundus angiography. Clinical studies with fluorescein fundus angiography demonstrated normal appearance soon after the trauma in commotio retinae. The retinal opacification gradually faded away and disappeared one week after the trauma. In contrast to commotio retinae in concussional necrosis dye leakage at the level of the retinal pigment epithelium was seen in the opaque lesion soon after the trauma. The opaque lesion also faded away and evidenced mottled pigmentary changes with hypopigmentation or hyperpigmentation. Two weeks after the trauma, there was no longer dye leakage but hyperfluorescence was observed in the area of hypopigmentation due to window defect in the retinal pigment epithelium. In retinochoroidal rupture, subretinal hemorrhage was often observed after the trauma. The lesion was repaired with formation of subretinal proliferative tissue. Histopathological studies revealed that the milky opaque lesion in commotio retinae showed swelling of the processes of the neural elements in the nerve fiber layer, inner and outer plexiform layers, outer segments of photoreceptor cells, retinal pigment epithelium and processes of Muller cells. These changes were due to intracellular edema. The opaque lesion in commotio retinae disappeared with a decrease in intracellular edema. On the other hand, in concussional necrosis the milky white opaque lesion showed marked degenerations in all layers of the retina. Vacuolar formation was observed in the inner layers of the retina and pyknotic changes in the outer layers. Electron microscopy revealed remarkable disorganization in the lamellar disk structure of the outer segments of the photoreceptor cells and degenerative changes of the retinal pigment epithelium cells. One week after the trauma, the lesion showed disappearance of the outer segments with infiltration of macrophages in the outer layer of the retina. Two weeks after the trauma the damaged outer layer of the retina was repaired by hyperplastic Muller cells and retinal pigment epithelium. Proliferation of the Muller cells with mitosis was observed in the outer nuclear layer one month after the trauma. Seven months after the trauma the damaged retina became extremely thin showing gliosis. The retinochoroidal rupture was healed with proliferation of Muller cells, retinal pigment epithelial cells, and fibroblasts in the choroid.