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Indirect choroidal ruptures result from blunt ocular trauma and have a pathognomonic fundal appearance. We analysed a group of 30 patients with indirect choroidal ruptures with specific reference to the circumstances of the injury, the pattern of ocular damage, the cause of any visual loss, and the final visual outcome. Using this analysis we deduce a pathogenetic explanation for the characteristic fundus signs in patients with indirect choroidal ruptures. The majority of cases were young males injured during sport or by an assault, a minority were injured at work. Diffuse nonfocal impact injuries due to punches were associated with ruptures concentric with and adjacent to the optic disc. Focal impact injuries, due to projectiles, showed more extensive ocular damage. Seventeen of 30 patients regained 6/12 vision after injury. Injuries due to projectiles and temporally situated ruptures were associated with a poorer visual outcome than others. Macular damage was the commonest cause of visual loss, principally due to pigmentary maculopathy, traumatic inner retinal damage, and choroidal neovascular membranes rather than direct focal damage by the rupture.

Chorioretinal neovascular membranes are a recognised but rare cause of late visual loss in eyes suffering contusional injuries. A series of eight cases is presented all with indirect choroidal ruptures involving the perifoveal region. Two main patterns of 'at risk' rupture were noted: a temporally situated rupture passing almost directly through the fovea, and a rupture which curves inferior or superior to the optic disc stopping just short of the fovea. In six of eight cases there was only a partial thickness rupture of the choroid. These neovascular membranes may present at any time after the original injury, either early (within six months of the injury), which could be related to persistence of the normal reparative neovascular response, or late (at least one year after the injury), which are more likely to have resulted from a secondary breakdown of the outer blood-retina barrier.

A series of comparative exposures to both argon and krypton lasers have been made at 3 locations in a human retina--the fovea, the macula, and intraretinal vessels. In the fovea argon irradiations resulted in damage to both the inner and outer retinal layers as a result of absorption within the pigment epithelium and the macular pigment, while krypton exposures damaged the outer retina and the choroid. In the macula both systems resulted in damage to the outer retina, and again sufficient krypton radiation passed into the choroid to induce blood vessel occlusion, haemorrhage, and oedema. When intraretinal vessels were irradiated, only with argon was sufficient energy absorbed within the vessels to damage them or their surroundings in the inner retina. The implications of these findings are discussed in relation to the therapeutic uses of lasers.

Retinal fluorescein angiographic and visual field studies were performed on 10 patients who had developed indireect choroidal tears, these procedures being repeated at intervals until the retinal disturbances stabilised. Fluorographic investigations revealed that a transient breakdown of the choroidoretinal barrier to fluorescein dye could be detected in cases investigated within 4 days of injury, and also that the late complication of neovascularisation, producing a serous maculopathy, may resolve and good central vision be retained without recourse to photocoagulation therapy. Patients who had visual field examinations performed within a few days of trauma were noted to have dense central scotomata, but some recovery occurred in most cases, although to a variable degree. Field defects away from fixation corresponded to an extent with areas of post-traumatic pigmentary retinopathy, but in some portions of retina with normal background appearances sensitivity was also noted to be reduced. Scotomata corresponding specifically to choroidal tears or nerve fibre bundle defects were not recorded. Improvement of visual acuity may be expected, except in cases where a choroidal tear has involved the fovea or progressive choroidal neovascularisation led to permanent macular damage.