A range finder can produce severe macular injury. The primary laser-tissue interaction mechanism seems to be explosive disruption of choroidal tissue. Intravitreal injection of TPA and C2F6 did not show a clear benefit to such laser lesions. A late complication can be secondary choroidal neovascularization.
The feasibility of small blood vessel occlusion by the argon laser was investigated on an animal experimental model, the vessels of the rat mesentery. Brief vascular occlusions could be achieved by producing endovascular thrombosis, mainly around altered erythrocytes. By summation of such individual effects, the duration of the occlusion could be decisively prolonged. This appears to be a way of delicately coagulating small vessels, i.e. with maintenance of vessel wall continuity.
During the last decade, five patients with laser injuries were examined at the University of Munich Eye Clinic, in addition to one laser-injury patient at the University of Erlangen Eye Clinic. From a review of these cases, it is possible to gain an insight into factors that led to the eye injuries and to predict the clinical sequelae of laser retinal injury. A possible means of treatment, using an ophthalmic Q-switched Nd:YAG laser, is suggested for some types of retinal injury involving vitreal hemorrhage.
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