Tolentino F I, Lapus J V, Novalis G, Trempe C L, Gutow G S, Ahmad A
Int Ophthalmol Clin. 1976 Spring;16(1):13-29. doi: 10.1097/00004397-197601610-00005.
Since the number of cases for each of the conditions in our study was small, only preliminary conclusions can be made; in order to establish the fluorescein pattern of each of these peripheral retinal lesions, additional studies will be required. The following summarizes our preliminary observations. 1. Areas of retinal white-with-pressure or without and peripheral retinal cystoid degeneration did not reveal remarkable fluorescein angiographic findings. One exception was in an area of pigment epithelial disturbance characterized by atrophy and proliferation, which showed a "window and masking" effect of choroidal fluorescence. 2. Fluorescein angiography of areas of the fundus with lattice retinal degeneration showed little or no findings in early or mild cases. In severe or advanced cases, the affected retina revealed poor or absent perfusion caused by vascular occlusion. The retinal and choroidal circulation was devoid of fluorescein leakage. Advanced lesions displayed choroidal hypofluorescence in areas of pigment proliferation and hyperfluorescence in areas of pigment atrophy. 3. In advanced cases, occlusive vascular changes over areas of acquired retinoschisis were observed. There was intraretinal leakage of the dye from deep capillaries and pooling of the dye in cystic cavities near the margin of the retinoschisis. 4. There was no perfusion of the choroid and retina in the area of the hole and in the retina surrounding it. This finding suggests choroidal and retinal ischemia in the pathogenesis of a retinal hole. 5. Fluorescein angiography of retinal tears revealed fluorescein leakage along the edge of the tear and absent perfusion of the retinal flap. The retinal and choroidal circulation-around the tear was otherwise unremarkable. The choroidal fluorescein underlying the retinal flap was not visible, perhaps because it was masked by the retinal flap. 6. Our fluorescein angiographic findings in cases of rhegmatogenous retinal detachment confirmed those of others [7, 8, 10]. Transit of fluorescein through the retinal circulation was sluggish. The retinal capillaries were dilated. 7. In cases of rhegmatogenous retinal detachment which had become reattached surgically, areas treated with diathermy or cryoapplications showed absent or diminished choroidal and retinal perfusion. Leakage of the fluorescein from capillaries in the optic disc and retina in the posterior pole was sometimes persistent several months postoperatively.
由于我们研究中每种病症的病例数量较少,只能得出初步结论;为了确定这些周边视网膜病变各自的荧光素模式,还需要进行更多研究。以下总结了我们的初步观察结果。1. 视网膜受压变白区或无受压变白区以及周边视网膜囊样变性区域,荧光素血管造影未显示明显异常。一个例外是一个以萎缩和增殖为特征的色素上皮紊乱区域,显示出脉络膜荧光的“窗样和遮蔽”效应。2. 眼底格子状视网膜变性区域的荧光素血管造影在早期或轻度病例中显示很少或没有异常发现。在严重或晚期病例中,受影响的视网膜显示因血管阻塞导致灌注不良或无灌注。视网膜和脉络膜循环无荧光素渗漏。晚期病变在色素增殖区域显示脉络膜低荧光,在色素萎缩区域显示高荧光。3. 在晚期病例中,观察到后天性视网膜劈裂区域的闭塞性血管改变。染料从深部毛细血管发生视网膜内渗漏,并在视网膜劈裂边缘附近的囊腔中积聚。4. 裂孔及其周围视网膜区域的脉络膜和视网膜无灌注。这一发现提示视网膜裂孔发病机制中存在脉络膜和视网膜缺血。5. 视网膜裂孔的荧光素血管造影显示沿裂孔边缘有荧光素渗漏,视网膜瓣无灌注。裂孔周围的视网膜和脉络膜循环无明显异常。视网膜瓣下方的脉络膜荧光不可见,可能是因为被视网膜瓣遮蔽。6. 我们对孔源性视网膜脱离病例的荧光素血管造影结果证实了其他研究[7, 8, 10]的结果。荧光素通过视网膜循环的过程缓慢。视网膜毛细血管扩张。7. 在手术复位的孔源性视网膜脱离病例中,接受透热疗法或冷冻治疗的区域显示脉络膜和视网膜灌注缺失或减少。术后有时视盘和后极部视网膜的毛细血管荧光素渗漏会持续数月。