In the mouse retina, a tridimensional model of retinal microcirculation was established, showing that most microvessel connections on the arteriolar side direct the flow from the superficial to the deep layer, and vice versa on the venular side. However, the presence of direct arteriovenous connections in the superficial layer and the longer vessel length in the deep layer offer the possibility of actively modulating intraretinal flow. Compared with other capillary beds, both the capillary velocity and microhematocrit are high, a situation that favors nutrient delivery to the inner retina.
Aims: To evaluate the characterics and surgical prognosis of macular holes that develop after rhegmatogenous retinal detachment repair. Design: Retrospective, interventional, consecutive case series. Methods: The case records of nine patients who developed a new full-thickness macular hole after prior RD repair were reviewed over 6 years. Optical coherence tomography (OCT) confirmed these holes. They were offered surgical repair with a median follow-up of 13.3 months (1-63 months). Main outcomes included preoperative vitreo-macular status, OCT evaluation and postoperative visual acuity. Results: 1007 eyes underwent surgery for prior retinal detachment between August 1999 and September 2005. Nine eyes developed a full-thickness macular hole (prevalence 0.9%): five developed after scleral buckling surgery, one after pneumatic retinopexy and three after primary vitrectomy. The mean time to macular hole diagnosis after RD was 2.9 months (0.5-18). All patients underwent macular hole surgery by the same surgeon. At 1 month, macular hole repair was noticed in eight eyes. In this group, visual acuity at a median of 11.9 months of follow-up was 20/125 (20/400 -20/63). Three eyes had an improvement of more than three Snellen lines. Conclusions: Macular holes developing after RD repair is a rare complication (less than 1%). Its physiopathological mechanisms are not well known. Conventional macular hole surgery including pars plana vitrectomy, inconstant internal limiting membrane delamination and long-acting gas tamponade seems to achieve to macular reattachment (89%). The visual outcome seems conditioned by the macular status noticed during the RD.Idiopathic macular hole is a well-known macular disease. Its origin has been attributed to tangential vitreofoveal traction responsible of centrofoveal defect.1 2 These data have been confirmed by optical coherence tomography (OCT). Thus, posterior vitreous detachment seems to be a protective factor to macular hole development. However, the occurrence of rhegmatogenous retinal detachment (RD) is often secondary to posterior vitreous detachment.Macular holes are an uncommon cause of rhegmatogenous RDs but can occur secondary to a retinal detachment associated with peripheral breaks.The condition has been described after scleral buckling, 4 pneumatic retinopexy 5 6 and vitrectomy. Many surgeons have attempted closure of such macular holes, but the results of surgery have not been widely published. We describe the characteristics of nine patients with a macular hole that develops after successful rhegmatogenous retinal detachment surgery. All patients underwent surgery to close the macular hole. METHODSThe medical records of all patients who had undergone retinal detachment surgery were reviewed from August 1999 to September 2005 retrospectively (1007 eyes). Following surgery, nine eyes developed a full-thickness macular hole (0.9%) as confirmed by OCT (OCT 3, StratusH, Carl Zeiss Meditec, Dublin, CA). All patients were offered surgery repair of their macular hole.The data...
Transient occlusion of a retinal vein in rats leads to short- and long-term microvascular remodeling upstream of the occlusion site. This study describes a model for the tridimensional arrangement of retinal microvessel that accounts for the topography of the early capillary closure and collateral vessel formation that occur after BRVO. In the long term, these changes regressed incompletely, with recanalization of the occluded vein, suggesting that after a short period of occlusion, microvascular changes may become at least partially independent of flow. Despite the intrinsically limited applicability of this model to human vein occlusion, the results suggest that even if therapeutic decompression of an occluded vein is performed early, it may not reverse capillary dropout completely.
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