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At least 199 records · Page 11Linked to original sources

Surgical management of retinal detachment associated with the acute retinal necrosis syndrome.

We operated on nine eyes in eight patients with retinal detachment associated with acute retinal necrosis (ARN) syndrome. The patients were treated with scleral buckling, vitreoretinal surgery, or a combination of these treatments. Vitrectomised eyes underwent combinations of lensectomy, membrane dissection, scleral buckling, air-fluid exchange, endolaser photocoagulation, cryotherapy, and retinal tamponade with C3F8 gas or SF6 gas. Macular attachment was achieved in eight (89%) eyes. Vision improved in seven (78%) eyes, of which five (56%) achieved 20/200 or better vision. Three eyes that had received laser treatment posterior to areas of retinitis suffered retinal detachment despite this prophylactic treatment. Poor visual outcome resulted from viral infection of the optic nerve or macular involvement, macular hole formation, macular pucker, or hypotony.

Adolescent↗

Vitrectomy for retinal detachment associated with acute retinal necrosis.

Six patients with retinal detachment associated with the acute retinal necrosis syndrome were treated by the combination of vitrectomy, gas injection, and laser photocoagulation. The retinas were successfully reattached in each patient with one operation. Five of the patients achieved a visual acuity of 20/200 or better, and three had a visual acuity of 20/40 or better.

Adolescent↗

Postoperative posterior retinal holes after pars plana vitrectomy for primary retinal detachment.

BACKGROUND: Although retinal breaks occur frequently during vitrectomy, the postoperative occurrence of new retinal holes close to the vascular arcade after vitrectomy for rhegmatogenous retinal detachment rarely has been reported. METHODS: Three patients with rhegmatogenous, retinal detachment were treated by vitrectomy. More than 49 days after vitrectomy, posterior retinal holes with no retinal detachment occurred halfway between the vascular arcade and the chorioretinal scar around the extrusion hole or the primary retinal tear. RESULTS: These new holes were effectively managed with photocoagulation. CONCLUSION: New hole formation could be caused by the technique of the internal drainage, the contraction of the photocoagulation scar, or epiretinal membrane contraction. Another possibility is that new holes occur through two opposite tangential traction contractile forces: one induced by the contraction of the photocoagulation scar, the other caused by the contraction of the premacular cortical vitreous attached to the vascular arcade.

Aged↗

Activation of signaling pathways and stress-response genes in an experimental model of retinal detachment.

PURPOSE: Despite the high metabolic demands of the neural retina, its detachment from the retinal pigment epithelium does not lead to immediate death for most of the cells. This study was undertaken to test the hypothesis that intrinsic protective mechanisms are activated in the neural retina during early stages of retinal detachment. METHODS: Retinal detachments were created in Brown Norway rats by injection of 1% hyaluronic acid into the subretinal space. Gene expression profiles of retinas detached for 24 hours were generated with a gene microarray (rat U34 GeneChips; Affymetrix, Santa Clara, CA) and compared to the profiles from control attached retinas in a robust multiarray protocol and false-discovery-rate analysis. Changes in individual, differentially expressed genes were validated by quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Additional qRT-PCR and immunoblot analyses were performed for additional selected genes. RESULTS: Genome-wide expression profiling revealed 27 genes that are differentially expressed in retinas detached for 24 hours. In silico analysis and functional clustering suggested that most genes belonged to three signaling pathways: interleukin-6/STAT, transforming growth factor-beta/Smad, and aryl hydrocarbon receptor oxidative stress response. Additional analyses of selected genes from these pathways demonstrated a time-dependent increase in their expression in detached retinas. CONCLUSIONS: Retinal detachment results in the early activation of stress-response genes and specific signaling pathways. This adaptive response may enable the photoreceptor cells to survive the acute phase of a retinal detachment, and it is the breakdown of these protective mechanisms in chronic disease that leads to the ultimate death of the cell.

Animals↗

Retinal breaks and rhegmatogenous retinal detachment in association with branch retinal vein occlusion.

BACKGROUND AND OBJECTIVE: To report the incidence and clinical characteristics of retinal breaks and/or rhegmatogenous retinal detachment (RRD) in patients with branch retinal vein occlusion (BRVO). PATIENTS AND METHODS: We reviewed the clinical records of 230 eyes of 214 patients with BRVO and identified eyes with retinal breaks and/or RRD. Patients had at least 6 months of follow-up. RESULTS: Seven of 230 eyes (3%) had retinal breaks and 3 eyes (1.3%) had RRD. One of the eyes with RRD had subclinical retinal detachment. All 7 eyes had ischemic disease documented by fluorescein angiography. Two of 7 eyes had concurrent retinal neovascularization. Four eyes with breaks, but without RRD, and the eye with subclinical RRD were managed by argon green laser. Two eyes with RRD were managed successfully with scleral buckling surgery and postoperative supplemental argon green laser. The mean follow-up period was 14.8 +/- 8.3 months. CONCLUSIONS: Patients with BRVO should be monitored closely for possible retinal break formation and RRD development.

Aged↗

[Acute retinal necrosis. Silicon oil tamponade in retinal detachment].

BACKGROUND: Because retinal necrosis syndrome seldom occurs, we present our results of silicone oil tamponade for associated retinal detachment. PATIENTS AND METHODS: Thirteen eyes from 13 patients undergoing retinal reattachment surgery for retinal detachment associated with acute retinal necrosis in a consecutive series between January 1988 and June 1995 were followed up. Patients were 25 to 56 years of age. Four patients had acquired immune deficiency syndrome (AIDS). Five eyes that were operated on with cryopexy and scleral buckling received vitrectomy, membrane peeling, silicone oil tamponade and endolaser treatment in a second operation. Eight eyes were primarily operated on with cryopexy, encircling buckle, vitrectomy with membrane peeling, silicone oil tamponade and endolaser treatment. All patients were treated with acyclovir. RESULTS: Postoperative complete reattachment was observed in 12 eyes and persistence of a peripheral detachment in one eye. Vision improved in eight eyes, but only five eyes achieved 20/200 or better vision. Limited functional results in our series were caused by retinal ischemia, optic atrophy and macula scars. After a median of 9.3 months silicone oil was removed in nine eyes. No retinal redetachment or recurrent retinitis was observed during a follow-up time of at least 6 months. CONCLUSIONS: Vitrectomy and silicone oil tamponade allowed all cases of retinal detachment associated with acute retinal necrosis to be successfully repaired. Further studies must be conducted to find out how we can improve the visual outcome-perhaps by earlier therapy with acyclovir or earlier vitrectomy.

Acquired Immunodeficiency Syndrome↗

Smad3 is required for dedifferentiation of retinal pigment epithelium following retinal detachment in mice.

Retinal pigment epithelial (RPE) cells dedifferentiate and undergo epithelial-mesenchymal transition (EMT) following retinal detachment, playing a central role in formation of fibrous tissue on the detached retina and vitreous retraction (proliferative vitreoretinopathy (PVR)). We have developed a mouse model of subretinal fibrosis with implications for PVR in which retinal detachment is induced without direct damage to the RPE cells. Transforming growth factor-beta (TGF-beta) has long been implicated both in EMT of RPEs and the development of PVR. Using mice null for Smad3, a key signaling intermediate downstream of TGF-beta and activin receptors, we show that Smad3 is essential for EMT of RPE cells induced by retinal detachment. De novo accumulation of fibrous tissue derived from multilayered RPE cells was seen following experimental retinal detachment in eyes of wild type, but not Smad3-null mice. Expression of alpha-smooth muscle actin, a hallmark of EMT in this cell type, and extracellular matrix components, lumican and collagen VI, were also not observed in eyes of Smad3-null mice. Our data show that induction of PDGF-BB by Smad3-dependent TGF-beta signaling is likely an important secondary proliferative component of the disease process. The results suggest that blocking the Smad3 pathway might be beneficial in prevention/treatment of PVR.

Actins↗

An animal model for studying cone function in retinal detachment.

In people, retinal detachment often leads to a significant loss in cone-based vision. Most of the animal models commonly used for studying the consequences of retinal detachment have rod-dominated retinas. The purpose of this investigation was to evaluate the possibility that the ground squirrel, a rodent with a heavily cone-dominated retina, might provide a useful model for studying cone function in retinal detachment. Corneal ERGs were recorded from ground squirrels for large-field temporal modulations presented on a computer-controlled color monitor. Modulations were chosen to selectively stimulate either of the two classes of cone found in the ground squirrel retina. Under these test conditions, large and reliable cone ERGs could be readily recorded. In animals in which the retina had been surgically detached, the loss of cone signal was directly related to the number of cones in the detachment zone relative to the total cone population and that relationship did not differ for short-wavelength sensitive (S) and middle-wavelength sensitive (M) cones. Surgical reattachment produced a progressive recovery of cone-based signals. The ground squirrel seems likely to provide a useful animal model for studying the dynamics of cone function in retinal detachment and subsequent events.

Animals↗

Surgical repair of rhegmatogenous retinal detachment in immunosuppressed patients with cytomegalovirus retinitis.

The authors performed retinal reattachment surgery in 29 eyes of 24 patients with acquired immune deficiency syndrome virus with retinal detachment associated with cytomegalovirus (CMV) retinitis and documented the course of eight additional untreated eyes. Retinal detachment repair using vitrectomy, posterior hyaloid removal, and intraocular tamponade with silicone oil or SF-6 gas resulted in a total retinal reattachment rate of 76% and a macular attachment rate of 90% in one operation. The mean postoperative visual acuity (best corrected) was 20/60, but, in some patients, the visual acuity decreased because of progressive retinitis. Prophylactic laser photocoagulation of fellow eyes to surround CMV lesions did not appear to prevent retinal detachment. The mean postoperative survival was 37 weeks (range, 8 to 127 weeks). The surgical techniques used and pathophysiology of these retinal detachments are discussed.

Acquired Immunodeficiency Syndrome↗

[Diabetic tractional retinal detachment].

Diabetic tractional retinal detachment is a severe complication in diabetic retinopathy. The decision for a surgical intervention has to consider the spontaneous course of the disease, intraoperative and postoperative complications and the expected functional results. An extramacular tractional detachment can remain stable for a long time and can be observed as long as the centre of the macula is not threatened. Traction to the macula can cause oedema and reduced vision, even if the macula itself is not detached. In these cases vitreous surgery can improve vision. Retinal breaks due to tractional membranes can cause a traction-rhegmatogenous retinal detachment which is usually rapidly progressive and requires early surgery. For cases with tractional detachment of the macula there is no alternative to surgery. In cases with long-standing and complete tractional detachment with severe retinal ischaemia the functional prognosis even after anatomically successful surgery is poor and it may be better not to operate.

Diabetic Retinopathy↗

Bupivacaine anesthesia in retinal detachment surgery.

Retinal detachment surgery and other long-duration ocular procedures can be performed safely with local anesthesia, but a long-acting anesthetic is required. A randomized and masked prospective series of 126 scleral buckling procedures was undertaken to test a mixture of bupivacaine (Marcaine), lidocaine (Xylocaine), and epinephrine against lidocaine and epinephrine. The data collected show a conclusive superiority of the bupivacaine mixture in longevity of action and overall performance. Also, there was significantly less variability in the quality of anesthesia with the mixture than with lidocaine (p = .0015).

Anesthesia, Local↗

Prophylaxis of retinal detachment.

Prophylactic treatment of retinal tears, holes, and degenerations has proved very effective in a convincing series of results. Ever since prophylactic treatment became available the number of patients treated prophylactically has been growing worldwide annually. While it will never be possible to prevent all retinal detachments, no significant fall in the rate of retinal detachment has been reported. Yet this is what we expect from prophylaxis. Most patients with manifest retinal detachment have not in fact received previous prophylactic treatment for various reasons. The ophthalmologist involved in prophylaxis is confronted with large numbers of patients. Preventive treatment has to be highly selective to be practicable and safe. Only lesions presenting a definite risk of retinal detachment should be treated. The criteria for treatment must be revised from time to time. Three types of failure should be noted: (a) Retinal detachment "because of" prophylaxis, (b) Retinal detachment "in spite of" prophylaxis, (c) Retinal detachment in cases in which prophylaxis was omitted because of a "false negative diagnosis". On the other hand overtreatment and misuse, i.e. prophylactic treatment of innocuous lesions, based on "false-positive diagnosis", apparently takes place without reducing the incidence of retinal detachment but resulting in expense and stress to the patient and in some cases even in complications of treatment. It seems unlikely that we have reached the final stage in the prevention of retinal detachment. Screening techniques, selection criteria, treatment, and follow-up should be improved. Until there are fewer detachments to operate upon, much remains to be done.

Humans↗

Cystic retinal tufts and their relationship to retinal detachment.

Cystic retinal tuft, a lesion of the peripheral retina that has been described histologically, is herein described clinically and illustrated by fundus photographs. It is a congenital developmental vitreoretinal abnormality associated with firm vitreoretinal adhesions and can lead to acute tractional retinal tears at the time of an acute posterior vitreous detachment. It has been reported to be present in 5% of autopsy cases. In a consecutive series of 200 retinal detachment cases, 6.5% seemed to be causally related to cystic retinal tufts. The risk of a cystic retinal tuft leading to retinal detachment was computed to be less than 1% (range, 0.18% to 0.28%). Prophylactic treatment of cystic retinal tufts is therefore not advised.

Adult↗