Evolution of a full-thickness macular hole

Autosomal recessive polycystic kidney disease (ARPCD) is a congenital kidney disease with severe prognosis. We present a male infant who was diagnosed prenatally by ultrasonography. He died at two months of age in a septic stage. The genetic defect for ARPCD has been mapped to chromosomal region of 6p21-cen. This represents the first study from this region of the world. The linkage studies up to this date fall to show genetic heterogeneity.     

Visual acuity and macular hole size after unsuccessful macular hole closure

We have identified and characterized a novel protein from adult zebrafish retina, which we named ES1. Database search revealed that the ES1 gene has significant similarity to two genes with unknown functions: the Escherichia coli sigma cross-reacting protein 27a (scrp27a) and the human KNP-I/GT335. In situ hybridization and immunohistochemistry experiments showed that both ES1 mRNA and protein are expressed specifically in adult photoreceptor cells. ES1 seems to be a cytoplasmic protein. An ES1-like antigen was also detected in photoreceptor cells of goldfish with anti-ES1 antibodies. The retina specific expression and the evolutionary conservation suggest that ES1 protein may be important for maintaining normal retina structure and function.     

Glaucoma after macular hole surgery

OBJECTIVE: The study aimed to report incidence and to assess risk factors of postoperative glaucoma in patients with stage 3 idiopathic macular hole treated with pars plana vitrectomy, removal of posterior hyaloid membrane, and perfluoropropane gas tamponade. DESIGN: The author performed a retrospective chart review and statistical analysis of risk factors of postoperative glaucoma by using chi-square statistics, Fisher's exact test, and logistic regression. PARTICIPANTS: Forty consecutive patients with stage 3 idiopathic macular hole who were operated on between January 1994 and December 1995 were studied. INTERVENTION: A pars plana vitrectomy, removal of posterior hyaloid membrane, and 14% perfluoropropane gas tamponade were done to all patients. MAIN OUTCOME MEASURES: Preoperative and postoperative intraocular pressure measurements were performed. RESULTS: Twenty-one (52%) of 40 patients experienced transient intraocular pressure elevation to more than 30 mmHg. Nine (22%) had pressure elevation within 2 to 4 hours, 6 (15%) in 24 hours, and 6 (15%) in 1 week after surgery. Three patients, including one with a history of preoperative ocular hypertension, required extended topical antiglaucoma medication. Factors of age, race, gender, lens status, preoperative intraocular pressure (all preoperative intraocular pressure were 25 mmHg or less), and success in closure of macular hole were not to any statistically significant degree associated with postoperative pressure elevation. CONCLUSION: Glaucoma is a significant complication after stage 3 macular hole surgery even without adjunctive therapy. Usually happening within the first postoperative week, elevation of intraocular pressure in most cases is transient and can be controlled by medication. However, extended medication might become necessary in some cases.     

Natural outcome of idiopathic macular hole

To ascertain the natural outcome of idiopathic macular holes, we studied 186 eyes with the disorder: stages 1 (48 eyes), 2 (30 eyes), 3 (71 eyes), and 4 (37 eyes), which were followed for over twelve months. In 11 (23%) eyes with stage 1 lesions full-thickness macular hole developed during the follow-up period, and in 12 (25%) eyes visual acuity decreased two or more Snellen lines. Twenty-five (83%) and 21 (70%) eyes with stage 2 lesions, 39 (55%) and 22 (31%) eyes with stage 3 lesions, and 7 (19%) and 5 (14%) eyes with stage 4 lesions had enlarged macular holes and decreased visual acuity during the follow-up, respectively. The present results suggest that different stages of macular holes have different natural outcomes and the treatment should be based on their stages.     

Ultrastructures of the glial epiretinal membrane induced by activated macrophages

A rabbit model of glial epiretinal membrane was established following the injection of activated macrophages into the vitreous. The membrane was composed entirely of cells with glial characteristics, ie, abundant intermediate filaments, microvilli, junctional complexes and basement membranes. The extracellular matrix of the mature membranes contained collagen fibrils of 10 to 15 and 20 to 25 nm in diameter. Fusiform densities were seen adjacent to the cell membrane and cells with indented nuclei were found in thick membranes. These observations demonstrate that glial cells in epiretinal membranes may synthesize collagen and possess myofibroblast-like properties.     

Distribution of iatrogenic retinal breaks in macular hole surgery

BACKGROUND: Intraoperative peripheral iatrogenic retinal breaks can be a serious complication of vitreous surgery. This study was undertaken to determine whether vitreous surgical techniques used for macular hole surgery were associated with a different incidence or distribution of retinal breaks. METHODS: The authors prospectively evaluated a series of 181 consecutive eyes undergoing macular hole surgery. Contemporaneous reporting of intraoperative and postoperative retinal breaks and postoperative retinal detachments was performed. Comparison was made to historic controls of two case series of patients undergoing vitreous surgery for other indications. RESULTS: Of 181 eyes, 10 (5.5%) had 15 intraoperative retinal breaks. Of the 15 breaks, 3 (20%) were in the quadrant near the surgeon's right-hand sclerotomy, 9 (60%) were in the two inferior quadrants, and 11 (73%) were in the two temporal quadrants. By comparison to previously reported case series, tears in our series were less likely to be near the right-hand sclerotomy (P = 0.00055) and more likely to occur in the two inferior retinal quadrants (P = 0.00015) and two temporal retinal quadrants (P = 0.0042). Two patients (1.1%) of 181 had postoperative retinal detachments. CONCLUSIONS: Patients undergoing vitreous surgery for macular hole have a similar incidence but different location of iatrogenic retinal breaks when compared with patients undergoing pars plana vitrectomy for other indications. These breaks are not distributed near sclerotomy sites and tend to be in the inferior and temporal retina. This establishes the need for greater intraoperative surveillance in these areas.     

Autologous platelet concentrate as an adjunct in macular hole healing: a pilot study

PURPOSE: A pilot study was undertaken to assess the efficacy of autologous platelets in macular hole healing. PATIENTS AND METHODS: Eight eyes of eight patients with stage 3 or 4 macular holes, two of which had failed to heal after previous vitrectomy and gas tamponade, were included. The procedure consisted of pars plana vitrectomy with removal of posterior cortical vitreous, stripping of associated epimacular membranes, 15% perfluoroethane-air tamponade, and instillation of autologous platelet concentrate onto the posterior pole. Strict postoperative facedown positioning was observed for 12 days. Postoperative evaluation included visual acuity measurement, biomicroscopic macular appearance and scanning laser ophthalmoscope examination. The follow-up period ranged from 3 to 13 months (mean, 7 months). RESULTS: Of eight eyes, flattening of the surrounding retina and closure of the hole were achieved in seven (87.5%). Visual acuity improved two lines or more in four eyes (50%) Four eyes (50%) reached a postoperative visual acuity of 20/50 or more. Increased nuclear sclerosis was observed in six eyes (75%), and retinal detachment occurred in two eyes (25%). CONCLUSIONS: Autologous platelet concentrate administered peroperatively in full-thickness macular holes seems to be a safe and effective adjunct to vitrectomy with removal of posterior hyaloid and gas tamponade. A larger multicenter randomized prospective study is underway to verify these encouraging results before advocating the use of autologous platelets in macular hole surgery.     

Effect of the vitreous on the prognosis of full-thickness idiopathic macular hole

Cancer is a genetic disease; tumor cells differ from their normal progenitors by genetic alterations that affect growth-regulatory genes. There exist 2 classes of such cancer genes: the oncogenes, which function as positive growth regulators, and the tumor suppressor genes, which function as negative growth regulators. Oncogenes are widely conserved among diverse forms of life and are active in transmitting growth signals from the cell periphery to the cell nucleus. These signaling functions can be disturbed by many types of genetic change; the result of an altered growth signal is often cancer. Tumor suppressor genes have an attenuating effect on cell growth that is lost as a result of inactivating mutations or deletion of the gene; in DNA virus-transformed cells, it is abrogated by neutralization of the tumor suppressor protein through a viral gene product. Tumor suppressor genes were first recognized in inherited cancers; defects in a tumor suppressor transmitted through the germ line can lead to increased tumor incidence in the offspring. Tumor suppressors also play important roles in nonheritable cancer, however; many tumors in humans show defects in tumor suppressor genes. Most cancers harbor multiple genetic changes in oncogenes as well as tumor suppressor genes. Oncogenes induce aberrant growth through a gain in function; tumor suppressor genes contribute to oncogenesis through a loss of function. Both types of mutation work together to produce cancer; the changes are not constant but increase in number as the tumor develops from benign to more and more malignant. Cancer results from the accumulation of genetic changes. Oncogenes and tumor suppressor genes provide important insights into the regulation of cell growth. This knowledge can now be used to develop gene-specific therapies for cancer.     

Late recurrences after successful surgery for retinal detachment with macular hole

Six myopic eyes affected by retinal detachment with macular hole which had been successfully reattached developed recurrent retinal detachment 7-78 months postoperatively. The mean interval between surgery and the recurrent retinal detachment was 13.4 months in five eyes managed with gas tamponade and no choroidal irritation. In an eye managed by scleral buckling with choroidal irritation, the recurrent retinal detachment occurred 78 months postoperatively. The retina was reattached following reoperation in all eyes. However, an eye successfully reattached without choroidal irritation developed four recurrences during the follow-up period. The pathogenesis of late recurrences after successful surgery for retinal detachment with macular hole remains speculative. A number of clinical findings suggest that vitreous traction plays a decisive role.     

The role of vitreoretinal surgery in the treatment of posttraumatic macular hole

PURPOSE: Purpose of this study was to test a triple slice saturation recovery turbo FLASH sequence for myocardial perfusion imaging. In addition data-evaluation-tools for qualitative and quantitative perfusion parameters are presented and preliminary tested. MATERIAL AND METHODS: We examined 8 healthy volunteers and 4 patients with myocardial infarction. Parameters of the saturation recovery turbo FLASH sequence were as follows: TR = 2.5 msec, TE = 1.2 msec, alpha = 8 degrees, 3 slices, thickness 10 mm. For data analysis signal-intensity time curves were calculated pixel by pixel and evaluated for signal-intensity-increase over baseline and signal-intensity-upslope. Images were displayed color-coded. For quantitative data analysis we used the indicator dilution theory and developed a deconvolution algorithm which takes the arterial input function into account to calculate the myocardial mean transit time (MTT). RESULTS: The color-coded parametermaps showed uniform conditions in normal myocardium of volunteers, but reduced signal-intensity-increase over baseline and signal-intensity-upslope for infarcted areas in patients. The MTTs calculated using our algorithm were significantly shorter than those assessed with previous methods and matched better with values derived from literature. Infarcted areas show prolonged MTTs in comparison to normal myocardium. CONCLUSION: A triple slice saturation recovery turbo FLASH sequence is suitable for myocardial perfusion imaging. Color-coded parametermaps can visualize hypoperfused areas. For calculating myocardial MTTs using indicator dilution therapy a deconvolution algorithm is necessary.     

Visual field defects after macular hole surgery. A new finding

PURPOSE: The purpose of the study is to report the problem of a temporal visual field defect occurring after macular hole surgery. METHODS: The authors reviewed the records of 13 patients found to have visual field defects after vitrectomy for macular holes. Fluorescein angiograms (13 patients), optic nerve photographs (13 patients), focal electroretinograms (3 patients), and nerve fiber analyses (8 patients) were performed in patients with visual field defects. RESULTS: An absolute, temporal, usually inferior field defect was noted in 13 patients. In eight patients, the defect was detected because of specific reports or retrospective field examination results. Five patients examined in a prospective manner were found to have field defects. No history of abnormal intraocular pressure or direct trauma to the optic nerve or retinal vessels was identified. Four patients showed optic nerve pallor and three had an anomalous-appearing disc. Focal electroretinograms were of similar amplitude in the involved retina compared to corresponding areas in the healthy fellow eye. Nerve fiber analysis showed a reduction in nerve fiber layer thickness correlating to the visual field defect in those eight patients in which this test was used. CONCLUSION: A significant temporal field defect may occur in patients after otherwise uncomplicated surgery for macular holes. The cause is unclear; however, reductions in nerve fiber layer thickness from the superior and nasal peripapillary area suggest that acute surgical release of the posterior hyaloid and the use of long-acting intraocular gas may in certain patients result in visual field defects.     

Dehydration injury as a possible cause of visual field defect after pars plana vitrectomy for macular hole

PURPOSE: To present the hypothesis that a visual field defect after pars plana vitrectomy for macular hole may be caused by dehydration injury to the nerve fiber layer during the fluid-air exchange. METHODS: In a consecutive nonrandomized series of 45 operations on 35 eyes of 34 patients with full-thickness macular hole, the surgical method was changed with postoperative visual field testing performed. RESULT: The incidence and location of the post-operative visual field defect was affected only by changing the location of the infusion cannula. CONCLUSION: Dehydration injury of the nerve fiber layer during the fluid-air exchange should be considered as a possible cause of visual field defect after pars plana vitrectomy for macular hole.     

Choroidal neovascular membrane in Best's vitelliform macular dystrophy

The right eye of a 9-year-old white boy with Best's vitelliform macular dystrophy had an intact egg-yolk lesion and a retinal pigment epithelial defect superiorly, suggesting an early pseudohypopyon stage. The disruptive phase of the left eye showed subretinal hemorrhages, a "signet ring," and a subretinal neovascular membrane.     

Outpatient postoperative fluid-gas exchange after early failed vitrectomy surgery for macular hole

BACKGROUND: Vitrectomy surgery with fluid-gas exchange and prone positioning has been shown to close macular holes and improve vision. In those eyes that have failed surgery, repeat vitrectomy has been advocated. As an alternative, the authors performed an outpatient postoperative fluid-gas exchange on eyes when the macular hole failed to close after vitrectomy surgery. METHODS: The authors reviewed all cases of failed vitrectomy surgery for macular holes that underwent a postoperative fluid-gas exchange. Eyes were considered to have failed initial surgery if a rim of subretinal fluid surrounded an open full-thickness macular hole. RESULTS: Twenty-three consecutive eyes underwent outpatient fluid-gas exchange 1 week to 8 weeks after vitrectomy surgery. In 17 eyes (74%), fluid-gas exchange resulted in flattening and closure of the macular hole. In all 17 eyes, visual acuity improved 2 or more lines, with 8 (35%) of the 23 eyes achieving 20/50 or better visual acuity. CONCLUSIONS: Postoperative fluid-gas exchange may achieve successful closure of macular holes and improve vision in eyes that have failed surgery for full-thickness macular holes and should be considered as a cost-effective alternative to repeat vitrectomy.     

The role of the premacular liquefied pocket and premacular vitreous cortex in idiopathic macular hole development

PURPOSE: To clarify the role of the vitreous in idiopathic macular hole formation. METHODS: We prospectively evaluated the vitreous before and during vitreous surgery in 64 consecutive eyes of 62 patients (stage 1B, four eyes; stage 2, ten eyes; stage 3, 43 eyes; stage 4, four eyes) with macular holes; another three eyes underwent a second vitrectomy. After core vitrectomy, the premacular vitreous cortex was examined by applying gentle suction. The detached posterior hyaloid face was observed under endoilluminiation. RESULTS: We observed in all eyes a liquefied lacuna anterior to the posterior fundus before and during vitreous surgery. The premacular vitreous cortex was extremely thin and elastic upon gentle suction. A premacular ring, the diameter two to four times that of the Weiss ring, was observed in 48 of 57 eyes (84%) with stages 1B, 2, and 3 macular hole. In most cases, the vitreous cortex within the premacular ring either was absent or had a break, resulting in a premacular round defect. The vitreous cortex peripheral to the premacular ring, which was thick and less deformed, never showed a break. In eyes that had undergone a second vitrectomy, we noted residual cortex or an epiretinal membrane around the macular hole. CONCLUSIONS: The premacular vitreous cortex is extremely thin and elastic. It is sharply demarcated by a ring from the thick peripheral vitreous cortex. Tangential traction, which causes macular holes, appears to originate exclusively in the premacular vitreous cortex that forms the posterior wall of the premacular liquefied pocket.