Refractory macular holes typically represent macular holes larger than 400 μm, macular holes in pathological myopic eyes or complicated with myopic schisis, chronic holes longer than 6 months, persistent macular holes after surgeries, and some subtypes of secondary macular holes. A routine pars plana vitrectomy combined with internal limiting membrane peeling yielded a lower closure rate and unsatisfying visual rehabilitation in patients with refractory macular holes, which raised concerns among vitreoretinal surgeons. This editorial reviewed the new upcoming surgical techniques which were reportedly to improve the anatomical and visual prognosis of major subtypes of refractory macular holes. Although with a great variability, these surgical techniques are based the following surgical strategies: firstly, to sufficiently unravel the epi-macular tractional force; secondly, to bridge the defect of neurosensory retina by tissue insertion or implantation and stimulate wound healing process; thirdly, proper tamponade of gas or silicone oil so that the surface tension can stabilize the inserted or implanted tissue and encourage closure of the holes. In conclusion, surgical strategies for refractory macular holes should be made after a comprehensive consideration and a customized design.
ObjectiveTo investigate the effects of limbal vitrectomy for persistent hyperplastic primary vitreous (PHPV) with disappeared anterior chamber and corneal opacity. MethodsSixteen eyes of 16 children with unilateral PHPV were included in this retrospective study. All the 16 eyes had both anterior and posterior disease, including opaque cornea, disappeared anterior chamber, pupil occlusion and extensive synechia, and lens opacity. The visual acuity was hand movement in 1 eye, and light perception in 15 eyes. There were 7 eyes with microphthalmia, 4 eyes with total retinal detachment, 3 eyes with retinal dysplasia, 1 eye with retinal folds, and 4 eyes with high intraocular pressure preoperatively. All the eyes underwent limbal vitrectomy, including dissection of synechia, pupil formation, lensectomy, posterior lens membrane peeling and vitrectomy. Four eyes with retinal detachment received long-acting gas tamponade following vitrectomy. The mean follow-up was 15.8 months (range from 9 to 21 months). ResultsNo eye had intraoperative complications. After surgery, all the 16 eyes had normal anterior chamber, round pupil and improved corneal transparency. Two eyes achieved a final visual acuity of 20/940 or better. Of the 4 eyes with retinal detachment, 3 eyes achieved retinal reattachment. Of the 4 eyes with preoperative high intraocular pressure, 3 eyes had controlled intraocular pressure postoperatively and the remaining 1 eye underwent glaucoma procedure at 6 months after the primary surgery. ConclusionPHPV eyes with disappeared anterior chamber and corneal opacity have a potential for developing better vision with improved cosmetic outcome and controlled intraocular pressure after vitrectomy by limbal approach.
Objective To investigate the histological changes of the internal limiting membrane (ILM) in pathological myopic eyes, and the relationships between those changes and the formation of macular hole.Methods The clinical data of 34 patients （34 eyes）with pathological myopia and macular hole, who had undergone vitrectomy were retrospectively analyzed. All the patients had a diopter over -6.00 D, their ocular axial length ranged from 26.00 to 33.12 mm with an average of 27.74 mm. There were 5 eyes without retinal detachment （macular hole group）while the other 29 eyes all had posterior retinal detachment（RD group）. A standard threeport pars plana vitrectomy was performed in all eyes. The existence of Weiss ring was considered as the sign of posterior vitreous detachment. The epiretinal membranes from 34 eyes and ILM specimens from 19 eyes were stained by hematoxylineosin (HE) and acetate uranyl acetatelead citrate, and then investigated under optical microscope and transmission electron microscope. Results The Weiss ring was observed in 5 eyes during the surgery, multilayer of vitreous tissue resides on the retinal surface in 24 eyes. The results of optical microscope showed that the epiretinal membranes were composed of vitreous collagen, astrocytes and extracellular matrixes. The results from transmission electron microscope showed a sandwich structure (ILMvitreous collagencells) in 5 eyes, and ILM damage, surface traction and astrocytes migration in 1 eye. Conclusions Splitting of posterior surface of vitreous and surface structure change of ILM are the major mechanisms for the formation and progression of macular holes, and even retinal detachment in high myopic eyes.
Objective To investigate the clinical manifestations and gene mutation of a pedigree with retinal lattice degeneration and granular corneal dystrophy (GCD) type 2. Methods Ten members in 3 generations of a pedigree with retinal lattice degeneration and GCD2 were included in the study, including 6 patients (3 males and 3 females) and 4 healthy family members. All members underwent visual acuity, slit lamp microscope, three-mirror lens, fundus color photography, optical coherence tomography, and corneal endothelial cells counting. Genomic DNA was extracted from peripheral venous blood (2 ml) from all the subjects and their spouses, who had no related inherited diseases. The next generation sequencing method was used to detect the mutation sites of transforming growth factor β (TGFBI), and all results underwent Sanger verification. Results Among the 12 eyes of 6 patients, the visual acuity was FC/20 cm-1.0. In the superficial central corneal stroma, snowflake-like deposits were observed in three cases (6 eyes), and a small amount of granular deposits were observed in three cases (6 eyes). Corneal endothelial cell counts were normal. Retinal lattice degeneration were observed in 3 cases, 6 eyes (including 3 cases of rhegmatogenous retinal detachment in 4 eyes); retinal thinning without obvious lattice degeneration in 4 eyes of 2 patients. Nystagmus in 1 patient and fundus examination showed no significant abnormalities. DNA sequencing results showed that the proband and 4 patients had missense mutation of TGFBI gene in exon 4 c.371G＞ A, the mutation site corresponding to the amino acid change encoded by TGFBI gene No. 124 Amino acids, from arginine to histidine (p.R124H). Patients with this mutation have varying degrees of clinical phenotype. Conclusions The mutation of c.701G＞ A (p.R124H) in TGFBI gene is the causative gene of GCD in this pedigree. The patients with this mutation have different clinical phenotypes.
Vitreous hemorrhage in children is caused by trauma or non-traumatic factors. Long-term vitreous hemorrhage not only affects children's vision, but also can lead secondary glaucoma, traumatic retinal detachment and other serious complications. Ocular trauma, some ocular and systemic diseases are the common etiology leading to vitreous hemorrhage in children. A small amount of vitreous hemorrhage can be treated by observation and conservative treatment. However, if the vitreous hemorrhage has no obvious absorption or serious complications appeared, it needs to be treated by surgery. The choice of treatment time and methods need to be further studied.