OBJECTIVE: To compare the incidence of secondary glaucoma after cataract surgery performed in infancy in children with congenital rubella syndrome (CRS) and children with non-rubella cataracts and to identify associated risk factors.
METHODS: Retrospective case control study.
METHODS: Children with CRS who had undergone cataract surgery in infancy and age matched infants who had undergone cataract surgery for infantile cataracts were included.
METHODS: Incidence of glaucoma and probability of survival was compared among the two groups. Risk factors for the development of glaucoma were assessed. The minimum follow up was 1 year after cataract surgery.
RESULTS: The study included 211 eyes of 115 children. The CRS group (cases) had 101 eyes (58 children) and the non-rubella cataract group (controls) included 110 eyes (57 children). There was no significant difference in the mean age at surgery among the two groups (p=0.96). Cumulative incidence of secondary childhood glaucoma for the entire study period of 14 years was 32.7% in the CRS group and 24.5% in the control group (p=0.19). Mean follow-up was 5.8 ± 3.7years for CRS group and 6.4± 3.4years for the non-rubella group. A significant difference in the cumulative probability of glaucoma free survival at 10 years after cataract surgery (cases 0.53 versus controls 0.8; log rank p-0.034) was present. Both groups had no significant difference in the time of onset of secondary glaucoma, average number of intraocular pressure lowering medications and number of eyes with surgical intervention for glaucoma (p>0.05). Microcornea was associated with the development of glaucoma (hazard ratio 2.83, 95% confidence interval 1.44-5.57; p=0.002) in CRS eyes.
CONCLUSIONS: There was no significant difference in the incidence of secondary glaucoma after cataract surgery performed in infants with CRS compared to infants who had undergone surgery for infantile cataracts. Since the ten year probability of glaucoma free survival was significantly less in children with CRS, a closer and longer follow up is recommended especially in eyes with at-risk features.

OBJECTIVE: Glaucoma management in pregnancy is a challenging task for the ophthalmologist. With limited studies due to ethical concerns, the exact management protocols are not well established. Surgery has been mentioned as an option in 2nd trimester and is avoided in 1st trimester due to the detrimental effect on organogenesis of fetus and the harmful effects of anaesthesia.
METHODS: A 26 year old woman with advanced glaucomatous damage underwent trabeculectomy without antifibrotic agent in first trimester of pregnancy.
RESULTS: The intraocular pressures (IOP) were well controlled during pregnancy with no need of addiitional antiglaucoma medications. She delivered a healthy baby at term with no congenital abnormality.
CONCLUSIONS: Trabeculectomy without antifibrotic agents can be done in first trimester of pregnancy in cases where IOP cannot be controlled with topical antiglaucoma drugs that are considered safe during this period. This is the first report in literature on trabeculectomy in first trimester of pregnancy.

UNASSIGNED: The dexamethasone (DEX) implant is an FDA approved treatment for diabetic macular edema, non-infectious posterior uveitis, and macular edema secondary to branch or central retinal vein occlusions. We describe a case of anterior chamber (AC) migration of a DEX implant in a patient with a history of congenital glaucoma and perform a review of the literature on this particular complication, summarizing the common risk factors, subsequent complications, and management options.
UNASSIGNED: A 46-year-old female with a history of congenital glaucoma, status post cataract extraction with insertion of intraocular lens, pars plana vitrectomy, and Baerveldt tube implant in the left eye was referred for post-operative cystoid macular edema (CME). The patient underwent insertion of a DEX implant, resulting in improvement in her CME. After the fourth implant was injected, the patient noticed a white line in her eye while looking in the mirror after doing jumping jacks. Slit lamp examination confirmed migration of the implant into the AC. Ultimately, the patient was taken to the operating room, where her implant was removed via bimanual vitrectomy through an anterior approach.
UNASSIGNED: This case report and literature review explores the ophthalmic structural changes specific to congenital glaucoma which may have predisposed this eye to anterior migration of the DEX implant. The purpose of this review is to detail the anatomic changes that may increase the risk of anterior chamber implant migration in patients with congenital glaucoma so that physicians may be aware of these risks when selecting patients for this implant.

Background: Chromosomal deletion involving the 6p25 region results in a clinically recognizable syndrome characterized by anterior eye chamber anomalies with risk of glaucoma and non-ocular malformations (6p25 deletion syndrome). We report a newborn infant case of childhood glaucoma with a combination of partial monosomy 6p25 and partial trisomy 18p11 due to an unbalanced translocation.Materials and methods: The patient was a 0-year-old girl. Both eyes showed aniridia and left eye Peters anomaly with multiple malformations. To identify the chromosomal aberrations in the patient with clinically suspected 6p25 deletion syndrome, we performed cytogenetic analysis (G-banding and multicolor fluorescent in-situ hybridization) and array-based comparative genomic hybridization (array-CGH) analysis.Results: Cytogenetic analyses revealed a derivative chromosome 6 with its distal short arm replaced by an extra copy of the short arm of chromosome 18. Array-CGH analysis detected a 4.6-Mb deletion at 6pter to 6p25.1 and 8.9-Mb duplication at 18pter to 18p11.22. To determine the breakpoint of the unbalanced rearrangement at the single-base level, we performed a long-range PCR for amplifying the junctional fragment of the translocation breakpoint. By sequencing the junctional fragment, we defined the unbalanced translocation as g.chr6:pter_4594783delinschr18:pter_8911541.Conclusions: A phenotype corresponding to combined monosomy 6p25 and trisomy 18p11 presented as childhood glaucoma associated with non-acquired (congenital) ocular anomalies consist of aniridia and Peters anomaly and other systemic malformations. To the best of our knowledge, this is the first report which demonstrated the breakpoint sequence of an unbalanced translocation in a Japanese infant with childhood glaucoma.