ABSTRACT
PURPOSE: Intra-operative and postoperative complications of the first 50 phacoemulsifications were evaluated. The procedures were performed by one, skilled at ECCE surgeon. The phaco-chop technique was carried out in all cases with use of anterior chamber maintainer (ACM). MATERIAL AND METHODS: Eyes for surgery met the requirements: normal comea, presence of red reflex from the fundus and correct lens position. The patients were divided into 2 groups: I group--25 eyes had first surgery, II group--25 eyes had second surgery. On the first day after surgery complications and uncorrected acuity were evaluated. RESULTS: 50 eyes of 48 patients underwent operation. The mean age was 69.4 years 5% eyes had previous surgical record: 4--underwent trabeculectomy, 1--pars plana vitrectomy. The 12 intra-operative complications appeared in 10 eyes (20%): posterior capsule rupture without vitreous loss in 4% and 10% with vitreous loss, Descemet membrane detachment in 4%, iris dialysis in 2%, and persistent iris damage without sphincter disruption in 4%. The 16 postoperative complications concerned 10 eyes (20%): corneal oedema in 20%, transient intra-ocular pressure raise in 8%, hyphaema in 2%, and fibrin exudation in 2%. The majority of complications concerned the I group of eyes. The uncorrected visual acuity was 0.5 or better in 80% of eyes, on the first day after the operation. CONCLUSIONS: The use of ACM made the first steps in phacoemulsification rate during the learning course.
Subject(s)
Clinical Competence , Intraoperative Complications/etiology , Phacoemulsification/adverse effects , Phacoemulsification/education , Postoperative Complications/etiology , Aged , Female , Humans , Learning , Male , Phacoemulsification/methods , Reoperation , Treatment Outcome , Visual AcuityABSTRACT
Leber hereditary optic neuropathy (LHON), which is a relatively rare disease, is an inherited form of bilateral atrophy of optic nerves. This atrophy is related to degeneration of retinal ganglion cells and optic nerve axons. The aetiology of this disease is complex and involves primary mutations of mitochondrial DNA, as well as secondary genetic and/or epigenetic changes. We compared the clinical course of LHON in the patients with identical mitochondrial mutations. The molecular PCR-diagnosis was performed in 8 patients, representing 2 generations of the tested family. The group included 2 women suspected of being carriers and 6 men, 3 of whom were diagnosed with LHON and 3 suspected of being at risk of LHON. The primary 11,778 mtDNA mutation was diagnosed in all tested patients with one exception of the son of a male with LHON, which is in agreement with inheritance of mtDNA mutations.
