Ethnic Differences in the Rates of Posterior Capsule Rupture and Long-Term Sequelae in Phacoemulsification Cataract Surgery.

Purpose The purpose of this study is to investigate the rates of posterior capsular rupture (PCR) and its sequelae during phacoemulsification across different ethnicities. Methods This is a retrospective cohort study of all consecutive phacoemulsification cases complicated by PCR that met the inclusion criteria over a four-year period at a single tertiary eye centre in the United Kingdom (UK). Results PCR occurred in 0.85% of cases overall (157/18,481). PCR rates were 1.8% (26/1485), 1.2% (51/4350), and 0.7% (75/10,927) in African-Caribbean, Indian subcontinent, and Caucasian patients, respectively (p < 0.001). Mean final corrected distance visual acuity improved (p < 0.05) in all ethnic groups (0.40 ± 0.57 logMAR) compared to pre-op (0.78 ± 0.61 logMAR). Post-operative cystoid macular oedema and unstable intraocular pressure rates following PCR did not statistically differ amongst ethnicities (p = 0.37 and p = 0.75, respectively). However, post-operative uveitis rates significantly differed at 11.5%, 15.7%, and 1.3% amongst the three ethnic groups, respectively (p = 0.01). Conclusion This is the first study to highlight a possible link between patient ethnicity and the risk of PCR during phacoemulsification cataract surgery. We observed significantly greater numbers of PCR cases amongst certain ethnic groups (highest in African-Caribbean eyes, then Indian subcontinental eyes, and lowest in Caucasian eyes) within the same multi-cultural urban population. Ethnicity may therefore be a contributing factor for PCR and should potentially be taken into consideration during preoperative risk stratification.

Association Between Keratoconus and Shoulder Dislocation: A Cross-Sectional Study.

Introduction Few studies have highlighted the correlation between shoulder dislocation and keratoconus (KC). This study aimed to examine the association between KC and shoulder dislocation using patients with KC and matched controls. Methods This cross-sectional study was conducted at Jordan University Hospital. We included patients diagnosed with KC from Jordan University Hospital's Ophthalmology Department between 2015 and 2018. We also included age- and sex-matched controls recruited randomly from fitness centers and shopping malls. All participants had complete ophthalmic and orthopedic assessments. KC was diagnosed by clinical examination followed by Pentacam (Scheimpflug Images, Oculyzer, WaveLight, Alcon, USA) confirmation. Results A total of 238 patients, with a mean age of 29.53 (±11.20) years, were included in this study. They were 144 (60.5%) men and 94 (39.5%) women. Moreover, 120 (50.4%) had KC while 118 (49.6%) did not have KC. Only 11 (4.6%) patients had previous shoulder dislocation. We did not find a significant difference in the frequency of shoulder dislocation between patients with and without KC (p = 0.512). Conclusion This study provides further evidence on the lack of association between shoulder dislocation and KC, an association that was presumed due to shared collagen characteristics.

Corneal neovascularization: updates on pathophysiology, investigations & management.

Objective. Corneal neovascularization is a sight-threatening condition affecting more than 1.4 million people per year. Left untreated, it can lead to tissue scarring, oedema, lipid deposition, and persistent inflammation that may significantly affect visual prognosis and quality of life. The aim was to review the recent evidence relating to the pathophysiology, investigations and management of corneal neovascularization. Methods. Literature review of prospective and retrospective studies, clinical trials and animal models relating to the pathophysiology, investigation and management of corneal neovascularization. Results. Corneal neovascularization is characterized by the invasion of new blood vessels into the cornea caused by an imbalance between angiogenic and antiangiogenic factors that preserve corneal transparency as a result of various ocular insults and hypoxic injuries. Risk factors that have been implicated in the pathogenesis of the disease include contact lens wear, ocular surface disease, trauma, previous surgery and herpes. The results highlighted the current and future management modalities of corneal neovascularization, which includes corneal transplantation, laser - phototherapy, injections and topical treatment. Conclusion. The future of corneal neovascularization is promising and this paper discusses the upcoming revolution in local gene therapy. Abbreviations. HSK = herpes stromal keratitis, VEGF = vascular endothelial growth factor, VEGFR-1 = VEGF Receptor-1, FGF = Fibroblast growth factor, PDGF = Platelet-derived growth factor, IL-6 = interleukin-6, IL-7 = interleukin-7, IL-8 = interleukin-8, IRS-1 = insulin receptor substrate-1.

Long term efficacy and stability of corneal collagen cross linking for post-LASIK ectasia: an average of 80mo follow-up.

This study was designed to evaluate efficacy and stability of corneal collagen crosslinking (CXL) in halting the progression of post-laser in situ keratomileusis (LASIK) ectasia and provide long-term follow-up results with an average of 80mo. Patients with post-LASIK ectasia were treated with CXL between December 2007 and January 2012. Main outcome measures were uncorrected distance visual acuities (UDVA) and corrected distance visual acuities (CDVA), minimum and maximum keratometry (K) values, spherical and cylindrical refraction, and corneal thickness. The study evaluated 17 eyes for 13 patients (8 men, 5 women) with mean age of 31y (range 23 to 39) and mean follow-up of 80.7±15 (range 57 to 102)mo. UDVA and CDVA improved from logMAR 0.53±0.36 (20/63) to 0.49±0.4 (20/50) (P=0.43) and from 0.18±0.17 (20/28) to 0.16±0.16 (20/27) (P=0.55) respectively. In 15 eyes UDVA and in 13 eyes CDVA either remained stable or improved ≥1 Snellen lines (88.2%) and (76.5%) respectively. Although statistically insignificant, spherical and cylindrical refraction decreased post-CXL from -1.26±2.87 to -0.38±2.32 diopters (D) (P=0.054) and from -3.80±2.47 to -3.04±2.18 D (P=0.13) respectively. Kmax significantly decreased from 44.23±3.76 to 42.85±3.08 D (P=0.013) and Kmin decreased from 41.07±3.61 to 40.00±2.65 D (P=0.057). Corneal thickness decreased from 470±42 to 460±41 µm, but was statistically non-significant (P=0.063). Therefore, CXL is effective in halting and partially reversing the progression of post-LASIK ectasia on the long-term (mean follow-up of more than 80mo), thus highlighting the stability and maintained effect of CXL for such cases.

Leber's congenital amaurosis and the role of gene therapy in congenital retinal disorders.

Leber's congenital amaurosis (LCA) and recent gene therapy advancement for treating inherited retinopathies were extensive literature reviewed using MEDLINE, PubMed and EMBASE. Adeno-associated viral vectors were the most utilised vectors for ocular gene therapy. Cone photoreceptor cells might use an alternate pathway which was not reliant of the retinal pigment epithelium (RPE) derived retinoid isomerohydrolase (RPE65) to access the 11-cis retinal dehydechromophore. Research efforts dedicated on the progression of a gene-based therapy for the treatment of LCA2. Such gene therapy approaches were extremely successful in canine, porcine and rodent LCA2 models. The recombinant AAV2.hRPE65v2 adeno-associated vector contained the RPE65 cDNA and was replication deficient. Its in vitro injection in target cells induced RPE65 protein production. The gene therapy trials that were so far conducted for inherited retinopathies have generated promising results. Phase I clinical trials to cure LCA and choroideremia demonstrated that adeno-associated viral vectors containing RPE genes and photoreceptors respectively, could be successfully administered to inherited retinopathy patients. A phase III trial is presently ongoing and if successful, it will lead the way to additional gene therapy attempts to cure monogenic, inherited retinopathies.

Nonarteritic anterior ischemic optic neuropathy associated with interferon and ribavirin in a patient with hepatitis C.

PURPOSE: To report a case of a temporal artery biopsy negative anterior ischemic optic neuropathy associated with a recently completed course of pegylated interferon 2 α with ribavirin for chronic hepatitis C. OBSERVATIONS: Despite the early presentation with symptoms and prompt treatment with systemic intravenous steroids the patient experienced deterioration of their optic neuropathy over the following few days. Although nonarteritic anterior ischemic optic neuropathy is a common disorder with known risk factors, the timing of onset of symptoms in our patient was suggestive of a possible etiology related to treatment with ribavirin and interferon 2 α, as found in the previously reported cases. CONCLUSIONS AND IMPORTANCE: There have been a few reported cases of the association between the use of interferon/ribavirin for treatment of chronic hepatitis with nonarteritic anterior ischemic optic neuropathy. In these cases stopping the drug caused some improvement of symptoms or halting the progression of optic neuropathy. Having reviewed the literature on previous cases, we postulate that there may be a dose related reaction to explain the delay and deterioration of vision in some cases despite stopping the drugs. We also advise that any person who is started on this treatment for chronic hepatitis are appropriately counselled as to the potential optic nerve side effect of the drug, based on the evidence reported in the literature.

A patient on long-term proton pump inhibitors develops sudden seizures and encephalopathy: an unusual presentation of hypomagnesaemia.

Objective. To present an unusual but known cause of hypomagnesaemia induced-hypocalcaemia in a chronic GORD patient with severe symptoms with a review of the current literature. Methods. Analysis of the clinical and laboratory findings of the patient and discussion of the multi-factorial nature of his disease and the underlying mechanisms. Results. Our patient described features of magnesium deficiency such as weakness, muscle twitches, and fits with clinical signs of hypocalcaemia: a carpal pedal spasm and paraesthesia. Preadmission blood results revealed low calcium and magnesium levels. He was admitted to ITU, when he presented with seizures and developed encephalopathy. The total vitamin D level was 52.4 nmol/L (>49.9). His U&Es and LFTs were within the normal range with the exception of potassium. He was on Omeprazole for his GORD. With omission of the PPI 1 day after admission and replacement therapy, his ion levels normalised. Conclusion. Hypomagnesaemia is often undiagnosed and is associated with multiple biochemical abnormalities. Treatment focus should be aimed at stopping the PPI and replacing the magnesium. Over use of PPIs is a problem in practice, with the FDA issuing a warning over long-term use. Continued monitoring and decision making on dose reduction/withdrawal is essential to avoid complications.