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130329 Static on the line: the interrupted conversation between nerve and muscle in congenital myasthenic syndromes
The congenital myasthenic syndromes are a body of inherited neuromuscular disorders caused by defects in the neuromuscular junction, posing a challenging differential with varied genotypes and phenotypes. With an incidence of 22.2 cases per million children, this condition can be easily overlooked and investigated as conditions with similar presentations, such as congenital fibrosis of extraocular muscles. Early diagnosis however, is crucial for optimal treatment given the potential systemic complications, such as respiratory distress, and potential long-term visual consequences such as amblyopia. This case series will discuss four patients with CMS and their presentation, diagnostic process, disease progression, and response to pyridostigmine.Four Slovakian patients presenting between the ages eleven months and seven years were referred into the local Ophthalmology services with poor vision and ptosis as primary complaints. On examination, all had ophthalmoplegia worse on upgaze initially which progressively involved other directions of gaze. All patients were referred to neurology for joint management and further investigations including EMG testing, anti-AChR and anti-MuSK antibodies, and genetic testing. There was an average time of presentation to genetic diagnosis of 26.5 months. On gene sequencing, all were homozygous for CHRNE, the gene accounting for over 50% of CMS cases. Of the four patients, three had partial or little improvement only in symptoms on pyridostigmine, with one not tolerating the side effects.CMS still presents diagnostic uncertainty to clinicians. An awareness of these conditions, however rare, is vital as an Ophthalmologist as they can be a first presentation to medical services via Ophthalmology.
Journal Article
Profound Vision Loss With Minimal Retinal Findings: A Case of Microvascular Ischemia Unraveled by Multimodal Imaging
An 80-year-old woman presented with sudden, profound vision loss in her left eye. Initial fundus examination showed only mild disc hyperemia, a few retinal hemorrhages, and venous dilation, findings insufficient to explain the severity of visual loss on their own. Optical coherence tomography (OCT) revealed hyperreflective bands in the inner nuclear layer consistent with paracentral acute middle maculopathy (PAMM), while en face OCT angiography demonstrated a fern-like perivenular pattern. A relative afferent pupillary defect (RAPD) was also noted at the 48-hour follow-up. Given the clinical-imaging discrepancy, fluorescein angiography, performed at the 48-hour follow-up, showed delayed arterial and venous filling, macular capillary dropout, and late optic disc leakage. Fundus autofluorescence revealed marked hypoautofluorescence in ischemic regions. Despite initial apparent anatomical resolution, vision remained poor, and the RAPD persisted. On the last follow-up, retinal atrophy had developed. Systemic evaluation identified previously undiagnosed atrial fibrillation, implicating microembolic retinal ischemia as the likely etiology. No emboli were visualized, but imaging suggested occlusion of small-caliber retinal vessels. No visual recovery was observed at follow-ups. To our knowledge, reports linking fern-like PAMM to newly discovered atrial fibrillation with this degree of vision loss are uncommon. This case underscores that profound vision loss may result from microvascular ischemia in the absence of overt fundus signs. It highlights the importance of multimodal imaging and cardiovascular assessment in unexplained acute visual loss.
Journal Article
Comparative Evaluation of Sodium Bicarbonate and Hyaluronidase as Adjuncts to Lignocaine in Peribulbar Block During Cataract Surgery
Background Peribulbar anaesthesia is widely used in cataract surgery to provide reliable analgesia, akinesia, and a low rate of complications. Hyaluronidase is conventionally added to local anaesthetic solutions to enhance diffusion and improve block quality. More recently, sodium bicarbonate has been suggested as an alternative adjunct, as its alkalinising effect increases the proportion of non-ionised lignocaine, potentially accelerating onset and improving efficacy. This study aimed to compare the effectiveness of sodium bicarbonate and hyaluronidase as adjuncts to lignocaine in peribulbar block during cataract surgery, with particular focus on pain perception, onset of anaesthesia, and onset of akinesia. Materials and methods A randomised interventional study was conducted on 80 patients undergoing cataract surgery, divided equally into two groups of 40. Group A received a mixture of lignocaine, bupivacaine, and hyaluronidase, while Group B received lignocaine, bupivacaine, and sodium bicarbonate. Pain intensity was assessed using the Visual Analogue Scale (VAS), and the onset of anaesthesia and akinesia were recorded at one-minute intervals for up to 10 minutes. Data were analysed using IBM SPSS Statistics for Windows, Version 22.0 (IBM Corp., Armonk, NY, USA), with statistical significance set at p < 0.05. Results Patients in Group B reported significantly lower pain scores (p < 0.05) and a faster onset of anaesthesia compared to Group A. In contrast, the onset of akinesia was significantly slower in Group B. Complication rates were comparable between the two groups, with no statistically significant differences observed. Conclusion The findings suggest that sodium bicarbonate is a useful adjunct to lignocaine in peribulbar anaesthesia, offering faster onset and reduced pain perception, though its effect on akinesia requires further evaluation.
Journal Article
Bilateral Cystoid Macular Edema After Light Treatment With Light-Adjustable Lens
Light-adjustable lenses (LALs) allow for visual acuity (VA) adjustment after cataract surgery, using ultraviolet (UV) light therapy. UV-induced cystoid macular edema (CME) is not well documented. We report the first case of bilateral CME after UV light therapy with LAL. An 81-year-old woman underwent uncomplicated staged bilateral cataract extraction with LAL implantation. Two days after the second UV light adjustment, she had bilateral decreased VA and a new-onset bilateral CME. UV treatments were halted, and she was started on topical nonsteroidal anti-inflammatory drug (NSAID) therapy and prednisolone. CME completely resolved within three weeks following onset. Topical NSAID and prednisone drops were continued until the completion of all light treatments, followed by a slow taper over one month. We hypothesize that UV light can contribute to CME via multiple mechanisms, including UV-activated macromer byproducts, direct UV-induced injury, or ultraviolet B (UVB) disrupting the blood-aqueous barrier. Clinicians should be aware of this complication and maintain a low threshold for deferring light therapy and initiating topical treatment.
Journal Article