Methodology: Initially, we interviewed 85 patients with established glaucoma who underwent Humphrey visual field (HVF) testing and also reviewed their medical notes. We looked for documentation of their driving status, specifically whether those with bilateral visual field (VF) defects recalled being given advice about the dangers of driving and whether this was documented in the notes. After this initial audit, doctors were educated on the availability of guidelines on visual requirements for driving, and reminder adhesive labels were put on the front of medical notes of driving glaucoma patients. A follow-up audit was then performed on 95 different patients.
Results: In the initial audit, none of the patients had their driving status recorded. Only 36% of drivers with bilateral VF defects recalled being advised of the dangers of driving, with no documentation of whether the advice was given to them. Following the interventions, documentation of driving status became 86%. All drivers with bilateral VF defects recalled being advised regarding the dangers of driving, with documentation of the advice being given recorded in 73% of the medical notes.
Conclusion: Eye doctors are inadequately identifying, advising, and documenting the dangers of driving in the medical notes of glaucoma patients with bilateral VF defects. This can be improved with simple interventions, such as the education of doctors and creating reminder labels, for the benefit of our glaucoma patients.
CASE PRESENTATION: A previously healthy 31-year-old man presented with a two-week history of left eye (OS) ptosis and diplopia, following botulinum toxin injection over the masseter area for masseter hypertrophy at an aesthetic centre. He had no proptosis or facial asymmetry. Visual acuity was 6/6 in the right eye (OD) and 6/9 in the OS. There was anisocoria, with pupils measuring 3 mm in the OD and 5 mm in the OS but no relative afferent pupillary defect. OS appeared hypertropic in primary gaze with impaired intorsion. Extraocular movement of the OS was restricted in all gazes, except for laevoversion; that of the OD was normal. This was associated with diplopia in all gazes except on laevoversion. Both eyes' anterior and posterior segment examinations were otherwise unremarkable. Besides the oculomotor and trochlear nerve, the other cranial nerves and neurological examinations were normal. Investigations including blood and cerebrospinal fluid, magnetic resonance imaging and angiography of the brain, were normal. Our impression was left oculomotor and trochlear nerve neuritis secondary to botulinum toxin injection. He was started on oral prednisolone 1 mg/kg daily and tapered by 5 mg per week. His condition improved gradually with no residual ptosis or anisocoria after three months. Extraocular movements normalised except for minimal residual restriction on depression.
CONCLUSION: Oculomotor and trochlear nerve neuritis can occur following botulinum toxin injection over the masseter area. Healthcare professionals should be aware of this potential complication before offering the injection.
METHODS: This retrospective study comprised 284 right eyes. Patients aged 18 years or older with myopia up to -12.00 D and/or astigmatism up to -6.00 DC and who underwent femtosecond LASIK were recruited. Patients were divided into three subgroups: low myopia (-0.50 to -3.00 D), moderate myopia (>-3.00 to ≤-6.00 D), and high myopia (>-6.00 D), according to their pre-LASIK spherical equivalent (SE). The variables included for analysis were PCC (central 0-3.0 mm, pericentral 3.0-6.0 mm, and peripheral region 6.0-9.0 mm), PCE, PCA, internal anterior chamber depth, intraocular pressure, and central cornea thickness at the pre- and post-LASIK stages.
RESULTS: The central PCC remained unchanged across all three myopia subgroups at 1 month when compared to the pre-LASIK stage and remained stable at 6 months. The pericentral regions became flatter across all myopia subgroups at 1 month postsurgery (P < 0.001) and remained unchanged at 6 months. This trend was not seen in the peripheral cornea regions, which remained unchanged at 1 and 6 months post-LASIK when compared to pre-LASIK mean readings. There were minimal changes in post-LASIK posterior cornea astigmatism throughout follow-up. There was no incidence of post-LASIK surgery ectasia in this study population.
CONCLUSION: Post-LASIK, the different cornea subregions behaved differently. Overall, the posterior cornea surface remained stable post-LASIK across all myopia subgroups throughout follow-up.
METHODS: We investigated the ocular permeation of topical tazocin after single drop application in normal rabbit eyes by estimating piperacillin and tazobactam concentrations in cornea, aqueous, and vitreous using a validated LC-MS/MS method. Furthermore, we determined the efficacy of repeated dose administration of tazocin against experimentally induced P. aeruginosa keratitis in rabbits in comparison to moxifloxacin. To determine the efficacy, clinical examination, histopathological examination, and estimation of bacterial load and inflammatory cytokines in cornea were done.
RESULTS: Significant corneal concentration of piperacillin and tazobactam was detected in normal rabbit corneas after single dose treatment with tazocin. In rabbits with Pseudomonas-induced keratitis, topical tazocin caused significant clinical and histopathological improvement. This improvement was associated with reduction in corneal bacterial load and inflammatory cytokines. Compared to moxifloxacin 0.5%, tazocin treated group showed greater clinical response which was associated with higher interleukin (IL)-1β, lower tumor necrosis factor (TNF)-α, a comparable level of IL-8, greater reduction in corneal bacterial load, and lesser inflammatory cell infiltration.
CONCLUSION: Tazocin showed good ocular penetration and was effective in treatment of Pseudomonas induced keratitis in rabbits.