Ocular ischaemia: signs, symptoms, and clinical considerations for primary eye care practitioners.

Ischaemic stroke is a major disease burden as well as a leading cause of death. Early signs of ischaemic stroke can manifest in the eye, placing primary eyecare practitioners in an important position to identify patients at risk of ischaemic stroke and initiate suitable referral pathways. The vascular supply to the brain is reviewed with reference to vision including the various retinal signs and ocular symptoms associated with transient ischaemic attacks and ischaemic stroke. Using a range of clinical cases, the diverse clinical presentations of retinal embolic events, as well as other forms of vascular occlusion, are highlighted and the underlying pathophysiology is discussed. A succinct scheme for the assessment and management of ischaemic events for primary eye care practitioners is provided.

Axial myopic progression following phakic intraocular lens implantation.

UNLABELLED: A 45-year-old woman presented to her ophthalmologist complaining of worsening uncorrected distance visual acuity following placement of an Implantable Collamer Lens phakic intraocular lens (pIOL) approximately 10 years earlier. Prior to the pIOL surgery, contact ultrasound axial length (AL) measurements of 28.28 mm in the right eye and 27.90 mm in the left eye indicated the presence of axial myopia. At review 10 years after the initial pIOL surgery, the AL measured by partial coherence interferometry had increased to 30.25 mm and 29.22 mm, respectively, indicating a progression of the axial myopia. This case suggests that in some patients, age and recent myopic stability are insufficient criteria to conclude that the high myopia is nonprogressive. In our patient, placement of a pIOL and induction of a stable, constant, and focused foveal image were not sufficient to prevent further axial myopic progression. FINANCIAL DISCLOSURE: No author has a financial or proprietary interest in any material or method mentioned.

Cobalt-chromium toxic retinopathy case study.

PURPOSE: To report the clinical case of a 65-year-old male who developed retinal dysfunction following cobalt-chromium toxicity. METHODS: A review of the clinical, haematological, radiological and electrophysiological investigations into a single patient was performed in order to form a case report. RESULTS: A 65-year-old male presented to his ophthalmologist with a 1-year history of worsening vision on the background of a multisystem illness including motor axonopathy, pericardiomyopathy and bulbar palsy. His medical history included hypertension, hypercholesterolaemia and a metallic hip prosthesis. Ocular examination revealed significantly reduced visual acuity bilaterally along with very poor colour vision. Cornea, fundi and optic discs all appeared normal. Bilateral moderate nuclear sclerosis was noted. Basic investigations including mitochondrial studies, auto-immune screen and MRI of brain were unremarkable. Further investigations showed significantly elevated plasma cobalt and chromium levels. Electrophysiological studies revealed an abnormality in all phases of the ERG including a negative b-waveform, suggestive of inner retinal pathology. Following subsequent revision of the hip, cobalt and chromium levels decreased and the patient's vision improved. Further electrophysiological testing indicates a persistent ERG abnormality despite a significant improvement in both the patient's visual acuity and colour vision. CONCLUSIONS: These results suggest that cobalt-chromium toxicity can cause inner retinal dysfunction.