Central retinal artery occlusion: a stroke of the eye.

Central retinal artery occlusion (CRAO), like a stroke in the brain, is a critical eye condition that requiring urgent medical attention. Patients with CRAO present with acute loss of vision and the visual prognosis is poor with low chance of spontaneous visual recovery. Moreover, the risk of developing ischaemic heart disease and cerebral stroke is increased due to the presence of underlying atherosclerotic risk factors. Currently, there is no officially recommended treatment for CRAO. This review will describe the anatomy, pathophysiology, clinical features of CRAO, as well as exploring existing and potential future approaches for managing the condition.

Pregnancy and the eye: What do we need to watch out for? A review.

Pregnancy causes changes in all body systems, including the eye. The eye can undergo physiological and pathological changes in pregnancy. Some changes exacerbate pre-existing eye conditions while other conditions manifest for the first-time during pregnancy. Early recognition and management are essential to prevent sight threatening complications. In addition, some obstetric complications can be associated with ophthalmic signs. Prompt recognition of these eye findings may be life saving for both the mother and the foetus. The aim of this article is to present potential ocular complications in pregnancy and outline the appropriate management to preserve sight and maintain maternal and foetal safety. The safety of the use of common ophthalmological medications will also be discussed.

A review of the management of central retinal artery occlusion.

Central retinal artery occlusion (CRAO), the ocular analog of a cerebral stroke, is an ophthalmic emergency. The visual prognosis for overall spontaneous visual recovery in CRAO is low. Furthermore, the risk of future ischemic heart disease and cerebral stroke is increased due to the underlying atherosclerotic risk factors. There is currently no guideline-endorsed treatment for CRAO. This review will describe the anatomy, pathophysiology, epidemiology, and clinical features of CRAO, and investigate the current and future management strategies.

Ophthalmic associations in pregnancy.

BACKGROUND: A range of ocular pathology exists during pregnancy. Some pre-existing eye conditions, such as diabetic retinopathy, can be exacerbated during pregnancy. Other conditions manifest for the first time during pregnancy as a result of complications such as pre-eclampsia and eclampsia. Early recognition and understanding of the management of ophthalmic conditions is crucial. OBJECTIVE: The aim of this article is to discuss the physiological and pathological changes in the eyes of pregnant women. Pathological changes are sub-divided into: 1) pre-existing eye conditions modified during pregnancy, 2) pathological conditions occurring for the first time and 3) ophthalmic associations due to complications in pregnancy. DISCUSSION: This article reviews the ophthalmic conditions that can manifest during pregnancy and discusses their pathophysiology and clinical implications. Recognition, history and examination of ophthalmic conditions and a diagnostic framework for referral are provided. Fundamental multidisciplinary care principles involving the primary care physician, ophthalmologist, rheumatologist or haematologist and obstetrician in the care of the pregnant patient are discussed.

Management of Retinal Vein Occlusion, Who Is Responsible?

Retinal vein occlusion (RVO) is a common retinal vascular occlusive disorder and is associated with a variety of systemic risk factors. The aim of this study was to investigate whether the underlying diseases were evaluated and managed appropriately by ophthalmologists. We performed a study of 1344 patients with retinal vein occlusion (RVO). Patients were evaluated with a questionnaire including ten closed questions to determine whether ophthalmologists evaluated and informed their patients about the underlying systemic diseases. None of the patients' homocysteine levels were measured. Only a small percentage of the patients were asked about the history of thrombotic diseases or family history of thrombotic diseases. We believe that most ophthalmologists are still not entirely convinced of their responsibility of managing the underlying predisposing factors of RVO. Ophthalmologists should either manage or engage other healthcare providers in the management of RVO to guarantee the patient the best care.

Cyclodialysis cleft with late hypotony maculopathy after inadvertent cannula detachment during cataract surgery.

We present the case of a 69-year-old woman who presented with hypotony several years after an inadvertent cannula detachment presumably formed a cyclodialysis cleft during phacoemulsification cataract extraction and posterior chamber intraocular lens implantation in her right eye. To our knowledge, this is the first report of late hypotony maculopathy as a result of inadvertent cannula release.

Orbital Varix Thrombosis and Review of Orbital Vascular Anomalies in Blue Rubber Bleb Nevus Syndrome.

A 57-year-old woman with cutaneous manifestations of (BRBNS) presented with acute left proptosis and venous congestion secondary to thrombosis within a superior ophthalmic vein varix. Multiple phleboliths were noted in the contralateral right orbit, and an incidental right middle cerebral artery aneurysm. Her symptoms spontaneously resolved within a few days. An English literature review found 7 reported cases of orbital vascular lesions in association with BRBNS from 1950 to 2012. All lesions showed contrast enhancement on CT or MRI: 4 had small orbital calcifications and 3 were distensible with raised venous pressure. The occurrence of a thrombosed orbital varix or cerebral artery aneurysm in BRBNS, to the best of the authors' knowledge, has not been previously reported. Although orbital vascular lesions in BRBNS have been described as hemangiomas, the biologic behavior and histology of most of the reported orbital lesions are most compatible with venous malformations.

Successful treatment of fingolimod-associated macular edema with intravitreal triamcinolone with continued fingolimod use.

The occurrence of macular edema as an adverse effect of fingolimod is well documented. Treatment modalities used to manage fingolimod-associated macular edema (FAME) have included nonsteroidal anti-inflammatory agents and sub-tenon injection. We describe two cases where intravitreal injection is used to successfully treat FAME in patients who were previously unsuccessfully treated with topical nonsteroidal anti-inflammatories.

Temporal arteritis.

Temporal or giant cell arteritis is an inflammation of medium and small extracranial vessels that may result in ocular ischemia, an aortitis followed by aortic dissection and peripheral limb ischemia. It should be considered a medical emergency due to the seriousness of end organ damage, in particular visual symptoms. While the presentation may be nonspecific, the presence of a tender temporal artery mandates a temporal artery biopsy. High-dose steroids should be begun the moment the diagnosis is considered and only withdrawn once it has been excluded. A gradual tapering of the steroid dose should occur over at least 1 year, with the consideration of the use of steroid-sparing agents if iatrogenic steroid complications occur. Careful monitoring of the response both clinically as well as with serial inflammatory markers is required.

Fingolimod and macular edema: Pathophysiology, diagnosis, and management.

Fingolimod causes macular edema (ME) by acting via the S1P3 receptor agonism, thereby reducing the tight junction between the endothelial cells of the retinal capillaries. This results in the breakdown of the inner blood retinal barrier, causing ME. Ophthalmologic evaluation including optical coherence tomography is recommended at baseline and then at 3 months, 6 months, and annually thereafter in all patients on fingolimod. The risk of ME increases in patients who are diabetic, have had uveitis, or who undergo intraocular procedures such as cataract surgery, and hence these patients need close monitoring. Cessation of the drug results in resolution of the ME. However, ME can also be treated using anti-inflammatory medication (steroids) in patients who opt to remain on fingolimod.

Three-year incidence and factors associated with posterior capsule opacification after cataract surgery: The Australian Prospective Cataract Surgery and Age-related Macular Degeneration Study.

PURPOSE: To assess 3-year incidence and associated factors of posterior capsule opacification (PCO) after phacoemulsification surgery. DESIGN: Cohort study. METHODS: A total of 1934 consecutive patients aged ≥64 years undergoing phacoemulsification surgery at Westmead Hospital were recruited, of whom 1495 (77.3%) had retroillumination anterior segment images taken of the surgical eyes after 1 month and at a further postoperative visit within 3 years. Severe PCO was defined if the view of the optic disc was obscured, or neodymium-yttrium-aluminum-garnet capsulotomy was performed. Cumulative incidence of PCO was estimated using Kaplan-Meier methods. Associations of PCO with surgeon groups and different types of implanted intraocular lenses (IOLs) were assessed, adjusting for age, sex, diabetes, and ethnicity. RESULTS: Three-year cumulative incidence of PCO was 38.5% (95% confidence interval [CI] 36.1%-40.9%) among the 1495 patients, including 4.7% (95% CI 3.5%-5.8%) with severe PCO. PCO incidence was higher in: (1) eyes operated on by junior trainees (49%) compared to those by senior ophthalmologist surgeons (36%) (adjusted odds ratio [OR] 1.6, 95% CI 1.2-2.0); and (2) eyes with hydrophobic, 3-piece (either square-edged [51%, OR 2.3, 95% CI 1.4-3.6] or partial-round-edged [39%, OR 1.5, 95% CI 1.1-2.1]), or hydrophilic IOLs (64%, OR 2.9, 95% CI 1.9-4.4) compared to those with single-piece, square-edged, hydrophobic IOLs (34%), after additional adjustment for surgeon group. CONCLUSIONS: Predominantly mild PCO occurred in one-third of eyes after phacoemulsification surgery. Possible predisposing factors associated with PCO development include surgery performed by ophthalmologic trainees and the use of hydrophilic or other hydrophobic IOLs apart from the single-piece, square-edged one.

Treatment options for central retinal artery occlusion.

OPINION STATEMENT: Central retinal artery occlusion (CRAO) is an ocular emergency and is the ocular analogue of cerebral stroke. It results in profound, usually monocular vision loss, and is associated with significant functional morbidity. The risk factors for CRAO are the same atherosclerotic risk factors as for stroke and heart disease. As such, individuals with CRAO may be at risk of ischemic end organ damage such as a cerebral stroke. Therefore, the management of CRAO is not only to restore vision, but at the same time to manage risk factors that may lead to other vascular conditions. There are a number of therapies that has been used in the treatment of CRAO in the past. These include carbogen inhalation, acetazolamide infusion, ocular massage and paracentesis, as well as various vasodilators such as intravenous glyceryl trinitrate. None of these "standard agents" have been shown to alter the natural history of disease definitively. There has been recent interest shown in the use of thrombolytic therapy, delivered either intravenously or intra-arterially by direct catheterisation of the ophthalmic artery. Whilst a number of observational series have shown that the recovery of vision can be quite dramatic, two recent randomised controlled trials have not demonstrated efficacy. On the contrary, intra-arterial delivery of thrombolytic may result in an increased risk of intracranial and systemic haemorrhage, while the intravenous use of tissue plasminogen activator (tPA) was not shown to be efficacious within 24 h of symptom onset. Nevertheless, both of these studies have shown one thing in common, and that is for treatment to be effective in CRAO, it must be deployed within a short time window, probably within 6 h of symptom onset. Therefore, while CRAO is a disease that does not have a treatment, nevertheless it needs to follow the same principles of treatment as any other vascular end organ ischaemic disease. That is, to attempt to reperfuse ischemic tissue as quickly as possible and to institute secondary prevention early.

Risk of age-related macular degeneration 3 years after cataract surgery: paired eye comparisons.

OBJECTIVE: To clarify possible associations between cataract surgery and progression of age-related macular degeneration (AMD). DESIGN: Clinic-based cohort. PARTICIPANTS: We followed cataract surgical patients aged 65+ years in the Australian Cataract Surgery and Age-related Macular Degeneration (CSAMD) study. Patients who remained unilaterally phakic for at least 24 months after recruitment were included. METHODS: We performed annual examinations with retinal photography. We assessed AMD using side-by-side grading of images from all visits. Paired comparisons between operated and nonoperated fellow eyes (defined as nonoperated or operated <12 months previously) were made using generalized estimating equation models. MAIN OUTCOME MEASURES: Incident early AMD was defined as the new appearance of soft indistinct/reticular drusen or coexisting retinal pigmentary abnormality and soft distinct drusen in eyes at risk of early AMD. Incident late AMD was defined as the new appearance of neovascular AMD or geographic atrophy (GA) in eyes at risk of late AMD. RESULTS: Among 2029 recruited, eligible participants, 1851 had cataract surgery performed at Westmead Hospital, Sydney, and 1244 (70.7%) had 36-month postoperative visits. Of these participants, 1178 had gradable photographs at baseline and at least 1 follow-up visit. Of 308 unilaterally operated participants at risk of late AMD, this developed in 4 (1.3%) operated and 7 (2.3%) nonoperated fellow eyes (odds ratio [OR], 0.74; 95% confidence interval [CI], 0.23-2.36) after adjusting for the presence of early AMD at baseline. Of 217 unilaterally operated participants at risk of early AMD, this developed in 23 (10.6%) operated and 21 (9.7%) nonoperated fellow eyes (OR, 1.07; 95% CI, 0.74-1.65). Incident retinal pigment abnormalities were more frequent in operated than nonoperated fellow eyes (15.3% vs. 9.9%; OR, 1.64; 95% CI, 1.07-2.52). There was no difference in the 3-year incidence of large soft indistinct or reticular drusen between the 2 eyes (8.8% vs. 7.9%; OR, 1.12; 95% CI, 0.79-1.60). CONCLUSIONS: Prospective follow-up data and paired eye comparisons of this older surgical cohort showed no increased risk of developing late AMD, early AMD, or soft/reticular drusen over 3 years. There was a 60% increased detection of retinal pigmentary changes in surgical eyes.