Acute retinal necrosis results in low vision in a young patient with a history of herpes simplex virus encephalitis

Acute retinal necrosis (ARN), secondary to herpes simplex encephalitis, is a rare syndrome that can present in healthy individuals, as well as immuno‐compromised patients. Most cases are caused by a secondary infection from the herpes virus family, with varicella zoster virus being the leading cause of this syndrome. Potential symptoms include blurry vision, floaters, ocular pain and photophobia. Ocular findings may consist of severe uveitis, retinal vasculitis, retinal necrosis, papillitis and retinal detachment. Clinical manifestations of this disease may include increased intraocular pressure, optic disc oedema, optic neuropathy and sheathed retinal arterioles. A complete work up is essential to rule out cytomegalovirus retinitis, herpes simplex encephalitis, herpes virus, syphilis, posterior uveitis and other conditions. Depending on the severity of the disease, the treatment options consist of anticoagulation therapy, cycloplegia, intravenous acyclovir, systemic steroids, prophylactic laser photocoagulation and pars plana vitrectomy with silicon oil for retinal detachment. An extensive history and clinical examination is crucial in making the correct diagnosis. Also, it is very important to be aware of low vision needs and refer the patients, if expressing any sort of functional issues with completing daily living skills, especially reading. In this article, we report one case of unilateral ARN 20 years after herpetic encephalitis.     

Monocular nystagmus with sectoral optic nerve hypoplasia in a patient with septo‐optic dysplasia

This case depicts an unusual presentation of septo‐optic dysplasia. A four‐year‐old female presented with monocular nystagmus and temporal optic disc pallor in her left eye. Despite a normal sized optic nerve head, magnetic resonance imaging (MRI) showed a hypoplastic intraorbital and intracranial left optic nerve in the absence of a septum pellucidum. She was subsequently diagnosed with septo‐optic dysplasia with sectoral optic nerve head hypoplasia.     

A medical device/drug delivery system for treatment of glaucoma

Background: The aim of this study was to investigate the uptake and release kinetics of two common glaucoma drugs delivered onto hydrogel contact lenses using analytical chemistry and to evaluate this device's ability to control intraocular pressure in a limited number of volunteers. Methods: Contact lenses were incubated in a source solution containing timolol maleate or brimonidine tartrate to determine uptake kinetics. The lenses were then immersed in fresh saline to determine release kinetics. Analysis was performed by high‐pressure liquid chromatography (HPLC). HPLC column retention times were determined for drugs released from the lens individually and under co‐elution conditions. To evaluate clinical feasibility and toxicity, three volunteers (patients being treated for glaucoma) were provided with contact lenses that had been passively impregnated with either drug. After a three‐week wash‐out period, the volunteers were instructed to wear the lenses for 30 minutes per day for two weeks. Results: HPLC analysis showed that maximum uptake and release of both drugs had occurred by approximately 60 minutes, with the slopes tending to flatten after this point. The retention time on the HPLC column was 8.08 minutes for timolol maleate and 2.16 minutes for brimonidine tartrate after incubation for one hour, with no changes after seven hours. Patient data showed that use of the lenses maintained IOP at levels equivalent to those obtained with previous treatment. No ocular toxicity was observed. Conclusion: Drugs commonly used for glaucoma treatment can be passively transferred to a hydrogel contact lens and then eluted from the polymer. Data obtained from a limited number of patients suggest that this contact lens/drug delivery system may be a feasible means of controlling IOP.     

Clinical imaging of macular pigment optical density and spatial distribution

Clinical research continues to provide an increasing number of studies that reveal an association between macular pigment optical density (MPOD) and both visual function and ocular health. As a result, there is a growing need for repeatable, accurate measures of MPOD that can describe peak optical density as well as spatial distribution. Measurement of MPOD in a research setting has an established history encompassing a number of both objective and subjective techniques. Transition of these techniques to a clinical setting has produced an array of commercial devices using three primary methods: heterochromatic flicker photometry, fundus autofluorescence and fundus reflectometry. The inherent differences among the techniques create difficulty in making direct comparisons between MPOD measurement devices. Understanding the limitations of each technique is critical in the clinical interpretation of MPOD results. Here, both the objective and subjective methods of MPOD measurement are reviewed with emphasis on the commercially available devices used in clinical settings.     

Release of xanthine oxidase to the systemic circulation during resuscitation from severe hypoxemia in newborn pigs

Xanthine oxidase may contribute to oxygen free radical formation during reoxygenation after hypoxia, but in humans the enzyme is present in substantial amounts only in the liver and intestine. We developed a sensitive assay for xanthine oxidase using ¹⁴C–xanthine as substrate and investigated whether xanthine oxidase was released into the systemic circulation when 19 newborn pigs were resuscitated after severe hypoxemia. In five piglets plasma xanthine oxidase concentrations increased from undetectable levels to a median value of 8 (range 4–18) μU/ml after 30 min of reoxygenation. In these pigs serum aspartate aminotransferase increased from 45 to 148 U/l, while alanine aminotransferase was unchanged (28–31 U/l). The release of xanthine oxidase did not seem to correlate with the severity of the histological brain damage after 4 days. We conclude that only low levels of xanthine oxidase are released to the systemic circulation after severe hypoxemia in newborn pigs.