Hesham Lakosha

Subretinal abscess due to Nocardia farcinica infection.

Purpose: Nocardia infection of the eye is uncommon. A case of choroidal abscess due to Nocardia farcinica infection is presented, and the literature is reviewed. Methods: A 41‐year‐old immunocompromised man with chronic myeloid leukemia developed a unilateral choroidal abscess. N. farcinica was isolated from a simultaneous subcutaneous abscess and both infections responded to systemic sulfonamide therapy. Results: Three weeks after discontinuation of the sulfonamides, the choroidal abscess recurred with involvement of the vitreous. The infection was brought under control after reinstitution of the same drug. Conclusions: Nocardiosis is a multisystem disease that has high mortality and ocular morbidity rates. The eyes of immunocompromised patients should be examined frequently as early detection and administration of the proper antibiotics may reduce the risk of this life‐threatening infection.

High-voltage electrical trauma to the eye

CAN J OPHTHALMOL—VOL. 44, NO. 5, 2009 605 uveal effusion syndrome inducing ciliary body rotation and narrowing of the anterior chambers, or pre-existing shallow anterior chambers, and the effusion devloped as a secondary event to the laser iridotomies. Ciliochoroidal effusion can develop following prophylactic laser iridotomy, though its mechanism is unknown. This report demonstrated the commonly misleading pseudo-melanoma presentation of uveal effusion and the value of ultrasound biomicroscopy as the investigation of choice in evaluating such a case.

Müller glia-derived PRSS56 is required to sustain ocular axial growth and prevent refractive error

A mismatch between optical power and ocular axial length results in refractive errors. Uncorrected refractive errors constitute the most common cause of vision loss and second leading cause of blindness worldwide. Although the retina is known to play a critical role in regulating ocular growth and refractive development, the precise factors and mechanisms involved are poorly defined. We have previously identified a role for the secreted serine protease PRSS56 in ocular size determination and PRSS56 variants have been implicated in the etiology of both hyperopia and myopia, highlighting its importance in refractive development. Here, we use a combination of genetic mouse models to demonstrate that Prss56 mutations leading to reduced ocular size and hyperopia act via a loss of function mechanism. Using a conditional gene targeting strategy, we show that PRSS56 derived from Müller glia contributes to ocular growth, implicating a new retinal cell type in ocular size determination. Importantly, we demonstrate that persistent activity of PRSS56 is required during distinct developmental stages spanning the pre- and post-eye opening periods to ensure optimal ocular growth. Thus, our mouse data provide evidence for the existence of a molecule contributing to both the prenatal and postnatal stages of human ocular growth. Finally, we demonstrate that genetic inactivation of Prss56 rescues axial elongation in a mouse model of myopia caused by a null mutation in Egr1. Overall, our findings identify PRSS56 as a potential therapeutic target for modulating ocular growth aimed at preventing or slowing down myopia, which is reaching epidemic proportions.

Choroidal melanoma and rhegmatogenous retinal detachment.

A 74-year-old woman was referred to the Ocular Oncology Service with retinal detachment in association with a choroidal melanoma in her left eye. Six months earlier she had noted photopsia in that eye, followed by progressive deterioration of vision. She reported that the vision in her left eye had been blurry for a long time and the cause was unclear. She had controlled hypertension. Ocular examination showed a visual acuity of 20/50 with +0.25 in the right eye and counting fingers with +0.25 in the left. The intraocular pressure, as measured by applanation tonometry, was 18 mm Hg bilaterally. There was a relative afferent pupillary defect in the left eye. Funduscopy of the left eye with the pupil dilated revealed a pigmented mass at the posterior pole measuring 10.5 mm by 6.5 mm in basal diameters. Lipofuscin pigment was visible on the surface of the lesion. An infe-

Transient myopic shift due to ciliary body detachment as the sole ocular manifestation of hypertensive emergency – A case report

Purpose Hypertensive emergency usually presents to ophthalmologists in the form of hypertensive retinopathy. We present a case of hypertensive emergency that presented as bilateral transient myopic shift due to ciliary body detachment in the absence of any retinal pathology. The purpose of this paper is to showcase another ocular manifestation of hypertensive emergency. Observations A 35 year-old female with a blood pressure of 192/114 mmHg presented to the emergency department with headache and acute onset blurry vision. Computed Tomography (CT) of the head, and lumbar puncture were within normal limits. Visual acuity was counting fingers in the right eye and 6/90 in the left eye, both of which improved to 6/9 with −5.00 diopters spherical correction in the right eye, and −4.75 diopters correction in the left eye. Intraocular pressures were normal. Anterior chambers were shallow, and there were no retinal changes on dilated fundus examination. Enhanced-depth optical coherence tomography (EDI-OCT) showed bilateral increased choroidal thickness and ultrasound biomicroscopy (UBM) showed 360° ciliary body detachment with angle closure. With improved blood pressure control, her ciliary body detachment resolved and her refractive error returned to baseline. Conclusions & Importance: Hypertensive emergency may present with choroidal thickening with anterior ciliary body rotation and detachment. A review of medications is important, as this presentation has also been reported as a rare side effect of sulphonamide drugs. In the absence of retinopathy, UBM and EDI-OCT imaging should be considered in the acutely hypertensive patient presenting with myopic shift.

Brachytherapy and anterior segment imaging in iris melanoma

A 40-year-old male presented to the ophthalmology clinic with a darkly pigmented infratemporal lesion in his right eye. The corrected visual acuity in both eyes was 6/6 and both pupils were equal and reactive. Slit lamp biomicroscopy showed a well-demarcated and heavily pigmented lesion in the peripheral iris between 6 and 8 o’clock. Ultrasound biomicroscopy (UBM) revealed a solid mass deriving from the iris stroma without ciliary body involvement, helping to classify the uveal melanoma and establishing the diagnosis of iris melanoma. Fine needle aspiration (FNA) confirmed melanoma with inactivation of the BAP1 gene. The patient was treated with brachytherapy using an I-125 plaque. Follow-up UBM, three years later, demonstrated significantly reduced dimensions of the tumour. UBM has become crucial to the differentiation of uveal melanomas from benign growths, and lesions <3 mm cannot be reliably visualised by other imaging modalities or localised to the correct uveal structure. Brachytherapy represents a safe and effective treatment option even in lesions that are BAP1 positive.