Punctate inner choroidopathy: A review.

Punctate inner choroidopathy (PIC), an idiopathic inflammatory multifocal chorioretinopathy that predominantly affects young myopic women, appears to be relatively rare, but there are limited data to support accurate estimates of prevalence, and it is likely that the condition is underdiagnosed. The etiological relationship between PIC and other conditions within the "white dot syndromes" group remains uncertain. We, like others, would suggest that PIC and multifocal choroiditis with panuveitis represent a single disease process that is modified by host factors (including host immunoregulation) to cause the range of clinical phenotypes seen. The impact of PIC on the patient is highly variable, with outcome ranging from complete spontaneous recovery to bilateral severe sight loss. Detection and monitoring have been greatly facilitated by modern scanning techniques, especially optical coherence tomography and autofluorescence imaging and may be enhanced by coregistration of sequential images to detect change over time. Depending on the course of disease and nature of complications, appropriate treatment may range from observation to systemic immunosuppression and antiangiogenic therapies. PIC is a challenging condition where treatment has to be tailored to the patient's individual circumstances, the extent of disease, and the risk of progression.

Adjunctive use of systematic retinal thickness map analysis to monitor disease activity in punctate inner choroidopathy.

A challenge in the management of 'white dot syndromes' is the lack of sensitive objective measures of disease activity. Retinal thickness maps from spectral domain optical coherence tomography (SD-OCT) inform treatment decisions in other retinal conditions such as age-related macular degeneration and diabetic maculopathy. In this report, we demonstrate their value in providing quantitative monitoring of a patient with punctate inner choroidopathy (PIC). Retinal thickness maps referenced against a baseline scan reliably detected focal areas of increased macular volume in active PIC lesions during symptomatic episodes, highlighting these as 'hot spots' that could be quantified, providing an objective basis for treatment decisions.

Wide-field fluorescein angiography in wet age-related macular degeneration.

PURPOSE: The aim of our study was to investigate if peripheral retinal ischaemia contributed to the pathogenesis of neovascular AMD (NvAMD), using wide-field fluorescein angiography (WFFA). METHODS: This prospective study included 30 consecutive patients with newly diagnosed NvAMD in the index eye. Wide-field colour fundus images and fluorescein angiograms were obtained using P200C optomap FA and analysed using a grid with three concentric circles of 50°, 100°, and 200° centred on the fovea to define zones Z1, Z2, and Z3. RESULTS: Areas of peripheral retinal nonperfusion were seen in 2 (7%) eyes, peripheral vascular leakage in 5 (17%) eyes, and diffuse dye leakage close to the ora in 5 (17%) eyes. A total of one-third of the study eyes showed changes on WFFA in Z2 and Z3. On comparing index eyes to nonindex eyes in these patients, the presence of NvAMD was associated with peripheral FA changes (P = 0.009, Fisher's test). CONCLUSION: Frank peripheral retinal non-perfusion does not appear to be associated with NvAMD. In some patients with active NvAMD there is degradation of the peripheral blood-retina barrier. Smoking was also found to be associated with the above-mentioned abnormalities.

Value of anti-VEGF treatment in choroidal neovascularization associated with autosomal recessive bestrophinopathy.

A 26-year-old white woman presented with a 1-year history of reduced vision in both eyes, bilateral yellowish deposits in the central macula, and pale yellow retinal flecks extending to midretinal periphery. Choroidal neovascularization (CNV) was confirmed in her left eye. On optical coherence tomography, both eyes showed diffuse intraretinal cystic spaces, thickening and separation of the photoreceptor layer from the retinal pigment epithelium (RPE), subretinal fluid, and focal thickening at the level of the RPE at the fovea. A diagnosis of autosomal recessive bestrophinopathy was confirmed by electrodiagnostic and molecular genetics testing. The CNV responded well to intravitreal ranibizumab therapy, and visual acuity in the left eye improved and stabilized; however, retinoschisis due to fluctuations in intraretinal fluid persisted. This case highlights the fact that current optical coherence tomography-driven protocols used widely to treat neovascular age-related macular degeneration may not be appropriate for CNV associated with other retinal diseases.

Pituitary apoplexy following shoulder arthroplasty: a case report.

INTRODUCTION: Pituitary apoplexy following a major surgical procedure is a catastrophic event and the diagnosis can be delayed in a previously asymptomatic patient. The decision on thromboprophylaxis in shoulder replacements in the absence of definite guidelines, rests on a careful clinical judgment. CASE PRESENTATION: A previously healthy 62-year-old Caucasian male patient who underwent shoulder arthroplasty developed hyponatremia resistant to correction with saline replacement. The patient had a positive family history of deep vein thrombosis and pulmonary embolism and heparin thromboprophylaxis was considered on clinical grounds. The patient developed hyponatremia resistant to conventional treatment and later developed ocular localizing signs with oculomotor nerve palsy. The diagnosis was delayed due to other confounding factors in the immediate post-operative period. Subsequent workup confirmed a pituitary adenoma with features of pituitary insufficiency. The patient was managed successfully on conservative lines with a multidisciplinary approach. CONCLUSIONS: A high index of suspicion is required in the presence of isolated post-operative hyponatremia resistant to medical correction. A central cause, in particular pituitary adenoma, should be suspected early. Thromboprophylaxis in shoulder replacements needs careful consideration as it may be a contributory factor in precipitating this life-threatening condition.

Fatal pulmonary embolism following shoulder arthroplasty: a case report.

INTRODUCTION: Fatal pulmonary embolism following a shoulder joint replacement is a rare event. The exact prevalence of shoulder arthroplasties is not clear. Unlike hip and knee joint replacements where some form of thromboprophylaxis is routinely prescribed, no such guidelines and practice exist for shoulder replacements. Other case reports have confirmed fatal and non-fatal pulmonary embolisms following shoulder replacements, but particular risk factors were identifiable in those patients. CASE PRESENTATION: We report the case of a 73-year-old Caucasian woman with fatal pulmonary embolism secondary to a calf deep vein thrombosis following a shoulder joint replacement procedure. The patient was otherwise healthy; there were no other risk factors directly contributing to deep vein thrombosis and pulmonary embolism except for a body mass index of 34. Post-mortem examination confirmed that the patient had a thrombus in the calf and a pulmonary embolus. CONCLUSIONS: Fatal deep vein thrombosis and pulmonary embolism can occur following shoulder joint replacements in otherwise normal patients. A high degree of suspicion should therefore be maintained in susceptible individuals. Thromboprophylaxis needs careful consideration in shoulder replacements in susceptible individuals.