Patients who are diagnosed with SCC should be screened for their calcium and phosphorus levels, complete blood count, and complete metabolic panel (paying attention to serum calcium and potassium) as well as magnesium, phosphorus, parathyroid hormone, blood pH, and urine calcium to distinguish from underlying systemic diagnoses. © the American Society of Retina Specialists." Available at Laboratory Tests Photographer Kristin Konecki, OcuSight Eye Care Center, Rochester, NY. Ĭopyright notice: “This image was originally published on the Retina Image Bank® website. Ophthalmoscopy can be unremarkable while ultrasound shows echogenic areas indicative of calcifications (hyperechoic lesion with acoustic shadow), due to deposition in the sclera not yet reaching the choroid. Calcifications can also be detected by B-scan ultrasonography, optical coherence tomography, orbital computed tomography, fundus autofluorescence, fluorescein angiography, and indocyanine green angiography. The lesions may be arranged in a ring-like configuration. There might be atrophy of the overlying choroid and/or retinal pigment epithelium. There may be multiple lesions which, however, are typically localized near the superotemporal arcade or at the equator. The fellow eye may also have a similar and symmetrical lesion. Ophthalmoscopy is sufficient for diagnosis. A long follow-up (mean 4 years) of these cases did not show enlargement of the lesion, hemorrhage, subretinal fluid, CNVM, vision loss, or decalcification. However, a large review of 179 eyes of 118 patients did not report hemorrhage, subretinal fluid, retinal pigment epithelial detachment, or choroidal neovascular membrane (CNVM) in any case. However, there are several case reports of macular SCC associated with choroidal neovascularization or exudative retinal detachment resulting in decreased visual acuity. Patients do not typically show a change in visual acuity. Patients are often asymptomatic and do not report ocular complaints. Lesions have been classified into 4 categories depending upon contour on optical coherence tomography: ĭue to the minimal symptoms associated with SCC, the condition is often found during unrelated clinical exams. ![]() According to the literature, around half of the cases diagnosed are bilateral. Lesions usually develop postequatorially and superotemporally some have speculated that calcifications correspond to the insertion sites of the oblique extraocular muscles. The white and yellow-colored calcium deposits manifest as yellow placoid lesions in diagnostic imaging. General PathologyĬalcium deposition begins in the sclera and expands to the choroid. Metastatic presentation is seen in patients with conditions that create an atypical calcium-phosphorus metabolism. Dystrophic calcification is seen following large amounts of tissue damage and/or chronic inflammation. Idiopathic presentation is seen in patients within the primary risk groups. Primarily, the pathogenesis of the disease is idiopathic. These include hyperparathyroidism, pseudohypoparathyroidism, parathyroid adenoma, chondrocalcinosis, sarcoidosis, Gitelman syndrome, Bartter syndrome, pseudo-gout, chronic renal disease, hypophosphatemia, hypervitaminosis, and metabolic imbalance after diuretic use. Patients with previous systemic disorders that impact calcium-phosphorus metabolism are at higher risk of developing sclerochoroidal calcifications. ![]() There is a slight female predisposition (approximately 60% of cases). The majority of patients diagnosed with SCC are Caucasian and elderly. The majority of cases are idiopathic and present with normal calcium-phosphorus metabolism and without associated ophthalmic or systemic conditions. ![]() Sclerochoroidal calcification (SCC) presents as flat or minimally elevated yellow placoid lesions, sometimes associated with gray lesions that are similar in appearance to senile scleral plaque.
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