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The resident must have been directly involved in the patient care of the case being presented. The resident does not have to initiate care but must have examined the patient as a resident.
Note: Those in an accredited Fellowship program are eligible to submit to the Residents Program in their first year of Fellowship. Those in their second year should submit to the Scientific Program.
The submission window will be open from August 5, 2024 until August 19, 2024, 5:00 PM ET. Final review and scheduling decisions will be sent via email by September 6, 2024.
Due to the large number of submissions, late submissions will NOT be considered. If you have any questions or difficulty with the online abstract submission process, contact Christina Velasquez at 321-319-4865 or ChristinaV@aaoptom.org.
Each case report is required to begin with a case summary, limited to 35 words (present tense), describing the uniqueness of the case that merits presentation. The below case report fields will be available within the submission form as separate text boxes – may use bullet points for Case History, Pertinent Findings and Differential Diagnosis, but must write in complete sentences for Diagnosis Discussion, Treatment/Management Discussion, and Conclusion. Image uploads are not permitted.
I. Case History (500 character limit including spaces)
II. Pertinent Findings (800 character limit including spaces)
III. Differential Diagnosis (200 character limit including spaces)
IV. Diagnosis Discussion (1000 character limit including spaces)
Write in complete sentences to elaborate on the condition, expound on unique features, and provide rationale.
V. Treatment/Management Discussion (1000 character limit including spaces)
Write in complete sentences to discuss the treatment/management, rationale for treatment, and response to treatment.
VI. Conclusion (500 character limit including spaces)
Write in complete sentences to provide take away points and/or “clinical pearls”
VII. Bibliography (no character limit)
Follow Optometry and Vision Science guidelines for citing. Use reliable, current, and primary sources referencing landmark studies or novel literature.
Primary Hyperaldosteronism Discovered in Persistent Chronic Bilateral CSCR with Uncontrolled HTN: Novel Pathogenesis Hypothesis and Treatment
Jennifer T. Chan, O.D.
A patient with persistent bilateral CSCR and uncontrolled hypertension (HTN) underwent workup for primary hyperaldosteronism (PA). With treatment for PA, CSCR and HTN improved. PA should be considered in CSCR and HTN of unknown origin.
I. Case History
II. Pertinent findings
III. Differential diagnosis
CSCR, polypoidal choroidal vasculopathy, CSCR-associated CNVM, pachychoroid neovasculopathy, dome-shaped macula with subfoveal detachment, optic disc pit, circumscribed choroidal hemangioma, ARMD.
IV. Diagnosis Discussion
There are multiple possible etiologies and risk factors of CSCR: idiopathic, HTN, PA, cardiovascular disease, exogeneous cortisol (corticosteroid), endogenous cortisol (pregnancy, Cushing Syndrome, type A personality), sympathetic drugs, sleep apnea. The pathogenesis of CSCR involves the dilation and leakage of choroidal vessels, increased choroidal thickness, disruption of RPE tight junctions, pigment epithelial detachment (PED), and subretinal fluid accumulation. Primary aldosteronism (PA) is characterized by overproduction of aldosterone by one or both adrenal glands, which can lead to hypertension. Both adrenal corticosteroid hormones (aldosterone and cortisol) bind to mineralocorticoid receptor (MR) with similar affinity. However, in the choroid, RPE, and neurosensory retina, MR is occupied and activated mainly by aldosterone rather than cortisol. In patients with PA, high aldosterone/MR signaling may affect the choroid vascular system and play a role in pathogenesis of CSCR.
V. Treatment / Management Discussion
This patient was worked up and referred to nephrology to evaluate for primary hyperaldosteronism due to chronicity of CSCR with long history of poorly controlled hypertension on maximum anti-hypertensive medication. Preliminary clinical studies have shown MR antagonists such as eplerenone and spironolactone have a beneficial effect on CSCR, but their exact role in treatment should be further evaluated. For systemic management of PA, the nephrologist initiated spironolactone and discontinued lisinopril. At follow-up, blood pressure was improved to 133/86mmHg. Additionally, improvement in CSCR was demonstrated on examination and with OCT.
The aldosterone/mineralocorticoid receptor pathway could be involved in CSCR pathogenesis. A diagnosis of primary hyperaldosteronism should be considered in patients with CSCR and hypertension of unknown origin. Co-management with nephrology for MR antagonism treatment with eplerenone and spironolactone are beneficial for CSCR.
Click here for the Residents Program grading rubric.