2023-24 residents are invited to submit Grand Rounds cases for presentation as both papers and posters.
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.
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.
Submission Window: July 31 – August 15, 5:00 PM ET
Guidelines & Sample
Submission Guidelines
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 resident can submit a maximum of one case as first author.
- Each submission can have only one first author. The first author MUST attend the Academy meeting and is solely responsible for presentation of accepted abstracts.
- Application is made by submitting a complete case report outline in the online submission system. The reviewers will determine whether the presentation style will be a poster or a paper (i.e., Grand Rounds presentation). Upon acceptance, paper presenters will need to submit a PowerPoint presentation.
- It is difficult to anticipate every clinical scenario for which a resident may submit to the Academy’s Residents Program. General criteria has been established by the Residents Program Committee for reviewing submissions. Three (3) committee members will independently review each submission, and final decisions will be made by consensus of the Residents Program Committee.
- The reviewers take into account the overall quality of each submission and consider:
- Uniqueness of the case
- Complexity of the case
- Pertinent details and appropriate ancillary testing to support the case
- Overall presentation of the case including writing skills
- Adherence to Residents Program abstract criteria
- Submissions may be screened using plagiarism software (iThenticate) to detect similarity with existing publications. Submissions determined to be plagiarized or judged as having too much similarity to existing published content will be rejected with no right to appeal. Responsible authors may be subject to penalties laid out by the Ethics Committee of the American Academy of Optometry. Self-plagiarism should also be avoided as original published text from authors may be under copyright at previous journals.
- Because of the limited time between receiving Residents Program results and the annual Academy meeting, residents are strongly advised to have posters and papers prepared before receiving Residents Program results.
- Paper presentations require PowerPoint and are limited to 15 minutes. If the abstract submission is accepted as a paper presentation the final PowerPoint must be submitted in advance of the meeting.
Submission Format
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)
- Patient demographics
- Chief complaint
- Ocular, medical history
- Medications
- Other salient information
II. Pertinent Findings (800 character limit including spaces)
- Clinical (ocular and/or systemic findings)
- Ancillary Testing
- Laboratory and/or radiology studies
- Others
III. Differential Diagnosis (200 character limit including spaces)
- Primary/leading
- Others
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.
Submission Sample
Primary Hyperaldosteronism Discovered in Persistent Chronic Bilateral CSCR with Uncontrolled HTN: Novel Pathogenesis Hypothesis and Treatment
Jennifer T. Chan, O.D.
Summary
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
- 70-year-old Hispanic male
- CC: Intermittent blur OU with long history of decreased vision OD
- POH: Central serous chorioretinopathy (CSCR) OU x 2000, s/p focal laser for CNVM OU, mild bilateral floppy eyelid syndrome, dry eye OU, mild cataract OU
- PMH: hypertension, hyperlipidemia, atrioventricular block, cardiac pacemaker, aortic valve insufficiency, sleep apnea
- Meds: amlodipine, atorvastatin, metoprolol, lisinopril, aspirin
II. Pertinent findings
- Clinical
- BCVA OD 20/400 EV, OS 20/20
- DFE: mild ERM OU, large area of macular atrophy OD, hypopigmented area sup/temp with scattered pinpoint hard drusen OS, no hemes OU
- Physical
- Recent BPs (mmHg): 157/88, 166/91, 156/87
- Laboratory Testings for PA
- Blood tests ordered: CBC, random aldosterone, renin activity, renal panel
- Urine tests ordered: random osmolarity, sodium and potassium to check transtubular potassium gradient (TTKG)
- Results: plasma renin activity low <1 (0.90 ng/mL/h); Aldosterone/renin ratio > 20 Serum sodium high: 146 mEq/L; metabolic alkalosis; elevated TTKG of 5
- OCT Macula: OD diffuse retinal pigment epitheliopathy with central retinal atrophy; OS pachychoroid pigment epitheliopathy with two areas of parafoveal serous sensory detachment
- Referral: Nephrology
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.
VI. Conclusion
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.
VII. Bibliography
- Daurich A, Matet A, Dirani A, et al. Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis. Prog Retin and Eye Res 2015;48:82-118.
- van Dijk EH, Nijhoff MF, de Jong EK, et al. Central serous chorioretinopathy in primary hyperaldosteronism. Graefes Arch Clin Exp Ophthalmol 2016;254:2033-2042.
- Gong Q, Sun X-H, Yuan S-T, Liu Q-H. The relation of the serum aldosterone level and central serous chorioretinoapathy – a pilot study. Eur Rev Med Pharmacol Sci 2017;21: 446-453.
- Kline GA, Prebtani AP, Leung AA, Schiffrin EL. Primary aldosteronism: a common cause of resistant hypertension. CMAJ 2017;189: E773-E778.
- Gruszka A. Potential involvement of mineralcorticoid receptor activation in the pathogenesis of central serous chorioretinopathy: a case report. Eur Rev Med Pharmacol Sci 2013;17:1369–1373.
- Behar-Cohen F, Zhao M. Corticosteroids and the retina. Curr Opin Neurol. 2016;29:49-54.
- Daruich A, Matet A, Dirani A, et al. Oral mineralocorticoid-receptor antagonists: real-life experience in clinical subtypes of nonresolving central serous chorioretinopathy with chronic epitheliopathy. Transl Vis Sci Technol 2016;5:2.
Reviewing Guidelines
Coming Soon!
