On this episode of Ready, Set, Retina, Daniel Epshtein, OD, FAAO, is joined by Jay M. Haynie, OD, FAAO, FORS, to review a case report of central serous chorioretinopathy (CSCR) secondary to testosterone use.
Dr. Haynie practices at Sound Retina in Tacoma, Washington, and is an adjunct assistant clinical professor at the Pacific University College of Optometry.
Overview of central serous chorioretinopathy
CSCR is a retinal disorder characterized by localized serous retinal detachment of the macula secondary to retinal pigment epithelium (RPE) decompensation and choroidal vascular changes.1 While most acute cases resolve spontaneously and patients regain normal vision, in chronic cases, intervention is required to prevent permanent vision loss.
Recurrence happens in around 31% of CSCR patients, although the rate has been identified as being as high as 50% in some studies.2 Typically, CSCR occurs in males aged 20 to 45 years, and patients tend to complain of central vision loss or distortion.2
Of note, CSCR is the fourth most common retinopathy after age-related macular degeneration, diabetic retinopathy, and branch retinal vein occlusion.3
Central serous chorioretinopathy case report
Case presentation
A 38-year-old white male patient was referred to the clinic with a 1-month history of central distortion and blurred vision in the left eye. He reported that this was the first episode of visual symptoms in his life. The patient’s medical history was remarkable for anxiety and low serum testosterone, for which he was being treated with bupropion and weekly testosterone injections.
The patient’s best-corrected visual acuity (BCVA) was 20/20 in the right eye (OD) and 20/20- in the left eye (OS). Dr. Haynie explained that based on his clinical experience treating CSCR patients, their Snellen acuity is often quite good, but patients tend to fear that they are going blind due to their visual symptoms, including metamorphopsia.
Retinal imaging at baseline
Figure 1: Color fundus photography (CFP) captured at the initial visit; a localized serous retinal detachment and sheen from the internal limiting membrane can be visualized; there is no evidence of hemorrhage, lipid, or pigmentary changes, and the retinal vasculature appears healthy.
Figure 1: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Figure 2: Optical coherence tomography (OCT) imaging OS taken at the initial visit; an area of subretinal fluid defining the focal neurosensory retinal detachment can be seen;4 additionally, the choroid appears thickened, which by definition places CSCR on the pachychoroid spectrum.1 Dr. Haynie emphasized the importance of paying attention to choroidal thickness in retinal imaging, as it has been implicated in various retinal and choroidal diseases.5
Figure 2: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Management of CSCR
Based on the findings from the retinal imaging, Dr. Haynie diagnosed the patient with CSCR, and he reviewed several of the common risk factors for CSCR, such as:1
- Exposure to corticosteroids
- Unaddressed stress or anxiety disorders in chronic cases
- Testosterone usage
- Sleep apnea in recurrent cases (61% incidence)6
- High caffeine consumption
He added that while patients are likely anxious about the visual symptoms, CSCR is often a self-limiting disease, and most patients recover vision over the course of 2 to 3 months.7
In chronic cases, or for patients who seek faster resolution of visual symptoms, CSCR therapies may include:2
- Topical dorzolamide 2% BID
- Oral acetazolamide 250mg PO qhs
- Eplerenone 50mg PO qAM
- Rifampicin 300/600mg daily
- Argon laser photocoagulation
- Photodynamic therapy
- Anti-vascular endothelial growth factor (VEGF)
Dr. Haynie remarked that he usually starts CSCR patients on acetazolamide, topical dorzolamide, or eplerenone (which is a medication similar to spironolactone). He added that rifampicin, an antimicrobial tuberculosis drug, has gained some momentum as an alternative treatment due to its effect on serum cortisol and low cost.8
For patients who do not respond to medical management, focal laser photocoagulation (if the lesion is extrafoveal) and half-fluence photodynamic therapy can work well to resolve the fluid accumulation, noted Dr. Haynie.9 He opts to reserve anti-VEGF injections for patients with secondary choroidal neovascular membranes (CNVMs), which can occur in patients with chronic CSCR.10
Dr. Haynie discussed with the patient how the testosterone injections may be connected to his visual symptoms. He added that, anecdotally, he has found that many patients with low testosterone prefer not to reduce their dosage—which was also true for this patient.
As such, the patient elected to pursue treatment, and Dr. Haynie subsequently prescribed 50mg of oral eplerenone daily. Since the patient reported an allergy to sulfa drugs, dorzolamide and acetazolamide were excluded as potential options.
1- and 3-month follow-up visits
At the 1-month follow-up visit, the neurosensory retinal detachment and subretinal fluid had fully resolved. Unfortunately, 2 months later, the patient returned with a second episode of CSCR. Knowing that he had responded well to eplerenone, Dr. Haynie prescribed a second course of the treatment, and the patient again responded well.
6-month follow-up visit
However, 6 months later, the patient returned with a third recurrence of CSCR, which suggested that the etiology was likely linked to his testosterone usage. To round out his comprehensive workup, Dr. Haynie referred the patient to a sleep specialist due to the relatively high incidence of recurrent CSCR (61%) in patients with sleep apnea.6
During this visit, Dr. Haynie ordered fluorescein and indocyanine green (ICG) angiography, which is not something he often does for patients with acute CSCR; however, for recurrent cases, he noted that it is important to identify where the focal leak is in the choroid and rule out CNVMs.
Figure 3: Fluorescein angiography imaging OS during the third recurrence of CSCR; a focal lesion just outside of the central macula can be seen.
Figure 3: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Figure 4: ICG angiography imaging OS during the third recurrence of CSCR; a focal extrafoveal leakage in the central macula can be visualized, there is no presence of choroidal neovascularization, but there is hypercyanesence, which is leaking in the choroid.
Figure 4: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Post-laser photocoagulation
The patient was subsequently referred for laser photocoagulation treatment, after which he remained stable with no additional recurrences over the next several years.
Figure 5: Near-infrared reflectance (NIR) imaging OS after laser photocoagulation; the yellow circle highlights where the laser treatment was performed, and mottling of the pigment can be visualized beneath the treated tissue.
Figure 5: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Figure 6: OCT imaging OS after laser photocoagulation; the neurosensory detachment is resolved, although there has been a slight alteration to the outer retinal/RPE complex due to the chronic presence of subretinal fluid.
Figure 6: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Comparing retinal imaging of acute and chronic CSCR
Dr. Haynie then compared CFP, fundus autofluorescence (FAF), and OCT imaging from patients with acute and chronic CSCR. He explained that even if it is his first interaction with a CSCR patient, he orders FAF imaging because it is helpful in differentiating between acute and chronic CSCR.11
Figure 7: CFP and FAF imaging OD in a patient with acute CSCR; serous elevation can be visualized in CFP, and relative foveal hyperautofluorescence is noted with FAF.
Figure 7: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Figure 8: OCT imaging OD in a patient with acute CSCR; the photoreceptor layer is smooth and subretinal fluid can be visualized.
Figure 8: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Figure 9: FAF imaging OS of a patient with chronic CSCR; serous-related RPE alteration can be visualized in the superior and inferior temporal arcades and scattered throughout the macula; in addition, there are drip lines of hyperautofluorescence, which indicates that subretinal fluid has tracked underneath the retina. Dr. Haynie noted that this patient likely had CSCR for decades.
Figure 9: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Figure 10: OCT imaging OD of a patient with chronic CSCR; accumulation of RPE outer segment shedding (known as “shaggy” photoreceptors) can be visualized.12 OCT is another important tool for identifying and monitoring CSCR patients and differentiating chronic from acute cases.12
Figure 10: Courtesy of Jay M. Haynie, OD, FAAO, FORS.
Conclusion
When treating a patient who presents with CSCR, optometrists can:
- Use CFP, FAF, and OCT to assess the extent of fluid accumulation and chronicity of the disease, as well as determine if there is choroidal neovascularization.
- Identify and address risk factors by educating patients on how they can limit associated factors that may cause CSCR.
- Make sure to ask CSCR patients if they have been diagnosed with sleep apnea, or if they seem to have any symptoms associated with the disease.
- If the case is mild, patients can be followed regularly to monitor resolution.
- Use fluorescein or ICG angiography to identify choroidal leakage and guide the treatment protocol moving forward.
- If the patient has recurrent CSCR, initiating treatment is recommended to preserve the quality of the photoreceptor outer segments and prevent potential vision loss.
- Monitor patients for choroidal neovascularization.
