Case study

1.
Case Report and Clinical Findings of Central Serous Retinopathy
Dan Mulder
dmulder@student.uiwtx.edu
Abstract
Central Serous Retinopathy (CSR) is a retinal disease that results in a serous detachment
of the neurosensory retina and/or the retinal pigmented epithelium (RPE). The etiology
of CSR is not clear, but may possibly be caused by hyperpermeability of the choroid
leading to serous detachment. CSR is normally a self-limiting disease that resolves
within six months. Diagnosis is normally straightforward and treatment is based upon
location of the detachment and severity of symptoms. This case report will present
common signs and symptoms, diagnostic tools, and possible treatments of CSR.

2.
2
2
Introduction
Central Serous Retinopathy (CSR) is a serous detachment of the neurosensory retina
and/or the retinal pigmented epithelium (RPE) in the posterior pole. The etiology of CSR
is unknown, but several mechanisms are believed to play a role. The most widely
accepted mechanism is hyperpermeability of the choroid 1,2
. The choroid becomes
hyperpermeable when it is subject to stasis, ischemia, or inflammation. The main
contributor to hyperpermeability is believed to be high systemic cortisol levels, which
causes vasoconstriction. The other possible mechanism is breakdown of the RPE pumps
leading to a disruption in the zona adherens between the RPE cells 1,2
. This results in a
breakdown of the blood retinal barrier and subsequent leakage of plasma into the retina.
Risk factors for CSR include any disease that increases systemic cortisol levels, including
but not limited to Cushing’s syndrome, pregnancy, type A personality, and hypertension.
Any systemically absorbed steroid can also increase the risk of CSR 3,4
. Topical
ophthalmic steroids are not a risk factor for CSR, but can exacerbate it once a detachment
has occurred 4
.
The classical presentation of CSR is men in their third and fourth decades of life. The
annual incidence of CSR is 9.9 cases per 100,000 men and 1.7 per 100,000 women 1,4
.
Patients often present with a loss of visual acuity (VA) due to the location of the serous
detachment, but may also be asymptomatic. A patient with a detachment affecting the
macula will have more severe VA loss as well as metamorphopsia and possible scotomas.
The majority of cases of CSR are monocular with an approximate 30% incidence of
occurrence in the fellow eye 1,4
. The incidence of bilateral CSR appears to increase in
patients that are over the age of fifty.
Case Report
The patient was evaluated on April 26, 2014 for the initial encounter. The patient was a
47-year-old Hispanic male presenting for his first ever eye exam. The chief complaint for
the visit was blurry vision at near in both eyes. The symptoms had been present for
several years and the patient had never used any spectacle correction. To compensate for
the blurred vision at near, the patient would increase his working distance. The patient
reported no visual complaints at distance. The patient had an unremarkable family and
personal ocular history.
The patients medical history consisted of type-II diabetes since 2011, hypertension since
2013, and the patient would go on to develop hypercholesterolemia and hypothyroidism
in 2015. The patient was also an everyday smoker for the past thirty years. The following
is a list of his medications: Metformin (Glucophage), Enalapril (Vasotec), Atorvastatin
(Lipitor), and Levothyroxine (Levoxyl). The patient was not taking any topical

3.
3
3
medications and reported no allergies to medications. He was oriented to time, place and
person.
His uncorrected visual acuity was 20/20-1 OD, 20/20-2 OS and 20/20 OU. Near
uncorrected visual acuities were 20/60 OD, OS, and OU. The preliminary exam results
are as follows:
Distance and Near Cover Tests: Ortho
Extra Ocular Movements: Smooth full range of motion without pain or diplopia
Pupils were equal round and responsive to light with no afferent pupillary defect
Confrontational fields were full to finger count with no scotomas
Intraocular Pressure (IOP): 10 mm Hg OD, OS taken with Goldmann Applanation
Tonometry
Refraction was performed and the patient achieved 20/20 vision at distance and near. A
final prescription of +1.75 SPH OU single vision reading only was issued. The anterior
segment was evaluated by slit lamp and the following results were obtained:
External lids: normal lid position, without obvious lesions OD, OS
Orbit and Adnexa: no proptosis, or visible mass OD, OS
Lids and Lashes: meibomian gland dysfunction, lashes without collarettes or scurf OD,
OS
Tear film: normal with a tear breakup time of >10 seconds OD, OS
Conjunctiva: normal bulbar conjunctiva, pinguecula nasal, diffuse injection that is greater
nasally OD, OS
Cornea: clear, no edema, no scarring OD, OS
Anterior Chamber: deep and quiet (Von Herrick of 3) with no cells or flare OD, OS
Iris: Normal appearing iris with no signs of neovascularization, atrophy or synechia OD,
OS
Lens: clear OD, OS
The patient was dilated using one drop 1% Tropicamide and one drop 2.5%
Phenylephrine OU. A fundus exam was then performed using a slit lamp with a 90 D lens
and Binocular Indirect Ophthalmoscope (BIO). The following results were obtained:
Optic Discs: normal appearing optic nerve with healthy pink rim and normal appearing
nerve fiber layer OD, OS. No neovascularization of the disc. Cup-to-disc ratio was
0.3/0.3 OD, OS.
Macula OD: pigment mottling, elevation ½ disc diameter (DD) from macula with a
diameter of 1 DD
Macula OS: pigment mottling, minor elevation ¼ DD from macula with a diameter of ¼
DD
Vessels: vessels are of normal caliber without arterio-venous nicking or significant
tortuosity OD, OS
Vitreous: normal and clear for age, no PVD OD, OS

4.
4
4
Periphery: pigment epithelial detachment adjacent to macula, with no diabetic
retinopathy
Fundus photo was captured OD (Figure 1). Fundus photo shows elevation temporal to
the macula with a clear dome where the detachment occurred. The elevation was clear
and the serous fluid within the dome appeared optically clear. Ocular coherence
tomography (OCT) was also performed OD (Figure 2) and OS (Figure 3). Pigmented
epithelial detachments (PED) were present in both eyes with the right being much greater
than the left.
Order Date: 4/26/14
Patient:
Interpretation:
Elevation temporal to the macula under pigment epithelium RTC with Dr. Sponsel May 19th for treatment options
Torres Victor, F DOB: 5/10/1966 Age: 50
Order Date: 4/26/14
Patient:
Interpretation:
Elevation temporal to the macula under pigment epithelium RTC with Dr. Sponsel May 19th for treatment options
Torres Victor, F DOB: 5/10/1966 Age: 50
Order Date: 4/26/14
Patient:
Interpretation:
Elevation temporal to the macula under pigment epithelium RTC with Dr. Sponsel May 19th for treatment options
Torres Victor, F DOB: 5/10/1966 Age: 50
Figure 1
Figure 2 Figure 3

5.
5
5
Assessment and Plan:
Central Serous Retinopathy OD>OS secondary to pigmented epithelial detachment.
Refer patient to the in-house retina specialist for further examination of OCT and
treatment options to prevent macular damage. Follow-up in two weeks was scheduled for
May 19, 2016.
The following differential diagnoses were considered in this case:
Age-related Macular Degeneration (AMD)
• Hemorrhages with detachment
• Soft/hard drusen
• Diffuse (not pinpoint) leakage on angiography
Presumed Ocular Histoplasmosis Syndrome
• Multiple choroidal lesions (macula or mid-periphery)
• Pallor/Peripapillary Atrophy (PPA)
• Choroidal Neovascular Membrane (CNVM) maculopathy
Idiopathic serous RPE detachments
• Young individuals (less than 50)
• No leakage on angiography
• Variant of CSR
Pathological Myopia
• Posterior staphyloma
• Macular holes
• Lacquer cracks
• CNVM
Diabetic Retinopathy
• Clinically Significant Macular Edema (CSME)
• Neovascularization of the disc, iris, and elsewhere
• Microaneurysms, dot and blot hemorrhages
In this patient there was no evidence of drusen or hemorrhage associated with the
detachment. The discs were pink and healthy without pallor or neovascularization and
the periphery was free of any choroidal lesions. There was also no peripheral holes or
macular holes in the retina. There were no other signs of diabetic retinopathy. The
macula was flat with no CSME. Most diseases that can cause a CNVM should be on the
list of differential diagnoses. In this case there was no CNVM present.

6.
6
6
1st
Follow-up
Patient failed to return for the two-week follow-up, but presented to the in-house retinal
specialist seven months later on November 3, 2014. The patient had no associated
symptoms, and denied any metamorphopsia, scotomas, or decrease in vision. Patient also
denied being stressed, and/or steroid use. All preliminary entrance test results and
corrected visual acuities were unchanged since initial visit.
An Amsler Test was administered and the patient reported temporal metamorphopsia in
the right eye. However, the visual disturbance did not correlate with the area of
detachment. There were no scotomas noted in the right or left eye and the patient
reported no metamorphopsia in the left eye. Dilated fundus exam was performed on this
visit and the patient presented with no resolution of the detachment with identical
fundoscopic findings as seven months previously.
OCT, 5 line raster, was performed OD (Figure 4) and OS (Figure 5). The OCT
confirmed that there had been no resolution in the detachment. The OCT further
demonstrated that the chronic nature of the PED led to a detachment of the neurosensory
retina in the right eye. The RPE is firmly attached to its underlying basement membrane
causing tension on the photoreceptor layer of the retina. This eventually caused the
photoreceptors to detach at the edge of the PED.
Figure 4 Figure 5
Plan:
Patient was given a prescription for Ketorolac (Acuvail) and instructed to use twice daily
for four weeks. The patient was also given an Amsler Grid and was instructed to monitor
daily for visual changes. The patient was scheduled to follow up in four weeks.
2nd
Follow-up
The patient neglected to follow up in four weeks and instead returned to the clinic for his
comprehensive exam May 30, 2015. It had now been thirteen months since the patient’s
Order Date: 11/03/14
Patient:
Interpretation:
Diagnosis: Cent Serous Retinopathy, OU. ... Impression: Abnormal OU. ... measurements taken on OCT shows that
OD CSR vertical height 533um, horizontal: 1574um OS vertical height: 90um, horizontal: 1052 um. Results: Stable. ...
Plan: NSAIDs. ... acuvail BID, OU. Repeat: 1 month. ...
Torres Victor, F DOB: 5/10/1966 Age: 50
Order Date: 11/03/14
Patient:
Interpretation:
Diagnosis: Cent Serous Retinopathy, OU. ... Impression: Abnormal OU. ... measurements taken on OCT shows that
OD CSR vertical height 533um, horizontal: 1574um OS vertical height: 90um, horizontal: 1052 um. Results: Stable. ...
Plan: NSAIDs. ... acuvail BID, OU. Repeat: 1 month. ...
Torres Victor, F DOB: 5/10/1966 Age: 50

7.
7
7
initial diagnosis of CSR. The patient did not have any ocular complaints and presented
for a diabetic evaluation. The patient was not compliant with the previous treatment of
Acuvail.
All preliminary entrance test results and corrected visual acuities were unchanged since
the initial visit. Amsler Grid was performed with normal results. On dilated fundus
exam, elevation temporal to macula was still present in the right eye. The left eye had
mottling of macula, but no elevation. There were also no signs of diabetic retinopathy.
Plan:
Return in six months for dilated fundus exam and monitor for resolution of the PED.
3rd
Follow-up
The patient again neglected to present for the six-month follow-up. The patient returned
for his comprehensive exam and diabetic evaluation one year later on May 4, 2016. It
had now been two years since the patient’s initial diagnosis of CSR. All preliminary
entrance test results and corrected visual acuities were unchanged since the initial visit.
Amsler Grid was performed with normal results. Upon dilation and examination of the
fundus, there was no elevation temporal to the macula in either eye. There was
hypopigmentation around macula in the right eye. There was no pigment mottling in the
left eye.
Plan:
Follow up in two weeks with the in-house retinal specialist and perform OCT. The
patient failed to comply and did not show for the follow-up.
Discussion
The etiology of Central Serous Retinopathy remains unknown, but it is clear that there is
a link to vascular disease. While the cause is unknown, the diagnosis of CSR is
straightforward. There are multiple diagnostic tools available to aid in diagnosis and
treatment. Many of those tools were used in the case presented, while others such as
angiography were not used because of the asymptomatic nature and location of
detachment. Dilated fundus examination is the most common initial tool used to find
CSR. Many patients with CSR will present with symptoms cueing the practitioner to
thoroughly evaluate the posterior pole. In some cases, such as the case presented, the
patient is asymptomatic and the signs of CSR are found on routine dilated examination.
Like in the presented case, dome-like elevation in the posterior pole is the most common
sign of CSR, along with pigment mottling and hypopigmentation of the retina. If the case
is chronic in nature, RPE atrophy causing exposure of the underlying choroidal vascular
may be present. Chronic CSR may also have areas of RPE pigment clumping, and bone
spicules on fundus examination 1,3,4,5
.

8.
8
8
Another valuable diagnostic tool of CSR is Spectral-Domain Optical Coherence
Tomography (OCT). An OCT will clearly portray the underlying serous detachment of
the retina. The classic form of CSR will have a serous neurosensory detachment of the
retina. In the case presented the patient had a pigmented epithelial detachment (PED) of
the retina, which is considered a variant of classical CSR.
While not preformed in the presented case, fluorescein angiography (FA) is the most
definitive diagnostic tool for CSR. Since CSR is caused by hyperpermeability of the
choroid, FA will detect leakage into the retina. The acute pattern of CSR is a single
pinpoint leak at the level of the RPE leading to a smokestack appearance (Figure 6) in
later stage of the angiogram1
. The chronic pattern of CSR is diffuse fluorescein leakage.
Multifocal Electroretinography (mfERG) can also be used to help with diagnosis and
prognosis. The mfERG is used to provide a topographical measure of retinal activity that
can be compared with the patient’s visual fields 6,7
. MfERG indicates that the foveal
cones and/or bipolar cells are dysfunctional and that they are the source of vision loss.
CSR will cause an increase in macular photostress recovery time recorded by mfERG.
After resolution, mfERG amplitudes improve greatly but do not reach normal levels.
MfERG can be a good diagnostic tool because the findings tend to correlate with function.
Treatment of CSR can be initiated once the proper diagnosis has been established and
possible differential diagnoses have been ruled out. Observation is the most common
initial treatment of CSR, as demonstrated in the presented case. CSR is typically a self-
limiting process with spontaneous recovery in six months. Approximately 95% of
patients with CSR will recover to a final visual acuity of 20/30 or better. The level of
regained visual acuity should coincide with reattachment of the neurosensory retina.
Once resolution has occurred approximately 30-50% of patients have recurrences within
the first year 1,3,4
. Careful observation and follow up is necessary even after resolution of
the detachment to ensure reoccurrences do not procure.
Initial treatment should also include discontinuation or tapering of steroids.
Corticosteroid use has been linked as a possible cause of CSR. Therefore,
limiting/discontinuing steroid use will aid in resolution and could prevent reoccurrences.
Topical non-steroidal anti-inflammatory drugs (NSAIDs) are a good treatment option for
Figure 6

9.
9
9
patients because of their non-invasive nature. In a study published by Alkin et al, topical
0.1% nepafenac was administered three times daily for four weeks and then was
continued until resolution. In the study 82% of treated patients resolved, and 42% of
untreated patients resolved spontaneously8
.
More aggressive treatment may be warranted in chronic CSR. Verteporfin photodynamic
therapy (PDT) is a good treatment option in such cases, or in cases that develop CNVM.
PDT causes short-term choriocapillaris hypoperfusion and long-term choroidal vascular
remodeling, leading to a reduction in vascular hyperpermeability and leakage 8
. Another
invasive treatment option is focal laser photocoagulation. Laser photocoagulation will
expedite the absorption of subretinal fluid and aid in more rapid resolution of the serous
detachment. The exact mechanism of laser photocoagulation is unknown, but it is
believed to seal focal defects in the RPE monolayer, promoting a healing response. This
response may cause recruitment of healthy RPE cells, or directly stimulate the pumping
function of RPE cells near the leak 1
.
Poor treatments include but are not limited to ketoconazole (antifungal), anti-VEGF
(Intravitreal bevacizumab), carbonic anhydrase inhibitors, and Aspirin. Antifungals may
appear to be a valid therapy because of their ability to lower endogenous cortisol, but it
has been shown to have little therapeutic effect 1,4
.
There are primarily two types of CSR: acute and chronic. Acute CSR is limited to cases
that spontaneously resolve in six months. Chronic CSR takes longer to resolve and may
not resolve spontaneously. Chronic CSR produces long-standing serous fluid that can
damage RPE and photoreceptor cells leading to atrophy and permanent damage. When
considering treatment options, duration and symptoms should be considered primarily.
There are several complications that can occur as a result of CSR. The most common
complication is permanent decreased visual acuity as a result of photoreceptor cell death
in the macula. Other complications include secondary choroidal neovascularization
(CNV), cystoid edema, and diffuse retinal pigment epitheliopathy (DRPE) 1,3,4
.
Conclusion
Central serous retinopathy is a common finding in men ages 30-60 years old and results
in a serous detachment of the neurosensory retina or a pigmented epithelial detachment.
It can be bilateral or unilateral. CSR has been linked to elevated systemic cortisol levels,
which are believed to cause hyperpermeability of the choroid. As demonstrated in the
case, CSR can be asymptomatic and resolve spontaneously with time. The overall
outcome following CSR is very good with most cases returning to 20/20 vision. Patients
may have increased risk of complication in the future due to permanent
RPE/photoreceptor damage caused by long-standing serous fluid and therefore should be
monitored yearly for changes.

10.
10
10
References
1. Nicholson, B., Noble, J., Forooghian, F., & Meyerle, C. (2013). Central Serous
Chorioretinopathy: Update on Pathophysiology and Treatment. Survey of
Ophthalmology, 58(2), 103–126. http://doi.org/10.1016/j.survophthal.2012.07.004
2. Yang, L., Jonas, J. B., & Wei, W. (2013). Choroidal vessel diameter in central serous
chorioretinopathy. Acta Ophthalmologica, 91(5). doi:10.1111/aos.12059
3. Colucciello, M. (2008, September). Central Serous Retinopathy. Retrieved June 08,
2016, from http://www.retinalphysician.com/articleviewer.aspx?articleid=102107
4. Shah, S., Desai, M., Desai, C., & Dikshit, R. (2011). Steroid-induced central serous
retinopathy. Indian Journal of Pharmacology Indian J Pharmacol, 43(5), 607.
doi:10.4103/0253-7613.84985
5. Tarabishy, A. B., Ahn, E., Mandell, B. F., & Lowder, C. Y. (2011). Central serous
retinopathy. Arthritis Care Res Arthritis Care & Research, 63(8), 1075-1082.
doi:10.1002/acr.20485
6. Nebbioso, M. (2014, August 26). Recommendations on Electroretinogram Testing in
Retinal Disorders. Retrieved June 20, 2016, from
http://www.jacobspublishers.com/index.php/journal-of-diabetes-and-endocrinology-
articles-in-press?id=1302
7. Maturi, R. (2004, December 15). Multifocal ERG in Practice. Retrieved June 08,
2016, from
http://www.reviewofophthalmology.com/content/d/cover_focus/i/1323/c/25418/
8. Alkin, Z., Osmanbasoglu, O. A., Ozkaya, A., Karatas, G., & Yazici, A. T. (2013).
Topical Nepafenac in Treatment of Acute Central Serous Chorioretinopathy.Medical
Hypothesis, Discovery and Innovation in Ophthalmology, 2(4), 96–101.
9. Siaudvytyte, L., Diliene, V., Miniauskiene, G., & Balciuniene, V. J. (2012).
Photodynamic Therapy and Central Serous Chorioretinopathy. Medical Hypothesis,
Discovery and Innovation in Ophthalmology, 1(4), 67–71.
10. Chakraborti, C., Samanta, S. K., Faiduddin, K., Choudhury, K. P., Kumar, S., &
Mondal, R. (2014). Bilateral central serous chorio-retinopathy in pregnancy
presenting with severe visual loss. Nepalese Journal of Ophthalmology Nep J Oph,
6(2). doi:10.3126/nepjoph.v6i2.11711
11. Fineman, M. S., & Ho, A. C. (2012). Retina. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins.