Central Serous Chorioretinopathy

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Article initiated by:
Cindy W. Mi, MD, Dong Won Lee, MD, Jing Sun, Murtaza Adam, MD, Nisarg Joshi, MD, Sunir J.Garg, MD, Vinay A. Shah M.D.
All contributors:
Jennifer I Lim MD, Dr John Davis Akkara (MBBS, MS, FAEH, FMRF), Dong Won Lee, MD, Vinay A. Shah M.D., Leo A. Kim, MD, PhD, Koushik Tripathy, MD (AIIMS), Murtaza Adam, MD, Francesc March de Ribot, MD, PhD, Christina Y. Weng, MD, MBA, Jonathan C. Tsui, MD
Assigned editor:
Mark P. Breazzano, MD, FACS
Review:
Assigned status Update Pending
 by Christina Y. Weng, MD, MBA on June 6, 2024.


Central Serous Chorioretinopathy
DiseasesDB
31277
ICD-10
H35.7
MedlinePlus
001612
MeSH
D056833


Disease Entity

Disease

Central serous chorioretinopathy (CSCR) is the fourth most common retinopathy after age-related macular degeneration, diabetic retinopathy, and branch retinal vein occlusion.[1] CSCR typically occurs in males in their 20s to 50s who exhibit acute or subacute central vision loss or distortion. Other common complaints include micropsia, metamorphopsia, hyperopic (most common) or myopic shift, central scotoma, and reduced contrast sensitivity and color saturation.[2] No underlying pathophysiologic mechanisms have been proven, but CSCR is thought to result from hyperpermeability in choroidal capillaries, which, in association with retinal pigment dysfunction, causes a serous detachment of the neurosensory retina. Recurrence occurs in about 31% of patients with CSCR,[3] although the recurrence rate has been cited as 50% in some texts.

The disease was first recognized by Albrecht von Graefe in 1866 and was termed central recurrent retinitis. Since then it has been reported under a variety of names, including idiopathic flat detachment of the macula by Walsh and colleagues, central angiospastic retinopathy by Gifford and colleagues, and central serous retinopathy by Straatsma and colleagues. The condition was termed Idiopathic central serous chorioretinopathy by Gass and colleagues in 1967.

Differential Diagnosis

CSCR causes unilateral vision loss, usually in males, due to development of subretinal fluid, typically between the ages of 20 and 50 years. In females, CSCR usually develops at an older age. The differential diagnosis for subretinal fluid is broad and encompasses all disease entities that can cause macular neurosensory detachment. These entities include neovascular age-related macular degeneration/polypoidal choroidal vasculopathy, myopic choroidal neovascular membrane, choroidal tumor, hypertensive choroidopathy, leukemic choroidal infiltration, choroidopathy due to multiple myeloma, retinal venous occlusion, unilateral acute idiopathic maculopathy, inflammatory conditions including posterior scleritis or Vogt-Koyanagi-Harada disease, optic nerve pit, and rhegmatogenous retinal detachment. Indeed, cases of bullous CSCR (which is usually seen in patients on systemic steroids), where a significant amount of subretinal fluid is found, can be mistaken for rhegmatogenous retinal detachments. Several associations for bullous CSCR include history of kidney disease or history of autoimmune disease. [4][5] In both acute and chronic cases that have resolved, the only clue that may be present on examination is macular retinal pigment epithelium (RPE) mottling. By definition, the patient’s retinal detachment cannot be due to another primary process. If suspected, those diagnoses should be ruled out. A thorough history, detailed examination, and appropriate imaging and laboratory tests can help differentiate these diagnoses.

Etiology

Although exact mechanisms behind CSCR have not been elucidated, many associations have been found. Steroids, both endogenous and exogenous, have the strongest known association with CSCR. Garg and colleagues found that patients with acute CSCR have higher levels of endogenous cortisol compared to age-matched controls.[6] Other studies have shown that exogenous steroid use for treatment of unrelated conditions is also associated with CSCR.[7] [8] [9][10] In patients with CSCR, the odds ratio of systemic steroid use was found to be 37.1 (95% confidence interval (CI), 6.2–221.8).[9] Exogenous hypercortisolism has been induced intravenously, cutaneously, or by nasal spray. Furthermore, the association of CSCR with having a "Type A" personality seems logical, given known increased glucocorticoid release with stress.[11] It is therefore the only "inflammatory" choroiditis not proven to be associated with infection that is precipitated or worsened by glucocorticoids.

Increased choroidal vascular permeability is postulated to occur as a response to epinephrine-mediated vasospasm that is potentiated by steroids, leading to choroidal ischemia and vascular hyperpermeability.[12] [13] Oncotic pressure in the choroidal space, combined with RPE dysfunction, leads to accumulation of fluid in the subretinal space.[14] [15] [16][17] The currently theorized role of the RPE involves the increased hydrostatic pressure in the choroid causing “micro-rips or blowouts” in the RPE, jeopardizing its barrier function.[18]

Other associations to CSCR have been described. Cotticelli determined that the odds ratio of Helicobacter pylori in CSCR patients is 4.6 (95% CI 1.28–16.9) and other prospective studies revealed that H. pylori infection was present in 53% and 69% of patients with CSCR.[19][20][21] Rahbani-Nobar demonstrated that treating the H. pylori infection is associated with more rapid subretinal fluid resorption.[22] Methylenedioxymethamphetamine (MDMA), also known as ecstasy, and sildenafil have also been associated with development of CSCR.[23][24] A case of CSCR has been reported in a patient with history of topiramate use.[25]

The RAF/MEK/ERK pathway is an intracellular cell-signaling pathway that is stimulated by growth factors and results in cell division. Medications that inhibit this pathway include sorafenib and vemurafenib. Sorafenib is used to treat hepatocellular carcinoma and renal cell carcinoma, whereas vemurafenib is used to treat melanoma and non-Hodgkin lymphoma. Use of MEK/ERK inhibitors has been associated with acute CSCR that resolves with cessation of medication.[26]

Central serous chorioretinopathy is associated with increased sympathetic activity, and obstructive sleep apnea is known to cause such increases. Yavas and colleagues showed in a prospective study that 61% of patients with CSCR had underlying obstructive sleep apnea that was diagnosed with overnight polysomnography.[27]

Epidemiology and Risk Factors

Most patients who present with CSCR are between the ages of 28 to 68 years with an average age of 43 years.[28] Those who are over 50 years of age are more likely to have bilateral disease (50%) with RPE loss and choroidal neovascularization compared to those less than 50 years of age (28.4%).[29] CSCR tends to affect males (9.9/100,000) about 6 times more than females (1.7/100,000).[3] Similar prevalence of CSCR was noted in White, Black, and Asian populations.[30][31] Studies have suggested that there may be a temporal predominance in spring months (March, April, May, and June), but the results were not statistically significant.[32][33]

Weenink and colleagues studied the family members of 27 patients with bilateral CSCR and found that in 52% of the families, at least 1 relative was affected.[34] Of the studied family members, 27.5% suffered from chronic CSCR in at least 1 eye, suggesting a genetic predisposition to central serous chorioretinopathy. Most CSC cases are diagnosed in patients with no refractive error or mild hyperopia. Common risk factors, apart from the ones described in the Etiology section, include pregnancy, antibiotic use, alcohol use, untreated hypertension, and obstructive sleep apnea.[9] Fok found that patients with psychiatric disorders such as depression are more likely to have a recurrence.[35] Other associations include Cushing syndrome, systemic lupus erythematosus (SLE), organ transplantation, and end-stage renal disease.

Neurosensory detachments and pigment epithelial detachments simulating CSCR may also be noted with choroidal ischemia in SLE, Goodpasture syndrome, polyarteritis nodosa, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, granulomatosis with polyangiitis (formerly Wegener granulomatosis), malignant hypertension, and pregnancy-induced hypertension.

Pathophysiology

While no pathophysiologic cause of CSCR has been identified, epidemiology, hormonal studies, fluorescein angiography (FA), and optical coherence tomography (OCT) imaging have elucidated some of the pathologic manifestations.

While RPE dysfunction was thought to be the primary etiology of CSR in the past, recent studies along with the advent of new imaging suggests that RPE dysfunction may not be the cause but rather is a sequela of CSCR. Microscopic evaluation of iatrogenic CSCR in monkeys showed damage and defects in endothelial cells of choriocapillaries with overlying degeneration of RPE cells. Indocyanine green angiography studies in humans have demonstrated choroidal staining, suggesting increased capillary permeability to be the cause of CSCR.[36] [37] Indocyanine green videoangiography shows choroidal hyperpermeability, irregular dilation of choroidal veins, and choroidal lobular ischemia.[15]Foveal or perifoveal leakage can be present in 50% of eyes. Prunte and Flammer demonstrated the presence of delayed arterial filling and ischemia, followed by capillary and venous congestion in areas of the choroid affected by CSCR, either or both of which could be the mechanism for increased permeability.[14] Autofluorescence studies show that in acute CSCR, there is increased autofluorescence in the area of leakage, suggesting elevated metabolic activity of the RPE.[38] However, in chronic CSCR, there is decreased or absent autofluorescence, suggesting reduced metabolic activity of the RPE and secondary RPE damage. Hypofluorescent or hyperfluorescent fundus autofluorescence is attributed to changes in subretinal and RPE lipofuscin content. Enhanced depth imaging OCT of the choroid shows thickening of the choroid in patients with CSCR, which further supports the idea of vascular congestion and elevated hydrostatic pressure.[39]

While pathophysiologic anatomy has been shown, the actual cause is still in speculation. Active CSCR has been correlated with elevated levels of endogenous and exogenous corticosteroids.[40] Intravitreal injections of corticosteroids and aldosterone in rats leads to choroidal enlargement,[41] suggesting that CSR-associated vasculopathy may in part be due to activation of the mineralocorticoid receptor, which has more recently become a new target for treatment.[41] [42] [43]

Some mechanisms of action of steroids on the choroid and RPE include potentiation of adrenergic hormones,[44] hypertension,[45] [46] and altered ion transport in RPE cells.[47] Glucocorticoids regulate the expression of adrenergic hormones and receptors, and therefore, said hormones may contribute to the pathophysiology of CSCR.[13] A study showed that patients with CSCR have increased sympathetic activity and decreased parasympathetic activity, based on tests of autonomic activity and reactivity.[12] Other theoretical causes of choriocapillary hyperpermeability and RPE damage include epinephrine,[36][48] ischemia,[36][14] inflammatory including H. pylori infection, and hormonal causes.[49] Epinephrine and norepinephrine have also been shown to be elevated in patients with active CSCR.[40][50]

Foveal attenuation, chronic macular edema, and damage of the foveal photoreceptor layer have been reported as causes of visual loss in CSCR.

Diagnosis

History

Typically, patients complain of central vision loss or distortion with a possible central scotoma. Other common complaints include micropsia, hyperopic or myopic shift, and reduced contrast sensitivity and color saturation.[2] Patients are generally healthy; however, hypercortisolism should be ruled out, especially in chronic cases. Type A personality, abdominal pain from H. pylori, and pregnancy, MDMA use, and sildenafil use may be associated as described above.

Clinical Diagnosis

On refractive examination, best corrected visual acuity (BCVA) can range from 20/20 to 20/200. Visual loss can partly be attributed to a hyperopic shift caused by the anterior displacement of the macular photoreceptors. Folk recorded that patients with CSCR can have minimal afferent pupillary defects and reduced critical flicker-fusion thresholds, both of which are the first to improve with resolution of the CSCR episode.[51] Ophthalmoscopy typically discloses a round or oval serous macular detachment without hemorrhage, with small, yellow subretinal deposits in the area of neurosensory detachment.[26] At times, the subretinal fluid may contain grey-white serofibrinous exudate.[52] An RPE detachment (PED) may be seen on OCT in up to 63% of eyes,[53] and it is better visible on retroillumination. The PED may touch the posterior aspect of the retina and there is usually a leak at this site.[25] The inner surface of retina may show a localized depression at this site. In CSCR with subretinal fibrin, an area of lucency may denote the site of the leak.

Macular RPE mottling can be found in cases of recurrent or chronic CSCR. Ophthalmoscopy may show a range from mono- or paucifocal RPE lesions with prominent elevation of the neurosensory retina by clear fluid--typical of cases of recent onset--to shallow detachments overlying large patches of irregularly depigmented RPE.

Diagnostic Procedures and Tests

The diagnosis of CSCR can be made clinically but diagnostic tests such as fluorescein angiography (FA) and optic coherence tomography (OCT) are often performed to rule out other differential diagnoses and guide treatment. Typical FA includes the ink blot appearance (31%), smokestack pattern (12%), and minimally enlarging spot (7%).[54] FA is also used to rule out subretinal neovascularization.[1] Disc leak is not present in CSCR. The leaking areas on fundus FA can correlate to hyperreflective areas on the infrared image in OCT in patients with CSCR.[55]

OCT can be helpful in cases of CSCR that show equivocal signs on clinical examination, and it can show detailed findings not appreciable on examination such as small PEDs and hyper-reflective, fibrinous subretinal fluid.[1] Furthermore, OCT can be helpful in following chronic CSCR patients to track resolution. Enhanced depth imaging OCT technology has been able to identify choroidal thickening bilaterally, even in patients with unilateral CSCR.[39] Typically, the RPE line is straight at the areas without serous PED compared to the wavy RPE in inflammatory condition.

Fundus autofluorescence (FAF) photography (488 nm) provides functional images of the fundus by employing the stimulated emission of light from endogenous fluorophores, the most significant being lipofuscin. In the case of RPE cells, the buildup of lipofuscin is related in large part to the phagocytosis of damaged photoreceptor outer segments and altered molecules retained within lysosomes, which eventually become lipofuscin. Moreover, near infrared fundus autofluorescence (NIA) imaging (787 nm) is able to study the RPE, the choriocapillaris, and the choroid by determining melanin fluorescence .

Natural Progression and Prognosis

Acute CSCR is a self-limited condition with resolution of neurosensory retinal detachment and generally good recovery of visual acuity within 3 months.[2] Of note, recurrences of CSCR have been documented in up to 50% of patients within 1 year.[56] Fifteen percent of patients may exhibit symptoms and show persistent subretinal fluid for greater than 6 months; these patients are diagnosed with chronic CSCR.[57] Limited studies investigating prognostic markers found that outer nuclear layer thickness at the fovea correlates with BCVA in patients with resolved CSCR[58] and that total foveal thickness correlates with BCVA in patients with chronic CSCR who have symptoms for 21.8 (7-36) months.[59]

Management

Overview of Treatment

As CSCR usually resolves spontaneously within 2 to 3 months, observation is currently standard of care for newly presenting cases.[11] For chronic CSCR, recurrent CSCR, and acute CSCR in functionally monocular patients, treatment should be discussed.[60]

Risk Factors and Risk Factor Modification

Exogenous steroids of any route (oral, intramuscular, intranasal, etc.) have been strongly linked to an increased risk of CSCR, even at doses as low as 10 mg per day. Discontinuation of steroids is highly recommended; however, if patients must remain on steroids, reductions in steroid dose have been shown to increase the speed of CSCR resolution. Because the eye care provider is typically not the person who prescribed these steroids, it is important to maintain close provider-to-provider communication so that the patient's systemic disease is concurrently managed.

While there are several other risk factors that have been associated with CSCR, modification strategies have not yielded consistent results like discontinuation of exogenous steroids. Patients with Type A personality should be addressed by lifestyle modification and stress management, although there is an absence of high-quality data to support this. H. pylori has been linked to CSCR[22]; its atherosclerosis-inducing cytotoxins are believed to lead to choroidal vessels damage. Several studies investigated the effects of screening and treating H. pylori in patients with CSCR, but resulted in discordant results on SRF reabsorption and VA improvement. Similarly, long-standing hypertension has been associated with CSCR; however, treatment with anti-hypertensive agents such as propranolol and metoprolol has yielded no beneficial effects. Eplerenone is not superior to placebo for improving chronic CSCR in a clinical trial.[61]   

Medical Therapy

Anti-corticosteroid therapy

As mineralocorticoid receptor action has been implicated in the pathogenesis of CSCR, Zhao and Bousquet treated patients with eplerenone, a mineralocorticoid antagonist, for 5 weeks. They found a significant and rapid improvement of retinal detachment with improvement in mean central macular thickness, subretinal fluid height, and visual acuity that persisted and was evident at 5 months' follow-up.[41][42] Similar studies have supported this potential treatment and have shown greater efficacy in patients with chronic CSCR.[42][43] Spironolactone, another anticorticosteroid, has been shown to decrease subretinal fluid, decrease central retinal thickness, and increase BCVA in patients with chronic CSCR.[62] A prospective, randomized, double-blind, and placebo-controlled study with a crossover design showed a reduction in subretinal fluid and subfoveal choroidal thickness.[63] A prospective, randomized, placebo-controlled trial studying the use of eplerenone for chronic CSCR found modest gains in BCVA and improvement in subretinal fluid height (in press).

Mineralocorticoid antagonists may raise serum potassium level, especially in patients with congestive heart failure and chronic kidney disease. Hyperkalemia can manifest as fatigue, muscle weakness, palpitations, and arrhythmias.[64] Prior to starting a medication in this class, reviewing medical history and discussing with the primary care doctor is recommended. Baseline serum potassium levels and renal function should be established, such as with a basic metabolic panel. Initiation of medication should be postponed or avoided if serum potassium concentration is >5.5 mEq/L, creatinine clearance is <50 mL/min, or serum creatinine is >2 mg/dL in men and >1.8 mg/dL in women.[64] Other anti-corticosteroid treatments have also been studied. Finasteride, a 5a-reductase inhibitor with anti-androgenic properties, was shown to improve central macular thickness (CMT) and sub-retinal volume in a study of five patients but these findings reversed when the drug was discontinued.[65] Mifepristone, an anti-progesterone and anti-glucocorticoid agent, was shown in a study of 16 patients to improve Snellen visual acuity.[66] Rifampin, an anti-tuberculous drug and cytochrome P450 3A4 inducer, accelerates the metabolism of steroids and has been shown to benefit patients with CSCR.[67]

However, its use may be avoided in countries with high prevalence of tuberculosis due to the risk of resistance.

A case study of patient with multifocal CSCR with persistent SRF of two years who was treated with rifampin showed complete resolution of SRF in one month.[67] Side effects of rifampin include orange-colored body fluids, anorexia, and hepatotoxicity.[67]

Melotonin is an endogenous neuromodulator that has been linked to circadian cycles and sleep regulation, aging, and neuroprotection via an antioxidant mechanism.[61]  Melotonin also has an inhibitory effect on corticosteroids and has a minimal side effect profile, making it a target for CSCR treatment. A study of eight patients showed significant improvements in CMT (87.5%) and BCVA (100%) compared to controls.[68] Furthermore, no side effects were observed.

Aspirin

Low-dose aspirin has been explored in treating CSCR. Elevated levels of plasminogen activator inhibitor 1 (PAI 1), a marker of platelet aggregation, have been linked to steroid use and have been measured in patients with CSCR.[69]A prospective study of 113 eyes with CSCR showed faster improvement in BCVA compared to control.[69]

Helicobacter pylori treatment

A randomized control trial (RCT) of patients tested positive for H. pylori studied the effect of treatment of H. pylori treatment of chronic CSCR.[22] This study found that patients treated for H. pylori infection has faster resolution of sub-retinal fluid (9 weeks) versus control (11 weeks) but no change in BCVA. A case series of treated biopsy positive H. pylori patients showed resolution of SRF in 14 of 15 patients.[70] However, another RCT tested the same hypothesis and found no statistical change in resolution of SRF and BCVA.[71] Dang and colleagues did find a statistically significant improvement in foveal sensitivity in the H. pylori treatment group. These studies with contradictory results indicate that larger RCTs are needed to elucidate the clinical significance of H. pylori treatment on resolution of CSCR.

Anti-adrenergic agents

The role of anti-adrenergic therapy for CSCR is unclear. A small case series in 1993 described 6 patients with CSCR treated with metoprolol, a non-selective beta-blocker, who improved symptomatically and had partial or complete resolution of retinal detachment.[72] Other studies have shown that both metipranolol (non-selective beta blocker) and metoprolol tartrate (selective beta-1 blocker) both induced remission of CSCR.[73][74] In contrast, a randomized controlled double blind study examining the impact of beta-blockade with metipranolol over the course of acute CSCR found no difference in the course of acute CSCR between the beta-blocker group and control group.[75] Since this RCT examined patients with acute CSCR, the conclusions are not readily applicable to patients with chronic CSCR. Although anti-adrenergic agents have been shown to be beneficial in CSCR in some studies, this therapy has not been widely implemented in treatment.

Intravitreal anti-VEGF therapy

The use of anti-vascular endothelial growth factor (VEGF) agents are based on the idea that VEGF levels may be elevated due to the choroidal pathology. However, studies have shown that VEGF levels are similar between CSCR patients and control patients.[76][77]A meta-analysis of four controlled studies with patients treated with intravitreal bevacizumab (IVB) compared to control showed no improvement in BCVA or CMT at six months.[78] Of note, patients with coexisting choroidal neovascularization and CSCR (confirmed on FA or OCT-angiography) do benefit from anti-VEGF therapy.[79]

Also, polypoidal choloridal vasculopathy which is an important differential of CSCR in patients older than 50 years, may benefit from anti-VEGF agents.

Surgical Management

Laser Photocoagulation

Patients that show persistent visual defects or lack of improvement on imaging after a few months may require alternative therapies. One option is laser photocoagulation, including focal argon laser and micropulse diode laser photocoagulation. Both rely on angiography to identify focal targets based on hyperfluorescence at sites of RPE detachment/disruption. It is hypothesized that destruction of these detached sites allow scarring that re-attaches the retina. During this process, healthy surrounding RPE cells are able to pump SRF back into the choroid and expedite healing.

For patients with focal RPE detachments not involving the fovea, focal argon laser photocoagulation may be considered[2]. It has been shown to reduce the duration of CSCR up to two months, with complete resolution of RPE detachment and increased speed of improvement of VA. However, long term benefits of focal argon laser photocoagulation remain unclear. Several studies showed significantly decreased rates of CSCR recurrence in treatment groups vs placebo groups after 9 to 18 months of follow-up[80][81]. Others have concluded there was no difference in CSCR recurrence rates between groups after 1 to 12 years of follow-up[80][82][2]. Although focal argon laser photocoagulation may lead to more rapid resorption of SRF and recovery of VA, patients should be made aware of its potential side effects. Because the laser destroys targeted retinal tissue, patients may develop symptomatic scotomas corresponding to these sites. Choroidal neovascularization (CNV) and further vision loss can result if Bruch’s membrane is ruptured by the laser, requiring additional therapy. Due to these potential complications, patients treated with focal argon laser photocoagulation should have regular ophthalmology follow-up.

Photodynamic therapy

Photodynamic therapy (PDT) with verteporfin, a photosensitizer that accumulates in vessels and helps target therapy, causes endothelial damage and vascular hypoperfusion to inhibit the choroidal hyperpermeability seen in CSCR. Several reports and studies have demonstrated that PDT can be used in chronic CSCR patients to decrease SRF and improve BCVA.[83] Unfavorable side effects, which include choroidal ischemia, RPE atrophy, RPE rip, retinal thinning, and secondary choroidal neovascular membrane (CNVM) have led to the development of safer versions of PDT, which are reduced-dose PDT and reduced-fluence PDT.[84][85][86][87] Bae demonstrated that reduced-fluence PDT was superior to intravitreal ranibizumab in a RCT for improving BCVA and central retinal thickness.[88] Half dose PDT versus half fluence PDT was compared in eyes with chronic CSCR, demonstrating that half dose PDT treatment allowed for faster SRF resolution and decreased recurrence compared to half-fluence PDT.[89] Further studies titrating dosage of verteporfin and laser fluence are needed to more precisely compare safety profiles and efficacy. PDT necessitates the avoidance of physical activity after treatment.

PDT may be used for subfoveal or diffuse leaks in CSCR.

Subthreshold Micropulse Laser Photocoagulation

The traditional argon laser is thought to work by activating the RPE cells at the periphery of the laser burn that are affected but not destroyed by thermal energy.[90] Subthreshold micropulse laser (SML), also known as “high density, low-intensity” laser, uses subthreshold energy that that selectively targets RPE cells without inducing chorioretinal damage or scarring. This allows exposure to a large area of RPE cells, which then down-regulate cytokine production and inflammation.[90] The laser is applied in pulses in a frequency that allows heat dissipation to prevent structural heat damage to the retina.[91] Unlike conventional laser, SML can be safely applied to the fovea. Fluorescein angiography and indocyanine green (ICG) angiography can be supplemented to determine areas of treatment.[92] Several wavelengths of pulse lasers including green 532 nm laser, yellow 577 nm laser, and infrared 810 nm laser have been used to target different cells in the retina.[93] For example, the 577 nm yellow laser has the highest hemoglobin to melanin ratio making it the best SML for vascular structures. Furthermore, the 577 nm laser allows for more concentrated light with a lower power compared to the 810 nm laser.[94] Several uncontrolled studies have shown the effectiveness of 810 nm and 577 nm SML therapy.[94][95][96] In a RCT, chronic CSCR patients treated with 810 nm SML showed significantly better BCVA, lack of scotoma, and improved contrast sensitivity compared to patients treated with argon laser photocoagulation.[97] A study comparing 577 nm SML with PDT in the treatment of chronic CSCR showed a better treatment response in the SML group and greater improvement in central retinal thickness in the SML group.[91] In addition to the superior outcomes with SML over PDT, SML avoids the potential side effects of PDT such as RPE atrophy, choroidal neovascularization, choriocapillary ischemia, and transient reduction of macular function.[91] Similar to PDT, there is no visible tissue response during treatment, which is why SML treatment guidelines for optimal laser, energy, and duty cycle parameters is a much needed area of investigation.

Scleral resection

Venkatesh and colleagues[98] have reported resolution of exudative retinal detachment from chronic CSCR/ diffuse retinal pigment epitheliopathy after scleral resection. This patient had borderline low axial length of the eyeball and thick ocular coats on ultrasonogram.

Summary

CSCR is a multifactorial disease without a known mechanism of action. It is most strongly associated with hypercortisolism and is hypothesized to occur because of choroidal hyperpermeability and secondary RPE dysfunction leading to serous retinal detachment. While acute CSCR can be observed and is self-resolving in most cases, progression to chronic CSCR warrants treatment. The mainstay of treatment is currently photodynamic therapy, however treatment with SML or mineralocorticoid antagonists such as eplerenone are gaining momentum.

Additional Resources

  1. American Academy of Ophthalmology. Central Serous Chorioretinopathy. Basic and Clinical Science Course, Section 12. Retina and Vitreous. San Francisco: American Academy of Ophthalmology; 2022-2023:215-221.
  2. Porter D, Gregori NZ. Central Serous Chorioretinopathy. American Academy of Ophthalmology. EyeSmart/Eye health. https://www.aao.org/eye-health/diseases/central-serous-retinopathy-3. Accessed January 06, 2023.
  3. Porter D, Vemulakonda GA. Blood Pressure. American Academy of Ophthalmology. EyeSmart/Eye health. https://www.aao.org/eye-health/anatomy/blood-pressure-list. Accessed January 06, 2023.
  4. AAO, Laser Photocoagulation of the Retina and Choroid, 1997, p. 237-240.
  5. Bousquet E, Beydoun T, Rothschild PR, et al. Spironolactone for Nonresolving Central Serous Chorioretinopathy: A Randomized Controlled Crossover Study. Retina. 2015 May 26.
  6. Bousquet E, et al. Mineralocorticoid receptor antagonism in the treatment of chronic central serous chorioretinopathy: a pilot study. Retina. 2013 Nov-Dec; 33(10):2096-102.
  7. Haimovici R, Koh S, Gagnon DR, et al. Risk factors for central serous Chorioretinopathy: a case-control study. Ophthalmology. 2004;111:244-9.
  8. Jampol LM, Weinreb R, Yannuzzi L. Involvement of corticosteroids and catecholamines in the pathogenesis of central serous Chorioretinopathy: a rationale for new treatment strategies. Ophthalmology. 2002;109:1765-6.
  9. Karakus SH, Basarir B, Pinarci EY, Kirandi EU, Demirok A. Long-term results of half-dose photodynamic therapy for chronic central serous chorioretinopathy with contrast sensitivity changes. Eye. 2013;27(5):612-620.
  10. Lai TY, Chan WM, Li H, et al. Safety enhanced photodynamic therapy with half dose verteporfin for chronic central serous retinopathy: as short term pilot study. Br J Ophthalmology. 2006;90:869-74.
  11. Nicholson B, Noble J, Forooghian F, Meyerle C. Central Serous Chorioretinopathy: Update on Pathophysiology and Treatment. Survey of ophthalmology. 2013;58(2):103-126.
  12. Piccolino FC, Borgia L. Central serous Chorioretinopathy and indocyanine angiography. Retina. 1994;14:231-42.
  13. Schaal KB, Hoeh AE, Scheuerle A, et al. Intravitreal bevacizumab for treatment of chronic central serous chorioretinopathy. Eur J Ophthalmol. 2009 Jul-Aug;19(4):613-7.
  14. Singh RP, Sears JE, Bedi R, Schachat AP, Ehlers JP, Kaiser PK. Oral eplerenone for the management of chronic central serous chorioretinopathy. International Journal of Ophthalmology. 2015;8(2):310-314.
  15. Taban M, Boyer DS, Thomas EL, Taban M. Chronic central serous Chorioretinopathy: photodynamic therapy. Am J Ophthalmol 2004: 1073-1080.

References

  1. ↑ 1.0 1.1 1.2 Wang M, Munch IC, Hasler PW, Prünte C, Larsen M. Central serous chorioretinopathy. Acta Ophthalmol (Copenh). 2008;86(2):126-145. doi:10.1111/j.1600-0420.2007.00889.x.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Liew G, Quin G, Gillies M, Fraser-Bell S. Central serous chorioretinopathy: a review of epidemiology and pathophysiology. Clin Experiment Ophthalmol. 2013;41(2):201-214. doi:10.1111/j.1442-9071.2012.02848.x.
  3. ↑ 3.0 3.1 Kitzmann AS, Pulido JS, Diehl NN, Hodge DO, Burke JP. The incidence of central serous chorioretinopathy in Olmsted County, Minnesota, 1980-2002. Ophthalmology. 2008;115(1):169-173. doi:10.1016/j.ophtha.2007.02.032.
  4. ↑ Kang HG, Woo SJ, Lee JY, et al. Pathogenic Risk Factors and Associated Outcomes in the Bullous Variant of Central Serous Chorioretinopathy. Ophthalmol Retina. 2022;6(10):939-948. doi:10.1016/j.oret.2022.04.015
  5. ↑ Tsui JC, Carroll RM, Brucker AJ, Kolomeyer AM. Bullous Variant of Central Serous Chorioretinopathy in Goodpasture's Disease - A Case Report and Review of Literature. Retin Cases Brief Rep. Published online December 5, 2023. doi:10.1097/ICB.0000000000001522
  6. ↑ Garg S, Dada T, Talwar D, Biswas N. Endogenous cortisol profile in patients with central serous chorioretinopathy. Br J Ophthalmol. 1997;81(11):962-964.
  7. ↑ Carvalho-Recchia CA, Yannuzzi LA, Negrão S, et al. Corticosteroids and central serous chorioretinopathy. Ophthalmology. 2002;109(10):1834-1837. doi:10.1016/S0161-6420(02)01117-X.
  8. ↑ Bouzas EA, Karadimas P, Pournaras CJ. Central Serous Chorioretinopathy and Glucocorticoids. Surv Ophthalmol. 2002;47(5):431-448. doi:10.1016/S0039-6257(02)00338-7.
  9. ↑ 9.0 9.1 9.2 Haimovici R, Koh S, Gagnon DR, Lehrfeld T, Wellik S. Risk factors for central serous chorioretinopathy: A case–control study. Ophthalmology. 2004;111(2):244-249. doi:10.1016/j.ophtha.2003.09.024.
  10. ↑ Tripathy K. Is Helicobacter pylori the culprit behind central serous chorioretinopathy? Graefes Arch Clin Exp Ophthalmol. 2016 Oct;254(10):2069-2070.  Epub 2016 Jun 30. PubMed PMID: 27364118.
  11. ↑ 11.0 11.1 Yannuzzi LA. Type A behavior and central serous chorioretinopathy. Trans Am Ophthalmol Soc. 1986;84:799-845.
  12. ↑ 12.0 12.1 Tewari HK, Gadia R, Kumar D, Venkatesh P, Garg SP. Sympathetic–Parasympathetic Activity and Reactivity in Central Serous Chorioretinopathy: A Case–Control Study. Invest Ophthalmol Vis Sci. 2006;47(8):3474-3478. doi:10.1167/iovs.05-1246.
  13. ↑ 13.0 13.1 Jampol LM, Weinreb R, Yannuzzi L. Involvement of corticosteroids and catecholamines in the pathogenesis of central serous chorioretinopathy: a rationale for new treatment strategies. Ophthalmology. 2002;109(10):1765-1766. doi:10.1016/S0161-6420(02)01303-9.
  14. ↑ 14.0 14.1 14.2 Prunte C, Flammer J. Choroidal Capillary and Venous Congestion in Central Serous Chorioretinopathy. Am J Ophthalmol. 1996;121(1):26-34. doi:10.1016/S0002-9394(14)70531-8.
  15. ↑ 15.0 15.1 Giovannini A, Scassellati-Sforzolini B, D’altobrando E, Mariotti C, Rutili T, Tittarelli R. Choroidal Findings In The Course Of Idiopathic Serous Pigment Epithelium Detachment Detected By Indocyanine Green Videoangiography. Retina. 1997;17(4):286-296.
  16. ↑ Spitznas M. Pathogenesis of central serous retinopathy: A new working hypothesis. Graefes Arch Clin Exp Ophthalmol. 1986;224:321-324.
  17. ↑ Marmor MF. New hypotheses on the pathogenesis and treatment of serous retinal detachment. Graefes Arch Clin Exp Ophthalmol. 1988;226(6):548-552. doi:10.1007/BF02169203.
  18. ↑ Nicholson B, Noble J, Forooghian F, Meyerle C. Central Serous Chorioretinopathy: Update on Pathophysiology and Treatment. Surv Ophthalmol. 2013;58(2):103-126. doi:10.1016/j.survophthal.2012.07.004.
  19. ↑ Cotticelli L, Borrelli M, D’ALESSIO AC, et al. Central serous chorioretinopathy and Helicobacter pylori. Eur J Ophthalmol. 2006;Vol. 16(2):274-278.
  20. ↑ Mauget-Faÿsse M, Kodjikian L, Quaranta M, et al. Helicobacter pylori in central serous chorioretinopathy and diffuse retinal epitheliopathy. Results of the first prospective pilot study. J Fr Ophtalmol. 2002;25(10):1021-1025.
  21. ↑ Asensio-Sánchez V, Rodríguez-Delgado B, García-Herrero E, Cabo-Vaquera V, García-Loygorri C. Central Serous Chorioretinopathy As An Extradigestive Manifestation Of Helicobacter Pylori Gastric Infection. Arch Soc Esp Oftalmol. 2008;83:177-182.
  22. ↑ 22.0 22.1 22.2 Rahbani-Nobar MB, Javadzadeh A, Ghojazadeh L, Rafeey M, Ghorbanihaghjo A. The effect of Helicobacter pylori treatment on remission of idiopathic central serous chorioretinopathy. Mol Vis. 2011;17:99-103.
  23. ↑ Fraunfelder FW, Fraunfelder FT. Central Serous Chorioretinopathy Associated With Sildenafil: Retina. 2008;28(4):606-609. doi:10.1097/IAE.0b013e31815ec2c8.
  24. ↑ Hassan L, Carvalho C, Yannuzzi LA, Iida T, NegrÃo S. Central serous chorioretinopathy in a patient using methylenedioxymethamphetamine (MDMA) or “ecstasy.” Retina. 2001;21(5):559–561.
  25. ↑ 25.0 25.1 Mazumdar S, Tripathy K, Sarma B, Agarwal N. Acquired myopia followed by acquired hyperopia due to serous neurosensory retinal detachment following topiramate intake. Eur J Ophthalmol. 2018 Sep 3:1120672118797286. doi: 10.1177/1120672118797286. [Epub ahead of print] PubMed PMID: 30175623.
  26. ↑ 26.0 26.1 Colucciello M. Update on Central Serous Chorioretinopathy. Retinal Physician. http://www.retinalphysician.com/articleviewer.aspx?articleID=107233. Published July 1, 2012. Accessed October 27, 2016.
  27. ↑ Yavaş GF, Küsbeci T, Kaşikci M, et al. Obstructive Sleep Apnea in Patients with Central Serous Chorioretinopathy. Curr Eye Res. 2014;39(1):88-92. doi:10.3109/02713683.2013.824986.
  28. ↑ Gäckle HC, Lang GE, Freissler KA, Lang GK. [Central serous chorioretinopathy. Clinical, fluorescein angiography and demographic aspects]. Ophthalmol Z Dtsch Ophthalmol Ges. 1998;95(8):529-533.
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  30. ↑ Desai UR, Alhalel AA, Campen TJ, Schiffman RM, Edwards PA, Jacobsen GR. Central serous chorioretinopathy in African Americans. J Natl Med Assoc. 2003;95(7):553-559.
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  32. ↑ Cassel GH, Brown GC, Annesley WH. Central serous chorioretinopathy: a seasonal variation? Br J Ophthalmol. 1984;68(10):724-726. doi:10.1136/bjo.68.10.724.
  33. ↑ Lee JK, Yoon BJ. A Seasonal Variation of Central Serous Chorioretinopathy. J Korean Ophthalmol Soc. 1986;27(5):801-803.
  34. ↑ Weenink AC, Borsje RA, Oosterhuis JA. Familial chronic central serous chorioretinopathy. Ophthalmol J Int Ophtalmol Int J Ophthalmol Z Für Augenheilkd. 2001;215(3):183-187. doi:50855.
  35. ↑ Fok ACT, Chan PPM, Lam DSC, Lai TYY. Risk Factors for Recurrence of Serous Macular Detachment in Untreated Patients with Central Serous Chorioretinopathy. Ophthalmic Res. 2011;46(3):160-163. doi:10.1159/000324599.
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  39. ↑ 39.0 39.1 Imamura Y, Fujiwara T, Margolis R, Spaide RF. Enhanced Depth Imaging Optical Coherence Tomography Of The Choroid In Central Serous Chorioretinopathy: Retina. 2009;29(10):1469-1473. doi:10.1097/IAE.0b013e3181be0a83.
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  43. ↑ 43.0 43.1 Chin EK, Almeida DR, Roybal CN, et al. Oral mineralocorticoid antagonists for recalcitrant central serous chorioretinopathy. Clin Ophthalmol Auckl NZ. 2015;9:1449-1456. doi:10.2147/OPTH.S86778.
  44. ↑ Barnes PJ. Corticosteroid effects on cell signalling. Eur Respir J. 2006;27(2):413-426. doi:10.1183/09031936.06.00125404.
  45. ↑ Tittl MK, Spaide RF, Wong D, et al. Systemic findings associated with central serous chorioretinopathy. Am J Ophthalmol. 1999;128(1):63-68.
  46. ↑ Yang S, Zhang L. Glucocorticoids and vascular reactivity. Curr Vasc Pharmacol. 2004;2(1):1-12.
  47. ↑ Arndt C, Sari A, Ferre M, et al. Electrophysiological effects of corticosteroids on the retinal pigment epithelium. Invest Ophthalmol Vis Sci. 2001;42(2):472-475.
  48. ↑ Sibayan SA, Kobuch K, Spiegel D, et al. Epinephrine, but not dexamethasone, induces apoptosis in retinal pigment epithelium cells in vitro: possible implications on the pathogenesis of central serous chorioretinopathy. Graefes Arch Clin Exp Ophthalmol Albrecht Von Graefes Arch Für Klin Exp Ophthalmol. 2000;238(6):515-519.
  49. ↑ Gemenetzi M, De Salvo G, Lotery AJ. Central serous chorioretinopathy: an update on pathogenesis and treatment. Eye Lond Engl. 2010;24(12):1743-1756. doi:10.1038/eye.2010.130.
  50. ↑ Jinghua S, Junfeng T, Zhitao W, Hong Y, Xuefei Z, Lingli L. Effect of catecholamine on central serous chorioretinopathy. J Huazhong Univ Sci Technolog Med Sci. 2003;23(3):313-316. doi:10.1007/BF02829525.
  51. ↑ Folk JC, Thompson HS, Han DP, Brown CK. Visual function abnormalities in central serous retinopathy. Arch Ophthalmol Chic Ill 1960. 1984;102(9):1299-1302.
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  54. ↑ Yamada K, Hayasaka S, Setogawa T. Fluorescein-angiographic patterns in patients with central serous chorioretinopathy at the initial visit. Ophthalmol J Int Ophtalmol Int J Ophthalmol Z Für Augenheilkd. 1992;205(2):69-76.
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  58. ↑ Matsumoto H, Sato T, Kishi S. Outer nuclear layer thickness at the fovea determines visual outcomes in resolved central serous chorioretinopathy. Am J Ophthalmol. 2009;148(1):105-110.e1. doi:10.1016/j.ajo.2009.01.018.
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  66. ↑ Nielsen JS, Jampol LM. Oral Mifepristone For Chronic Central Serous Chorioretinopathy: Retina. 2011;31(9):1928-1936. doi:10.1097/IAE.0b013e31821c3ef6.
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  68. ↑ Gramajo AL, Marquez GE, Torres VE, Juárez CP, Rosenstein RE, Luna JD. Therapeutic benefit of melatonin in refractory central serous chorioretinopathy. Eye. 2015;29(8):1036-1045. doi:10.1038/eye.2015.104.
  69. ↑ 69.0 69.1 Caccavale A, Romanazzi F, Imparato M, Negri A, Morano A, Ferentini F. Low-dose aspirin as treatment for central serous chorioretinopathy. Clin Ophthalmol Auckl NZ. 2010;4:899.
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  76. ↑ Lim JW, Kim MU, Shin M-C. Aqueous Humor And Plasma Levels Of Vascular Endothelial Growth Factor And Interleukin-8 In Patients With Central Serous Chorioretinopathy: Retina. 2010;30(9):1465-1471. doi:10.1097/IAE.0b013e3181d8e7fe.
  77. ↑ Shin MC, Lim JW. Concentration of Cytokines in the Aqueous Humor of Patietns with Central Serous Chorioretinopathy. Retina. 2011;31(9):1937-1943. doi:10.1097/IAE.0b013e31820a6a17.
  78. ↑ Chung Y-R, Seo EJ, Lew HM, Lee KH. Lack of positive effect of intravitreal bevacizumab in central serous chorioretinopathy: meta-analysis and review. Eye. 2013;27(12):1339-1346. doi:10.1038/eye.2013.236.
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  84. ↑ Lai TYY, Chan W-M, Li H, Lai RYK, Liu DTL, Lam DSC. Safety enhanced photodynamic therapy with half dose verteporfin for chronic central serous chorioretinopathy: a short term pilot study. Br J Ophthalmol. 2006;90(7):869-874. doi:10.1136/bjo.2006.090282.
  85. ↑ Kim S-W, Oh J, Oh IK, Huh K. Retinal Pigment Epithelial Tear After Half Fluence PDT for Serous Pigment Epithelial Detachment in Central Serous Chorioretinopathy. Ophthalmic Surg Lasers Imaging. 2009;40(3):300-303. doi:10.3928/15428877-20090430-14.
  86. ↑ Lee PY, Kim KS, Lee WK. Severe choroidal ischemia following Photodynamic Therapy for pigment epithelial detachment and chronic central serous chorioretinopathy. Jpn J Ophthalmol. 2009;53(1):52-56. doi:10.1007/s10384-008-0613-z.
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  88. ↑ Bae SH, Heo J, Kim C, et al. Low-Fluence Photodynamic Therapy versus Ranibizumab for Chronic Central Serous Chorioretinopathy: One-Year Results of a Randomized Trial. Ophthalmology. 2014;121(2):558-565. doi:10.1016/j.ophtha.2013.09.024.
  89. ↑ Nicoló M, Eandi CM, Alovisi C, et al. Half-Fluence Versus Half-Dose Photodynamic Therapy in Chronic Central Serous Chorioretinopathy. Am J Ophthalmol. 2014;157(5):1033-1037.e2. doi:10.1016/j.ajo.2014.01.022.
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  92. ↑ Ricci F, Missiroli F, Regine F, Grossi M, Dorin G. Indocyanine green enhanced subthreshold diode-laser micropulse photocoagulation treatment of chronic central serous chorioretinopathy. Graefes Arch Clin Exp Ophthalmol. 2008;247(5):597-607. doi:10.1007/s00417-008-1014-1.
  93. ↑ Yadav NK, Jayadev C, Rajendran A, Nagpal M. Recent developments in retinal lasers and delivery systems. Indian J Ophthalmol. 2014;62(1):50. doi:10.4103/0301-4738.126179.
  94. ↑ 94.0 94.1 Yadav NK, Jayadev C, Mohan A, et al. Subthreshold micropulse yellow laser (577 nm) in chronic central serous chorioretinopathy: safety profile and treatment outcome. Eye. 2015;29(2):258-265. doi:10.1038/eye.2014.315.
  95. ↑ Chen S-N, Hwang J-F, Tseng L-F, Lin C-J. Subthreshold Diode Micropulse Photocoagulation for the Treatment of Chronic Central Serous Chorioretinopathy with Juxtafoveal Leakage. Ophthalmology. 2008;115(12):2229-2234. doi:10.1016/j.ophtha.2008.08.026.
  96. ↑ Malik KJ, Sampat KM, Mansouri A, Steiner JN, Glaser BM. Low-Intensity/High-Density Subthreshold Micropulse Diode Laser For Chronic Central Serous Chorioretinopathy: Retina. 2015;35(3):532-536. doi:10.1097/IAE.0000000000000285.
  97. ↑ Verma L, Sinha R, Venkatesh P, Tewari H. Comparative evaluation of diode laser versus argon laser photocoagulation in patients with central serous retinopathy: A pilot, randomized controlled trial [ISRCTN84128484]. BMC Ophthalmol. 2004;4(1). doi:10.1186/1471-2415-4-15.
  98. ↑ Venkatesh P, Chawla R, Tripathy K, et al. Scleral resection in chronic central serous chorioretinopathy complicated by exudative retinal detachment. Eye Vis Lond Engl2016;3:23. doi:10.1186/s40662-016-0055-5
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