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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. If suspected, those diagnoses should be ruled out. A thorough history, detailed exam and appropriate imaging and laboratory tests can help delineate between these diagnoses. 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 CSR.

Garg and colleagues found that patients with acute CSCR have higher levels of endogenous cortisol compared to age-matched controls. 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 hyper-permeability. Other associations to CSCR have been described. Medications that inhibit this pathway include sorafenib and vemurafenib. Central serous chorioretinopathy is associated with increased sympathetic activity, and obstructive sleep apnea is known to cause such increases.

Most patients who present with CSCR are between the ages of 28 to 68 years with an average age of 43 years. Most CSC cases are diagnosed in patients with no refractive error or mild hyperopia. Neurosensory detachments and pigment epithelial detachments simulating CSCR may also be noted with choroidal ishcemia in SLE, Goodpasture syndrome, polyarteritis nodosa, thrombotic thrombocytopenic parpura, disseminated intravascular coagulation, granulomatosis with polyangiitis formerly Wegener granulomatosis , malignant hypertension, and pregnancy induced hypertension.

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.

Microscopic evaluation of iatrogenic CSCR in monkeys showed damage and defects endothelial cells of choriocapillaries with overlying degeneration of RPE cells and indocyanine green angiography studies in humans have demonstrated choroidal staining, suggesting increased capillary permeability to be the cause of CSCR.

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.

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. 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. Some mechanisms of action of steroids on the choroid and RPE include potentiation of adrenergic hormones, [42] hypertension, [43] [44] and altered ion transport in RPE cells. Foveal attenuation, chronic macular edema, and damage of the foveal photoreceptor layer have been reported as causes of visual loss in CSC. 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. Type A personality, abdominal pain from H. 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. The PED may touch the posterior aspect of the retina and there is usually a leak at this site.

In CSCR with subretinal fibrin, an area of lucency may denote the site of leak. 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.

The leaking areas on fundus fluorescein angiography can correlate to hyperreflective areas on the infrared image in OCT in patients with CSCR. OCT can be helpful in cases of CSCR that show equivocal signs on clinical exam, and can show detailed findings not appreciable on exam such as small PEDs and hyper-reflective, fibrinous sub-retinal fluid. Enhanced depth imaging OCT technology has been able to identify choroidal thickening bilaterally, even in patients with unilateral CSCR.

Fundus autofluorescence FAF photography 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 nm is able to study the RPE, the choriocapillaris, and choroid, by determining melanin fluorescence.

Acute CSCR is a self-limited condition with resolution of neurosensory retinal detachment and generally good recovery of visual acuity within three months.

As CSCR usually resolves spontaneously within 2 to 3 months, observation is currently standard of care for newly presenting cases. Exogenous steroids of any route oral, intramuscular, intranasal, etc. 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.

Several studies investigated the effects of screening and treating H. 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. As mineralocorticoid receptor action has been implicated in the pathogenesis of CSCR, Zhao and Bousquet treated patients with eplerenone, a mineralocorticoid antagonist, for five weeks and found a significant and rapid improvement of retinal detachment with improvement in mean central macular thickness, sub-retinal fluid height, and visual acuity that persisted at five month follow up.

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. Baseline serum potassium levels and renal function should be established, such as with a basic metabolic panel. 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.

However, its use may be avoided in countries with high prevalence of tuberculosis due to the risk of resistance. Melotonin is an endogenous neuromodulator that has been linked to circadian cycles and sleep regulation, aging, and neuroprotection via an antioxidant mechanism.

A study of eight patients showed significant improvements in CMT 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.

A randomized control trial RCT of patients tested positive for H. A case series of treated biopsy positive H. These studies with contradictory results indicate that larger RCTs are needed to elucidate the clinical significance of H. The role of anti-adrenergic therapy for CSCR is unclear.

A small case series in 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. Although anti-adrenergic agents have been shown to be beneficial in CSCR in some studies, this therapy has not been widely implemented in treatment. Also, polypoidal choloridal vasculopathy which is an important differential of CSCR in patients older than 50 years, may benefit from anti-VEGF agents.

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. It is hypothesized that destruction of these detached sites allow scarring that re-attaches the retina.

For patients with focal RPE detachments not involving the fovea, focal argon laser photocoagulation may be considered [2]. 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 [78] [79]. Others have concluded there was no difference in CSCR recurrence rates between groups after 1 to 12 years of follow-up [78] [80] [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. Due to these potential complications, patients treated with focal argon laser photocoagulation should have regular ophthalmology follow-up.

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.

PDT necessitates the avoidance of physical activity after treatment. 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. This allows exposure to a large area of RPE cells, which then down-regulate cytokine production and inflammation.

Fluorescein angiography and indocyanine green ICG angiography can be supplemented to determine areas of treatment. Furthermore, the nm laser allows for more concentrated light with a lower power compared to the nm laser. Big 10 The Vault — "—" denotes albums that did not chart or were not released in that territory. Accessed July 8, Hung Medien. Retrieved 24 February Top peaks between January and December Ryan, Gavin Australia's Music Charts London: Guinness World Records Limited.

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