Central serous chorioretinopathy (CSCR) is a retinal disorder characterized by the accumulation of subretinal fluid, leading to retinal detachment and visual impairment. Despite being a relatively common condition, CSCR presents diagnostic and management challenges due to its variable clinical course and multifactorial etiology. This article aims to provide a thorough overview of CSCR, encompassing its pathophysiology, clinical manifestations, diagnostic approaches, treatment strategies, and recent advancements in research.

Introduction: Central serous chorioretinopathy (CSCR) is a retinal disorder characterized by the accumulation of subretinal fluid, resulting in neurosensory retinal detachment. While typically self-limiting, CSCR can cause significant visual impairment and impact quality of life, necessitating timely diagnosis and appropriate management. Despite being well-recognized, the exact etiology and optimal management of CSCR remain subjects of ongoing research and debate.

Pathophysiology: The pathophysiology of CSCR involves dysfunction of the choroid and retinal pigment epithelium (RPE), leading to impaired fluid transport and accumulation beneath the neurosensory retina. Risk factors such as systemic hypertension, corticosteroid use, and Type A personality traits have been implicated in CSCR pathogenesis. Emerging evidence also suggests a role for genetic predisposition and dysregulation of the hypothalamic-pituitary-adrenal axis in disease development.

Clinical Manifestations: Clinical manifestations of CSCR vary widely and may include blurred or distorted vision, central scotoma, metamorphopsia, and micropsia. Fundoscopic examination typically reveals serous retinal detachment, often localized in the macular region. Optical coherence tomography (OCT) imaging is invaluable for visualizing subretinal fluid and assessing structural changes in the retina and choroid.

Diagnostic Approaches: Diagnosing CSCR relies on a combination of clinical evaluation and imaging modalities, including OCT, fluorescein angiography (FA), and indocyanine green angiography (ICGA). OCT findings such as subretinal fluid accumulation and RPE detachment are characteristic of CSCR and aid in distinguishing it from other retinal pathologies. FA and ICGA can further delineate choroidal vascular abnormalities and leakage patterns.

Treatment Strategies: Management of CSCR aims to promote fluid resorption, restore retinal anatomy, and preserve visual function. While observation may suffice for some cases of acute CSCR with spontaneous resolution, persistent or recurrent cases may require intervention. Treatment modalities include focal laser photocoagulation, photodynamic therapy, intravitreal anti-vascular endothelial growth factor (anti-VEGF) agents, and mineralocorticoid receptor antagonists.

Recent Advancements: Recent advancements in CSCR research have expanded our understanding of disease pathogenesis and treatment options. Novel imaging techniques such as swept-source OCT and enhanced-depth imaging OCT have improved visualization of choroidal and retinal structures, facilitating early diagnosis and monitoring of CSCR. Emerging therapies targeting inflammatory pathways, oxidative stress, and choroidal vasculature hold promise for more targeted and effective management of CSCR.

Conclusion: In conclusion, central serous chorioretinopathy remains a complex and multifaceted retinal disorder with variable clinical manifestations and treatment responses. By staying abreast of the latest research findings and leveraging advanced diagnostic modalities and treatment options, clinicians can optimize patient outcomes and improve the management of this challenging condition.

Reference Links:

• American Academy of Ophthalmology: Central Serous Chorioretinopathy
• PubMed: Advances in Central Serous Chorioretinopathy
• National Eye Institute: Central Serous Chorioretinopathy
• Review of Ophthalmology: Current Concepts in Central Serous Chorioretinopathy
• Retina Today: Recent Advances in Central Serous Chorioretinopathy