Summary of Macular Diseases: Diagnosis and Treatment
Macular Diseases: Diagnosis and Treatment for Students
Introduction
Central serous chorioretinopathy (CSCR) is an exudative chorioretinopathy characterized by localized serous detachment of the neurosensory retina at the macula, often associated with a thickened choroid and focal retinal pigment epithelium (RPE) dysfunction. It most commonly affects working-age adults and typically causes unilateral, painless central vision disturbance.
Definition: Central serous chorioretinopathy is an exudative condition in which hyperpermeability of the choriocapillaris and focal defects in the RPE lead to accumulation of subretinal fluid beneath the macula, producing a serous neurosensory retinal detachment.
Pathophysiology — step by step
1. Primary choroidal abnormality
- Pachychoroid: thickened choroid with dilated Haller layer vessels (pachyvessels). This increases hydrostatic pressure and choroidal hyperpermeability.
2. RPE dysfunction
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Focal or diffuse hyperpermeability of the choriocapillaris leads to increased fluid and protein leaking through the RPE.
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Loss of normal RPE active fluid transport and breakdown of intercellular (zonular) adhesions in RPE allow fluid to accumulate in the subretinal space.
3. Neurosensory retinal detachment
- Fluid accumulates between the RPE and photoreceptor layer producing a blister-like (round/oval) detachment at the macula. Photoreceptor separation and disruption of the ellipsoid zone cause visual symptoms.
Box: Key mechanism — choroidal hyperpermeability + RPE barrier failure = subretinal fluid accumulation
Epidemiology & risk factors
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Typical age: peak incidence between 25 and 50 years (working-age adults).
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Sex: more common in males than females.
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Bilaterality: can be bilateral; reported up to ~42%, more common over age 50.
Major risk factors
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Psychological stress and Type A personality
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Endogenous cortisol elevation and exogenous corticosteroids (oral, inhaled, topical, intravitreal, injection/IV)
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Pregnancy
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Helicobacter pylori infection (association reported)
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Sleep apnea
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Phosphodiesterase type 5 inhibitors (eg, sildenafil/Viagra) — possible association
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Recreational drugs (eg, MDMA/ecstasy)
Clinical presentation
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Unilateral, painless central visual disturbance: blurring, central scotoma, metamorphopsia, micropsia
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Visual acuity ranges from near normal to markedly reduced (commonly 20/20 to 20/200)
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Color vision changes and reduced contrast sensitivity
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No relative afferent pupillary defect (RAPD) unless severe/other pathology
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Hyperopic shift (transient increase in hyperopia) due to elevation of the macula
Examination findings (signs)
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Fundus: round or oval “blister-like” serous neurosensory retinal detachment at the macula; subretinal fluid may be clear, turbid, or fibrinous
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RPE often intact in simple CSCR (contrast with RPE detachments)
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OCT: subretinal fluid with neurosensory detachment; pachyvessels and increased subfoveal choroidal thickness on enhanced-depth imaging
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FA (fluorescein angiography): characteristic leakage patterns
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Ink-blot: a pinpoint leak that enlarges and becomes more intense
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Smoke-stack: an early pinpoint leak that rises vertically then spreads (less common)
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ICGA (indocyanine green angiography): demonstrates choroidal hyperpermeability and large pachyvessels
Table: FA patterns in CSCR vs. PED
| Feature | CSCR (subretinal fluid) | Serous PED |
|---|---|---|
| Lesion shape | Blister-like neurosensory detachment | Dome-shaped, sharply demarcated elevation of RPE |
| FA early | Pinpoint leak (ink-blot) or smoke-stack | Early pooling confined to PED area |
| FA late | Increasing size and intensity of leak | Persistent hyperfluorescence within PED without diffuse spread |
Disease course
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Spontaneous resolution occurs in 80–90% within 3–6 months.
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Visual acui
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Central Serous Chorioretinopathy
Klíčové pojmy: CSCR is caused by choroidal hyperpermeability plus RPE barrier failure leading to subretinal fluid., Typical presentation: unilateral painless central blur, metamorphopsia, and micropsia in 25–50-year-olds., Acute CSCR often resolves spontaneously within 3–6 months; observe with OCT every 6–8 weeks., Persistent subretinal fluid beyond ~3–4 months defines chronic CSCR and prompts treatment., FA patterns: ink-blot (common) and smoke-stack (less common) pinpoint leaks; ICGA shows choroidal hyperpermeability., First-line interventions for chronic CSCR: reduced-fluence or half-dose photodynamic therapy (PDT) and focal laser for extrafoveal leaks., Risk factors include systemic/exogenous corticosteroids, stress, pregnancy, sleep apnea, H. pylori, and PDE-5 inhibitors., Differentiate CSCR from serous PED, ARMD, optic pit maculopathy, and rhegmatogenous detachment; use OCT, FA, and ICGA., Pachychoroid spectrum includes PPE, CSCR, PNV, PCV, FCE, and PPS; CSCR often coexists with PPE and pachyvessels., Refer when VA <20/70, atypical features, persistent fluid >4–6 months, bilateral severe disease, or suspected CNV/PCV