Introduction
Commonly found in people ages 40-50
- 6x more likely in males than females (9.9 vs 1.7 per 100,000)
- Bias decreases with age
- Age of onset varies between 7 to 83 years
- Is the 4th most common retinopathy associated with fluid leakage, behind neovascular AMD, diabetic macular oedema and RVO
- Occurs more often in stressed individuals, and high levels of cortisol
Dead Giveaways
Acute CSCR:
Typically spontaneously resolves in 3-6 months
In this case, there is a subretinal detachment, and a noticeable elevation on fundus images
Px may report hyperopic shift, blur and metamorphopsia
Really nice photo from Retinal Image Bank shows the smooth contours superiorly, and bright borders inferiorly, creating a blister On the OCT:
Whilst PED can be present, this image is mainly to show the difference between PED and SRF
Non-resolving CSCR
Not exactly chronic, and describes persistent SRF longer than 4 months, and is typically associated with elongated PR outer segments, along with subretinal fibrin deevelopment.
Note the extensions of the PR at the top of the SRF, and the subretinal fibrin at the bottom, originating from the choroid, to reattach the neurosensory retina On the fundus, can appear as hyper-reflective dots:
Note the yellow dots. Thought to consist of macrophages, plasma, proteins and inflammatory cell debris
Chronic CSCR:
Can be recurrent, but is usually classified with atrophic RPE changes, with or without activity
Here, the biggest giveaway is FAF:
Shown slightly in the left and more so in the right, there is a vertical gravitational tract, defined by widespread pigmentary changes The gravitational tract occurs due to the subretinal space being dragged as fluid moves down via gravity.
RPE atrophy appears hypo-AF
Should be noted that 85% of non-resolving CSCR also have gravitational tracts
Initially, they can appear hyper-AF, but overtime, it mottles and becomes hypo.
On the OCT, RPE and retinal atrophy may be observed, leading to a slight increase in choroidal transmission
Inactive CSCR:
Gravitational tract can be present indicating chronic CSCR, though there is no SRF
OCT may reveal loss of outer retina layers and OCT
Increased transmission of the choroid seen, along with loss of ELM, shrinking of ONL, loss of RPE
Posterior Cystoid Retinal Degeneration:
Occurs in long standing CSCR, typically after 5 years
Associated with intraretinal hypo-reflective spaces, potentially due to fluid leakage into the inner retinal layers.
Hyper-reflective areas indicate CSCR longer than 4 months
Note the cystic spaces
diagnostic features
Risks: (most associated with increased cortisol)
Type A personality type
Someone who is very anxious, tense and drives to overachieve
Very competitive or emotionally unstable
Systemic corticosteroid use
Stressful events and personalities
Less significant factors:
pregnancy and pre-eclampsia
Hypertension
Hypercortisolism from Cushing's syndrome
Poor sleep
Disrupted circadian rhythm
Asian ethnicity
Acute CSCR Sequelae
It is possible for the SRF to dissipate, recombining the neurosensory retina and the RPE, but if the transport system is overhwelmed again, it leads to recurrent CSCR
Chronic CSCR Sequelae:
CSCR can show FIPED
Type-1 sub-RPE CNV associated with flat irregular PED (OCT-A indicated)
FIPED's can be avascular or vascular, depending on if the interior is hypo or hyper-reflective
Avascular 
Vascular Ignoring the SRF in both images, the avascular displays a dark line just under the FIPED, but the vascular shows a considerably more hyper-reflective area, indicating the presence of vessels
FIPEDs are not a classic feature of CSCR, indicating OCT-A is needed. It is however good to differentiate against PNV which does have FIPEDs
CSCR's involvement of the macular, during cystoid degeneration, can greatly affect vision