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The differential diagnosis for a serous (exudative) retinal detachment includes:

• Central serous chorioretinopathy
  
• Inflammatory (Vogt-Koyanagi-Harada disease, posterior scleritis, choroiditis)
  
• Choroidal neovascular membrane (AMD, myopic CNV)
  
• Malignant hypertensive retinopathy
  
• Neoplastic lesions (choroidal melanoma, choroidal haemangioma)

Optical coherence tomography (OCT) through the left macula demonstrated subretinal (subsensory) fluid (Figure 2). An accumulation of material was noted on the underside of the detached retina. Hyperreflective dots were noted within this material and also within the retina itself. Fundus autofluorescence imaging demonstrated hyperautofluorescent dots within the serous retinal detachment (Figure 3).

The patient was advised of the association between corticosteroids and CSC. As his hayfever symptoms were not especially severe he was happy to stop using the Rhinocort® steroid nasal spray. Review was scheduled for 3 months. At this time there was no improvement in the degree of subretinal fluid as measured by OCT and the patient was still very troubled by his symptoms. Vision remained 6/15 (pinhole 6/12+).

As the CSC was not improving and the patient remained symptomatic, combined fluorescein and indocyanine green (ICG) angiography was performed in an effort to plan treatment. The fluorescein angiogram demonstrated focal leakage just inferonasal to the fovea (Figure 4A). The ICG angiogram demonstrated midphase choroidal hyperpermeability and hypercyanescence within the area of the serous detachment (Figure 4B). As there was an area of focal leakage, after informed consent light focal argon laser was used to ablate this area (Figure 5A). Two months following laser treatment the subretinal fluid had resolved (Figure 5B, 6) and visual acuity improved to 6/6-.

Central serous chorioretinopathy is a disease of the choroid and retinal pigment epithelium (RPE).(1) Choroidal dilation and hyperpermeability, which can be increased by risk factors such as corticosteroids, results in increased choroidal hydrostatic pressure. This increased pressure overcomes the barrier function of RPE and results in fluid accumulation underneath the retina and a serous (exudative) sensory detachment.

Patients with CSC are typically men aged 20-50 years. Presenting symptoms include central disturbance of vision, micropsia, metamorphopsia and altered colour perception.(1) A hypermetropic shift often occurs due to anterior displacement of the photoreceptors by the subretinal fluid. The hallmark finding in CSC is of a serous retinal detachment, often at the macula.1 Yellow precipitates often seen on the under surface of the retina are felt to represent shed outer photoreceptor segments.(2,3)

Optical coherence tomography (OCT) is a valuable tool in the diagnosis and monitoring of CSC. OCT findings include:

• Subretinal fluid.
  
• Serous pigment epithelial detachment (PED) (Figure 7A).
  
• Subretinal hyperreflective material (shed photoreceptor outer segments, engorged macrophages, and other inflammatory debris such as fibrin).(2,3)
  
• Hyperreflective intra and subretinal deposits.(2,3)
  
• Increased subfoveal choroidal thickness (this reflects choroidal hyperpermeability)5 (Figure 7B).

Red flags in the diagnosis of CSC include:

• Age over 50 years (need to consider neovascular AMD).
  
• Female patient unless pregnant (CSC is 6-8 times more common in men).(4)
  
• Presence of macular haemorrhage (consider CNV or polyps). However, in some cases CSC may be complicated by CNV.(6)
  
• Pathological myopia. While CSC can occur in myopia(7) it is more common in hypermetropes. In high myopes, myopic CNV or a dome shape macula configuration need to be considered.

Most cases of CSC will resolve spontaneously within 3-4 months.(8) There is however a high recurrence rate with almost 50% of patients having a further episode within the next year.(9) The most important and easily reversible risk factor for the condition is corticosteroid usage (oral, topical, inhaled, nasal spray, intra-articular). Eyecare professionals should liase with the patient’s physician to stop or minimise the dose of the medication where it is safe to do so. Other described risk factors include type A personality, phosphodiesterase inhibitors (e.g. Cialis and Viagra), obstructive sleep apnea, hypertension and pregnancy.(1) Since most cases resolve spontaneously within 4 months, modification of reversible risk factors and observation is the usual management.(1)

Persistent submacular fluid can cause irreversible macular damage.(1) Accordingly most retinal specialists intervene if there has been no improvement following 3-6 months of observation. Fluorescein and indocyanine green (ICG) angiography is used to guide treatment. If angiography demonstrates focal leakage away from the foveal centre, argon laser can be used to promote subretinal fluid reabsorption. Although the precise mechanism is not known, it may seal focal RPE defects, promote the recruitment of nearby RPE cells or improve the pumping function of RPE cells.(1)

If there is no focal leakage, or it is too close to safely treat with argon laser, reduced fluence photodynamic therapy (PDT) has been reported to have a close to 95% success in resolving subretinal fluid.(10,11) It has a good safety profile but risks include choroidal ischaemia and RPE damage, both of which can result in irreversible vision loss.(1) An intravenous medication (Visudyne® (verteporfin)) is injected intravenously before being activated by the PDT laser. In Australia, verteporfin is only listed for treatment of neovascular AMD and an application for compassionate usage has to be made to the Therapeutic Goods Administration (TGA) and manufacturer for its supply in patients with CSC.