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Symptoms

Central scotoma, blurred or dim vision, objects may appear distorted (metamorphopsia) and miniaturized (micropsia), colors may appear faded. Usually unilateral, but can be bilateral (more likely in older patients, may not be symptomatic at the same time). May be asymptomatic.

Signs

(See Figure 11.15.1.)

Figure 11.15.1: Central serous chorioretinopathy.

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Critical

Localized serous detachment of the neurosensory retina in the macula without subretinal blood or lipid exudates. The margins of the detachment are sloping and merge gradually into the attached retina.

Other

Visual acuity usually ranges from 20/20 to 20/200. Amsler grid testing reveals relative scotoma and distortion of straight lines. May have a small serous RPE detachment or subretinal fibrin. Focal RPE changes may indicate sites of previous episodes. (Neither blood or lipid should be present. If so, CNV should be ruled out.)

Differential Diagnosis

These entities may produce a serous detachment of the neurosensory retina in the macula.

Etiology

Workup

  1. Amsler grid test to document the area of field involved. See Appendix 4, Amsler Grid.

  2. Slit-lamp examination of the macula with a handheld lens to rule out concomitant CNV. In addition, search for an optic pit of the disc.

  3. Dilated fundus examination with indirect ophthalmoscopy to rule out a choroidal tumor or RRD.

  4. OCT is helpful in demonstrating SRF or PEDs and for monitoring purposes. Enhanced-depth imaging OCT often demonstrates choroidal thickening and may be a useful adjunct in diagnosis (See Figures 11.15.2 and 11.15.3).

    Figure 11.15.2: Intravenous fluorescein angiography of central serous chorioretinopathy showing “smoke-stack” pattern of dye leakage.

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    Figure 11.15.3: Enhanced-depth imaging optical coherence tomography of central serous chorioretinopathy showing subretinal fluid and choroidal thickening.

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  5. IVFA and ICGA if the diagnosis is uncertain or presentation atypical, CNV is suspected, or laser treatment is to be considered. IVFA shows the nearly pathognomonic “smoke-stack” pattern of dye leakage in 10% to 20% of cases. ICGA shows multifocal hyperfluorescent patches in the early phase. OCTA is useful for detecting any CNV which can occur secondarily in chronic/recurrent CSCR.

  6. In cases of chronic CSCR, a systemic workup including cortisol levels and renal function should be considered.

Treatment

  1. Observation: Acute CSCR is usually self-limited with good visual prognosis. Worse prognosis for patients with recurrent disease, multiple areas of detachment, or prolonged course.

  2. Stop corticosteroids, if possible, including topical skin and nasal spray preparations.

  3. Laser photocoagulation: May accelerate visual recovery, but long-term benefit and safety are unclear. May increase risk of CNV formation. Given the CNV risk, use low laser intensity. Subthreshold laser has also been used with variable success. Consider laser for:

    • Persistence of a serous detachment for several months. 

    • Recurrence of the condition in an eye that sustained a permanent visual deficit from a previous episode.

    • Occurrence in the contralateral eye after a permanent visual deficit resulted from a previous episode.

    • Patient requires prompt restoration of vision (e.g., occupational necessity).

  4. Photodynamic therapy (PDT) with verteporfin: May be helpful for chronic CSCR. Half-dose PDT may be considered for rapid SRF resolution in patients with acute CSCR.

  5. Mineralocorticoid receptor antagonists: Case reports have suggested eplerenone and spironolactone as treatments, but larger studies question their utility.

  6. If CNV develops, consider anti-VEGF therapy.

Follow-Up

  1. Examine patients every 6 to 8 weeks until resolution.