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Retina When and How to Treat Central Serous ChorioretinopathyThough we don’t know a great deal about its etiology, we do know some solid, effective ways to treat this condition.Edward B. Feinberg,
MD, MPH, and Vito R. LaRocca, MD, MPH , The Disease CSC is a syndrome characterized by idiopathic serous detachment of the macula caused by a focal loss 
of the blood-retina barrier function of the retinal pigment epithelium (RPE).
Traditionally, CSC has been thought of as a disease affecting young, 20- to
45-year-old males.1 However, recently it’s diagnosed with
increasing frequency among patients over 50. In this population, the male to
female ratio diminishes to 2:1 from the 10:1 ratio seen in younger
patients.2 It’s critical to differentiate CSC from age-related
macular degeneration (AMD) amongst these older patients. CSC is uncommon among
African Americans, but frequent in Caucasians, Hispanics and
Asians.3 Upon retinal examination, the CSC patient will characteristically show a serous retinal detachment. Clinical Findings and Diagnosis The most frequent symptom of CSC is a unilateral decrease of central vision. On questioning, patients with CSC frequently describe metamorphopsia or micropsia, as well as color desaturation and a prolonged dark adaptation time. Occasionally, patients will experience a migraine-like prodrome. Patients with CSC frequently have a type-A personality or have recently experienced unusual stress.4 Exogenous and endogenous ster-oid excess is well-documented as both a risk factor and a poor prognostic indicator for CSC.5,6 Patients receiving immunosuppressive therapy and pregnant women are at a higher risk. On examination, patients suffering from CSC may have a visual acuity ranging from 20/20 to 20/200.7 Amsler grid testing may reveal a relative central scotoma with associated metamorphopsia, and recovery of acuity after bright light exposure may be delayed.8 The anterior segment, vitreous and optic nerve are typically normal. Retinal examination characteristically reveals serous retinal detachment. There may be visible underlying serous detachment of the retinal pigment epithelium (RPE). You may notice subretinal precipitates on the outer surface of the retina, as well as RPE atrophic changes. Fluorescein angiography (FA) is definitive, with the leak or leaks forming a variety of patterns. The more common pattern shows diffuse and progressive hyperfluoresence over the surface of RPE detachment(s). This gradually diffuses into the subretinal space. In a minority of cases there is a single-point leak of dye through the RPE into the subretinal space.9 This dye is pulled upward by convection current in the serous subretinal fluid and forms a classic “smokestack” pattern. There may be multiple such point leaks. Indocyanine green (ICG) angiography has revealed hyperpermeability of the choroidal circulation under the pigment epithelial detachment (PED). These areas of hyperfluorescence remain after the resolution of the serous detachment.10 They may also be seen outside the detachment and in the fellow eye. They don’t occur in patients with the point leak and “smokestack” pattern.
Fluorescein will usually show progressive hyperfluorescence such as that shown here at the 40-second frame (left) and the four-minute frame (right). Diseases such as presumed ocular histoplasmosis syndrome and AMD, which are associated with choroidal neovascularization, must be excluded. There are other causes of serous retinal detachment that should be considered, also. Ocular diseases that may cause central serous detachments include optic nerve pit, Harada’s disease, choroidal tumor located in the periphery, peripheral retinal breaks and choroidal or scleral inflammatory disease. Systemic causes are usually evident from the history. They include choroidal vascular disease associated with acute hypertension, collagen vascular disease or disseminated intravascular coagulation. Prognosis/Clinical Course The majority of patients with CSC recover spontaneously within several months of onset, and residual visual deficits can continue to improve for up to a year.11 The most common residual problems include decreased contrast sensitivity, scotomas, impaired color vision, metamorphopsia and nyctalopia.12 Approximately 5 percent of patients have more serious complications. Findings of cystoid macular edema, RPE atrophy and choroidal neovascularization are associated with an increased incidence of permanent decreased visual acuity, which may be as poor as 20/200.13 Though the majority of patients have a good prognosis, a large number of cases—as many as half within the first year—recur.14 Medical Treatment Physicians and researchers have attempted to use a variety of medical therapies directed at the relationship of stress and type-A personality characteristics to CSC, including barbiturates, tranquilizers and beta blockers. None have shortened the duration of the foveal detachment or improved the long-term prognosis.15 Some have proposed acetazolamide as therapy for CSC, because it’s known to increase transport of ions and fluid across the RPE.16 This use is anecdotal and has not been tested in a clinical trial, however. When you diagnose a patient with CSC who is being treated with steroids, consider decreasing or discontinuing the steroids. Since steroid use is usually reserved for diseases with serious consequences or in support of organ transplantation, the risks of discontinuing the steroids must be carefully weighed against the potential benefits, which are unproven. You must involve both the patient and the physician who is treating the underlying disease in the decision. Laser Photocoagulation-Patient Selection Photocoagulation therapy for CSC has long been controversial. Excellent evidence exists that photocoagulation of the PED or of the location of the RPE leak will produce resolution of the serous retinal detachment more quickly than in untreated eyes. However, there is no evidence of a corresponding improvement in the rate of recurrence or the long-term prognosis for visual function. It would be valuable to know if photocoagulation decreased the incidence of severe visual loss. However, this would require a large clinical trial.
The complications of laser treatment are relatively uncommon, but potentially threatening to recovery of good acuity.17 They include choroidal neovascularization, choroidal scarring with foveal distortion and inadvertent foveal photocoagulation. The cumulative incidence of these complications is as high as 5 percent in Gass’ series,18 closely approximating the incidence of poor visual outcome in untreated cases.7 Although other series report lower rates of complications,19 I utilize the guidelines in Figure 1 for selecting patients for treatment. Laser Photocoagulation-Technique Argon green photocoagulation is the standard wavelength, and some authors have suggested red and yellow.20 However, there is no evidence of a best wavelength. Treat the site of leakage. Treatment of RPE detachments is associated with a much higher risk of being complicated by choroidal neovascularization. Digital angiographic systems can help treatment planning by making a composite image of the retina with the leaks marked. Then, display the images during the treatment. We prefer a 200-µm spot size. Avoid spots smaller than 100 µm, due to the risk of creating RPE defects and inducing choroidal neovascularization with small spots. The use of low energy is critical to successful treatment with minimal risk. For the treatment itself, we begin by training the patient to fixate the fixation target with the opposite eye. Our personal preference is argon green at 0.2 second’s duration. We then place a test spot of under 100 Mw in a location similar in pigmentation to the area to be treated, but outside the posterior pole. Energy levels delivered vary somewhat with the individual laser. We then raise the energy level in increments of 50 milliwatts until the laser makes a very light burn in the test area. This energy will produce almost no visible reaction in the choroid in the actual treatment area, where the retina is detached. However, it will tell you the appropriate energy for use there, with a low risk of creating traction lines or choroidal neovascularization. Three to six spots will cover a point leak. In the postop period, we don’t restrict the patient’s activity, instead believing that activity restrictions are counterproductive given the usual type-A personality of the CSC patient. We will give the patient an Amsler grid to use daily, with instructions to report any increase in scotoma size. Should choroidal neovascularization occur, the use of the Amsler grid will catch it early. We’ve found the typical CSC patient to be meticulously compliant. We see the patient a month later. At the one-month follow-up visit, if the serous detachment has resolved and there are no complications, even if the acuity hasn’t fully recovered, the patient may continue to be observed at one-month intervals for several months, then less frequently. We’ll discharge the patient from further follow-up at six months, arming him with the knowledge that recurrence in either eye is possible and that he should return if he notices symptoms. If there’s no resolution at one month, we consider repeating fluorescein angiography. If the leak is present but less than at pretreatment, we’ll consider continued observation. If it’s the same or worse, we’ll consider retreatment. As clinical experience and research have shown, you don’t need to know the answers to all of the mysteries surrounding CSC in order to treat it, and preserve patients’ vision. Supported in part by grants from Research to Prevent Blindness, the Massachusetts Lions Eye Research Fund, and the Lenore and Harold Larkin Philanthropic Foundation. Dr. Feinberg is an associate professor and acting director of the retina service at the department of ophthalmology, Boston University School of Medicine. Dr. LaRocca is an intern in the department of internal medicine.
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