Central serous retinopathy (CSR), also known as central serous chorioretinopathy (CSC), is an eye disease which causes visual impairment, often temporary, usually in one eye, mostly affecting males in the age group 20 to 50 but which may also affect women. When the disorder is active it is characterized by leakage of fluid under the retina that has a propensity to accumulate under the central macula. This results in blurred or distorted vision (metamorphopsia). A blurred or gray spot in the central visual field is common when the retina is detached. Reduced visual acuity may persist after the fluid has disappeared.
The diagnosis usually starts with a dilated examination of the retina, followed with confirmation by optical coherence tomography and fluorescein angiography. The angiography test will usually show one or more fluorescent spots with fluid leakage. In 10%-15% of the cases these will appear in a "classic" smoke stack shape. Indocyanine green angiography can be used to assess the health of the retina in the affected area which can be useful in making a treatment decision. An Amsler grid could be useful in documenting the precise area of the visual field involved.
CSR is a fluid detachment of macula layers from their supporting tissue. This allows choroidal fluid to leak into the subretinal space. The build-up of fluid seems to occur because of small breaks in the retinal pigment epithelium.
CSR is sometimes called idiopathic CSR which means that its cause is unknown. Nevertheless, stress appears to play an important role. An oft-cited but potentially inaccurate conclusion is that persons in stressful occupations, such as airplane pilots, have a higher incidence of CSR.
CSR has also been associated with cortisol and corticosteroids. Persons with CSR have higher levels of cortisol. Cortisol is a hormone secreted by the adrenal cortex which allows the body to deal with stress, which may explain the CSR-stress association. There is extensive evidence to the effect that corticosteroids (e.g. cortisone) — commonly used to treat inflammations, allergies, skin conditions and even certain eye conditions — can trigger CSR, aggravate it and cause relapses. A study of 60 persons with Cushing's syndrome found CSR in 3 (5%). Cushing's syndrome is characterized by very high cortisol levels. Certain Sympathomimetic drugs have also been associated with causing the disease.
Recently found evidence has also implicated Helicobacter pylori (see gastritis) as playing a role. It would appear that the presence of the bacteria is well correlated with visual acuity and other retinal findings following an attack.
Recent evidence also shows that sufferers of MPGN Type II kidney disease can develop retinal abnormalities including CSR caused by deposits of the same material that originally damaged the glomerular basement membrane in the kidneys.
The prognosis for CSR is generally excellent. Whilst immediate vision loss may be as poor as 20/200, clinically over 90% of patients regain 20/30 vision or better within 6 months.
Once the fluid has resolved, by itself or through treatment, visual acuity should continue to improve and distortion should reduce as the eye heals. However, some visual abnormalities can remain even if visual acuity is measured at 20/20, and lasting problems include decreased night vision, reduced color discrimination, and localized distortion caused by scarring of the sub-retinal layers.
Complications include subretinal neovascularization and pigment epitheliopathy.
The disease can re-occur causing progressive vision loss.
There is also a chronic form, titled as Type II Central Serous Retinopathy, this occurs in approximately 5% of cases. This exhibits diffuse rather than focalized abnormality of the pigment epithelium, producing a persistent subretinal fluid. The serous fluid in these cases tends to be shallow rather than dome shaped. Prognosis for this condition is less favorable and continued clinical consultation is advised.
Differential diagnosis should be immediately performed to rule out retinal detachment, which is a medical emergency. Additionally, a clinical record should be taken to keep a timeline of the detachment.
Most eyes with CSR undergo spontaneous resorption of subretinal fluid within 3-4 months, recovery of visual acuity usually follows. Any ongoing corticosteroid treatment should be tapered and stopped, where possible. It is important to check current medication, including nasal sprays and creams, for ingredients of corticosteroids, if found seek advice from a medical practitioner for an alternative.
Patients sometimes present with an obvious history of psychosocial stress, in which case counselling and expectancy is relevant.
Treatment should be considered if it does not disappear within 3-4 months, spontaneously or as the result of counselling.
Laser photocoagulation, which effectively burns the leak area shut, may be considered in cases where there is little improvement in a 3 to 4 month duration, and the leakage is confined to a single or a few sources of leakage at a safe distance from the fovea. However, for many cases the leak is very near the central macula, where photocoagulation would leave a blind spot or the leakage is widespread and its source is difficult to identify. Foveal attenuation has been associated with more than 4 months' duration of symptoms, however a better long-term outcome has not been demonstrated with laser photocoagulation than without photocoagulation. Laser photocoagulation can permanently damage vision where applied. Carefully tuned lasers can limit this damage. Even so laser photocoagulation is not a preferred treatment for leaks in the central vision and is considered an outdated treatment by some doctors.
In chronic case Transpupillary thermotherapy has been suggested as an alternative to laser photocoagulation where the leak is in the central macula.
Photodynamic therapy (PDT) with verteporfin has been shown promise as an effective treatment with minimal complications. Follow up studies have confirmed the treatment's long-term effectiveness. Indocyanine green angiography can be used to predict how the patient will respond to PDT.
Other experimental treatments include anti-VEGFs and several oral medications.