Central serous retinopathy

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Central serous retinopathy
Classification and external resources

An occurrence of central serous retinopathy of the fovea centralis imaged using Optical coherence tomography.
ICD-10 H35.7
ICD-9 362.41
DiseasesDB 31277
eMedicine oph/689

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.[1][2] 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.[1]

Contents

[edit] Diagnosis

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. An Amsler grid could be useful in documenting the precise area of the visual field involved.

[edit] Causes

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.

The "type A personality" has also been linked to this condition.[1] However, the statistics may be skewed by the fact that CSR often goes undiagnosed or misdiagnosed; airline pilots and so-called "type A" people are demonstrably exacting, demanding people with (certainly in the case of pilots) better-than-average vision. They are more likely than the general population to notice the sometimes-subtle degradation of vision caused by CSR and insist on a believable diagnosis of it.[citation needed] People who need glasses may assume that the blurriness caused by CSR is simply a change in their prescription, and fail to have the condition assessed by a retinal specialist. These statistic-skewing factors undermine the conclusion that CSR is a condition specific to "type A" people.[citation needed]

CSR has also been associated with cortisol and corticosteroids. Persons with CSR have higher levels of cortisol.[3] 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.[4][5][6] A study of 60 persons with Cushing's syndrome found CSR in 3 (5%).[7] Cushing's syndrome is characterized by very high cortisol levels.

Recently found evidence has also implicated Helicobacter pylori (see gastritis) as playing a role.[8][9][10] 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.[11]

[edit] Prognosis

The prognosis for CSR is generally excellent.[1] Whilst immediate vision loss maybe as poor as 20/200, clinically over 90% of patients regain 20/30 vision or better within 6 months.

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.[12]

Complications include subretinal neovascularization and pigment epitheliopathy.[13]

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.

[edit] Treatment

Differential diagnosis should be immediately performed to rule out retinal detachment, which is a medical emergency. Additionally, a clinical record should be taken to give a timeline of the detachment.

Any ongoing corticosteroid treatment should be 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.

Low-dose aspirin has been shown to speed recovery.[14]

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 a few months,[15] spontaneously or as the result of counselling.[1]

Laser photocoagulation (hot laser), 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.[1] Laser photocoagulation can permanently damage vision where applied. Carefully tuned lasers can limit this damage.[16] Even so laser photocoagulation is not a preferred treatment for leaks in the central vision and is considered an outdated treatment by some doctors.[15]

Transpupillary thermotherapy (cold laser) has been suggested as a lower-risk alternative to laser photocoagulation in cases where the leak is in the central macula.[17]

Photodynamic therapy (PDT) with verteporfin has been shown promise as an effective treatment with minimal complications.[18] Follow up studies have confirmed the treatment's long-term effectiveness.[19] Indocyanine green angiography can be used to predict how the patient will respond to PDT.[20][15]

Nutritional supplements commonly recommended for macular degeneration, such as lutein and zeaxanthin, may assist healing.[citation needed]

[edit] See also

[edit] References

  1. ^ a b c d e f Wang M, Munch IC, Hasler PW, Prünte C, Larsen M (2008). "Central serous chorioretinopathy". Acta Ophthalmologica 86 (2): 126–45. doi:10.1111/j.1600-0420.2007.00889.x. PMID 17662099. 
  2. ^ QUILLEN D. A., GASS J. D. M., BROD R.D., GARDNER T. W., BLANKENSHIP G. W. and GOTTLIEB J. L. ; (1996). "Central serous chorioretinopathy in women". Ophthalmology 103 (1): 72–79. PMID 8628563. 
  3. ^ Garg SP, Dada T, Talwar D, Biswas NR (November 1997). "Endogenous cortisol profile in patients with central serous chorioretinopathy". Br J Ophthalmol 81 (11): 962–4. doi:10.1136/bjo.81.11.962. PMC 1722041. PMID 9505819. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1722041. 
  4. ^ Pizzimenti JJ, Daniel KP (2005). "Central serous chorioretinopathy after epidural steroid injection". Pharmacotherapy 25 (8): 1141–6. doi:10.1592/phco.2005.25.8.1141. PMID 16207106. 
  5. ^ Bevis T, Ratnakaram R, Smith MF, Bhatti MT (2005). "Visual loss due to central serous chorioretinopathy during corticosteroid treatment for giant cell arteritis". Clin. Experiment. Ophthalmol. 33 (4): 437–9. doi:10.1111/j.1442-9071.2005.01017.x. PMID 16033370. 
  6. ^ Fernández Hortelano A, Sádaba LM, Heras Mulero H, García Layana A (2005). "[Central serous chorioretinopathy as a complication of epitheliopathy under treatment with glucocorticoids]" (in Spanish; Castilian). Arch Soc Esp Oftalmol 80 (4): 255–8. PMID 15852168. 
  7. ^ Bouzas EA, Scott MH, Mastorakos G, Chrousos GP, Kaiser-Kupfer MI (September 1993). "Central serous chorioretinopathy in endogenous hypercortisolism". Arch. Ophthalmol. 111 (9): 1229–33. PMID 8363466. 
  8. ^ Giusti C (2004). "Association of Helicobacter pylori with central serous chorioretinopathy: hypotheses regarding pathogenesis". Med. Hypotheses 63 (3): 524–7. doi:10.1016/j.mehy.2004.02.020. PMID 15288381. 
  9. ^ Ahnoux-Zabsonre A, Quaranta M, Mauget-Faÿsse M (2004). "[Prevalence of Helicobacter pylori in central serous chorioretinopathy and diffuse retinal epitheliopathy: a complementary study]" (in French). J Fr Ophtalmol 27 (10): 1129–33. PMID 15687922. 
  10. ^ Cotticelli L, Borrelli M, D'Alessio AC, et al. (2006). "Central serous chorioretinopathy and Helicobacter pylori". Eur J Ophthalmol 16 (2): 274–8. PMID 16703546. 
  11. ^ Colville D, Guymer R, Sinclair RA, Savige J (2003). Visual impairment caused by retinal abnormalities in mesangiocapillary (membranoproliferative) glomerulonephritis type II (dense deposit disease). 42. American Journal of Kidney Diseases. pp. e2-e5. S0272-6386(03)00665-6. http://www.ajkd.org/article/S0272-6386(03)00665-6/. 
  12. ^ Baran NV, Gürlü VP, Esgin H (2005). "Long-term macular function in eyes with central serous chorioretinopathy". Clin. Experiment. Ophthalmol. 33 (4): 369–72. doi:10.1111/j.1442-9071.2005.01027.x. PMID 16033348. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=1442-6404&date=2005&volume=33&issue=4&spage=369. 
  13. ^ Kanyange ML, De Laey JJ (2002). "Long-term follow-up of central serous chorioretinopathy (CSCR)". Bull Soc Belge Ophtalmol (284): 39–44. PMID 12161989. 
  14. ^ Filippo Romanazzi; Manuela Imparato; Angelo Negri; Anna Morano; Fabio Ferentini (2010-08-09), Low-dose aspirin as treatment for central serous chorioretinopathy, Dove Medical Press, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921298/, retrieved 2012-01-05 
  15. ^ a b c Francesco Boscia (2010-04). When to Treat and Not to Treat Patients With Central Serous Retinopathy. Retina Today. 
  16. ^ Johann Roider et. al.. Retinal Sparing by Selective Retinal Pigment Epithelial Photocoagulation. Ophthalmology. http://archopht.ama-assn.org/cgi/content/abstract/117/8/1028. 
  17. ^ Wei SY, Yang CM (2005). "Transpupillary thermotherapy in the treatment of central serous chorioretinopathy". Ophthalmic Surg Lasers Imaging 36 (5): 412–5. PMID 16238041. 
  18. ^ Michael D. Ober et. al. (2005-12). Photodynamic Therapy for Focal Retinal Pigment Epithelial Leaks Secondary to Central Serous Chorioretinopathy. Ophthalmology. http://www.sciencedirect.com/science/article/pii/S0161642005009000. 
  19. ^ Wai-Man Chan et. al. (2008-06-05). Half-Dose Verteporfin Photodynamic Therapy for Acute Central Serous Chorioretinopathy: One-Year Results of a Randomized Controlled Trial. Ophthalmology. http://www.ophsource.org/periodicals/ophtha/article/S0161-6420(08)00373-4/abstract. 
  20. ^ Inoue R et. al. (2010-03). Association between the efficacy of photodynamic therapy and indocyanine green angiography findings for central serous chorioretinopathy. Am J Ophthalmol. http://www.ncbi.nlm.nih.gov/pubmed/20172070. 

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