Alejandro Lavaque, MD

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,” a blog series featuring contributions from members of the ophthalmic community. These blogs are an opportunity for ophthalmic bloggers to engage with readers with about a topic that is top of mind, whether it is practice management, experiences with patients, the industry, medicine in general, or healthcare reform. The series continues with this blog by Alejandro Lavaque, MD. The views expressed in these blogs are those of their respective contributors and do not represent the views of 

, fluid accumulates under the retina, causing a serous detachment and vision loss. The condition occurs most often in young and middle-aged adults (20 to 50 years of age), with men being affected more often than women. Although vision loss with CSR is usually temporary, it can recur and become chronic anywhere from 30% to 50% of the time.


	
	The most common symptom that patients present with is blurry central vision in one eye. Patients may also complain of micropsia, metamorphosia, hyperopic shift, central scotoma, and reduced contrast sensitivity.

 Upon examination, the patient will often have some involvement in the other eye. Depending on the location and amount of 

, patients may not have any symptoms.
	
	The exact causes of CSR are not fully understood. However, it is known that systemic exposure to corticosteroids is a risk factor.

An association has also been made between CSC and patients with so-called type A personalities.

 It has been hypothesized that the body’s natural corticosteroids produced when under stress may trigger CSR in prone individuals. This makes the condition a “reactive choroiditis.”

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It has been reported that about 50% of CSR patients have at least one relative with findings upon retinal examination, indicating some genetic inheritance is at play.

Hypertension and heart disease as well as current or recent pregnancy can increase one’s risk for CSR. 

 such as stimulants, decongestants, erectile dysfunction medications, and some anti-cancer agents.


	
	CSR is typically a self-limiting disease, and visual recovery usually occurs spontaneously within 2 to 3 months without treatment. Patients should discontinue or limit corticosteroids, and patients with type A personality can be offered lifestyle modifications and stress management.


	
	Although observation is the standard initial treatment for CSR, there are instances where treatment is appropriate. For acute, chronic, and recurrent CSR, various treatments have been used including medical therapies, 

intravitreal antivascular growth factor agents

, and surgical management. Photodynamic therapy has been used focally to treat leakage. Several reports and studies have demonstrated that reduced-dose and reduced fluence PDT can be used in chronic CSR patients to decrease subretinal fluid and improve best-corrected visual acuity (BCVA).


	
	Focal laser photocoagulation and subthreshold approaches have been used to speed up resolution of subretinal fluid. Spots are applied to areas of leakage identified on fluorescein angiography and/or 

optical coherence tomography angiography (OCTA)

.
	
	In my practice, I have found that early detection of CSR and the use of laser treatment using 

PASCAL with Endpoint Management (EpM; Topcon)

 is safe and effective and leads to quick restoration of vision without macular damage in most cases.
	
	I evaluated the safety and efficacy of PASCAL EpM in 23 eyes of 21 patients with acute of CSCR (average follow-up = 26 months). The short-pulse laser treatment was applied to the area of hyperactivity in the choroid seen on optical coherence tomography-angiography. No other topical or systemic treatment was prescribed.
	
	Before treatment, mean 

 was 20/80, the mean central macular thickness (CMT) was 549 µm, and the mean choroidal thickness (CT) was 289 µm. After laser treatment, mean BCVA improved to 20/30, mean CMT to needing two treatments and one needed three.
	
	


	
	PASCAL laser with EpM appears to be a safe and effective treatment in patients diagnosed with the acute form of CSR. 
	
	

*PASCAL laser with EpM is not FDA cleared to treat CSR.

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Dr. Lavaque is chief executive officer of Centro de Especialidades OftalmolÃ³gicas, TucumÃ¡n, Argentina. He is a consultant to Topcon.

1. Kitzmann AS, Pulido JS, Diehl NN, Hodge DO, Burke JP. The incidence of central serous chorioretinopathy in Olmsted County, Minnesota, 1980-2002. 

. 2008;115:169-173. doi:10.1016/j.ophtha.2007.02.032.

2. Garg S, Dada T, Talwar D, Biswas N. Endogenous cortisol profile in patients with central serous chorioretinopathy. 

3. Yannuzzi LA. Type A behavior and central serous chorioretinopathy. 

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Ophthalmol J Int Ophtalmol Int J Ophthalmol Z FÃ¼r Augenheilkd

5. ASRS. Retina Health Series. https://www.asrs.org/patients/retinal-diseases/21/central-serous-chorioretinopathy[SS1] .

6. Lai TYY, Chan W-M, Li H, Lai RYK, Liu DTL, Lam DSC. Safety enhanced photodynamic therapy with half dose verteporfin for chronic central serous chorioretinopathy: a short-term pilot study. 

. 2006;90:869-874. doi:10.1136/bjo.2006.090282.

7. Kim S-W, Oh J, Oh IK, Huh K. Retinal pigment epithelial tear after half fluence pdt for serous pigment epithelial detachment in central serous chorioretinopathy. 

. 2009;40:300-303. doi:10.3928/15428877-20090430-14.

8. Lee PY, Kim KS, Lee WK. Severe choroidal ischemia following Photodynamic Therapy for pigment epithelial detachment and chronic central serous chorioretinopathy.

. 2009;53:52-56. doi:10.1007/s10384-008-0613-z.

9. Reibaldi M, Cardascia N, Longo A, et al. Standard-fluence versus low-fluence photodynamic therapy in chronic central serous chorioretinopathy: a nonrandomized clinical trial. 

. 2010;149:307-315.e2. doi:10.1016/j.ajo.2009.08.026.

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Quick visual recovery is important for this young population

Alejandro Lavaque, MD

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