Evaluating subthreshold laser technique for CSCR patients


Ongoing study aims to clarify patient selection for endpoint management

Chronic CSCR patients who have less RPE scarring stand to benefit the most from EpM laser therapy. They have the best chance for a quick and complete resolution of subretinal fluid.

Among the more common retinopathies in the United States-along with age-related macular degeneration, diabetic retinopathy, hypertensive retinopathy, and retinal vein occlusion-central serous chorioretinopathy (CSCR) has no treatment that is considered the gold standard.1 Unlike the other conditions, CSCR tends to affect working-age individuals-the mean onset being 45 years of age-and it occurs more frequently in men.1

The exact etiology and pathogenesis is not well understood, but it has been reportedly associated with a range of factors such as corticosteroid exposure, phosphodiesterase inhibitor use, and obstructive sleep apnea.2-4 Interestingly CSCR has also been associated with “type A personality” and those experiencing psychological stress.5,6

An inciting event is thought to trigger an increased permeability of the choroidal vessels and retinal pigment epithelium (RPE) dysfunction-subsequently allowing for the accumulation of exudative fluid in the subretinal space.2,7

It has been reported that more than 80% of CSCR patients will have spontaneous resolution of symptoms within three months, nevertheless, the other 20% often require treatment.7-9 These individuals may have persistent serous macular detachment, vision loss, and subjective impairment.10,11

Although definitions of chronicity vary, a patient can be considered to have chronic CSCR if subretinal fluid has not resolved by three months. In practice, the classic patient with chronic CSCR presents with reduced visual acuity and contrast sensitivity, visual distortions, and a change in color vision.

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CSCR presentation

Clinically, the retina will have subretinal fluid and RPE irregularities that can also be seen with infrared imaging and optical coherence tomography (OCT). Most RPE irregularities will be seen over a central leakage point. In patients who have had the condition longer, damage will extend into the outer retinal layers.

In a very progressed form of the disease, the patient may have a complete loss of photoreceptors with only the external limiting membrane visible on OCT. Microperimetry on these patients will reveal small scotomas in these areas.

To identify patients with the signs of secondary neovascularization, we take care to look for double layer signs on OCT and typical signs on fluorescein and ICG angiography.

A double layer of the RPE and Bruch’s membrane filled with hyper-reflective material is an indicator for secondary choroidal neovascularization (CNV). These secondary CNVs in double layers can be visualized more distinctly with OCT angiography. A secondary neovascularization calls for a treatment approach using intravitreal anti-vascular endothelial growth factor (VEGF) agents.

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Treatment options

In the absence of a gold standard treatment, various strategies have been attempted in CSCR management. Specialists frequently apply laser photocoagulation to the leaking RPE, as directed by fluorescein angiography. Xenon, krypton, and more currently, argon laser has been used.12-14

The development of subthreshold laser therapy has garnered growing interest as these techniques-including micropulse, selective retinal therapy, and Topcon’s PASCAL with endpoint management (EpM)-can deliver the similar therapeutic benefits without causing visible damage.15Photodynamic therapy (PDT) with verteporfin has been used to treat chronic and acute CSCR in patients, as well as, to reduce potential recurrences.

We find that PDT with reduced dose (half-dose) is the preferred approach for this method.16-19 Other drug treatments that have been used for CSCR include intravitreal anti-VEGF, mineralocorticoid receptor antagonists, adrenergic blockers, systemic carbonic anhydrase inhibitors, aspirin, Helicobacter pylori treatment, and methotrexate.20

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Our investigation

My colleagues and I have initiated an investigation evaluating patients with chronic central serous chorioretinopathy, who are good candidates for EpM. Currently, we treat CSCR patients every three months if they present with subretinal fluid, a protocol that was also suggested by the technology’s inventors.

To see how suitable EpM is in the day-today practice of a clinical outpatient service, we have set up trial conditions to follow patients and gather more detail.

We will be looking closely at the anatomical outcomes on OCT as well as patients’ functional vision through visual acuity testing and microperimetry. We hope to include at least 50 patients. Currently, there are 30 are enrolled.

The follow-up period will be a year, and we would like to extend that out to longer intervals so we can examine recurrence after one year. We know that one of the difficulties in treating CSCR is that it is likely to recur with subretinal fluid-even after other therapies like half-fluence PDT.

We observe this on a regular basis. During our investigation, we want to determine which patients seem to improve the most and if there also are specific subgroups who will derive the most benefit from it.

Eventually, we will randomly assign patients to treatment and no treatment or treatment versus another type of treatment to show superiority. First, we want to evaluate the treatment’s effectiveness and improve our technique with the procedure. We want to ensure it does no harm. We had observed no adverse effects, burns, or scars. It is clearly safe.

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Through our observations, we believe that chronic CSCR patients who have less RPE scarring stand to benefit the most from EpM laser therapy. These patients tend to have the best chance of a relatively quick and complete resolution of subretinal fluid. We suspect that if the subretinal fluid bubble is not very large and is centrally located, this approach likely will be significantly beneficial.

Patients with leakage points within a 3-mm radius from the fovea appear to do well with EpM’s macular laser pattern. Patients who have chronic CSCRs with fluid accumulation in multiple locations are more difficult to treat. An extended recruitment period and a longer follow-up will allow us to include patients with different disease presentation and investigate our data in more detail.

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Benedikt Schworm, MD
E: benedikt.schworm@med.uni-muenchen.de
Dr. Schworm is with the Eye Clinic of the University of Munich, Germany. He did not indicate anay proprietary interest. Topcon’s PASCAL laser with EpM is not FDA approved for CSCR.


1. Wang M, Munch IC, Hasler PW, Prunte C, Larsen M. Central serous chorioretinopathy. Acta Ophthalmol. 2008;86:126-145.

2. Bouzas EA, Karadimas P, Pournaras CJ. Central serous chorioretinopathy and glucocorticoids. Surv Ophthalmol. 2002;47:431-448.

3. Nicholson B, Noble J, Forooghian F, Meyerle C. Central serous chorioretinopathy: update on pathophysiology and treatment. Surv Ophthalmol. 2013;58:103-126.

4. Wong KH, Lau K, Chhablani J, Tao Y, Li Q, Wong IY. Central serous chrioretinopathy: what we have learnt so far. Acta Ophthal. 2016;94:321-325.

5. Yannuzzi LA. Type A behavior and central serous chorioretinopathy. Trans Am Ophthalmol Soc. 1986;84:799-845.

6. Yannuzzi LA. Type-A behavior and central serous chorioretinopathy. Retina. 1987;7:111-131.

7. Ross A, Ross AH, Mohamed Q. Review and update of central serous chorioretinopathy. Curr Opin Ophthalmol. 2011:22;166-173.

8. Sharma T, Shah N, Rao M, et al. Visual outcome after discontinuation of corticosteroids in atypical severe central serous chorioretinopathy. Ophthalmology. 2004;111:1708-1714.

9. Gilbert CM, Owens SL, Smith PD, Fine SL. Long-term follow-up of central serous chorioretinopathy. Br J Ophthalmol. 1984;68:815-820.

10. Bujarborua D. Long-term follow-up of idiopathic central serous chorioretinopathy without laser. Acta Ophthalmologica Scandinavica. 2001;79:417-421.

11. Singer M, et al. Non-steroidal anti-inflammatory topical therapy speeds recovery in central serous chorioretinopathy. Paper presented at: AAO 2013 meeting, New Orleans. Unpublished data.

12. Mitsui Y, Matsubara M, Kanagawa M. Xenon light-exposure as a treatment of central serous retinopathy (a preliminary report). Nihon Ganka Kiyo. 1969;20:291-294.

13. Slusher M.M. Krypton red laser photocoagulation in selected cases of central serous chorioretinopathy. Retina. 1986;6:81-84.

14. Novak MA, Singerman LJ, Rice TA. Krypton and argon laser photocoagulation for central serous chorioretinopathy. Retina. 1987;7(3):162-169.

15. Karth PA, Madadi S. AAO. Subthreashold laser. Available at. http://eyewiki.aao.org/Sub-threshold_ Laser. Accessed Sept. 24, 2018.

16. Ohkuma Y, Hayashi T, Sakai T, Watanabe A, Tsuneoka H. One-year results of reduced fluence photodynamic therapy for central serous chorioretinopathy: the outer nuclear layer thickness is associated with visual prognosis. Graefes Arch Clin Exp Ophthalmol. 2013;251:1909-1917.

17. Kang NH, Kim YT. Change in subfoveal choroidal thickness in central serous chorioretinopathy following spontaneous resolution and low-fluence photodynamic therapy. Eye(Lond). 2013;27:387-391.

18. Nicoló M, Eandi CM, Alovisi C. Half-fluence versus half-dose photodynamic therapy in chronic central serous chorioretinopathy. Am J Ophthalmol. 2014;157:1033-1037.

19. van Dijk EHC, Fauser S, Breukink MB, et al. Halfdose photodynamic therapy versus high-density subthreshold micropulse laser treatmentin patients with chronic central serous chorioretinopathy: The PLACE Trial. Ophthalmology. 2018;125:1547-1555. doi:10.1016/j.ophtha.2018.04.021

20. Abouammoh MA. Advances in the treatment of central serous chorioretinopathy. Saudi J Ophthalmol. 2015;29:278-286. doi:10.1016/j.sjopt.2015.01.007

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