A case of macular damage following micropulse laser treatment for central serous chorioretinopathy

Abstract

Subthreshold micropulse laser treatment has proven to be an effective treatment for central serous chorioretinopathy. We report a rare case of localized macular damage following 577-nm subthreshold micropulse laser therapy in a patient with central serous chorioretinopathy in his early 40s, with 3-year longitudinal follow-up data. Pretreatment optical coherence tomography demonstrated the presence of subretinal hyperreflective material in the macular area. Despite adherence to validated fixed safety parameters during subthreshold micropulse laser application, post-treatment optical coherence tomography revealed partial macular damage characterized by disruption and atrophy of the ellipsoid and interdigitation zones. Fundus examination revealed localized lesions precisely corresponding to the subthreshold micropulse laser spot distribution patterns, confirming treatment-induced damage. These findings suggest that 577-nm subthreshold micropulse laser therapy for central serous chorioretinopathy induces macular damage, especially in patients with optical coherence tomography-detectable subretinal hyperreflective material. When subretinal hyperreflective material is present, careful energy adjustment is crucial. We recommend using reduced power settings (250–300 mW, 5% duty cycle) for subretinal hyperreflective material-associated central serous chorioretinopathy to enhance safety.

Introduction

Central serous chorioretinopathy (CSC) is a common macular disorder primarily affecting young to middle-aged adults. To date, the pathogenesis of CSC has not been completely clarified.

CSC generally has a self-limiting characteristic; however, there are clinical cases with a prolonged course and recurrent episodes. If the disease persists for >3 months, persistent subretinal fluid may progressively and irreversibly impair photoreceptors. This results in an unfavorable visual prognosis and a significant deterioration in the quality of life. ¹

Clinically, the common therapeutic approaches for CSC include photodynamic therapy (PDT), traditional laser photocoagulation, subthreshold micropulse laser (SML), and antivascular endothelial growth factor therapy. PDT has been effectively applied in the treatment of CSC. Owing to the severe global verteporfin shortage in recent years (although supply has now been restored), SML—which is favored for its safety, minimal invasiveness, and low cost—has become the mainstream treatment modality for CSC in both Chinese and international ophthalmic practice. The validated fixed SML parameters—including a spot diameter of 200 μm, a duration of 0.2 ms, a duty cycle of 5%, and an energy of 400 mW—are generally regarded safe and are widely used in Chinese ophthalmic clinical practice. ² Cases of localized macular damage following SML treatment for CSC have been rarely reported, although recent evidence has identified structural complications such as retinal pigment epithelium (RPE) hyperplasia in a prospective series of patients undergoing SML for chronic CSC. ³ Herein, we present a case of macular damage with pigment proliferation despite adherence to validated safety parameters, with 3-year longitudinal follow-up data, providing further confirmation of this phenomenon.

Case report

The patient, a male in his early 40s, visited the outpatient clinic of Ningbo Eye Hospital, Zhejiang Province, China, in mid-2021 and reported a 1-week history of distorted vision in the left eye. He stated that there were no other concomitant symptoms, including eye redness or pain. His medical history did not disclose any instances of ocular trauma or significant systemic diseases. Best-corrected visual acuity (BCVA) was 1.0 in the right eye (OD) and 0.6 in the left eye (OS), and intraocular pressure (IOP) was within normal limits (20 mmHg OD and 19 mmHg OS). Examination of the anterior segment of the left eye was normal. Fundoscopy of OS revealed that the vitreous body was clear, the cup-to-disc ratio of the optic disc was 0.3, and there was a disc-shaped detachment in the macular area. Optomap fundus photograph (Figure 1(a)) revealed a disc-shaped elevation measuring 8–9 disc diameters (DD) within the macular area. Optical coherence tomography (OCT; Spectralis OCT; Heidelberg Engineering, Germany) of OS (Figure 1(b)) revealed a notable presence of macular subretinal fluid, accompanied with temporal neurosensory retinal thickening (“retinal dipping”) and subretinal hyperreflective material (SHRM). In the sub-RPE space, the choroidal vessels exhibited prominent dilation compared with adjacent areas. Simultaneously, optical coherence tomography angiography (OCTA) was performed to rule out choroidal neovascularization (CNV). Fluorescein fundus angiography (FFA; Spectralis HRA; Heidelberg Engineering, Germany) demonstrated localized hyperfluorescent leakage points on the temporal macular area during the early phase. Subsequently, these leakage points exhibited expansion during the late phase. Indocyanine green angiography (ICGA; Spectralis HRA; Heidelberg Engineering, Germany) revealed dilated choroidal vessels, increased choroidal vascular permeability, and late-phase hyperfluorescence (Figure 1(c)). A diagnosis of CSC in the left eye was established, and the patient was advised to rest adequately and visit for a reexamination within 2 weeks.

Figure 1.

Initial diagnostic imaging of a CSC patient. (a) Optomap fundus photograph of the left eye showed an 8–9 DD disc-shaped elevation. (b) OCT of the left eye revealed marked elevation of macular subretinal fluid with temporal neurosensory retinal thickening (“retinal dipping,” star), and SHRM (arrow). Sub-RPE choroidal vessels showed prominent dilation compared with adjacent areas (triangle) and (c) FFA (12 min) revealed a circular macular fluorescence pooling with localized hyperfluorescent leakage points (arrow). ICGA (12 min) showed increased choroidal vascular permeability and hyperfluorescence (arrow) surrounding the corresponding FFA leakage sites. CSC: central serous chorioretinopathy; DD: disc diameters; OCT: optical coherence tomography; SHRM: subretinal hyperreflective material; RPE: retinal pigment epithelium; FFA: fluorescein fundus angiography; ICGA: indocyanine green angiography.

Three months following the initial visit, the patient returned to the clinic presenting with persistent distorted vision and requested further treatment. BCVA was 1.0 OD and 0.8 OS. IOP was 19 mmHg in each of the two eyes. Fundoscopy revealed a persistent disc-shaped detachment in the macular area. Concurrently, the elevation of the neurosensory retina showed a tendency to flatten, and no other abnormalities were detected during the comprehensive ophthalmic assessment. OCT (Figure 2(a)) revealed a marked decrease in subretinal fluid and the presence of a distinct SHRM on the temporal macular area. OCTA still showed no signs of CNV (Figure 2(a)).

Figure 2.

Multimodal imaging of a CSC patient before and after SML treatment. (a) Pre-SML OCT revealed persistent subretinal fluid with a distinct SHRM (arrow). En face OCTA showed no signs of CNV. (b) One-month post-SML fundus photograph revealed faint punctate lesions in a matrix pattern (arrow) and scattered faint punctate marks in the inferior macula. (c) One-month post-SML OCT infrared image revealed well-defined faint punctate lesions in a matrix pattern (arrow), with scattered marks inferior to the macula. Corresponding OCT demonstrated disruption and atrophy in the EZ and IZ, while the RPE displayed a rough appearance (arrow). (d) Three-year follow-up fundus photograph showed temporal macular pigment proliferation (arrow) and (e) three-year follow-up OCT revealed outer nuclear layer cystic changes (star), disruption and defects in the EZ and IZ (arrow), and local RPE hyperplasia (triangle); concurrent infrared image revealed white punctate changes (arrow). CSC: central serous chorioretinopathy; SML: subthreshold micropulse laser; OCT: optical coherence tomography; SHRM: subretinal hyperreflective material; OCTA: optical coherence tomography angiography; CNV: choroidal neovascularization; EZ: ellipsoid zone; IZ: interdigitation zone; RPE: retinal pigment epithelium.

After providing informed consent, the patient underwent SML treatment in the left eye under topical anesthesia at Ningbo Eye Hospital in late 2021. The SML treatment area encompassed the entire subretinal fluid region, excluding the fovea. It included the dilated choroidal vessels and hyperpermeability observed on ICGA as well as the leakage points identified on FFA. The SML parameter was set as follows: a 5% duty cycle, spot size of 200 μm, pulse duration of 200 ms, and power of 400 mW (laser device: IRIDEX brand, model: IQ 577™ micropulse laser, USA). A six-spot matrix mode with no spacing between two spots was applied. The total number of SML dots was 150. No medications were prescribed. Immediately after the SML procedure, faint punctate lesions in a matrix pattern were visible under the Volk Area Centralis laser lens in the treated temporal macular area. One month after the SML treatment, the patient reported a reduction in visual distortion and an improvement in the clarity of vision. BCVA was 1.0 in both eyes. Fundoscopy revealed a flattened retina in the macula, with a diminished foveal reflex and faint punctate pigment changes in the temporal macular area. No other abnormalities were noted in the comprehensive ophthalmic assessment. Color fundus photograph (Figure 2(b)) revealed faint punctate lesions in a matrix pattern on the temporal macular area corresponding to the SML marks observed directly under the laser lens 1 month ago. OCT (Figure 2(c)) revealed well-defined faint punctate lesions in a matrix pattern on the infrared image (this is in contrast to the dot-like precipitates with nonuniform sizes and discoid distribution, as reported by Maruko et al.⁴ in their study on yellow precipitates and subretinal yellow materials in CSC), consistent with the findings observed in the color fundus photograph. There was disruption and atrophy of the ellipsoid zone (EZ) and interdigitation zone (IZ) in the corresponding temporal macular area, and the underlying RPE had a rough appearance. Given the patient’s recovery of vision and substantial resolution of subretinal fluid, no further treatment was administered. In early 2025, 3 years after the SML treatment, the patient returned to the clinic due to dry eye. The BCVA of OS was maintained at 1.0. The fundus color photograph (Figure 2(d)) showed pigment proliferation (retinal scar) in the temporal macular area. OCT (Figure 2(e)) showed cystic lesions in the outer nuclear layer of the temporal macular area, disruption and defects in the EZ and IZ, and local hyperplasia of the RPE. Infrared image revealed faint punctate changes in the temporal macular area.

The reporting of this study conforms to the Case Report (CARE) guidelines. ⁵

Discussion

Multiple studies^2,6 have demonstrated the effectiveness and safety of SML in treating CSC. The therapeutic benefits of SML stem from the thermal stimulation of RPE cells without causing their death, which leads to increased activity of heat-shock proteins in the RPE. ²

Currently, there are no standardized SML parameters for reference. Recent studies on chronic CSC have revealed substantial variability in the optimal power settings required for effective 577-nm SML therapy, underscoring the importance of personalized dose titration to achieve optimal therapeutic outcomes. ⁷ The Subthreshold Laser Ophthalmic Society (SOLS) supports titration and the use of half the titrated power for treatment; it further recommends a 5% duty cycle, 200 ms pulse duration, and a 100–200 μm spot size for SML application. ⁸ Some researchers use fixed parameters; the International Retina Laser Society advocates the use of validated fixed parameters, specifically the published “fixed” settings (e.g. 250 mW for 577-nm SML), in micropulse laser treatments while discouraging titration to minimize the risk of accidental retinal damage. ⁹ The fixed parameters for 577-nm micropulse laser treatment used in this study—5% duty cycle, 200 µm spot size, 200 ms pulse duration, and 400 mW energy—are considered safe and are commonly used in the clinical management of CSC in China ⁶ and at our center.

Regarding the treatment area of SML, experts from the SOLS suggest that for acute CSC, the localized leakage site and surrounding regions on FFA should be treated; for chronic CSC, it is recommended to treat the areas of focal and diffuse hyperfluorescence on FFA. ⁸ The International Retinal Laser Society recommends that a substantial area of the RPE should be treated to optimize clinical benefits. ⁹ In the current case, the treatment area was the entire site of subretinal fluid accumulation, excluding the fovea centralis. This area encompassed regions of dilated choroidal vessels, hyperpermeability on ICGA, and leakage points on FFA.

Under these validated fixed safety parameters (400 mW, 5% duty cycle), immediately after the SML treatment, faint punctate lesions in a matrix pattern could be observed under the Volk Area Centralis laser lens in the SML-treated temporal macular area. Thirty days following the SML procedure, fundus photographs and OCT confirmed persistent faint punctate lesions in a matrix pattern in the treated temporal macular area, with associated EZ and IZ disruption and atrophy. Three years after SML treatment, pigment proliferation (retinal scar) was evident at the SML-treated site, resembling conventional laser-induced scarring. These findings support the occurrence of SML-induced macular damage, although the absence of fundus autofluorescence (FAF) imaging limited the evaluation of RPE integrity and functional changes. Wood et al.¹⁰ reported that in two studies on the treatment of CSC with micropulse laser, six cases developed RPE pigmentation alterations due to excessively high energy settings. Zhou et al.¹¹ conducted a 6-month follow-up and reported that in the 577-nm SML group, 27.3% (15/55) of the patients had mild impairment of the RPE, and 3.64% (2/55) showed distinct impairment of the RPE. In addition, a recent study (12- to 16-week follow-up) on 577-nm SML treatment for chronic CSC reported RPE hyperplasia in 7 of the 149 treated eyes (4.7%) following subthreshold laser therapy. ³ These studies indicate that although SML treatment causes less damage to the RPE and fewer side effects, it is not entirely safe. If the SML energy exceeds the threshold that can be tolerated by the retina in this area, RPE cells will be damaged.

Titration is critical for establishing appropriate SML power parameters during SML therapy. However, due to variations in the RPE and choroidal melanocytes across different locations, even after rigorous titration, the actual treatment power still cannot be uniformly applied to all retinas. ¹¹ Based on the abovementioned reasons, some researchers have indicated that precise titration within the vascular arcades is critical for achieving foveal-comparable pigment density during SML treatment for CSC. ⁷ Gawęcki et al. ¹² presented an overtreated case of CSC treated with 577-nm SML under careful titration. They highlighted that the energy requirements for edematous retina vary depending on the underlying etiology due to differences in power transmission. In the case under discussion, the SHRM in the temporal macular area, as observed on OCT, distinguishes this case from most CSC cases previously treated with SML without macular damage. Thus, the SHRM may explain the post-treatment macular injury in this patient. This hypothesis is supported by the colocalization of matrix pattern changes with SHRM in the temporal macular area.

SHRM represents a prevalent and significant biomarker detectable via OCT. On OCT, SHRM is characterized by substance deposits exhibiting varying degrees of homogeneous or heterogeneous hyperreflectivity, predominantly determined by their composition. ¹³ It mainly consists of type 2 macular neovascularization (MNV), fibrotic tissue, fibrin, subretinal hyperreflective exudates, vitelliform substances, hemorrhagic components, and subretinal drusenoid accumulation. ¹⁴ OCTA can noninvasively detect microvascular flow, allowing differentiation of vascular from nonvascular SHRM. Given the exclusion of vascular SHRM via OCTA, the SHRM discussed in this study is nonvascular. Although the composition of nonvascular SHRM in CSC remains incompletely characterized, current evidence suggests that it primarily consists of fibrin aggregates and/or degenerated photoreceptor outer segments and exhibits RPE shedding. ¹⁵

Vujosevic et al.¹⁶ conducted scaling law analysis by comparing parameters at 577 nm and 810 nm and revealed that the therapeutic range of 810-nm laser was six times wider than that of 577-nm laser. This difference reflects the higher energy and RPE melanin absorption rate of 577-nm laser compared with those of 810-nm laser, making 577-nm laser more likely to cause inadvertent retinal damage. Potential contributing factors include flawed titration algorithms as well as medium absorption or scattering effects. ¹⁷ Owing to its shorter wavelength, the 577-nm laser exhibits increased light scattering in opaque ocular media (e.g. fibrin deposits and photoreceptor outer segment debris) and edematous retinal tissues compared with lasers at longer wavelengths. ¹⁸ This phenomenon substantially elevates the risk of thermally induced retinal injury, potentially accounting for the macular damage observed in the current case despite rigorous compliance with standard SML therapy safety protocols. Nevertheless, as this is a single case observation, further validation through larger-scale investigations is imperative.

In vascular SHRM, the higher hemoglobin absorption and lower xanthophyll absorption of the 577-nm laser permit treatment at reduced energy levels, improving focal precision and minimizing damage to the macular inner retinal layers.^18,19

Furthermore, the 810-nm diode laser exhibits negligible energy absorption and limited thermal diffusion in both normal neurosensory retina and pathological conditions, including intraretinal hemorrhage, cataractous changes, vitreous hemorrhage, and severely edematous retinal tissue. ¹⁸ Compared with the 577-nm laser, the 810-nm laser exhibits a significantly broader therapeutic window and superior safety profile, with substantially reduced risk of iatrogenic retinal injury. ¹⁷ Therefore, the 810-nm micropulse laser offers higher safety, especially for treating SHRM-associated CSC cases, including the current case.

Conclusion

This report presents a rare 3-year follow-up case documenting macular damage following 577-nm SML therapy in a patient with CSC complicated with SHRM. Our findings demonstrate that the selection of energy parameters is a critical safety determinant in 577-nm SML treatment for SHRM-associated CSC. Based on these observations, we recommend using conservative 577-nm SML energy parameters (250–300 mW with 5% duty cycle) for SHRM-associated CSC. However, these preliminary findings require validation in larger-scale prospective studies.

Supplemental Material

sj-pdf-1-imr-10.1177_03000605251363514 - Supplemental material for A case of macular damage following micropulse laser treatment for central serous chorioretinopathy

Supplemental material, sj-pdf-1-imr-10.1177_03000605251363514 for A case of macular damage following micropulse laser treatment for central serous chorioretinopathy by Jianli Wei and Lishuang Chen in Journal of International Medical Research