Rhegmatogenous Retinal Detachment with Extensive Proliferative Vitreoretinopathy following High-Voltage Electrical Shock Injury: A Case Report

Abstract

Introduction

Rhegmatogenous retinal detachment (RRD) following electrical shock injury is rare, particularly when accompanied by extensive proliferative vitreoretinopathy (PVR). We report a case of RRD with extensive PVR, and cataract following a high-voltage electrical shock injury and discuss its clinical course, surgical management, and visual prognosis.

Case Presentation

A 67-year-old male sustained a high-voltage electrical shock to the trunk, resulting in severe systemic injury and prolonged loss of consciousness. Two months after the injury, he presented with decreased vision in the left eye and underwent bilateral cataract surgery at another ophthalmology clinic. Because of persistent visual impairment, he was referred to our hospital 3 months after the electrical injury. Fundus examination revealed total RRD with extensive PVR in the left eye, without an identifiable retinal break. Visual acuity in the left eye was limited to hand motion. The patient underwent pars plana vitrectomy with scleral encircling and silicone oil tamponade. Although anatomical retinal reattachment was successfully achieved, the final visual acuity remained poor.

Conclusion

RRD following electrical shock injury is rare and may be overlooked due to delayed presentation or concomitant systemic injuries. Furthermore, severe PVR associated with delayed diagnosis may result in poor visual outcomes despite successful anatomical repair. Early and comprehensive retinal evaluation is essential in patients with electrical shock injuries.

Introduction

Electrical shock injuries can result in a wide spectrum of ocular complications, ranging from anterior segment involvement such as a cataract formation, to posterior segment disorders, including optic neuropathy, macular pathology, retinal tears, and retinal detachment [1–5]. Among these, rhegmatogenous retinal detachment (RRD) is a rare but vision-threatening complication of electrical injury [4, 5].

The proposed mechanisms of retinal damage after electrical injury include direct electrical current-induced cellular damage, thermal injury resulting from heat generation within the retinal pigment epithelium (RPE), ischemic injury secondary to vascular compromise, and vitreoretinal traction caused by concussive forces and thermal shrinkage of the vitreous [3–5]. Although several retinal manifestations of electrical injury have been reported, RRD complicated by proliferative vitreoretinopathy (PVR) remains rare [4, 5]. PVR is an abnormal wound healing response after retinal detachment or ocular trauma that involves cellular proliferation, migration, epithelial-mesenchymal transition, extracellular matrix deposition, and contraction of fibrovascular membranes [6, 7].

We report a case of total RRD with extensive PVR and cataract formation following a high-voltage electrical shock injury, emphasizing the diagnostic challenges, surgical management, possible mechanisms of PVR development, and visual prognosis associated with this uncommon complication. This case report was prepared in accordance with the CARE guidelines, and the completed CARE Checklist is provided as online supplementary Material (for all online suppl. material, see https://doi.org/10.1159/cop/acaag021).

Case Presentation

A 67-year-old male with no history of hypertension or diabetes mellitus sustained a high-voltage (25,000 V) electrical shock at the workplace in January 2025. The injury resulted in extensive generalized burns, especially to the neck and trunk, and a comatose state, requiring intensive care unit (ICU) management for approximately 2 months.

After regaining consciousness, the patient experienced marked visual deterioration in the left eye. He visited a local ophthalmology clinic in March 2025, where he was diagnosed with bilateral complicated cataracts with multiple stellate opacities in the peripheral lens (Fig. 1). In addition, retinal detachment with macular involvement was identified in the left eye using optical coherence tomography and ocular ultrasound (Fig. 1). Full-field electroretinography demonstrated markedly decreased amplitudes in the light-adapted 3 electroretinography of the left eye (Fig. 1). A retinal tear was found on the superonasal retina of the right eye, and barrier laser photocoagulation was immediately performed.

Fig. 1.

Initial clinical manifestation observed at a local clinic in a 67-year-old male patient following high-voltage electrical injury. Retinal tear in the right eye (a) and rhegmatogenous retinal detachment (RRD) in the left eye (b, d) were found. Complicated cataract with multiple stellate opacities was also identified in the left eye (b, e, arrows). RRD was confirmed by OCT scan (d) and ocular ultrasound (f) in the left eye, while there was no detachment in the right eye (c). Markedly decreased amplitudes were noted in the light-adapted 3 electroretinogram of the left eye (g). OCT, optical coherence tomography.

Owing to the poor general condition of the patient, cataract surgery was performed first rather than retinal surgery. Sequential cataract surgery with intraocular lens implantation was performed in both eyes. However, visual improvement in the left eye was limited, and the patient was referred to our tertiary hospital approximately 2 months after the electrical shock injury and 1 week after the cataract surgery for management of the RRD.

Before the electrical injury, the patient had no known previous ophthalmologic surgery, ocular trauma, previous retinal detachment history, or family history of retinal detachment. No preexisting retinal disease or systemic connective tissue disease was identified from the available history of the patient. Axial length was 23.51 mm and refractive error with spherical equivalent was −0.75 diopters in the left eye before initial cataract surgery.

Best-corrected visual acuity was 20/20 in the right eye and hand motion in the left eye on presentation at our hospital. Intraocular pressure was 10 mm Hg in the right eye and 7 mm Hg in the left eye. Anterior segment examination revealed well-positioned posterior chamber intraocular lens in both eyes. Dilated fundus examination of the left eye revealed total RRD with extensive PVR, especially involving the entire posterior pole and inferior retina. No definite retinal tear was identified on the posterior pole owing to the dense PVR membranes, and no identifiable retinal breaks were found in the peripheral retina. No signs of retinal inflammation were observed. In contrast, the right eye showed no abnormal retinal findings other than previous laser scars around the treated retinal tear.

Surgical management consisted of a 25-gauge three-port pars plana vitrectomy, scleral encircling using a silicone band, extensive membrane peeling, internal limiting membrane peeling, and intravitreal silicone oil tamponade. No obvious retinal breaks were detected intraoperatively. Multiple tractional components were relieved, and barrier endolaser photocoagulation was applied on the peripheral retina.

Postoperatively, the retina remained anatomically attached without recurrence of RRD for 1 month. Optical coherence tomography confirmed the absence of subretinal fluid, but retinal thinning with atrophic changes in the outer retina progressed, reflecting poor functional recovery (Fig. 2). Despite the anatomical success of retinal attachment, the final best-corrected visual acuity in the left eye remained at hand motion for 3 months after the surgery.

Fig. 2.

Consecutive changes in the fundus before (a) and after surgery for RRD with extensive PVR (b–d). Postoperatively, the retina remained anatomically attached without recurrence of RRD for 1 month. However, progressive retinal atrophic changes (b–d) were observed, consistent with poor visual prognosis. BCVA remained at hand motion (HM) for 1 month after the surgery. BCVA, best-corrected visual acuity.

Discussion

RRD or retinal tears following electrical shock injury are uncommon but serious complications [4, 5]. Previous reports have suggested that retinal detachment after electrical injury may result from vitreoretinal traction induced by concussive forces or thermal shrinkage of the vitreous, even in cases of relatively low-voltage exposure [4, 5]. In high-voltage injuries, additional mechanisms such as direct RPE damage, ischemia, and extensive retinal necrosis may further exacerbate retinal vulnerability [3]. Electrical currents travel through the RPE cells, where energy is absorbed and converted into heat, resulting in tissue damage and subsequent damage to the overlying retina [3].

Previous studies have reported that electrical damage to the ocular tissues depends on the intensity of the electrical current, the entrance and exit sites of the current, and the electrical current pathway through the body [1, 3, 4]. Moreover, tissue resistance to the electrical current and the duration of exposure are associated with electrical damage [3, 4]. In this case, the patient sustained a high-voltage injury, and the electrical current passed through the neck and trunk of the body. Based on these findings, it is likely that the patient’s retina inevitably sustained severe damage from the electrical injury, and the visual prognosis was expected to be extremely poor.

The most distinctive feature of the present case was the development of extensive PVR. Current concepts regard PVR as an exaggerated wound healing and fibrotic response that occurs after breakdown of the blood-retinal barrier and dispersion of RPE cells, glial cells, macrophages, fibroblasts, and inflammatory mediators into the vitreous cavity and subretinal space [6, 7]. RPE cells play a critical role by losing their normal polarity and undergoing epithelial-mesenchymal transition, acquiring fibroblast- and myofibroblast-like characteristics [6, 7]. Cytokines and growth factors, including transforming growth factor-beta, platelet-derived growth factor, vascular endothelial growth factor, interleukins, and other inflammatory mediators, promote cellular proliferation, migration, extracellular matrix deposition, and contraction [6–8]. These processes lead to epiretinal, intraretinal, and subretinal membrane formation, fixed retinal folds, retinal shortening, and recurrent or persistent retinal detachment [6, 7].

In this case, several factors may have promoted severe PVR. First, the left eye had total, macula-involving RRD before referral, suggesting a prolonged period of retinal detachment. Second, delayed ophthalmic management was unavoidable because of coma, ICU care, and severe systemic burns. Third, high-voltage electrical injury may have induced extensive RPE and retinal damage, ischemia, and necrosis, thereby increasing the inflammatory and cellular substrate for PVR formation. Forth, cataract and poor systemic status complicated early visualization and timely vitreoretinal intervention. These factors together may explain why dense posterior and inferior PVR developed despite the absence of preexisting systemic or ocular risk factors for retinal detachment.

No retinal break was identified preoperatively and intraoperatively despite scleral indentation. Several explanations are possible. Dense PVR membranes and chronic retinal folds may have obscured a small causative break, particularly in the posterior pole or peripheral retina. An occult anterior break may have been hidden by the vitreous base or by peripheral contraction. Alternatively, focal retinal necrosis and tissue contraction caused by electrical injury could have created small atrophic breaks that later became indistinguishable within the chronic detached and proliferative retina. Similar reports of electrical injury-associated retinal breaks and RRD have proposed vitreoretinal traction, thermal shrinkage of the vitreous, and retinal ischemia or necrosis as potential mechanisms [3–5].

The surgical strategy in this case was selected according to the chronic total RRD and extensive PVR. Although no definite retinal break was seen, scleral encircling was used to support the vitreous base, reduce residual peripheral traction, and provide coverage for possible occult peripheral retinal breaks. Extensive membrane peeling was required to relieve tangential and anteroposterior traction. ILM peeling was performed at the posterior pole because the PVR involved the macular area and because the ILM can serve as a scaffold for recurrent epiretinal membrane proliferation or posterior pole PVR recurrence. Silicone oil tamponade was chosen because of the severity of PVR, the chronicity of the detachment, and the need for long-term tamponade effect.

Pharmacologic treatment for PVR prevention remains an active area of investigation. At present, surgical removal of membranes and adequate retinal tamponade are considered as a mainstay of treatment, and no pharmacologic agent has been universally accepted as standard adjunctive therapy for PVR [6, 8]. Anti-inflammatory and antiproliferative approaches, including corticosteroids, 5-fluorouracil with low-molecular-weight heparin, daunorubicin, anti-vascular endothelial growth factor agents, retinoids, kinase inhibitors, and biologic approaches, have been evaluated with variable or inconclusive clinical benefit [8, 9].

Methotrexate (MTX) has recently applied for PVR prevention or treatment because of its antiproliferative and anti-inflammatory effects, including inhibition of DNA synthesis in proliferating cells and modulation of inflammatory pathways [8, 9]. Clinical studies have explored intraoperative infusion, single intravitreal or intra-silicone oil injection, and repeated postoperative intravitreal injections, most commonly at doses ranging from 100 to 400 µg of MTX [9]. Melphalan is another adjunctive treatment option. Moreira-Neto et al. [10] reported intraoperative intravitreal melphalan for recurrent PVR prevention in which 5 µg/0.1 mL melphalan was administered at the end of vitrectomy, and no ocular toxicity or PVR recurrence was observed during the 90-day follow-up. However, the available evidence of these agents remains limited by small sample sizes, heterogeneous dosing protocols, and nonrandomized study designs; therefore, further randomized clinical trials are needed.

No adjuvant pharmacologic therapy for PVR was administered in this case. Given the patient’s advanced chronic PVR at presentation, severe systemic injury, limited visual potential from long-standing macular detachment and retinal atrophy, and the lack of an approved pharmacologic standard for PVR, we chose surgical management alone. Nevertheless, this case illustrates why adjunctive pharmacologic approaches may be relevant in selected eyes with severe or high-risk PVR in the future.

One of the most important factors contributing to this patient’s poor visual prognosis was the delayed diagnosis. The development of severe PVR in this case strongly suggests a prolonged disease course and delayed diagnosis because of patient’s prolonged comatose mental status and ICU care. Several factors contributed to this delay, including the prioritization of life-threatening systemic injuries, delayed ophthalmic assessment, and late referral to a retinal specialist. The presence of extensive PVR is a well-established predictor of poor visual prognosis in RRD patients, even when anatomical reattachment is achieved after a surgery. Therefore, this case highlights the importance of early retinal examination in patients with electrical shock injuries, regardless of the voltage level or apparent ocular symptoms [3–5].

This case highlights total RRD with extensive PVR and cataract formation as a rare but devastating complication of high-voltage electrical shock injury. Moreover, RRD following electrical injury may be overlooked because of delayed presentation or concomitant systemic injury. Diagnostic delays can result in advanced PVR and irreversible visual loss despite successful surgical intervention and anatomical repair. Comprehensive early retinal evaluation should be performed in all patients with electrical injuries as soon as their systemic condition permits.

Acknowledgments

During the preparation of this work, the authors used AI-assisted tools for language translation from Korean to English and editing support. The author reviewed and edited the manuscript and take full responsibility for the content of the article.

Statement of Ethics

This study was conducted in accordance with the Declaration of Helsinki. Written informed consent was obtained from the patient for publication of clinical data and images. This study was approved by the Institutional Reviewer Board (IRB) of Soonchunhyang University Cheonan Hospital (IRB 2026-07-015).

Conflict of Interest Statement

The authors declare no conflicts of interest relevant to this article.

Funding Sources

This work was supported by the Soonchunhyang University Research Fund. The funding source had no role in the design or conduct of the study, data analysis or interpretation, manuscript preparation, or the decision to submit the manuscript for publication.

Author Contributions

J.L.: acquisition, analysis, or interpretation of data, writing – original draft, and final approval. H.D.K.: conceptualization, reference review, figure editing, supervision, writing – original draft, review, and editing, and final approval.

Funding Statement

This work was supported by the Soonchunhyang University Research Fund. The funding source had no role in the design or conduct of the study, data analysis or interpretation, manuscript preparation, or the decision to submit the manuscript for publication.

Data Availability Statement

All relevant data supporting the findings of this case report are included in the article. Additional data are not publicly available due to patient privacy and confidentiality but may be obtained from the corresponding author upon reasonable request, subject to ethical and institutional approval.