Suprachoroidal hemorrhage and detachment in the non-laser photocoagulation posterior pole after intravitreal Anti-VEGF injection: A case report

Abstract

Intravitreal anti-vascular endothelial growth factor (anti-VEGF) injections are widely used for diabetic macular edema (DME) and neovascular ocular diseases. Suprachoroidal hemorrhage and detachment (SCHD) in the posterior pole non-laser photocoagulation area is an extremely rare complication after anti-VEGF injection, with no standardized management. We report a 56-year-old male with a 20-year history of type 2 diabetes, bilateral proliferative diabetic retinopathy (DR), neovascular glaucoma (NVG), and prior pars plana vitrectomy who developed SCHD in the right eye after intravitreal Conbercept injection. He was treated with retrobulbar triamcinolone acetonide injection. During follow-up, SCHD resolved completely with significant improvement in best-corrected visual acuity and stable intraocular pressure. Pathogenesis may involve low intraocular pressure, anti-VEGF-related vascular effects, diabetic vascular fragility, and chronic high intraocular pressure injury. Retrobulbar triamcinolone acetonide injection may represent a promising treatment option for this complication, although further evidence is needed to establish its efficacy. Strict perioperative blood glucose and intraocular pressure control, standardized injection technique, and close postoperative monitoring may be beneficial for high-risk patients.

Plain language summary

Anti-VEGF eye injections are a standard treatment for diabetic macular edema and eye diseases involving abnormal neovascular growth. A very rare but serious complication is suprachoroidal hemorrhage and detachment (SCHD), especially when it occurs at the posterior pole of the eye. We describe one such case in a man with long-term diabetes, severe diabetic eye disease, neovascular glaucoma, and multiple prior eye surgeries. He developed SCHD shortly after an anti-VEGF injection. He was treated with a retrobulbar steroid injection. Over weeks of follow-up, the hemorrhage and detachment fully resolved, and his vision improved noticeably. This case shows that SCHD can occur in high-risk patients even in non-lasered posterior pole regions. Retrobulbar triamcinolone acetonide injection appears to be a promising treatment option, though further evidence is needed. Clinicians should pay close attention to high-risk patients, control blood glucose and eye pressure before injection, use careful injection technique, and monitor patients closely after injection to detect and manage this rare complication early.

Introduction

Intravitreal anti-vascular endothelial growth factor (anti-VEGF) injections are the gold standard first-line therapy for diabetic macular edema (DME) and various neovascular ocular diseases, characterized by good efficacy and an overall favorable safety profile in clinical practice. ¹ Although rare, severe ocular complications can occur after anti-VEGF injection, among which suprachoroidal hemorrhage and detachment (SCHD) is a serious adverse event that may lead to significant visual loss. ² Most reported cases of SCHD after anti-VEGF injection involve the peripheral choroid, and SCHD occurring in the posterior pole non-laser photocoagulation area is extremely uncommon. To the best of our knowledge, no such case has been previously described in the literature, and standardized clinical diagnosis and management guidelines remain unavailable.

Diabetic retinopathy (DR) complicated by neovascular glaucoma (NVG) is a severe end-stage ocular complication of diabetes, associated with multiple vitreoretinal surgeries, repeated anti-VEGF injections, and unstable intraocular pressure (IOP). ³ Patients in this population have fragile ocular vascular structures due to long-term hyperglycemia-induced microangiopathy, and are at potentially higher risk of rare complications after intraocular interventions. Here, we report a case of SCHD in the posterior pole non-laser photocoagulation area after intravitreal Conbercept injection in a 56-year-old male with long-term type 2 diabetes, bilateral proliferative DR, NVG, and multiple vitreoretinal surgeries. We explore the potential pathogenesis of this rare complication and report our experience with retrobulbar triamcinolone acetonide injection as a treatment attempt, aiming to provide clinical reference for the diagnosis, treatment and prevention of this underrecognized complication in high-risk patients.

Case presentation

This case report was prepared in accordance with the CARE guidelines. ⁴ A flowchart summarizing the clinical course and outcome of this case is presented in Figure 1.

Figure 1.

Timeline figure of the case history. Black boxes: relevant past medical history of this case. Green boxes: current illness, physical exam, diagnostic evaluations, diagnoses. Red boxes: interventions and follow-ups. Gray arrow: dates. PDR, proliferative diabetic retinopathy; PPV, pars plana vitrectomy; PRP, panretinal photocoagulation; NVG, neovascular glaucoma; T2DM, type 2 diabetes mellitus; OCTA, optical coherence tomography angiography; IOL, intraocular lens; NVI, neovascularization of the iris; VEGF, vascular endothelial growth factor; OD, oculus dexter; OCT, optical coherence tomography; DME, diabetic macular edema; SCHD, suprachoroidal hemorrhage and detachment.

Medical history, initial evaluation and treatment

A 56-year-old male with a 20-year history of type 2 diabetes was referred to our hospital for bilateral visual loss and ocular pain with pressure sensation. He had previously undergone bilateral pars plana vitrectomy (PPV) combined with phacoemulsification for DR-related vitreous hemorrhage, followed by multiple intravitreal anti-VEGF injections with poor efficacy, and subsequently developed bilateral NVG. On initial presentation, his OD IOP was uncontrolled at 39mmHg despite topical hypotensive medications, and ophthalmic examination confirmed iris neovascularization, panretinal photocoagulation (PRP) spots, and normal macular morphology without edema (Figure 2). He was diagnosed with bilateral proliferative DR (post-PRP), bilateral NVG, bilateral pseudophakia, and type 2 diabetes mellitus. He received an intravitreal anti-VEGF injection and PPV combined with peripheral retinal/cyclophotocoagulation in the OD, and subsequent follow-up showed resolved iris neovascularization, stabilized IOP at 11–12mmHg, and a flat retina.

Figure 2.

Initial and early postoperative OD imaging findings (November 26, 2025 – December 24, 2025). A. November 26, 2025 iris OCTA: Extensive peripheral and pupillary iris neovascularization (white arrows). B. November 26, 2025 infrared fundus image: Panretinal photocoagulation spots with a flat retina in the posterior pole of the right eye. C. December 24, 2025 iris OCTA: Complete resolution of iris neovascularization after surgery and anti-VEGF injection. D. December 24, 2025 macular OCT: Epiretinal membrane with focal linear hyperreflectivity in the macular area (white arrow), no macular edema. OCTA, optical coherence tomography angiography; OCT, optical coherence tomography; OD, right eye (oculus dexter); anti-VEGF, anti-vascular endothelial growth factor.

Onset of SCHD following anti-VEGF injection for DME

On January 14, 2026, the patient presented with further visual loss in the OD during follow-up, and re-examination indicated an IOP of 11mmHg, a BCVA of 20/200 with ineffective correction, and recurrent iris neovascularization in the OD, as well as DME with cystoid changes confirmed by macular OCT, so intravitreal Conbercept 0.5 mg was immediately administered in the OD for anti-angiogenesis and edema reduction (Table 1, Figure 3). The injection was performed using a 30-gauge needle via a superotemporal approach, with the injection site located 3.5–4.0 mm posterior to the corneoscleral limbus. A tunneled technique was employed: the needle was first inserted at a 15° oblique angle and then redirected perpendicularly through the sclera to create a self-sealing tract, facilitating watertight closure. The needle was left in place for approximately 5–10 seconds after injection to minimize reflux; no additional cotton tip compression or scleral massage was applied, consistent with routine practice. Manual IOP assessment by digital palpation immediately after injection revealed a normotensive to firm eye, and the patient tolerated the procedure with mild discomfort. Systemic blood glucose and blood pressure were within acceptable ranges per internal medicine consultation prior to the injection. Severe visual loss in the OD occurred on the next day after the injection, and the patient was re-admitted to our hospital for a comprehensive examination on January 23, 2026, which showed that the UCVA of the OD was 20/2000 and the BCVA was 20/400 with a refractive error of +7.25 DS/-2.25 DC ×55°, and the IOP was 10mmHg in the OD; imaging examinations revealed choroidal elevation around the optic disc on fundus photography, severe choroidal elevation with an unclear retinal structure in the posterior pole on OCT, and dense hyperreflectivity protruding into the vitreous cavity with shortened axial length on B-scan, leading to the final diagnosis of SCHD in the non-laser photocoagulation area of the posterior pole in the OD (Figure 4).

Table 1.

Serial changes in visual acuity, IOP, and key imaging findings of the right eye from pre-Conbercept injection through post-retrobulbar triamcinolone acetonide treatment.

Follow-up date	IOP (mm Hg)	UCVA	BCVA	Key imaging findings
January 14, 2026	11	20/200	20/200 (+0.75 DS/-1.75DC ×85°)	Recurrence of NVI and development of DME
January 23, 2026	10	20/2000	20/400 (+7.25 DS/-2.25 DC ×55°)	Development of SCHD
February 5, 2026	9	CF/30cm	20/330 (+8.75 DS/-2.75 DC ×45°)	Unchanged SCHD
February 9, 2026	10	CF/20cm	No improvement (+7.75 DS/-1.75 DC ×50°)	Mild choroidal elevation reduction
February 25, 2026	9	20/200	No improvement (+2.00 DS/-1.25 DC ×55°)	Marked SCHD regression
March 11, 2026	13	20/200	20/125 (+1.50 DS/-2.25 DC ×55°)	Complete SCHD resolution
March 25, 2026	13	20/200	20/125 (+1.25 DS/-2.25 DC ×75°)	Stable, no recurrence

IOP, intraocular pressure; UCVA, uncorrected visual acuity; BCVA, best-corrected visual acuity; NVI, neovascularization of the iris; DME, diabetic macular edema; CF, counting fingers; DS, diopter sphere; DC, diopter cylinder; SCHD, suprachoroidal hemorrhage and detachment.

Figure 3.

OCT imaging findings of diabetic macular edema in OD (January 14, 2026). A. Schematic diagram indicating the OCT scanning location in the macular area. B. Macular OCT image: Diabetic macular edema with typical cystoid changes (white star), macular thickening and nasal linear hyperreflectivity (white arrow). OCT, optical coherence tomography; OD, right eye (oculus dexter).

Figure 4.

SCHD diagnostic imaging findings in OD (January 23, 2026). A. Fundus photograph: Obvious choroidal elevation around the optic disc (posterior pole non-laser photocoagulation area, white arrow). B. Schematic diagram indicating the OCT scanning location in the posterior pole. C. Posterior pole OCT image: Severe choroidal elevation with unclear retinal layer structure (white arrow). D. B-scan ultrasonography: Dense hyperreflective lesions protruding into the vitreous cavity (white arrows) with shortened ocular axial length, consistent with SCHD. OCT, optical coherence tomography; OD, right eye (oculus dexter); SCHD, suprachoroidal hemorrhage and detachment.

SCHD treatment and follow-up

Considering the severe SCHD and significant visual loss, retrobulbar injection of triamcinolone acetonide 20 mg (combined with lidocaine 1 mL as a local anesthetic adjuvant) was performed in the OD on February 2, 2026 to exert anti-inflammatory effects, promote hemorrhage absorption and relieve pain. Of note, observation alone was not considered appropriate given the large volume of hemorrhage, which was unlikely to resolve spontaneously in a timely manner; systemic steroids were avoided due to the patient’s type 2 diabetes, and surgical drainage was deemed overly invasive in light of the recent vitreoretinal surgery in the same eye. The patient received weekly follow-ups after treatment with gradual improvement in ocular signs and visual acuity as recorded in Table 1. By March 11, 2026, fundus photography, OCT and B-scan confirmed complete resolution of SCHD in the OD, flat retina and normal macular foveal structure; the BCVA of the OD improved to 20/125 with a refractive error of +1.50 DS/-2.25 DC ×55°, and the IOP recovered to 13mmHg (Figure 5). A second follow-up on March 25, 2026 showed stable clinical findings, with a BCVA of 20/125 and an IOP of 13mmHg in the OD, and no recurrence of SCHD or new ocular complications.

Figure 5.

Post-treatment OD imaging findings following retrobulbar triamcinolone acetonide injection, with complete SCHD resolution (March 11, 2026). A. Fundus photograph: Complete resolution of SCHD with a flat posterior pole around the optic disc (white arrow). B. Schematic diagram indicating the OCT scanning location in the macular/posterior pole area. C. Macular OCT image: Normal macular foveal structure with a flat choroid and no obvious elevation. D. B-scan ultrasonography: Resolution of dense hyperreflective lesions (white arrows), no abnormal protrusion into the vitreous cavity, and normal ocular axial length. OCT, optical coherence tomography; OD, right eye (oculus dexter); SCHD, suprachoroidal hemorrhage and detachment.

Discussion

This case reports a rare complication of SCHD in the posterior pole non-laser photocoagulation area after intravitreal anti-VEGF injection, occurring in a high-risk patient with 20-year type 2 diabetes, bilateral proliferative DR, NVG, and multiple vitreoretinal surgeries. To the best of our knowledge, this is the first reported case of posterior pole non-laser area SCHD associated with anti-VEGF injection, thereby offering important clinical educational value.

A systematic literature search retrieved only three peer-reviewed publications describing SCHD secondary to intravitreal anti-VEGF injection, none of which reported lesions predominantly confined to the laser-spared posterior pole.^1,5,6 The two documented cases presented peripheral or 360° annular choroidal lesions induced by aflibercept or faricimab,^1,6 while large-scale pharmacovigilance data confirmed that faricimab carries a disproportionate risk of choroidal hemorrhagic adverse events, although case profiles were not detailed. ⁵ Moreover, none of these prior cases involved patients complicated with proliferative DR or NVG, nor did they include patients with PPV or cyclophotocoagulation; their management strategies consisted of conservative observation or sub-Tenon triamcinolone acetonide injection.^1,6 In contrast, full peripheral photocoagulation had stabilized the peripheral chorioretinal architecture in our patient, with SCHD predominantly developing at the laser-spared posterior pole. The intravitreal agent administered here was Conbercept, which has never been linked to SCHD in the aforementioned three published works. Our patient also presented a unique clinical profile characterized by repeated vitreoretinal operations for proliferative DR complications and chronically fluctuating IOP caused by refractory NVG. In this case, retrobulbar triamcinolone acetonide injection was performed, which completely resolved the posterior pole lesions and yielded substantial visual recovery, providing novel clinical insights into this underrecognized rare complication.

Pathogenic factors of SCHD in this case

The occurrence of this rare SCHD may be attributed to the combined effects of multiple interrelated factors, which are presumed to be closely associated with the patient’s high-risk clinical background and intraocular interventions. ① Low IOP caused by scleral leakage: The patient underwent OD PPV + cyclophotocoagulation prior to the incident, and the vitreous cavity was filled with aqueous humor postoperatively, leading to a non-watertight anti-VEGF injection puncture site. Aqueous humor leakage caused sustained low IOP (10mmHg), which increased the choroidal vascular pressure gradient and may have raised the risk of vascular rupture and hemorrhage. ⁷ ②Vascular regulatory effects of anti-VEGF drugs: Anti-VEGF drugs not only inhibit neovascularization but also disrupt the normal vascular tone and blood flow regulation of the choroid. ¹ In the eye with diabetic microangiopathy, this effect may further impair choroidal vascular stability and potentially increases the risk of vascular rupture. ③ Diabetic vascular fragility: Long-term hyperglycemia induced diabetic microangiopathy, characterized by vascular basement membrane thickening, endothelial cell loss and reduced vascular elasticity. ⁸ The choroidal blood vessels of the patient may have been in a fragile state, and could have been highly susceptible to mechanical damage and IOP fluctuations during intraocular injection. ④ Reperfusion injury from chronic high IOP damage: The patient had long-term uncontrolled high IOP (39mmHg) in the OD due to NVG, which caused chronic ischemia and hypoxia of choroidal blood vessels. The sudden reduction of IOP after surgery and injection may have triggered vascular reperfusion injury, potentially leading to vascular dilation, rupture and subsequent SCHD (3).

Clinical management and prevention of the complication

At present, there is no standardized treatment protocol for SCHD after anti-VEGF injection due to its low incidence. Conservative treatment (e.g., bed rest, IOP control) is sufficient for mild SCHD with no obvious visual loss, while active intervention is required for severe SCHD with significant choroidal elevation and severe visual loss. In this case, retrobulbar injection of triamcinolone acetonide was attempted based on the consideration that the patient’s SCHD may have been driven by choroidal inflammation and vascular hyperpermeability triggered by anti-VEGF injection trauma, hypotony, and diabetic microangiopathy. As a long-acting local corticosteroid, triamcinolone acetonide is theoretically capable of suppressing inflammation, stabilizing vascular endothelium, and promoting resorption of hemorrhage and exudation. ⁹ Retrobulbar administration was also preferred over systemic corticosteroids in this patient with comorbid T2D and NVG, given its higher intraocular bioavailability and lower systemic side-effect profile. Several previous reports have described the use of local corticosteroid injections for similar conditions: Nilforushan et al. and Sato et al. successfully managed choroidal detachment after glaucoma surgery or anti-VEGF therapy with sub-Tenon’s triamcinolone acetonide injection, with most cases resolving within 1–4 weeks^6,10; Sun et al. also observed gradual fluid absorption in a patient with panuveitis and bilateral choroidal detachment using a combination regimen including retrobulbar triamcinolone acetonide. ¹¹ In our patient, the complete resolution of posterior pole SCHD and marked visual improvement at 1 month post-injection represent an observed association with recovery that supports the plausibility of this therapeutic rationale, although the efficacy and safety of this approach warrant further validation in larger studies.

For high-risk patients (long-term diabetes, proliferative DR, NVG, multiple vitreoretinal surgeries), preventive measures may be considered to reduce the occurrence of such rare complications: strict pre-injection control of blood glucose and IOP may help stabilize the systemic and ocular microcirculation; careful anti-VEGF injection technique, with attention to puncture and confirmation of the watertightness of the puncture site to avoid scleral leakage and low IOP, is advisable; close post-injection monitoring of IOP and visual acuity, with timely comprehensive imaging examinations (OCT, B-scan) for patients with sudden visual loss to achieve early diagnosis and intervention, are also recommended.

Limitations

Several limitations of this case report should be acknowledged. First, as a single case report, the findings may not be generalizable to all patients with SCHD following anti-VEGF injection, given the variability in clinical presentation and underlying risk factors. Second, the lack of indocyanine green angiography or fluorescein angiography limited a more comprehensive characterization of choroidal vascular changes and perfusion status during the acute phase. Third, although we hypothesize that multiple factors contributed to the pathogenesis of SCHD in this case, the specific contribution of each factor remains speculative due to the absence of invasive hemodynamic monitoring and histopathological confirmation. Fourth, the follow-up duration was relatively short, and long-term outcomes, including the durability of visual improvement and the potential for SCHD recurrence, remain unknown. Despite these limitations, this case provides valuable clinical insights into a rare but vision-threatening complication in high-risk patients.

Conclusions

In conclusion, SCHD in the posterior pole non-laser photocoagulation area is an extremely rare severe complication of intravitreal anti-VEGF injection, which mainly occurs in high-risk DR patients with long-term diabetes, multiple vitreoretinal surgeries and NVG. The combined action of low IOP from scleral leakage, anti-VEGF vascular effects, diabetic vascular fragility, and chronic high IOP damage is likely to be the primary pathogenic mechanism of this complication. Retrobulbar triamcinolone acetonide injection may represent a promising treatment option for this rare SCHD, and in this case timely clinical intervention can achieve complete resolution of SCHD and significant improvement of BCVA, with favorable clinical outcomes. However, given the rarity of this condition, further evidence is needed to establish its efficacy. Clinicians should recognize the high-risk factors of this rare complication, implement standardized preventive measures in clinical practice, and perform early diagnosis and active intervention for suspected cases to avoid permanent visual loss in patients.

Appendix.

List of abbreviations

anti-VEGF

Anti-vascular endothelial growth factor

BCVA

Best-corrected visual acuity

DME

Diabetic macular edema

DR

Diabetic retinopathy

IOP

Intraocular pressure

NVG

Neovascular glaucoma

OD

Oculus dexter (right eye)

OCT

Optical coherence tomography

OCTA

Optical coherence tomography angiography

PPV

Pars plana vitrectomy

PRP

Panretinal photocoagulation

SCHD

Suprachoroidal hemorrhage and detachment

UCVA

Uncorrected visual acuity

VEGF

Vascular endothelial growth factor.

ORCID iDs

Yikeng Huang https://orcid.org/0000-0002-2534-9466

Xionggao Huang https://orcid.org/0000-0002-9979-9750

Ethical considerations

This case report was approved by the Ethics Committee of The First Affiliated Hospital of Hainan Medical University (Approval Number: 2026-KYL-187). All clinical procedures conformed to the ethical standards of the Declaration of Helsinki.

Consent to participate

Written informed consent was obtained from the patient for all clinical treatments and participation in the study.

Consent for publication

Written informed consent for the publication of this case report, including all clinical details, imaging data and follow-up results, was obtained from the patient. The consent form is kept in the medical record department of The First Affiliated Hospital of Hainan Medical University and is available for review by the journal editorial office upon request.

Data Availability Statement

All data and materials supporting the findings of this case report are included in the manuscript and the accompanying imaging figures/tables. The original medical records and imaging data are kept in the Department of Ophthalmology, The First Affiliated Hospital of Hainan Medical University, and are available from the corresponding author on reasonable request.*