Toxic posterior segment syndrome induced by silicone oil tamponade after surgery for rhegmatogenous retinal detachment: a case report

Abstract

Purpose

To report a clinical case of silicone oil-induced toxic posterior segment syndrome (TPSS) after rhegmatogenous retinal detachment (RRD) surgery.

Case description

A 75-year-old female developed TPSS with retinal hemorrhage and vessel sheathing after 25-G pars plana vitrectomy with silicone oil tamponade for left-eye RRD, had recurrent RRD after silicone oil removal, and achieved complete resolution of inflammation at 1-month follow-up after reoperation with 12% C₃F₈ gas tamponade instead of silicone oil, with laboratory tests confirming silicone oil-induced intense intraocular inflammation.

Conclusion

Silicone oil can induce early postoperative toxic posterior segment syndrome (TPSS), and 12% C₃F₈ inert gas is a viable alternative tamponade material for such cases.

Introduction

Silicone oil, as a long-acting intraocular tamponade material with stable physicochemical properties, is one of the core consumables in vitreoretinal surgery for the treatment of complex rhegmatogenous retinal detachment (RRD) [1, 2]. Its clinical application has been highly refined with a well-documented favorable safety profile in routine clinical practice [2, 3]. However, rare silicone oil-induced complications still occur occasionally, among which toxic posterior segment syndrome (TPSS) represents a challenging and underrecognized entity [4–6]. TPSS is typically accompanied by minimal or mild anterior segment inflammation, with the core features being sterile inflammation of the ocular posterior segment characterized by retinal vasculitis and retinal hemorrhage [7].

Herein, we report a rare case of silicone oil-induced TPSS after RRD surgery. More notably, the patient developed recurrent retinal detachment, and was successfully treated with 12% C₃F₈ inert gas tamponade instead of silicone oil, which provides a valuable clinical reference for the management of similar cases.

Case presentation

A 75-year-old female presented to our clinic with decreased visual acuity in her left eye for 2 months. She had a medical history of systemic sclerosis diagnosed 35 years prior and pulmonary fibrosis diagnosed 15 years ago, and she was on oral acetylcysteine for maintenance treatment. On examination, the best-corrected visual acuity (BCVA) was 20/40 in the right eye and 20/200 in the left eye. Slit-lamp examination showed grade 2 senile cataracts in both eyes. Fundus examination revealed a supranasal retinal degenerative area with a round retinal break within the degenerative region, accompanied by extensive inferior retinal detachment in the left eye.

The patient underwent a standard 25-G pars plana vitrectomy for the left eye under retrobulbar anesthesia with lidocaine. During the operation, silicone oil (RT SIL-OL 5000, Zeiss, Berlin, Germany) was used for intraocular tamponade. In addition, other routine auxiliary materials were administered intraoperatively, including triamcinolone acetonide (TA) and perfluorocarbon liquids (PFCL). Intraoperative perfusion pressure was maintained at approximately 22 mmHg during vitrectomy. During fluid-air exchange, IOP was elevated to 35 mmHg, and silicone oil was injected with a maximum pressure of 50 psi. No additional ocular compression was applied. At the end of the surgery, the intraocular pressure was adjusted to approximately 17 mmHg, which was measured by a Schiotz tonometer (Riester, Germany).

On postoperative day 1, the patient’s visual acuity was 20/100, intraocular pressure was 16 mmHg, the retina was well-attached, and laser photocoagulation spots were visible around the retinal break and degenerative area. On postoperative day 2, visual acuity remained 20/100, and intraocular pressure was 17 mmHg. No significant anterior segment inflammation was observed. However, fundus examination revealed extensive patchy retinal hemorrhage with central fibrinous exudation and localized retinal vessel sheathing (Fig. 1a). Optical coherence tomography (OCT) revealed only a small amount of subfoveal fluid (Fig. 1b). And fluorescein fundus angiography (FFA) showed simultaneous arteriovenous filling without prolongation of transit time (Fig. 1c), followed by capillary dilation and vessel wall staining (Fig. 1d). A preliminary diagnosis of TPSS was made, and the patient received a peribulbar injection of TA 40 mg.

Fig. 1.

(a) Fundus photograph of the left eye on postoperative day 2. The retina is well-attached, and extensive intraretinal patchy hemorrhage with central fibrinous exudation (*) and localized sheathing of retinal vessels (arrow) are clearly visible. (b) Optical coherence tomography (OCT) of the left eye on postoperative day 2, showing a small amount of subfoveal fluid. (c) Fluorescein fundus angiography (FFA) at 20s of the left eye on postoperative day 2, showing simultaneous filling of arteries and veins without arteriovenous transit delay. (d) Fluorescein fundus angiography (FFA) at 61s of the left eye on postoperative day 2, showing abnormal capillary dilation, fluorescein staining of vessel walls (arrow), and fluorescence masking in the areas of retinal hemorrhage (*)

On postoperative day 10, the patient’s visual acuity remained 20/100. Fundus examination showed that the retinal hemorrhage had partially absorbed compared with the previous examination, and the sheathing of retinal vessels had basically subsided (Fig. 2).

Fig. 2.

Fundus photograph of the left eye on postoperative day 10. Compared with Fig. 1(a), the intraretinal hemorrhage (*) and retinal vessel sheathing (arrow) are partially absorbed

On postoperative day 14, fundus examination confirmed that the retina remained well‑attached and that the laser photocoagulation spots around the retinal break exhibited a solid pigmented response. Given this stable retinal adhesion and the concern that silicone oil was the persistent inflammatory trigger, we decided to perform silicone oil removal combined with cataract surgery at this time rather than delay further. After this operation, the patient’s visual acuity recovered to 20/33.

Nevertheless, 5 days after silicone oil removal, the patient complained of decreased visual acuity again. Fundus examination revealed recurrent retinal detachment in the left eye. The patient underwent 25-G pars plana vitrectomy again, with TA and PFCL used as auxiliary materials. However, 12% C₃F₈ was selected as the intraocular tamponade instead of silicone oil this time, and the patient maintained a prone position after the operation. Meanwhile, we collected the patient’s aqueous humor and peripheral blood for laboratory testing, and the results revealed immunological abnormalities. Specifically, the level of interleukin-6 (IL-6) in the aqueous humor was markedly elevated to 118.85 pg/mL (reference range: 0–11.09 pg/mL); the proportion of highly suppressive regulatory T (Treg) cells in the blood increased abnormally to 48.4% (reference range: 2.6–29.1%); and the peripheral blood levels of tumor necrosis factor-alpha (TNF-α) and interleukin-2 (IL-2) were also elevated.

No retinal hemorrhage or retinal vessel sheathing was observed in the patient after this operation. At the 1-month follow-up, complete absorption of retinal hemorrhage was noted, and the patient’s visual acuity recovered to 20/25 (Fig. 3).

Fig. 3.

(a) Fundus photograph of the left eye 1 month after the second vitrectomy with 12% C₃F₈ gas tamponade for recurrent retinal detachment. The retina is well-attached, a small amount of residual gas is visible in the superior fundus, and the intraretinal hemorrhage and retinal vessel sheathing have been absorbed. (b) OCT of the left eye 1 month after the second vitrectomy, showing the macular retina is well-attached

Discussion

In this case, we observed the occurrence of extensive intraretinal hemorrhage and retinal vessel sheathing at the early stage after silicone oil tamponade surgery. This clinical manifestation is consistent with the characteristics of toxic posterior segment syndrome (TPSS) reported in previous literature. For instance, Sriram et al. reported a case of early postoperative retinal vasculitis [5]; Niroj et al. described three cases of occlusive retinal vasculitis [4]; and Miho et al. documented a case of early retinal vascular occlusion as manifestations of silicone oil-induced TPSS [6]. And a well-recognized potential cause of silicone oil-induced TPSS is the inherent impurities in silicone oil, including linear and cyclic low-molecular-weight components (LMWCs), which are known to induce ocular toxic reactions and trigger inflammatory responses in the ocular posterior segment [8–10]. Another thing to note is that, in contrast to previous reports where retinal vasculitis appeared on the first postoperative day, our patient developed clinical signs on day 2. This difference may reflect that a mild degree of inflammation was already present on day 1 but was too subtle to detect clinically and it became more apparent by day 2 as the inflammatory response progressed. We also considered infectious causes but cautiously excluded them based on the clinical findings: minimal anterior chamber inflammation, no hypopyon, no fibrinous exudate, and no signs of progressive infection. Furthermore, the patient did not receive any intraocular anti-infective therapy, yet the inflammation did not worsen and responded favorably to corticosteroids, supporting a sterile inflammatory etiology. Decompression retinopathy was considered as a differential diagnosis, but this was excluded based on the following: (1) intraoperative IOP was not excessively elevated; (2) postoperative IOP remained stable, with no hypotony or significant IOP fluctuation observed during the period when the retinal hemorrhage and vasculitis were developing; and (3) the presence of retinal vessel sheathing and capillary staining on FFA is more consistent with vasculitis than with a purely pressure-related hemorrhagic event. Based on the typical clinical features and relevant literature evidence, we made a diagnosis of TPSS in this patient.

We performed laboratory tests of aqueous humor and peripheral blood for two reasons: to objectively verify the presence of intraocular inflammation, and to preliminarily investigate whether the patient’s underlying systemic immune dysregulation—given her long-standing scleroderma and pulmonary fibrosis—might predispose her to silicone oil hypersensitivity. This remains a speculative hypothesis, offered only as a clinical clue for further consideration. IL-6 and TNF-α are key pro-inflammatory cytokines that play crucial roles in mediating acute inflammatory responses, promoting vascular endothelial damage, and inducing inflammatory cell infiltration [11, 12]; In this case, the level of interleukin-6 (IL-6) in the aqueous humor was markedly elevated to 118.85 pg/mL (reference range: 0–11.09 pg/mL), despite minimal anterior chamber inflammation clinically. It might be because IL-6 is a more sensitive marker of inflammation, and its elevation may not have reached a threshold sufficient to cause clinically overt anterior chamber cells or flare. Meanwhile, a direct comparison with reference values for aqueous IL-6 after retinal detachment surgery is limited, and surgical trauma itself may theoretically induce a certain degree of postoperative cytokine elevation. Therefore, the markedly elevated IL 6 level in this patient may not just represent inflammatory response and TPSS. As for other indicators, IL-2 is involved in regulating T cell activation and proliferation [13], while highly suppressive Treg cells function to maintain immune homeostasis and inhibit excessive inflammatory reactions [14]. These abnormal immunological indicators, combined with the patient’s long-standing history of systemic sclerosis and pulmonary fibrosis suggest that the patient was in a state of systemic immune dysregulation. This existing immune disorder background may have rendered the patient more susceptible to ocular inflammatory reactions induced by silicone oil, thus serving as a contributing factor to the development of TPSS.

Furthermore, TPSS has been reported to be induced by various intraoperative factors, including different intraocular materials (e.g., perfluorocarbon liquids), retrobulbar anesthesia, and even contaminated surgical instruments [7, 15]. However, in this case, the patient underwent two separate 25-G pars plana vitrectomy procedures due to recurrent retinal detachment, and the surgical instruments, anesthetic techniques and all auxiliary materials used in the two operations were completely consistent, including PFCL and TA. The only critical difference between the two surgeries was the intraocular tamponade material: silicone oil was used in the first surgery, while 12% C₃F₈ inert gas was adopted as the alternative in the second surgery. Notably, TPSS occurred only after the first surgery, and no similar inflammatory manifestations were observed after the second surgery with C₃F₈ gas tamponade. This clear comparison confirms that silicone oil was the primary inducer of TPSS in this case, and also suggests that 12% C₃F₈ inert gas may be a feasible alternative tamponade material for patients of silicone oil-induced TPSS.

In summary, two key clinical inferences can be drawn from this case. First, when extensive retinal hemorrhage and retinal vascular inflammatory changes occur in the early postoperative period after silicone oil tamponade, especially in patients with pre-existing systemic immune dysregulation, TPSS should be highly suspected as a potential diagnosis. Second, for patients diagnosed with silicone oil-induced TPSS, early silicone oil removal combined with the use of 12% C₃F₈ inert gas as an alternative intraocular tamponade material may be a clinically effective management strategy.

Author contributions

Y.H.D-collecting the patient data, writing the manuscript; H.J- performing the clinical management of the patient, interpreting the findings, and revising the manuscript. All authors commented on and approved the manuscript.

Funding

Technological Innovation and Cultivation Fund for Medical Youth of Peking University (BMU2020PYB014). The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or decision to submit the manuscript for publication.

Data availability

No datasets were generated or analyzed during the current study.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and the accompanying clinical images. All identifying information has been removed.

Competing interests

The authors declare no competing interests.