Anterior Chamber Sulfur Hexafluoride Injection for Hypotony Management: Case Report and Literature Review

Abstract

Introduction

Hypotony is a potentially vision-threatening condition that may persist despite conservative management, often necessitating surgical or interventional treatment. We present a case where a minimally invasive injection of 100% sulfur hexafluoride (SF6) into the anterior chamber (AC) successfully reversed refractory hypotony secondary to ciliary body shut-down.

Case Presentation

A 72-year-old male with advanced pseudoexfoliation glaucoma and a nonfunctioning trabeculectomy presented with hypotony, decreased vision, a deep AC, and 360° serous choroidal effusions. After excluding other etiologies, ciliary body shutdown was presumed. Conventional measures, including topical steroids, cycloplegia, and AC viscoelastic injection, failed to restore intraocular pressure (IOP). Given the refractory course, 100% SF6 gas was injected into the AC. Within 24 h, a reverse pupillary block developed, leading to a rapid IOP increase. The gas fully reabsorbed within weeks, with resolution of the choroidal effusions and normalization of IOP. At 6 months, the patient maintained stable IOP and visual acuity without further intervention.

Conclusion

This case highlights the potential of SF6 gas injection as a minimally invasive and effective treatment for refractory hypotony, even when the underlying mechanism is not over-filtration.

Introduction

Hypotony is a potentially vision-threatening condition and can lead to corneal folds, flat anterior chamber (AC), choroidal effusions, and hypotony maculopathy [1, 2]. It is a well-recognized complication following glaucoma filtration surgery [3], with rates ranging from 1.3% to 32.7% [4–6]. However, hypotony secondary to other causes is less well described in the literature [7].

A variety of techniques have been suggested to conservatively manage filtration-related hypotony, including cycloplegic and steroid eye drops, and filling a flat AC using BSS or ophthalmic viscosurgical devices, such as sodium hyaluronate 1.0% (Healon) [8, 9]. The use of gas, such as air, perfluoropropane (C3F8) and sulfur hexafluoride (SF6) in such cases was first described as early as the 1980s [10–13].

These gases, commonly used in retinal detachment and macular hole surgeries, expand by drawing dissolved N₂, O₂, and CO₂ from the vitreous into the bubble, thus expanding the initial gas volume. In the vitreous, 100% SF6 more than doubles its volume within 48 h, after which it begins to gradually reabsorb over 7–10 days [14]. A similar timeframe has been suggested for gas resorption from the AC [10, 15].

We present a case demonstrating the efficacy of 100% SF6 gas injection into the AC to treat hypotony secondary to ciliary body shutdown. This intervention induced a reverse pupillary block, leading to intraocular pressure (IOP) elevation [16, 17]. This approach is shown here to be effective in an eye with a deep AC and a nonfunctioning trabeculectomy.

Case Presentation

We present a healthy 72-year-old African male with a history of bilateral advanced pseudoexfoliation glaucoma. His left eye (LE) underwent uneventful cataract phacoemulsification surgery 5 years earlier. He reported no use of glasses prior to cataract surgery, and postoperative biometry revealed normal values (axial length: 23.6 mm; AC depth: 4.66 mm; K1: 42.82 D; K2: 43.78 D). He had a good central vision of 20/40; however, his visual field had advanced arcuate defects (shown in Fig. 1). Due to a suboptimal IOP (IOP of 20 mm Hg) on maximal medical treatment, the patient underwent LE trabeculectomy augmented with mitomycin C, with normal postoperative management and good IOP control of 10 mm Hg. He had a known chronic flat serous inferior retinal detachment that was first identified during post-trabeculectomy follow-up visits. The patient declined any treatment for this condition, as it did not impact his visual function.

Fig. 1.

Visual field and OCT RNFL at presentation: on the left, Humphrey 24-2 FASTPAC visual field (stimulus size V) demonstrating a residual central island of vision. On the right, optical coherence tomography (OCT) retinal nerve fiber layer (RNFL) scan (Zeiss) showing marked superior and inferior thinning of the optic nerve in the left eye.

After 7 months, he presented to our clinic with an IOP of 19 mm Hg in both eyes, with a flat bleb in his LE. He was treated by needling and a 5-Fluorouracil injection into the LE at the slit lamp. Two days after, he developed decreased vision, ocular pain, and conjunctival injection. His best-corrected visual acuity (BCVA) reduced to 20/100. Examination revealed an IOP of 4 mm Hg, corneal Descemet’s folds, shallow AC, and serous choroidal effusions (i.e., choroidal detachments; CDs) confirmed by ultrasonography. He was admitted to the ophthalmology department and received 3 injections of hyaluronic acid-based viscoelastic (Biolon, Altacor Ltd, Berkshire, England) into the AC over the next few days, resulting in normalization of IOP (12 mm Hg), with complete symptom resolution. He was discharged using topical steroids (Dexamethasone Sodium Phosphate 0.1%, Sterodex, Dr. Fischer Ltd, Bnei Brak, Israel), instructed to gradually taper down the dosage to twice daily.

Four months later, IOP spiked to 28 mm Hg in his LE. The LE bleb was flat, appeared scarred and non-functional. He was treated in the ophthalmology emergency department until IOP normalized and was discharged home with full topical glaucoma treatment. The topical steroids were discontinued due to suspected steroid response.

Another month later, the patient presented with 3 days of ocular pain in the LE. His BCVA reduced to 20/200. The patient denied any ocular trauma. Examination showed a scarred nonfunctioning bleb; corneal Descemet’s folds without Keratic precipitates; a deep and quiet AC (shown in Fig. 2a, b); and a mildly dilated pupil showing a minimal light response (attributable to PXF) but no cells or flare. The IOP was 3 mm Hg. There were no signs of vitritis or retinitis, but 360° CD were noted (shown in Fig. 3a). Gonioscopy illustrated a normal open angle, without a ciliary cleft or other abnormal findings. Macular ocular coherence tomography (OCT) revealed macular folds. Ultrasound biomicroscopy also illustrated a normal position of the ciliary body (images unavailable).

Fig. 2.

Slit-lamp photographs of the anterior segment at various time points. a Scarred, flat bleb at presentation. b Deep AC at presentation. c Immediately post-injection, showing an excessively deep AC with an SF6 gas bubble occupying approximately 80% of the chamber and inducing reverse pupillary block. d Nearly complete absorption of the gas bubble.

Fig. 3.

Fundus images of the patient’s left eye at different time points. a At presentation, demonstrating 360° CDs. b On day 11 post-SF6 injection. c On day 19 post-injection, showing complete resolution of CDs.

The mechanism for the hypotony was unclear, and ciliary shutdown was suspected. All topical glaucoma therapy was stopped, and steroid drops (fluorometholone 0.1%, FML; Allergan Ltd, Irvine, CA, USA) and cycloplegia (atropine sulfate 1%, Atrospan, Dr. Fischer Ltd, Bnei Brak, Israel) were initiated. Over the next 2 weeks, conservative management, including an injection of a cohesive viscoelastic substance into the AC (Provisc, Alcon Ltd, Geneva, Switzerland), failed to increase IOP to normal levels. It is noteworthy that repeat gonioscopy was performed after the injection of viscoelastic, as this can enhance visualization of a cyclodialysis cleft; however, no cleft was identified in this case.

Given the refractory nature of the patient’s hypotony, and his refusal for any surgical intervention, such as choroidals drainage, we decided to try the minimally invasive treatment of SF6 injection into the AC. The patient was appropriately informed of the technique and gave written informed consent before treatment.

Surgical Technique

The procedure was conducted at the slit lamp, after instilling topical anesthetic drops and gel (Oxybuprocaine HCl, Localin, Dr. Fischer Ltd, Bnei Brak, Israel; Esracain Gel, Lidocaine HCL 2%, Jerusalem, Israel) and topical Minims Povidone iodine 5% (Bausch & Lomb, Rochester, NY, USA). 1 mL of pure 100% concentration SF6 was prepared in an insulin syringe, under sterile conditions. An eyelid speculum was placed with a 30-G needle, and then used to enter the AC at the 3 o’clock position through the peripheral cornea. After ensuring a complete AC entry, the gas was slowly injected until it filled the AC (approximately 0.4–0.6 mL). A long needle track is advantageous to prevent gas leakage and to create a self-sealing tunnel. The patient was not instructed to maintain a specific position.

Immediately after the procedure, IOP was measured at 17 mm Hg. The AC deepened significantly, and the goal of creating a reverse pupillary block was achieved, with posterior iris displacement observed (shown in Fig. 2c). The patient received antibiotic, corticosteroid and miotic drops (Sterodex and Oflox QDS; Pilocarpine 2% TDS [pilocarpine hydrochloride 2%, Vitamed Pharmaceutical Industries Ltd, Binyamina, Israel]).

Follow-Up

The patient was examined daily. On day one post injection, IOP peaked at 40 mm Hg, requiring medical control with oral acetazolamide 250 mg QDS and full topical glaucoma therapy. Under this regimen, IOP stabilized at 21 mm Hg, with residual gas in the AC and persistent choroidal effusions. Repeat B-SCANs showed no evidence of gas migration to the posterior segment.

In the subsequent days, IOP stabilized between 9 and 14 mm Hg while BCVA improved to 20/70. Glaucoma medications were progressively tapered and discontinued. The injected SF6 gas fully resorbed within 12 days, resulting in an anatomically deep and quiet AC (shown in Fig. 2d). The choroidal effusions gradually resolved (shown in Fig. 3b, c).

At 6-month follow-up, the patient maintained good vision of 20/50 with stable IOP in the low teens without topical therapy. The AC remained deep and quiet, and the choroidal effusions had fully resolved. Interestingly, the chronic inferior serous retinal detachment had also resolved.

Discussion

This case illustrates the successful use of 100% SF6 gas injection in managing refractory hypotony. Similar to previous reports [9, 10, 13] focusing on post-surgical hypotony secondary to over-filtration with a flat AC, the technique was successful in this case, with presumed ciliary body shutdown as the underlying mechanism. The SF6 gas injection induced a reverse pupillary block and contributed to IOP normalization.

The normal AC volume is 0.2 mL, and we injected about 0.4 mL to create an abnormally deep AC. This is important because the aim of the gas tamponade is twofold: first, to create a reverse pupillary block [16] by preventing aqueous humor (AH) outflow into the AC. To achieve this block, it is critical to fill the AC to the point that the gas bubble completely covers the pupil, a mechanism we reinforced in our case with the administration of pilocarpine drops. Second, the gas may displace the ciliary body, restore AH production, stretch the iris base and surrounding tissues, and simultaneously block the trabecular meshwork.

We injected the gas at the slit lamp using a 30-G needle at the 3 O'clock position. As this was the patient’s LE, we found this position most comfortable for a right-handed injector, and the procedure was simple with no observed leakage of the gas during or after the procedure. Previous reports suggested injecting the gas in the 6 o’clock position, as its nature is to float upward [12, 18]. We found this unnecessary, as a long corneal tunnel was enough to prevent backflow leakage.

As the gas bubble expanded, IOP rose to 40 mm Hg. Such a spike may be harmful to an already glaucomatous optic nerve. Although IOP was effectively controlled with medication, we recommend frequent follow-up visits to detect and manage this complication. A smaller gas fill, limited to 60–70% of the AC, may help reduce this risk.

In our case, the 100% pure gas bubble absorbed completely only 12 days after the injection, which seems longer than previously reported as 7–10 days for complete absorption [10, 15]. One possible explanation is the absence of a functioning bleb in our case so no gas was leaking through the sclerostomy. It took approximately 19 days after IOP normalization to achieve complete resolution of the CDs. Previous reports suggested a 1–3 weeks interval for CD resolution after hypotony is corrected [19]. However, others reported a much faster recovery following gas injection; four to 7 days [12, 18]. The hypotony in our patient may have resulted from multiple factors. The differential diagnosis of ocular hypotony can be divided into three categories or a combination thereof: decreased AH production; increased AH outflow and reversed osmotic gradient [7]. In our case, potential contributors included prior filtration surgery, medication-induced aqueous suppression, and chronic serous retinal detachment. It is important to note that the patient did not undergo cyclophotocoagulation treatment, which is a known cause for hypotony, at any point.

The absence of a functioning bleb suggests that excessive AH outflow was not the primary mechanism. Prior to his hypotony, our patient was treated with maximal topical IOP-lowering agents for 4 weeks. However, hypotony secondary to glaucoma medications is rarely reported and their effect alone is unlikely to explain the severe hypotony of 3 mm Hg, as episcleral venous pressure limits IOP reduction [7]. In addition, eliminating all IOP-lowering medications for 2 weeks did not reverse the hypotony. Reports of topical medication-induced hypotony typically involve additional risk factors such as systemic medications, prior filtration surgery, or laser trabeculoplasty [7, 20]. On the other hand, in combination with other risk factors, it may have contributed to the clinical picture.

Our patient had a chronic flat serous inferior retinal detachment, which could be considered a potential factor contributing to hypotony [7, 21]. Solberg et al. [22] described two possible mechanisms for hypotony following retinal detachment: reduced AH production, or an abnormal posterior outflow through the vitreous and retinal hole into the subretinal space. However, in our case, retinal detachment is a less likely cause of hypotony, as the patient previously had significantly elevated IOP despite the presence of the detachment. In addition, no retinal tear was seen at any point during follow-up, as well as the fact that his choroidal effusion was absorbed once the pressure was elevated. Moreover, the retinal detachment improved over time and did not worsen, and eventually resorbed.

Given these factors, we suggest that ciliary body shutdown is the most plausible explanation. However, he had no signs of inflammation, ocular ischemia, and denied any trauma. Decreased AH production can also occur as an idiosyncratic response to ocular surgery, but the last ocular intervention he had (bleb needling) occurred 5 months prior to hypotony.

It is worth mentioning that AC injection of SF6 has been linked in animal models to significant endothelial loss and stromal edema, attributable to a prolonged mechanical barrier between AH and the corneal endothelium [23, 24]. In contrast, most human series have not documented corneal toxicity, yet every phakic eye developed a full cataract formation within 6 months [18]. These findings suggest that alternative tamponade techniques should be considered for phakic patients.

To conclude, the success of this surgical technique in our patient highlights the potential role of 100% pure SF6 gas injection in cases of hypotony secondary to causes other than over-filtration. This minimally invasive office procedure appears effective and safe, and may allow avoidance of more invasive surgical interventions. However, further studies are needed to explore the long-term safety and efficacy in broader clinical settings.

The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000550117).

Statement of Ethics

This case report was reviewed and granted exemption from ethics approval by the Edith Wolfson Institutional Review Board (IRB), in accordance with institutional policy for single case reports that do not contain identifying information. Written informed consent was obtained from the patient for publication of the details of their medical case and any accompanying images.

Conflict of Interest Statement

The authors declare that they have no competing interests.

Funding Sources

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Author Contributions

M.N.: drafting the work and interpretation of data; M.K.-L.: interpretation of data and revised the manuscript; R.E.: conception and revised the manuscript; L.M.-V.: performed the procedures, figures photographer, interpretation of data, and revised the manuscript.

Funding Statement

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Data Availability Statement

All data generated or analyzed during this case report are included in this article. Further inquiries can be directed to the corresponding author.