Fig. 1. Ultrasonic biomicroscopy showing no cyclodialysis cleft at the surgical site
Рис. 1. Ультразвуковая биомикроскопия не выявила зоны циклодиализа в проекции операционного вмешательства
Fig. 2. Follow-up examination of the left eye showing intraocular lens dislocation secondary to chronic hypotony
Рис. 2. Состояние левого глаза при контрольном осмотре, свидетельствующее о дислокации интраокулярной линзы вследствие хронической гипотонии
Topicality
Trabeculectomy (TRAB) is a widely performed glaucoma surgery but carries the risk of postoperative hypotony, which can lead to vision-threatening complications such as choroidal effusion, maculopathy, optic neuropathy, and cataract formation [1]. While early hypotony is relatively common and often self-limiting, late-onset hypotony—developing months or even years after surgery—is rare and more challenging to diagnose and manage [2].
Late hypotony is generally attributed to excessive aqueous outflow due to bleb leakage or reduced aqueous production from ciliary body dysfunction. However, in some cases, no clear etiology can be identified, making diagnosis and management particularly difficult. When bleb leakage is absent, alternative mechanisms should be considered, including subclinical cyclodialysis clefts, increased uveoscleral outflow, chronic inflammation, or prolonged use of aqueous suppressants. Additionally, Mitomycin-C (MMC), commonly used in TRAB, has been implicated in long-term changes in scleral permeability and ciliary body function, potentially contributing to persistent hypotony [3, 4].
Purpose.
This study presents three cases of unexplained late-onset hypotony following trabeculectomy (TRAB), highlighting the diagnostic complexity and management challenges when conventional causes such as overfiltration and bleb leaks are ruled out. In addition to analyzing these cases, we conducted a comprehensive review of the literature to explore potential mechanisms, risk factors, and treatment strategies for persistent hypotony in post-TRAB patients.
Material and methods.
We analyzed three patients who developed late-onset hypotony after undergoing TRAB. Each case was evaluated based on best-corrected visual acuity (BCVA), intraocular pressure (IOP) trends, ultrasound biomicroscopy (UBM), optical coherence tomography (OCT) findings, visual field (VF) analysis, use of antiglaucoma medications, bleb morphology, and surgical history. Additionally, the patients’ responses to various medical interventions, including cycloplegics, corticosteroids, cataract surgery, and gas tamponade, were assessed. The diagnosis of hypotony was confirmed by IOP <5 mmHg with associated anatomical changes (e.g., choroidal effusion, macular folds). The primary challenge was identifying the cause in the absence of overfiltration or bleb leaks on Seidel testing and UBM findings.
Case presentations
Case 1
A 65-year-old male with pseudoexfoliative (PEX) glaucoma in the left eye had been under follow-up for 10 years. Preoperatively, BCVA was full in the right eye and 0.8 in the left eye. IOP was 17 mmHg (right, no medication) and 22 mmHg (left, on brimonidine, timolol, dorzolamide, and latanoprost). The left eye exhibited advanced glaucoma with a mean deviation of –18.72 dB, an arcuate scotoma, and a retinal nerve fiber layer (RNFL) thickness of 98 μm in the right eye and 55 μm in the left. In March 2020, he underwent MMC-augmented TRAB on the left eye. For three years, IOP remained stable without symptomatic hypotony, despite ongoing medication adjustments. OCT showed no progression, and IOP fluctuations were managed with antiglaucoma therapy modifications.
In the third postoperative year, IOP in the left eye dropped to 0–1 mmHg, marking the onset of recurrent hypotony episodes. The anterior chamber depth was adequate, the bleb was flat without leakage. However, upon initiating tropicamide and dexamethasone (3x1), IOP sharply increased to 30 mmHg, suggesting a steroid response. When steroids were discontinued, IOP dropped again to 12/0 mmHg within two months. UBM revealed no cyclodialysis cleft (Fig. 1).
One month later, the patient experienced an IOP spike to 32 mmHg in the left eye. The anterior chamber depth (ACD) remained adequate, with a flat bleb and a small iridectomy.
In response, dorzolamide-timolol (2×1) was added to the regimen, while tropicamide and dexamethasone were discontinued. However, three months l
Fig. 3. The left eye exhibited a well-formed anterior chamber with no bleb formation. Optical coherence tomography revealed the presence of an epiretinal membrane and choroidal folds, associated with chronic hypotony
Рис. 3. Левый глаз: передняя камера определяется, плоская фильтрационная подушка. ОКТ: эпиретинальная мембрана и хориоидальные складки на фоне хронической гипотонии
Fig. 4. Ultrasound biomicroscopy of the left eye, demonstrating mild leakage beneath the scleral flap but no detectable cyclodialysis cleft
Рис. 4. Ультразвуковая биомикроскопия (УБМ) левого глаза: незначительная фильтрация под склеральный лоскут, без признаков отслойки сосудистой оболочки
Case 2
A 68-year-old female with PEX glaucoma was diagnosed in 2018. Despite one year of treatment with brimonidine, brinzolamide, timolol, and bimatoprost, her IOP remained uncontrolled (24 mmHg right, 36 mmHg left), leading to TRAB with MMC on the left eye in 2019. For 2.5 years postoperatively, IOP remained stable between 10– 18 mmHg without signs of hypotony. However, six months after undergoing phacoemulsification with IOL implantation in 2021, gonioscopy revealed iris obstruction of the TRAB ostium, necessitating a revision with MMC. Six months after TRAB revision with MMC in 2021, multiple severe hypotony episodes (IOP: 0–1 mmHg) were occured, each lasting several weeks. Despite the marked reduction in IOP, the ACD was well-maintained, and no bleb formation was observed. Given the hypotony, brinzolamide and brimonidine were discontinued. During this period, epiretinal membrane (ERM) and choroidal folds were noted in the left eye (Fig. 3).
Although IOP initially stabilized, the patient experienced a second and third hypotony episode, with spontaneous recovery after cessation of aqueous suppressants. Throughout these episodes, the bleb remained absent, Seidel’s test was negative, and the iridectomy site remained open. UBM did not reveal a cyclodialysis cleft, but mild leakage beneath the scleral flap was detected (Fig. 4).
Each hypotony episode responded dramatically to cycloplegics and corticosteroids, leading to a rapid IOP increase. However, once steroids were tapered, IOP again dropped to hypotonic levels, repeating this cycle three times over the course of a year. For six years, the right eye had been treated with brimonidine, brinzolamide, and timolol. In July 2024, the patient underwent gonioscopy-assisted transluminal trabeculotomy surgery in the right eye, allowing for the discontinuation of all IOP-lowering medications. Interestingly, shortly after stopping treatment in the right eye, the left-eye IOP—previously prone to hypotony—spontaneously increased to 22 mmHg, requiring the reintroduction of bimatoprost.
At the last visit, the patient remained hypotony-free, with an IOP of 18 mmHg (right, medication-free) and 12 mmHg (left, on bimatoprost). Despite stable IOP, the left eye showed no bleb formation, and the iridectomy site exhibited anterior displacement of the iris pigment epithelium and ciliary body. Additionally, progressive ERM formation led to a decline in VA to 0.1 (Fig. 5).
Case 3
A 79-year-old male with PEX glaucoma underwent TRAB with MMC in the left eye (2004) and right eye (2007). Until 2015, the right eye remained medication-free, while the left eye was treated with dorzolamide-timolol. After cataract surgeries in both eyes (2015, 2018), all glaucoma medications were discontinued, and the patient remained stable without treatment until 2024. His VA was: 1.0/0.9, RNFL: 79/59 without pr
Fig. 5. At the final visit, the anterior chamber depth was well-maintained, but there was no bleb formation in the left eye. Top right photo showing anterior displacement of the iris pigment epithelium and ciliary body at the iridectomy site. Optical coherence tomography revealed a macular epiretinal membrane
Рис. 5. Последний визит пациента: глубокая передняя камера, отсутствие фильтрационной подушки в левом глазу. Вверху справа: переднее смещение пигментного эпителия радужной оболочки и цилиарного тела в месте иридэктомии. По данным ОКТ, сохраняется макулярная эпиретинальная мембрана
Fig. 6. Ultrasonography illustrating 360-degree choroidal effusion and choroidal detachment
Рис. 6. Ультразвуковое исследование: наличие субхориодальной жидкости по всему периметру 3600 и отслойка сосудистой оболочки
In April 2024, IOP was 6 mmHg (right) and 25 mmHg (left), prompting the reintroduction of brinzolamide, brimonidine, and latanoprost in the left eye. One month later, IOP dropped to 8 mmHg. By January 2025, he developed 360-degree uveal effusion, and IOP further declined to 5 mmHg (Fig. 6).
Anterior segment examination showed a flat bleb, a closed iridectomy, and mild anterior chamber shallowing. Scleral thinning was noted, with the scleral flap margins visibly outlined externally (Fig. 7).
Glaucoma medications were stopped, and treatment with atropine 1% (2×1) and dexamethasone (5×1) was initiated. Despite treatment, IOP remained critically low (2–4 mmHg), and the anterior chamber progressively shallowed. By January 31, 2025, he developed maculopathy with choroidal folds, leading to a decline in VA to 0.1 (Fig. 8).
Fundoscopic examination suggested a possible exudative retinal detachment, likely secondary to prolonged choroidal detachment, though no retinal tears were observed (Fig. 9).
However, the presence of severe hypotony may have masked small retinal breaks. On February 3, 2025, 20% sulfur hexafluoride (SF6 ) gas was injected into the anterior chamber. The following day, IOP improved to 8 mmHg, accompanied by anterior chamber deepening, although VA was reduced to counting fingers. By February 6, 2025, choroidal detachments had become less bullous, and retinal detachment was ruled out due to the absence of outer retinal discontinuity on imaging (Fig. 10).
Discussion
These three cases presented illustrate that hypotony can develop at any time following TRAB, ranging from as early as the sixth postoperative month (Case 1) to as late as the 22nd year (Case 3). While cystic bleb formation and overfiltration are often cited as the primary causes of post-TRAB hypotony, none of our patients exhibited a well-formed filtering bleb, ruling out excessive filtration as the primary mechanism. Additionally, UBM failed to identify a cyclodialysis cleft in two cases, and in the third, detailed gonioscopy showed no evidence of cleft formation.
Hypotony is a well-recognized complication of glaucoma filtration surgery, with reported incidence rates ranging from 1% to 31%. However, late-onset hypotony is considerably less common [1]. A study demonstrated that persistent hypotony can occur as late as 720 days postoperatively, reinforcing the unpredictable nature of this condition [2].
In our cases, the absence of bleb leakage and the loss of well-formed blebs were particularly notable. When bleb leakage is ruled out, increased aqueous outflow through a cyclodialysis cleft becomes a potential cause of hypotony [5]. Even as small as 50 µm cleft can induce significant hypotony, potentially resulting from surgical trauma [6]. Martinez-Bello et al. identified persistent choroidal effusion in 28 eyes using UBM conducted 4 to 6 months post-TRAB, suggesting that scleral spur excision may disrupt the barrier between the anterior chamber and supraciliary space, leading to cyclodialysis and increased uveoscleral o
Fig. 7. Anterior segment exam showing flat bleb, closed iridectomy, and scleral thinning with externally visible scleral flap margins
Рис. 7. Биомикроскопия переднего сегмента: плоская фильтрационная подушка, закрытое иридэктомическое отверстие и истончение склеры с внешне видимыми краями склерального лоскута
Fig. 8. Optical coherence tomography scan demonstrating persistent choroidal folds, despite treatment
Рис. 8. ОКТ заднего отрезка глаза: сохранение хориоидальных складок на фоне лечения
Mitomycin-C (MMC) is well-documented as a risk factor for post-TRAB hypotony [3]. The absence of bleb formation or overt leakage in our cases suggests that MMC-induced toxicity may have contributed to late-onset hypotony through scleral weakening and ciliary body dysfunction [9]. Histological studies have shown that MMC thins the sclera, increasing aqueous permeability and allowing for diffuse transscleral leakage, even when Seidel’s test is negative [10]. In case 2, UBM revealed an intrascleral aqueous flow, supporting this hypothesis. However, due to the thickness of the upper scleral flap, fluid permeability appears to occur through the lower scleral flap into the sclera, rather than forming a visible bleb. Additionally, MMC has been reported to cause direct toxic effects on the ciliary body epithelium, leading to aqueous hyposecretion, which may explain persistent hypotony in the absence of overfiltration [9].
Emerging evidence suggests that aqueous suppressant medications may contribute to late-onset hypotony following TRAB [11]. A study investigating five patients who developed choroidal effusion after cataract surgery found that all had previously used carbonic anhydrase inhibitors, and their effusions resolved with corticosteroids and cycloplegics, indicating a potentially reversible mechanism [12]. In our cases, the use of topical aqueous suppressants was a common factor, raising concerns about their role in postoperative hypotony. Similarly, Rachmiel et al. described two cases of postoperative late-onset hypotony, both occurring while patients were on IOP-lowering medications, despite the absence of bleb leakage or inflammation [13]. One proposed mechanism is that prolonged aqueous suppression may lead to progressive ciliary body dysfunction, particularly in eyes that have undergone filtration surgery. Over time, the ciliary body may become unable to maintain sufficient aqueous production, predisposing the eye to hypotony episodes [14]. Latanoprost has also been implicated in cases of hypotony and choroidal detachment following filtration surgery, likely due to its enhancement of uveoscleral outflow [15]. Additionally, systemic absorption of aqueous suppressants from the contralateral eye has been suggested as a possible contributor to bilateral regulatory changes in aqueous production, even in the absence of direct treatment in the affected eye [16]. In our cases, the use of aqueous suppressants in the contralateral eye was a notable finding. These findings suggest that aqueous suppressant medications should be carefully considered as a potential contributing factor in cases of unexplained late hypotony following TRAB [17].
Another potential cause of aqueous hyposecretion is anterior segment inflammation following intraocular surgery.
Inflammation can induce ciliary shutdown, leading to hypotony by reducing aqueous production and increasing uveoscleral outflow [7, 18]. The presence of PEX is also known to further increase the risk of postoperative inflammation, particularly in association with IOL implantation. Notably, all of our cases had PEX glaucoma and had undergone multiple ocular surgeries, which may have contributed to the development of late hypotony [19].
In our cases, the rapid IOP elevation in response to steroids was a notable finding. Similarly, a study on late-onset hypotony fol
Fig. 9. Fundoscopy showing possible exudative retinal detachment, likely secondary to prolonged choroidal detachment. Ultrasonography shows persistent bullous choroidal detachments
Рис. 9. Офтальмоскопия глазного дна: возможная экссудативная отслойка сетчатки на фоне длительной отслойки сосудистой оболочки и гипотонии. Ультразвуковое исследование: наличие пузыревидной отслойки сосудистой оболочки
Fig. 10. Post-SF6 injection, anterior chamber deepening with persistent choroidal folds on Optical coherence tomography, though bullous choroidal detachment reduced on US
Рис. 10. Состояние глаза после введения газа SF6, углубление передней камеры, сохраняющиеся хориоидальные складки по данным ОКТ. УЗИ: уменьшение высоты пузыревидной отслойки сосудистой оболочки
Conclusion.
Late-onset hypotony following TRAB remains a complex and multifactorial condition, particularly in cases without detectable bleb leakage. Our findings suggest that MMC-induced scleral and ciliary body toxicity, increased uveoscleral outflow, aqueous hyposecretion, and prolonged use of aqueous suppressants may play key roles in its development [17]. Additionally, subclinical cyclodialysis clefts, steroid responses, and chronic low-grade inflammation could further disrupt aqueous dynamics, perpetuating hypotony.
Despite advances in imaging and treatment, late-onset hypotony remains a significant challenge, underscoring the need for further research to refine diagnostic approaches and develop more effective long-term management strategies.
Information about the authors
Umay Güvenç — MD, Ankara training and research hospital, Ankara, umay.guvenc@gmail.com, https://orcid.org/0000-0002-8993-1674
Gülizar Soyugelen — Assoc prof, Ankara training and research hospital, Ankara, gulizardemirok@hotmail.com, https://orcid.org/0000-0003-4655-4669
Информация об авторах
Умай Гювенч — доктор медицины, Учебно-исследовательская клиника г. Анкары, Анкара, Турция, umay.guvenc@gmail.com, https://orcid.org/0000-0002-8993-1674
Гюлизар Союгелен — доцент, Учебно-исследовательская клиника г. Анкары, Анкара, Турция, gulizardemirok@hotmail.com, https://orcid.org/0000-0003-4655-4669
Authors’ contributions:
Umai Güvenç — material set, article writing and literary review
Gulizar Soyugelen — basic concept research, writing section discussion, editing
Вклад авторов:
Умай Гювенч — набор материала, написание статьи и литературный обзор.
Гюлизар Союгелен — основная концепция исследования, написание раздела обсуждение, редактирование.
Financial transparency: The authors have not declared a specific grant for this research from any funding agency in the public, commercial, or non-profit sector.
Финансирование. Авторы не получали конкретный грант на это исследование от какого-либо финансирующего агентства в государственном, коммерческом и некоммерческом секторах.
Conflict of interest: None.
Конфликт интересов: Отсутствует.
Поступила: 15.10.2025
Переработана: 14.11.2025
Принята к печати: 18.11.2025
Received: 15.10.2025
Revision: 14.11.2025
Accepted: 18.11.2025
