Should We Fear Wipe-Out in Glaucoma Surgery?
Abstract
:1. Introduction
2. Materials and Methods
3. Results
3.1. Incidence of Wipe-Out in Glaucoma Surgery
3.2. Risk Factors Associated with Wipe-Out
- Advanced visual field loss (split fixation): By definition, wipe-out has been observed almost exclusively in advanced or end-stage glaucoma eyes [24]. A classic risk factor is a preoperative visual field showing central vision involvement, such as a split fixation or only a small central island remaining [10]. Costa et al. found that eyes with preoperative “macular splitting” on the visual field (i.e., the horizontal meridian through the central 5° had a defect in one hemifield) were significantly more likely to experience wipe-out [10]. Essentially, if the glaucoma has encroached on the central 10° of the field, the optic nerve’s reserve is minimal, and any further insult may abolish the remaining vision. A recent study in Japan also identified specific central visual subfield sensitivity as being predictive of future central vision loss in advanced glaucoma, reinforcing that the involvement of the central field is a red flag (though that study was about progression in general, and not just post-op occurrences) [28]. In practical terms, surgeons recognize that an eye with only a “tubular” field or a lone temporal island is at potential risk—these are exactly the scenarios in which wipe-out has been reported [29]. Patients with split fixation were the focus of Bhadra et al.’s 2022 prospective study; while none of their patients ended up with wipe-out, the fact that such a study was deemed important shows that this subgroup is considered high-risk [24]. Case reports of wipe-out (including MIGS cases) invariably involve eyes that had severe glaucomatous damage pre-surgery [25].
- Older age: Age-related factors appear to play a role. Costa et al. noted that older patients were more likely to suffer wipe-out, with the average age of wipe-out cases being higher than that for cases without [10]. Aging may contribute to less resilient optic nerve perfusion or greater susceptibility to IOP changes and ischemia [8,30]. An older optic nerve head might have impaired autoregulatory capacity, for instance [2]. However, age is likely a proxy for other factors (long-standing disease, vascular health, etc.) rather than a direct cause.
- Early postoperative hypotony: Several findings point to a low intraocular pressure in the immediate postoperative period as a risk factor. In Costa’s study, eyes that had severe hypotony on day 1 (IOP ≤2 mmHg) were significantly more likely to experience wipe-out [10]. Hypotony—an extremely low IOP—can compromise ocular perfusion pressure or cause structural changes (e.g., choroidal effusions and retinal folds) that might damage central vision [29]. In Topouzis et al.’s series, they carefully avoided sustained hypotony, which may partly explain the absence of wipe-out [9]. The association between immediate hypotony and wipe-out risk suggests that a sudden, drastic drop in the IOP could precipitate the phenomenon in a susceptible eye [10,29]. This has parallels to decompression retinopathy, a condition where a sharp IOP reduction causes retinal hemorrhages and can affect vision [18,31]. Indeed, case reports exist of decompression retinopathy after glaucoma surgery causing central vision loss (Karadimas 2002), which may overlap with what we call wipe-out [18]. Hypotony might lead to temporary retinal/choroidal changes which, in an end-stage eye, become permanent vision loss [10]
- Perioperative ocular ischemia: Wipe-out might sometimes result from a vascular insult to the optic nerve or retina during surgery [1]. One often-cited risk factor is the use of retrobulbar anesthesia, which in rare cases can cause optic nerve or central retinal artery compromise (for example, via injection pressure or vasospasm) [31]. There is a documented instance of a patient who had a central retinal artery occlusion presumably from a retrobulbar block during glaucoma surgery, leading to irreversible vision loss [31]. While modern anesthesia techniques (sub-Tenon’s or topical anesthesia) have largely mitigated this, it remains a consideration [18]. Patients with known vascular risk factors (e.g., severe hypertension, diabetes, and carotid artery disease) might have less capacity to tolerate fluctuations in ocular perfusion [1,2]. Some authors have postulated that an acute ischemic optic neuropathy (an infarct in the remaining neuroretinal rim) could underlie wipe-out in certain cases, analogous to how some cardiac surgeries can cause anterior ischemic optic neuropathy in susceptible patients [18,30]. However, concrete evidence linking systemic vascular health to wipe-out is limited. One retrospective finding was that patients with systemic cardiovascular disease had a higher incidence of hypotony maculopathy (not wipe-out per se), which suggests that vascular issues could exacerbate hypotony effects [2].
- Optic nerve vulnerability: Not surprisingly, an optic nerve that is already severely damaged (thin neuroretinal rim and pale appearance) is at risk [4]. Some glaucoma specialists anecdotally mention that an extremely “fragile” optic disk (for example, very advanced cupping with barely any rim) raises concern. While difficult to quantify, this speaks to the intrinsic robustness of the remaining ganglion cells [22]. It is possible that certain optic nerves—due to genetic or structural factors—are less tolerant of surgical perturbations [4]. For instance, eyes with high myopia have stretched optic nerves and poorer blood flow; the wipe-out case in a degenerative myope from the GATT series supports that high myopia might amplify risk [25].
- Type of surgery and surgical technique: Traditional full-thickness filtering surgeries (like older trephinations or uncontrolled full-thickness procedures) carry a higher hypotony risk than modern guarded trabeculectomy, and indeed, wipe-out was mostly discussed in the era of full-thickness procedures [11,12]. Modern trabeculectomy with adjustable sutures and anti-fibrotics allows for better IOP titration [6,32]. Non-penetrating surgeries (deep sclerectomy and canaloplasty) inherently avoid sudden decompression, which likely lowers wipe-out risk—Leleu et al. (2019) found no wipe-out cases after deep sclerectomy in a series of severe glaucoma patients [19]. MIGS procedures vary: ab-interno trabecular bypass (iStent, Trabectome) produce gradual IOP reduction and have essentially no wipe-out reports, whereas procedures that can cause larger immediate outflow (GATT and XEN stent) theoretically have a bit more risk (and indeed, the rare MIGS wipe-outs were observed with GATT and a bleb shunt) [17,20,25,33]. Combined surgeries (e.g., phacoemulsification + glaucoma surgery) could have an interplay: cataract surgery can induce inflammation or IOP changes, but generally, phaco tends to improve perfusion by gradually lowering the IOP [16,17]. A British survey (Ramsden et al. 2023) even looked at wipe-out after cataract surgery alone in glaucoma patients and found it exceedingly rare, reinforcing that the surgical IOP drop is a key factor [23].
3.3. Pathophysiological Mechanisms
- Acute retinal ganglion cell death (neurotoxicity or apoptosis): One theory is that the stress of surgery (or the immediate postoperative environment) triggers a wave of retinal ganglion cell (RGC) death in an already compromised optic nerve. Unlike an infarction that happens all at once, this could be a cascading process of apoptosis in the remaining RGCs. A fascinating insight into this came from Mohammadzadeh et al. (2019), who used optical coherence tomography (OCT) to observe the macula in two eyes that had lost vision after glaucoma surgery [34]. They found progressive thinning of the macular ganglion cell layer over time, corresponding to the period of vision loss. This indicates that the wipe-out phenomenon in those cases was due to ongoing RGC degeneration (the central-most RGCs dying off), rather than an instantaneous event at the moment of surgery [34]. In other words, the surgery may have initiated a process that continued in the postoperative weeks—perhaps via loss of neurotrophic support, glutamate excitotoxicity, or some kind of optic nerve “shock” that caused cells already on the brink to perish [3,34]. The authors pointed out that progressive macular OCT changes can be a sign of snuff-out and provide evidence that wipe-out is essentially extreme glaucoma progression accelerated by surgical intervention [34]. This aligns with the clinical observation that sometimes the vision does not disappear immediately on post-op day 1 but declines over days to weeks and then stabilizes at no light perception [28,30].
- Ischemia–reperfusion injury: The act of drastically lowering the IOP in an eye that has adapted to a high IOP could cause a form of ischemia–reperfusion injury [8,30]. In advanced glaucoma, the optic nerve head may have chronically reduced perfusion due to a high IOP. When the IOP is suddenly normalized (or drops below normal in the case of hypotony), the sudden increase in perfusion pressure might paradoxically lead to damage—akin to reperfusion injury in other tissues [8,9]. Alternatively, if the IOP drops too low, transient optic nerve ischemia could occur due to insufficient intraocular pressure to support circulation (especially if blood pressure is low or autoregulation is impaired) [29]. This mechanism is hard to prove, but it is consistent with why extreme hypotony is dangerous and why gradual IOP reduction (say by staged procedures) might be safer in some cases. It has been likened to decompression sickness for the eye [18]. Decompression retinopathy, noted earlier, is one manifestation with retinal hemorrhages; wipe-out might be a variant where the damage primarily hits the optic nerve axons instead of manifesting hemorrhage [18,31].
- Optic nerve head circulation compromise: Related to the above, any factor that compromises the delicate blood supply to the optic nerve head can cause irreversible loss of the remaining function [8,31]. We mentioned retrobulbar anesthetic injections as a risk—these can cause direct trauma through the injection of anesthetic into the optic nerve sheath, leading to infarction of the optic nerve head or the occlusion of the central retinal artery [31]. Such an event would immediately wipe out vision. While this is not the classic mechanism in most wipe-out cases (most of which have uncomplicated anesthesia), it is a potential pathophysiology for some [18,31]. More broadly, patients with poor cardiovascular status might not tolerate fluctuations in ocular perfusion well [9,30]. No definitive studies show, for example, that low blood pressure intraoperatively causes wipe-out, but it is something surgeons keep in mind (maintaining adequate systemic blood pressure during sedation) [9].
- Choroidal effusion or maculopathy: If the surgery leads to a serous choroidal detachment or significant choroidal effusions (from hypotony), the macula can be distorted or the central retina compromised [10,29]. In most cases, hypotony maculopathy or choroidal detachments cause reversible vision loss (vision improves after the IOP normalizes and the retina reattaches). However, in an eye with advanced glaucoma, even a temporary insult to the macula might irreversibly silence the fragile remaining neurons [10,29]. Karadimas’s report of decompression retinopathy and other cases of massive choroidal effusions causing prolonged foveal dysfunction might overlap with wipe-out [18]. Essentially, structural changes from hypotony could conceivably push an already ischemic central retina over the edge [10,18,24].
- Pre-existing momentum of disease: One further consideration is that some eyes might have been destined to lose vision due to end-stage glaucoma progression, and surgery’s timing was coincidental [8,12]. The natural history of end-stage glaucoma can include sudden central loss (for example, from acute angle closure or late-stage optic disk changes). It is difficult to prove cause and effect. However, the temporal association with surgery in wipe-out cases (and the relative rarity of spontaneous “terminal events” in glaucoma without surgery) suggests that surgery is indeed a trigger in true wipe-out [10]. Mohammadzadeh’s OCT evidence strongly points to a causative role of surgery as the timing lined up and was bilateral in one of their patients only after surgeries [34].
3.4. Management and Prevention Strategies
- Careful patient selection and counseling: The surgeon must weigh the necessity of surgery in a patient with advanced glaucoma and very limited vision. If the eye in question is the patient’s only seeing eye (the other eye being blind), the decision is even more critical [10,24]. Modern evidence indicates that one should not categorically deny surgery due to fear of wipe-out—if glaucoma progression is threatening the remaining vision, surgery should be performed to control the IOP given the low incidence of wipe-out [9,18]. However, it is crucial to counsel the patient preoperatively about the small risk of catastrophic vision loss. Patients with advanced disease often understand that without surgery, they will also likely go blind; framing the discussion around relative risks is helpful [8]. In essence, “the risk of doing nothing is loss of vision from glaucoma, the risk of doing surgery includes a very small chance of immediate vision loss (wipe-out), but a much higher chance of preserving vision long-term.” Informed consent should include wipe-out as a potential complication in end-stage cases (even if one emphasizes its rarity). This conversation prepares the patient and manages expectations [8,10].
- Optimization of modifiable factors: Prior to surgery, any modifiable risk factors should be addressed [1,2]. For instance, if the patient has poorly controlled blood pressure, it should be optimized to ensure adequate ocular perfusion (avoiding extreme hypertension or hypotension) [30]. If the patient is on systemic beta-blockers or other meds that could lower blood pressure at night, the timing could be adjusted around the surgery to maintain perfusion. Some surgeons ensure the patient is well hydrated and has stable blood pressure on the day of surgery to reduce intraoperative ischemia risk. There is also a practice (anecdotally) of pre-treating with oral acetazolamide for a few days to gently lower the IOP before a big surgery so that the drop on the day of surgery is not so drastic—essentially to “soften the landing” for the optic nerve [18,29]. While not evidence-based by trials, this approach addresses the hypothetical reperfusion injury mechanism [1,2].
- Choice of anesthesia: To avoid potential optic nerve compromise from injections, many surgeons prefer sub-Tenon’s (subconjunctival) anesthesia or topical anesthesia for high-risk glaucoma cases [31]. Sub-Tenon’s (a blunt cannula infusion of anesthetic) anesthesia has a much lower risk of orbital hemorrhage or direct nerve trauma than retrobulbar injection [31]. Topical anesthesia with intravenous sedation avoids orbital injections entirely, though the patient must be cooperative. By eliminating retrobulbar needles, one removes a known, albeit rare, cause of catastrophic optic nerve injury [18]. If deeper anesthesia is needed (for instance, if a superior rectus bridle block is to be placed or the case is complex), many will still avoid inserting the needle too deeply [31]. In short, the anesthetic technique should be tailored to minimize risk in these eyes [18,31].
- Surgical technique to minimize hypotony: In an eye at risk for wipe-out, the surgeon can employ measures to prevent extreme IOP lows [10]. For trabeculectomy, this might include using a smaller scleral flap or leaving more sutures tied, with a plan to gradually lower the IOP [6]. The use of releasable or adjustable sutures is invaluable—one can leave the flap fairly secure on day 1 (to avoid very low pressures) and then incrementally loosen sutures in the clinic to reach the target IOP over a week or two [32]. Anti-fibrotic use (mitomycin-C) should be balanced: enough should be used to achieve long-term IOP control but not so much that the flap undergoes filtration too fast [6,32]. In very high-risk eyes, some surgeons even stage the procedure: for example, they first perform cataract extraction, which often lowers the IOP a bit in glaucoma patients, and then trabeculectomy is conducted a few weeks later once the eye has healed [21]. The idea is to reduce the IOP in multiple steps rather than all at once. Another approach described is performing a limited pars plana vitrectomy at the time of trabeculectomy to absorb some fluid and avoid sudden shallowing of the anterior chamber (though this is not common practice). In tube shunt surgery, one can choose a valved implant (e.g., Ahmed valve) that prevents hypotony [35], or if using a non-valved implant (e.g., Baerveldt), the tube is ligated for the first 4–6 weeks so that the IOP is gradually reduced as the ligature dissolves [26]. These techniques ensure that the IOP does not plummet to near-zero on day 1, thus protecting against hypotony-related mechanisms [10,29]. The importance of this is highlighted by Costa’s finding of wipe-out in eyes with a day-1 IOP of 2 mmHg—something we now have the tools to avoid [10].
- Consideration of MIGS or alternate surgery: For some advanced patients, especially if the IOP is not extremely high, a surgeon might consider an MIGS or less invasive procedure in lieu of a trabeculectomy, specifically to mitigate wipe-out risk [13,14]. For example, some case series have tried GATT or canaloplasty in advanced glaucoma as a primary surgical option, precisely because these ab interno approaches do not typically cause hypotony [20,25]. A 24-month GATT study in advanced glaucoma showed good IOP control in ~77% of eyes and only one wipe-out case (2.3%), suggesting that it can be a viable alternative to trabeculectomy for certain patients [25]. Another example is deep sclerectomy or viscocanalostomy in advanced glaucoma—by avoiding entering the eye, these have a smoother postoperative course (Leleu et al. reported no sudden vision loss in severe glaucoma with non-penetrating surgery) [19]. Cyclophoto-coagulation (laser treatment to ciliary body) is also an option to lower the IOP without incisional surgery; micropulse transscleral laser in particular has a milder effect and could be considered for frail eyes [36]. However, one must balance efficacy—MIGS or laser might not lower the IOP enough in very advanced cases, risking ongoing glaucoma damage [15,37]. Increasingly, glaucoma specialists individualize the plan (as advocated by Mégevand and Bron’s personalized surgery approach): an ab interno MIGS might be attempted first for moderate control, and a filtering surgery can be reserved as a second step if needed [15,33]. The good news is that MIGS has expanded our surgical toolkit so we can attempt lower-risk interventions first in many cases [16,17].
- Intraoperative and postoperative vigilance: During surgery, the surgeon will be attentive to avoid long hypotensive episodes or excessive manipulation. For instance, preventing a long period of eyeball compression is relevant—older anesthesia involved a Honan balloon to soften the eye, but one wouldn’t use that in an end-stage eye for long [31]. Postoperatively, close monitoring is critical. The surgeon should see the patient early (often on day 1 and day 3 rather than waiting a week) to check the IOP and the eye’s status. If the IOP is very low and the patient has choroidal effusion or complains of vision decline, one should intervene promptly (e.g., place a suture in the trabeculectomy flap, inject viscoelastic to raise the IOP, etc.) [10,29]. Treating any complications aggressively—such as through choroidal detachments, bleb leaks, or hypotony—may prevent a transient problem from becoming permanent [2,18,38]. There is some evidence that even if central vision is lost immediately, visual recovery can occur if the cause is transient. Francis et al. (2011) observed that transient vision loss after trabeculectomy is common and may take up to 1–2 years for recovery, whereas truly permanent vision loss is less common [38]. This means that some patients who seem to have a “wipe-out” initially might actually improve if the issue was hypotony maculopathy or cataract [5,6]. Therefore, distinguishing true wipe-out (irreversible) from temporary loss (reversible) is part of management [29,38]. In practice, if a patient’s vision drops after surgery, one would conduct a thorough exam to rule out the possible causes, determining whether the cornea is cloudy, whether the lens is swollen, whether there is vitreous hemorrhage, whether the retina is attached, the nerve’s appearance, etc. If nothing is obvious and the IOP is adequate, observation is warranted with supportive measures like corticosteroids (to reduce any inflammation) and perhaps neuroprotective vitamins [3,4]. Unfortunately, if after a few months there is no improvement and no pathology, one has to conclude that it was wipe-out [10].
- Rehabilitation and support: In the unfortunate event that a wipe-out does occur, management should focus on low vision rehabilitation and patient support. The patient will need counseling to cope with sudden blindness. Orientation and mobility training, low-vision aids (if any vision remains in the periphery or light perception), and connecting with vision loss resources are crucial [29,39]. While this is outside the scope of surgical management, it is an important aspect of caring for the patient post-complication. Psychologically, wipe-out can be devastating (the patient often questions why they had surgery). It is incumbent on the clinician to provide empathy, a clear explanation (while acknowledging the limits of our understanding), and continued care, including perhaps second opinions to confirm nothing treatable was missed [8,24].
4. Discussion
5. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Risk Factor | Description/Mechanism |
---|---|
Advanced visual field loss (split fixation) | Glaucoma encroaching on the central field (e.g., split fixation or only a small central island) leaves the optic nerve with minimal reserve; any further insult (e.g., sudden IOP drop) can abolish the remaining vision [5,29]. |
Older age | Older patients are more likely to experience wipe-out; aging may reduce optic nerve autoregulation and perfusion resilience, making nerves more susceptible to IOP fluctuations [5]. |
Early postoperative hypotony | Immediate postoperative hypotony (very low IOP) can severely compromise ocular perfusion and induce structural changes (e.g., choroidal effusions and retinal folds) that damage central vision [5,6]. |
Perioperative ocular ischemia | Ischemic insults during or after surgery (e.g., optic nerve or retinal artery compromise from anesthesia or systemic vascular disease) can further reduce perfusion to an already compromised optic nerve, precipitating wipe-out [1,7]. |
Optic nerve vulnerability | Severely damaged optic nerves (thin neuroretinal rim and extreme cupping) are intrinsically fragile; even minor surgical stress can cause an abrupt loss of the remaining ganglion cells (especially in high myopia) [25]. |
Type of surgery/surgical technique | Procedures causing abrupt IOP reduction (e.g., uncontrolled full-thickness trabeculectomy) historically had a higher wipe-out risk; modern guarded or non-penetrating techniques (adjustable-suture trabeculectomy, deep sclerectomy, and MIGS) allow gradual decompression and have much lower risk [3,4,17]. |
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Zeppieri, M.; Cannizzaro, L.; Gagliano, G.; Cappellani, F.; Rapisarda, L.; Spinello, A.; Longo, A.; Russo, A.; Avitabile, A. Should We Fear Wipe-Out in Glaucoma Surgery? Diagnostics 2025, 15, 1571. https://doi.org/10.3390/diagnostics15131571
Zeppieri M, Cannizzaro L, Gagliano G, Cappellani F, Rapisarda L, Spinello A, Longo A, Russo A, Avitabile A. Should We Fear Wipe-Out in Glaucoma Surgery? Diagnostics. 2025; 15(13):1571. https://doi.org/10.3390/diagnostics15131571
Chicago/Turabian StyleZeppieri, Marco, Ludovica Cannizzaro, Giuseppe Gagliano, Francesco Cappellani, Lorenzo Rapisarda, Alfonso Spinello, Antonio Longo, Andrea Russo, and Alessandro Avitabile. 2025. "Should We Fear Wipe-Out in Glaucoma Surgery?" Diagnostics 15, no. 13: 1571. https://doi.org/10.3390/diagnostics15131571
APA StyleZeppieri, M., Cannizzaro, L., Gagliano, G., Cappellani, F., Rapisarda, L., Spinello, A., Longo, A., Russo, A., & Avitabile, A. (2025). Should We Fear Wipe-Out in Glaucoma Surgery? Diagnostics, 15(13), 1571. https://doi.org/10.3390/diagnostics15131571