Management of positive and negative dysphotopsia postcataract surgery – A literature review

Abstract

The objective of this review was to provide a summary of the literature on the etiologies and management of positive (PD) and negative dysphotopsia (ND) which are optical phenomena that occur after routine cataract surgery. A search of PubMed and Google Scholar identified 36 relevant papers. There is a consensus on the etiology of PD, which is attributed to the edge design of the intraocular lens (IOL). A truncated square edge can cause light of an oblique incidence to reflect onto the retinal surface and cause streaks and haloes in the visual field. Other causes of PD include diffractive multifocal IOLs and IOLs with a high index of refraction. The causes of ND are multifactorial; however, the majority of the evidence from experimental and clinical studies supports the “illumination gap” of the nasal retina which may arise from the anterior capsule overlying the IOL. Other factors such as pupil size, a high-angle kappa, and increased posterior chamber depth may also play a role. Regarding surgical management, ND has been successfully treated with reverse optic capture, neodymium-doped yttrium aluminum garnet laser capsulectomy, nasal IOL optic truncation, piggyback IOL, and an ND ring. Both PD and ND can be surgically managed by replacing the IOL using in-the-bag exchange or bag-to-sulcus exchange. Technological advancements have presented new avenues for developing antidysphotopsia lenses. Novel approaches utilize anterior capsulotomy fixation using IOL phalanges and a recent diffractive spiral lens that provides smooth full-range vision without dysphotopsia.

Introduction

Cataract surgery is the most commonly performed surgical procedure worldwide.[1] Over decades, improved surgical techniques and intraocular lens (IOL) design have afforded cataract surgery high success rates as a safe outpatient procedure. However, even in a seemingly “perfect operation”, one source of continued patient and clinician dissatisfaction is the presence of unwanted optical phenomena and dysphotopsia. Tester et al.[2] were the first to coin the term which refers to the presence of various subjective visual phenomena, and dysphotopsia have been classified into two main types: positive and negative. Positive dysphotopsia (PD) is the introduction of bright artifacts onto the retinal image, such as arcs, streaks, rings, and halos produced by an oblique light source (approximately 35°). In contrast, negative dysphotopsia (ND) is reported as the presence of a dark arc of shadow usually in the temporal visual field and attributed to a narrow band of nonilluminated nasal retina.[3]

Published literature provides varying estimates of the prevalence of ND and PD. It is useful to draw a distinction between transient (<6 weeks) and persistent dysphotopsia (>6 weeks). PD is estimated to be experienced by as many as 67% of patients immediately after surgery but only 2.2% of patients have persistent symptoms after 1 year.[4] Importantly, if PD is caused by a diffractive multifocal IOL, the symptoms are typically persistent.[5]

ND is estimated to occur in between 15% and 26% of patients in the 1^st week after cataract surgery[6,7] but can persist at 1 year in 0.13–3.2% of patients[7,8] and after 5 years, this may fall to 1.5%.[9] The improvement in ND symptoms over time has been attributed to neuroadaptation, although causal mechanisms have not been established.[10] Rarely, patients may experience both PD and ND concurrently. The rarity of persistent symptoms and the need for surgical intervention have previously limited the study of dysphotopsia to case reports and case series. More recently, further prospective trials have been published.[11,12,13] Despite the low rates of PD and ND, the prevalence of cataract surgery means these patients will be encountered in the routine practice of most cataract surgeons,[8] thus this is an issue of relevance.

The subjective nature of symptoms coupled with the multifactorial etiology has made the study and management of dysphotopsia challenging. Few patients spontaneously report such visual phenomena which are only elicited using various interviewing techniques or questionnaires, such as the QoV Questionnaire[14] or the photographic questionnaire by Aslam et al.[15] Attempts to quantify dysphotopsia have yielded mixed success, and no single, validated approach currently exists.[16] Standardized tests or simulations can be used to assess a patient’s visual perception. For example, glare and halo simulators (halometry) are used to measure disability glare by quantifying the impact of light scatter.[17] This is achieved by measuring the patient’s contrast sensitivity or threshold detection. The C-Quant (OCULUS Optikgerate GmbH, Wetzlar-Dutenhofen, Germany) is a device that has been applied to measure intraocular straylight objectively. However, C-Quant was shown to be poorly representative of dysphotopsia.[16,18] Makhotkina et al.[19] attempted to objectively evaluate ND using Goldmann kinetic perimetry to measure the change in peripheral vision before and after surgery, however, this quantitative assessment has been demonstrated to only pick up the ND shadow in up to 30% of patients. Furthermore, light-distortion analysis techniques have been used to evaluate the extent of light scatter between monofocal IOLs and diffractive bifocal and trifocal lenses[20] using a light-distortion analyzer (HLMP-CW47-RU000, Agilent Technologies). However, light-scatter analysis techniques have not been widely adopted or evaluated.[16] In this way, dysphotopsia is likely underreported leading to an unclear picture of the full extent of the problem. Furthermore, although the cause of PD has been better established than ND which remains enigmatic, the different etiologies (discussed below) are likely to occur to varying degrees in different patients.

Several previous reviews[3,5,21,22,23] have outlined the management strategies for positive and negative dysphotopsia. This review hopes to add to the discussion by summarizing the more recent literature on the causes and management of dysphotopsia.

Etiology of Positive Dysphotopsia

The leading cause of PD has been widely attributed to diffractive multifocal IOLs, the edge design of the IOL, and the index of refraction of the optic material. Ray-tracing models have demonstrated how the truncated square edge of IOL can cause light of an oblique incidence to reflect onto the retinal surface and lead to PD symptoms (arcs, streaks, and halos).[24] In contrast, round-edged IOLs disperse stray light over a larger portion of the retina, reducing PD symptoms.[25] Despite the association with PD, square-edged IOLs gained popularity as they were associated with lower rates of posterior capsule opacification by inhibiting the migration of equatorial lens epithelial cells along the posterior capsule.[26] This trade-off has left PD a frustrating consequence of otherwise highly successful and uncomplicated cataract surgery. In addition, the high index of refraction (I/R) of some IOLs has been implicated in PD due to high surface reflectivity and a greater chance of internal reflection.[27] However, other studies have not found a statistically significant difference in PD rates between varying I/R IOLs.[28]

Diffractive multifocal IOLs are associated with higher rates of PD.[29] Unlike monofocal IOLs, multifocal IOLs have multiple focal points which can split incoming light into different pathways. While this design improved vision at various distances, it can also lead to unintended light scatter.[5] Monaco et al.[29] compared visual acuity and side effects of two trifocal lenses and one monofocal lens in 76 patients and found that although visual acuity was significantly better in the trifocal group, these patients experienced higher rates of dysphotopsia (25%) compared to the monofocal IOL group (15%) when measured using a Quality of Vision Questionnaire.[14] Equally, the additional split of light into multiple foci decreases contrast sensitivity and increases the difficulty of seeing clearly in low-light situations with larger pupil sizes.[5]

Furthermore, creases in the posterior capsule can generate PD, giving rise to the Maddox rod effect on vision in one patient as demonstrated in Figure 1.

Figure 1.

Both photos are taken from a patient with a crease in the posterior capsule experiencing positive dysphotopsia (Maddox rod effect on vision. Crease is most evident with retroillumination (right image)

Etiology of Negative Dysphotopsia

The underlying etiology of ND has been studied extensively and although significant advancements have been made, we are yet to completely understand this phenomenon. Initially, it was theorized that ND was related to acrylic IOL with truncated edges,[8] however, ND has since been experienced in a wide range of IOLs including both acrylic and silicone IOLs and those with rounded and truncated edges.[30] While highly refractive IOLs such as those composed of acrylic are more frequently associated with ND,[30,31] the consensus is moving toward placing more importance on the position of the IOL in relation to the capsule rather than the material or design of the optic.

The leading explanation for ND is the “Illumination gap” of the nasal retina, first explained by Holladay and Simpson[32] in their ray tracing analysis on computer eye models. They showed that temporal field shadow could be attributed to the different refraction of rays that hit the IOL optic periphery to those that miss the IOL. The illumination gap is bounded posteriorly by the rays refracting on the IOL optic periphery as intended and anteriorly by the rays missing the IOL which are not refracted. They divided the underlying causes of the illumination gap into primary (smaller photopic pupil, larger positive angle k, shape of IOL, and nasal anterior capsule overlying anterior nasal IOL) and secondary factors (edge design, material of IOL, and negative aspheric surfaces),[32] while others have compared lens factors to patient’s anatomy.[5,33]

A case series from Masket and Fram[34] provided the most convincing theory that ND could arise from the anterior capsule coverage of the IOL. They reviewed 12 eyes with ND and all patients underwent piggyback IOL placement in the sulcus or reverse optic capture (ROC) (discussed below) and experienced a resolution of symptoms. This theory is supported clinically as ND has only been reported with in-the-bag IOLs, not with ciliary sulcus/anterior chamber or scleral fixated IOLs.[34] Surgical approaches that remove the nasal capsule edge or place the optic over the capsule largely resolve ND symptoms.[35,36]

Equally, many associations between a patient’s anatomical features and ND have been made, though their relative importance is unclear. First, the pivotal ray tracing optical models highlighted that a smaller pupil increases ND occurrence.[32,37] The temporal retinal shadow occurred with a small 2.5 mm pupil diameter but disappeared when the pupil was 5 mm wide. This was attributed mostly to larger ray dispersion in wider pupils, reducing the chances for the illumination gap to occur. This has been supported by clinical studies demonstrating an increase in ND symptoms with miotic agents and improvements with mydriatic agents.[34]

Furthermore, a high-angle kappa may increase ND symptoms. Angle kappa is the angle between the visual axis (an imaginary line connecting the point of gaze fixation and the fovea) and the pupil axis (an imaginary line running through the pupil center perpendicular to the cornea. In one study of 95 patients, hyperopic subjects, in whom angle kappa was larger, were more susceptible to ND development.[6] van Vught et al.[38] compared 27 patients with ND to 25 pseudophakic controls and corroborated the association between ND and an increased angle kappa.

Other researchers have suggested that ND may be the result of an increased posterior chamber depth[39] and Holladay et al.[31] used ray-tracing analysis to hypothesize that acrylic lenses may have a larger range of posterior chamber depths than silicone lenses, in which ND can occur which may explain the difference in ND incidence between the two IOLs. However, others such as Vamosi et al.[40] found no association between posterior chamber depth between symptomatic ND patients and asymptomatic patients using ultrasound biomicroscopy.

In this way, the causes of ND are likely multifactorial, with a complex interplay between IOL and personal factors. This may partly explain the lack of reliability in resolving the problem and the diversity of treatment approaches discussed below.

Search Methods

A literature review was conducted in PubMed and Google Scholar searches using the keywords “dysphotopsia” and “management OR treatment” for all articles published since 2000. This review focused on interventional studies, cohort studies, case series, case reports, and review articles. 154 results were produced from the initial search, and 36 were included following the screening. Papers discussing phakic IOL dysphotopsia and dysphotopsia postiridotomy were excluded. Figures are operative images taken by the author (JSM) from patients reporting dysphotopsia symptoms. The required consent to use patient data and figures were obtained.

Discussion – Management

For transient dysphotopsia, clinicians can take a conservative approach, and the initial steps involve patient education and reassurance. This includes correcting refractive errors and treating any complications, such as posterior capsule opacification.[21] This helps patients tolerate symptoms and facilitates the process of neuroadaptation. The management of persistent dysphotopsia can be divided into pharmacological and surgical approaches.

Pharmacologic Management of Negative Dysphotopsia

The utility of pharmacological management for ND is equivocal. Given the association between ND and smaller pupil sizes, mydriatic therapy could be utilized to improve the illumination of the peripheral retina.[34,41] However, most patients cannot tolerate long periods of voluntary pupillary dilation, which is inconvenient for normal daily activities. A case report (Ernest 2006) found limited utility of pilocarpine (cholinergic agent) therapy for severe dysphotopsia. Limitations to pharmacological therapy include frequent administration/poor patient compliance and side effects such as ciliary spasm, vision blurring, and reduced night vision.[42,43] Interestingly, Marques and Marques[44] found that miotic therapy with brimonidine tartrate (alpha-2 adrenergic agonist) was effective in a patient with unilateral ND after implantation with an acrylic lens with a sharp posterior edge, though the relative contribution of the miotic therapy and neuroadaptation is unclear. Nonetheless, for patients with persistent ND, long-term pharmacological management is inadequate and surgical management is indicated.

Surgical Management of Negative Dysphotopsia

Several surgical approaches for ND have been developed with varying levels of success. There is an overlap in the surgical treatment of ND and PD.

Reverse Optic Capture

ROC is one of the better-established surgical approaches [Figure 2] for ND management[45] devised by Masket and Fram in 2011. It is based on the concept that the anterior capsule coverage or overlap of the IOL is the chief contributor to ND. This surgical technique involves elevating the edge of the IOL optic above the anterior capsule while leaving the IOL haptics in the capsular bag. Typically, ROC is undertaken as a secondary procedure to treat ND but could be done primarily at the time of phacoemulsification to prevent ND in the second eye of a patient with known ND.[46] ROC requires that anterior capsulotomy be smaller than the diameter of the lens optic and, if too large, may provide insufficient support to hold the optic in front of the capsulotomy. Further, if the capsulotomy is not symmetric, there is a risk of lens tilt, and alternative surgical approaches should be pursued.

Figure 2.

Intraoperative photograph of reverse optic capture technique. Both images show how the intraocular lens (IOL) is elevated above the anterior capsule while leaving the IOL haptic in the capsular bag

In the original study, all 3 patients that underwent ROC had complete resolution of symptoms at 3-month evaluation. In one patient, the temporal aspect of the optic slipped into the capsular bag resulting in the resolution of symptoms and simultaneously confirming the visual disturbance etiology.[34] Another study found that primary ROC helped prevent ND in all 21 patients when evaluated at 3 months and 21 out of 22 patients who underwent secondary ROC.[30] ROC is a largely successful procedure but can be linked to postoperative complications such as earlier opacification of the posterior lens capsule, capsular block syndrome, iris chafe, and postoperative myopic refractive error.[4] One complication of primary ROC is accelerated posterior capsule opacification and all eyes in the preventative group of one study required neodymium-doped yttrium aluminum garnet (Nd: YAG) capsulotomy by 3 months postoperatively and two cases experienced capsular block syndrome.[30]

Neodymium-doped Yttrium Aluminum Garnet Laser Capsulectomy and Nasal Intraocular Lens Optic Truncation

Adopting a similar principle to ND etiology as ROC, Nd: YAG capsulotomy uses a laser to remove the nasal portion of the anterior capsule, which may overlie the optic. Alternatively, others suggest this technique may also decrease the distance between the back of the iris and the IOL, as capsulectomy of the anterior capsule rim is expected to cause anterior movement of the IOL[36] which underlies ND resolution. Nevertheless, Nd: YAG capsulectomy is one of the least invasive surgical techniques that preserves intraocular anatomy and has been clinically validated. Nd: YAG capsulectomy improved ND symptoms in 83% (5/6) of patients in one case series[35] and another case report.[36] One case report used the Nd: YAG laser to induce nasal light scattering through targeted lens pitting and found symptoms of ND reduced,[47] though this could lead to irreversible side effects such as glare.

Alapati et al.[48] describe a new approach termed “in-the-bag nasal IOL optic truncation” on one patient with recurrent ND after ROC. In this case, the nasal optic edge was surgically truncated (without laser) and they hypothesized that the resolution of ND was also aided by the irregular edge promoting light scattering.

Piggyback Intraocular Lens

Based on the principle that greater posterior chamber distances are associated with ND, the placement of an additional lens (piggyback lens) with no spherical power in the ciliary sulcus in front of the posterior chamber lens could reduce the effective depth of the posterior chamber.[46] Equally, the piggyback IOL could provide another surface for internal reflection and thus create more scattering of light rays at the IOL edge, preventing a shadow from developing. Piggyback IOLs carry fewer surgical risks than IOL exchange procedures. One study treated 7 patients with piggyback IOLs, including one patient who failed IOL exchange, and all patients experienced complete resolution of symptoms.[34] In another study, improvement or resolution of ND by 3 months was found in 72% of patients (8/11) following piggyback IOL.[30] Support has also been provided by ray tracing analysis in 3 patients following piggyback IOLs, which demonstrated that the second IOL shafted the iris anteriorly allowing additional light to miss the primary IOL and illuminate larger areas of the peripheral retina.[49]

Negative Dysphotopsia Ring

The “negative dysphotopsia ring” is a novel device designed for implantation in the sulcus of a pseudophakic eye with posterior chamber IOL in situ within the capsular bag. The ring of the implant has a biconcave cross-section which actively diverges the light incident on its inner edge such that the light rays distribute to the area of the ND shadow. The ring can be injected through a 2.2 mm incision. Roop et al.[13] conducted a prospective interventional cohort study on 22 patients with ND who received the ND ring either therapeutically or prophylactically. Ninety-three percent of patients in the therapeutic group reported complete resolution of ND on the first postoperative day, and no ND was reported in any of the 7 eyes treated prophylactically. The procedure is quick and easy, taking around 3 min compared to a long IOL exchange. Currently, the ND ring has not been approved by the US FDA and further studies are required to evaluate its utility.

Lens Orientation – A Preventative Approach

The orientation of the IOL at the time of implantation may also play a role in ND development. One single-center prospective randomized control trial on 201 participants randomized patients to receive their IOL either orientated with the optic-haptic junctions at 180 degrees (horizontal) or without manipulation following implantation (control).[11] They found that orientating the IOL optic-haptic junctions horizontally halved the incidence of ND by the 4^th week postoperatively. This has been corroborated by another more recent randomized control trial on 163 patients which found significant differences between orientations (vertically, horizontally, superonasally, or inferonasally) and ND incidence at 1 week and 4–6 weeks postoperatively.[50] They too found the horizontal orientation performing best at 4–6 weeks. However, further studies have not found statistically significant differences between IOL orientation and ND at 1 month.[12] It is currently unclear whether haptic orientation should be considered an intraoperative strategy to prevent ND.

Intraocular Lens Exchange for Positive Dysphotopsia and Negative Dysphotopsia

IOL exchange has been utilized as a management strategy for both PD and ND. For PD, where the etiology is closely related to the characteristics of the lens, the benefits of switching IOL characteristics are clear. Hydrophobic acrylic IOLs were the most commonly inciting IOL (79%), although silicone (9%), copolymer (5%), and hydrophilic acrylic (7%) make minor contributions.[11] For ND, where a highly refractive IOL contributes to ND symptoms, changing the lens may confer benefits too. Previous studies have found that using a lens of different materials, lens design and implant location yields more success than changing only one variable.[46]

There are two main types of IOL exchange: in-the-bag exchange [Figure 3] and bag-to-sulcus exchange. Indications for the type of IOL exchange depend on the presence of PD or combined ND/PD symptoms and the integrity of the capsular bag. In a bag-to-bag exchange, the original IOL is removed and replaced with a different IOL in the capsular bag. This technique is used only for patients with PD symptoms with an intact capsulotomy and posterior capsule. Masket et al.[27] found that exchanging the original IOL lens for a lens with lower RI improved PD symptoms in 84% of patients (n = 56 cases). However, they found an indistinguishable difference in the improvement of switching from acrylic IOL to either silicone IOL (87%) or Collamer IOL (88%).

Figure 3.

Ultrasound biomicroscopy demonstrating the difference between “in-the-bag” intraocular lens exchange (b and d) and anterior capsule clipped lens (Femtis) (a and c)

If the capsular bag is unstable or compromised, a sulcus-fixated lens exchange may be attempted. This involves removing an IOL from the capsular bag and placing a 3-piece IOL in the ciliary sulcus. This technique has been used in patients with combined ND/PD. Masket et al.[30] found that bag-to-sulcus IOL exchange was successful in 7/8 eyes and resolved ND symptoms in two cases in another study.[40] However, the approach is limited by an increased rate of iris depigmentation scatter and glaucoma.[6,48,49] In this way, IOL exchange for PD is related more to changes in IOL material in design, whereas for ND, it is more associated with the position of the optic.

Textured Intraocular Lens Edge

Preoperatively, some have suggested using square-edge IOL with a textured edge to prevent unwanted glare symptoms in PD.[51] However, further studies using a square-edge IOL with a frosted edge did not decrease PD symptoms and could result in decreased contrast sensitivity.[52]

Development of an Antidysphotopsia Lens

Finally, the development of a specific antidysphotopsia lens is a potential avenue for treating these patients and could help minimize the aforementioned surgical complications.[30] Given the association of PD with high I/R and flat IOL surfaces, the ophthalmic industry has responded by reducing the thickness of square-edged IOLs, rounding the anterior edge, moving the IOL’s optical power to the anterior surface of the optic, and using materials with lower I/R.[3] Anterior capsulotomy fixation is also a key factor in achieving long-term alignment of the optical axis of the IOL and the visual axis of the eye to avoid decentration which can induce optical aberrations, dysphotopsia, and other visual effects.[3] Figure 4 demonstrates the nonaxial movement of a diffractive IOL in a patient reporting PD symptoms. In one study, the 6-month visual outcomes of an antidysphotopsia lens (FEMTIS Comfort MF15) were evaluated.[53] The plate haptic lens features four phalanges that fixate the optic to the anterior capsulotomy. None of the 25 participants reported negative dysphotopsia symptoms.[53] The Morcher (Masket) 90S IOL is another lens designed to prevent ND with a circumferential groove on the optic that captures the anterior capsulotomy. By improving the accuracy of effective lens position, the use of enhanced refractive optics could help reduce ND occurrence.

Figure 4.

Slit-lamp examination demonstrating nonaxial movement of a diffractive lens. The patient reported positive dysphotopsiae (PD). In the nondilated pupil (a), diffractive rings are not visible. Dilated pupil shows decentrated irregular capsulorrhexis with posterior capsule opacification (b). Retroillumination demonstrates the nonaxial vertical displacement of the diffractive intraocular lens causing the PD (c)

Furthermore, although diffractive multifocal IOLs are associated with enhanced visual acuity compared to monofocal lenses, their use is limited by the increased incidence of dysphotopsia such as haloes and glare.[29] Recently developed, the RayOne Galaxy, may overcome this problem. It has a unique spiral optic design developed using artificial intelligence. Instead of a series of rings that create three separate focal points as seen with multifocal IOLs,[48] the spiral design reduces surface steps/discontinuities which provides a smooth optic surface. This new nondiffractive optic is proposed to reduce dysphotopsia, particularly in low-light conditions while producing a smooth full range of vision.[48] Clinical study data presented at the European Society of Cataract and Refractive Surgeons, (September 2024), involved 30 participants and compared the acuity, contrast sensitivity, and haloes of 3 lenses using the Real Artificial Lens Vision device (DEZIMAL GmbH).[49] This device enabled participants to experience postoperative vision with an IOL before implantation. The Galaxy spiral lens demonstrated a halo size closer to an enhanced monofocal IOL than standard diffractive trifocal IOL.[49] In this way, advancements in lens technology may afford enhanced visual acuity alongside a reduction in dysphotopsia symptoms.

Neuroadaptation Strategies

Neuroadaptation strategies could also provide an avenue for dysphotopsia management. One randomized placebo-controlled trial evaluated a 3-week visual rehabilitation program based on Gabor patches in patients undergoing bilateral cataract surgery with trifocal diffractive IOL implantation.[54] Gabor patches consist of alternating dark and light patterns which can be orientated at different angles, spatial frequency, size, and contrast to help patients better process and adapt to complex visual stimuli. Dysphotopsia was not directly evaluated, however, the study group had greater distance and near contrast sensitivity than the control group.[54] Further research is necessary to fully understand the effectiveness of neuroadaptation strategies and refine treatment protocols.

Conclusion

Dysphotopsia is the most common complication after “routine cataract surgery”. It is important to recognize and not dismiss the subjective symptoms patients report. Future studies utilizing a standardized survey or objective measurements will enable us to understand the full extent of dysphotopsia. Several decades of research into the common causes of dysphotopsia have advanced our understanding of the etiology of PD and helped slowly uncover the pathophysiology of ND. For both types, the initial management involves patient reassurance and validation. The primary rationale for the surgical management of ND involves clipping of the lens to the anterior capsule which helps resolve symptoms. For PD, enhanced refractive optics and changing IOL material and/or design are the mainstay of surgical management. The development of new IOL technologies presents an exciting avenue for preventing dysphotopsia.

Data availability statement

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Conflicts of interest

Prof. Jodhbir S. Mehta, an editorial board member at Taiwan Journal of Ophthalmology, had no role in the peer review process of or decision to publish this article. All authors declared no conflicts of interest in writing this paper.

Funding Statement

Nil.