Understanding and Managing the Dysphotopsias

41   Understanding and Managing the Dysphotopsias


Samuel Masket and Nicole R. Fram


The dysphotopsias, both positive dysphotopsia (PD) and negative dysphotopsia (ND), represent subjective undesired optical phenomena that are associated with otherwise uncomplicated cataract and lens implant surgery. They are unanticipated photic consequences that are, at least in part, related to intraocular lens (IOL) design and, to some extent, surgical methods. No significant physical or demographic characteristics have been attributed to symptomatic patients. PD is typically described by patients as light streaks, arcs of light, central light flashes, and starbursts; these observations are induced by external light sources. PD is to be distinguished from entoptic light flashes resulting from vitreoretinal traction. In contrast, ND is observed by the patient as a temporal dark shadow much like the effect of wearing “horse blinders.” The etiology and symptomatology may be somewhat different between the two conditions, although there can be some crossover and both conditions can coexist in the same patient, as described by Davison.1 Indeed temporal light “flickering” is commonly associated with ND. Adding to the clinician’s frustration with evaluating these conditions is that there are no objective tests to qualify or quantify symptoms; we rely solely on patient-reported outcomes (PROs). Furthermore, there are no “absolutes” with the dysphotopsias; although most cases can be codified, some are atypical in symptoms, causes, and cures.


Olson’s group2 has reported that dysphotopsia represents the chief cause of dissatisfaction following routine cataract surgery. In fact, the term dysphotopsia was coined in a publication from Olson’s department. In that report, 49% of patients had a degree of dysphotopsia, either ND or PD, at some time following surgery. Additionally, Bournas et al3 reported that 19.5% of patients complained of dysphotopsia at 1 day after surgery. Specific to ND, Osher4 reported a 15.2% incidence at 1 day postoperatively, which was reduced to 3.2% at 1 year postoperatively.


Given that the volume of cataract surgery in the United States is 3 million eyes annually, somewhere between 30,000 and 100,000 new cases of chronic dysphotopsia occur each year. As mentioned, evaluating the patient with dysphotopsia is very difficult. However, in the optical laboratory setting, one can use ray-tracing analysis and reflectometry of IOL materials, surfaces, shapes, and edge designs.


Dysphotopic complaints should also be distinguished from Purkinje images, which are a series of reflections from the corneal and lens surfaces. The accentuated third Purkinje images may be associated with lens implants and represent purely a cosmetic blemish, as they are not associated with functional vision deficits. Additionally, patients may notice a Maddox rod effect (with point sources of light) from striae in the posterior capsule; this undesired optical phenomenon is not specific to the intraocular lens and may be managed by laser capsulotomy, as necessary.


Traditionally, the nonsequential ray tracing from Zemax (Kirkland, WA) has been used to analyze optical pathways, surfaces and edges; Franchini et al5 found good laboratory evidence that the square edge of IOLs is associated with the production of halos, rings, and arcs of light. In fact, edge-induced positive dysphotopsia was first reported by one of us (S.M.) and coworkers6 in 1993 with regard to the truncated squared edge of ovoid IOLs. At that time, prior to wide acceptance and distribution of foldable IOLs, oval polymethylmethacrylate (PMMA) IOLs were in wide use as a means to reduce incision size. The vast majority of implanted IOLs were made of PMMA and typically had round or thin (knife) edges. Oval lens implants were created by truncating the parallel edges of the optic, reducing one dimension from 6 to 5 mm, and hereby allowing implantation through a smaller incision. However, an optical effect of truncating the edge was creation of a flat surface that induced internal reflection from oblique illumination. This effect was investigated by reflectometry and ray tracing in the 1993 publication.6 A clinical example of internal light reflection is provided in Fig. 41.1, in which the oblique slit-lamp beam strikes the surface of a square-edged acrylic IOL, and the edge becomes highly luminescent. Given the above, we remain concerned about the recent reintroduction of ovoid IOLs. However, the square-edge design reduces posterior capsule opacification (PCO) by inhibiting migration of equatorial lens epithelial cells (LECs) along the posterior capsule. This aspect of the square edge was established by the work of Nishi et al.7 As a result, the (posterior) square edge has been maintained as a feature of most IOLs to limit PCO. The trade-off, however, can be induction of positive dysphotopsia.


Other facets of IOL design may induce PD. According to the work Erie et al,8 positive dysphotopsia may be caused by internal reflection from the posterior surface of the front of the IOL. In keeping with their theory, the occurrence of PD is more likely with IOLs that have relatively flat surfaces associated with a high index of refraction optic material.


The ophthalmic industry has responded to PD in several ways:



  1. Modifying the square edge of the IOL by reducing its thickness and by rounding the anterior edge
  2. Leaving the edge unpolished or frosted; one wonders, however, how this modification reduces internal light reflection
  3. Moving more of the IOL optical power to the anterior rather than posterior surface of the optic

Other opportunities to reduce PD might include using materials with a lower index of refraction or reduced surface reflectivity. The latter property has not been addressed by the manufacturing sector and may be an important consideration with both ND and PD.


Negative dysphotopsia is perhaps a less well understood phenomenon. As mentioned, it is typically manifest as a temporal dark crescent, similar to wearing “horse blinders,” which may be very disconcerting and annoying to the patient. Temporal “shimmering” or “smudging” of vision may also be present, suggesting an occurrence of both ND and PD in the same eye. Interestingly, although PD symptoms may be improved with pharmacological pupil constriction, the opposite is true of ND symptoms, which almost invariably improve with pupil dilation.



The etiology of ND remains a topic of debate, and there are a few theories about its origin. Osher4 suggests that edema surrounding a temporal corneal incision could be responsible for the high early incidence of ND. But the fact that ND has been reported with superiorly oriented cataract incisions makes that theory less likely. Furthermore, the corneal cataract incision is seemingly not a likely source, as ND has never been reported with radial or arcuate keratotomies, nor has it been reported with penetrating keratoplasty or laser-assisted in situ keratomileusis (LASIK) flaps. But it is well recognized that ND symptoms improve over time, suggesting that neuro-adaptation reduces the severity and incidence of ND over time.


Another theory about the etiology of ND is offered by Holladay et al.9 Their premise is that ND represents a penumbra primarily associated with IOL edge design but is also related to posterior chamber depth and the index of refraction of the IOL material. However, their theory cannot explain the clinical phenomena that we reported.10 Corroborating our suggestions is the study from Burke and Benjamin,11 in which five patients with ND and a variety of “in-the-bag” IOLs were relieved of their symptoms when the IOLs were exchanged for sulcus-placed AcrySof IOLs (Alcon Labs, Fort Worth, TX). Interestingly, that particular IOL has been impugned as causal for ND when placed in the capsule bag.


Our experience, in agreement with other reports in the literature, strongly suggests that the final common path for ND is the presence of the IOL within the confines of the capsule bag, irrespective of lens material or design.12 Frustrating for both surgeon and patient is the fact that ND seemingly only occurs with what we consider to be “perfect” surgery with a well-centered IOL with the edge fully covered by the anterior capsulotomy. Interestingly, and in concurrence, ND has not been associated with anterior chamber IOLs or sulcus-fixated IOLs. Furthermore, Vámosi et al13 first reported that ND symptoms could only be relieved surgically by elevating the IOL from the capsule bag to the sulcus; when the bag-placed IOL was exchanged for an IOL of different material and design, ND symptoms persisted. We have had a similar experience. In one of our reported cases, the patient was highly symptomatic with a square-edged acrylic IOL in the capsule bag. At surgery the acrylic IOL was exchanged for a round-edged silicone IOL placed in the capsule bag; symptoms persisted without change. However, when that same IOL was brought anterior to the capsule bag in a subsequent surgery, the ND symptoms fully abated. We also have reported that placing a piggyback IOL atop the existing implant may relieve or improve symptoms in roughly 75% of patients. We particularly noted improvement (in 13 of 14 eyes) in ND symptoms when the previously implanted optic edge was elevated above the anterior capsulotomy, leaving the haptics in the capsule bag. This orientation is referred to as reverse (or anterior) optic capture (ROC). We have also employed ROC with universal success (11 eyes) for second eyes of patients who were significantly bothered by ND in the previously operated eye; however, one cannot be certain that the second eyes would be equally symptomatic.


In our investigation we employed ultrasound biomicroscopy (UBM) to evaluate the relationship of posterior chamber depth and ND.10 Interestingly, and in distinction to the Holladay et al9 report, we did not find that increased posterior chamber depth was associated with ND. Two cases are illustrative: In one case the patient complained of ND following surgery with a single-piece acrylic IOL. A second surgeon exchanged the offending lens for a round-edged silicone IOL and added a capsule tension ring as diffuse zonulopathy was noted. The patient’s symptoms were unchanged and he was referred to one of us (S.M.) for evaluation and management. UBM testing revealed exaggerated posterior chamber depth. At a subsequent surgery the bag/IOL/capsular tension ring (CTR) complex was suture fixated to the iris, significantly collapsing the posterior chamber depth; however, the ND symptoms persisted unchanged. In another patient with severe ND, the UBM demonstrated a remarkably shallow posterior chamber in accord with high hyperopia preoperatively and the need for a +30 D IOL implant.


The above observations have led us to believe that the optical interaction between the anterior capsulotomy and anterior surface of the IOL is a potential contributing factor for ND or even a causative factor. Toward that end, certain features of the IOL might enhance the risk of ND, among them a high index of refraction and high surface reflectivity. It is interesting to note two reports in the literature indicating relief of ND symptoms in some patients after neodymium:yttrium-aluminum-garnet (Nd:YAG) laser anterior capsulectomy over the nasal aspect of the IOL.14,15 Although not uniformly successful, this finding seems to corroborate the concept that the anterior capsule/IOL interface may be causal of ND. This finding also speaks against progressive anterior capsule opacification as responsible for reduction of ND symptoms with time. Moreover, given no movement of the IOL after anterior laser capsulotomy, it is not likely that the “penumbra” has been shifted away from visible retina. All these considerations point to an optical relationship between the anterior capsulotomy and anterior surface of the IOL as contributing to ND. Nevertheless, the etiology of ND remains unsettled and is likely multifactorial.


Unlike PD, to date there has been no significant response from the manufacturing sector regarding an IOL design specific for reducing the incidence of ND. However, there have been unsubstantiated reports that a given oval IOL precludes ND. Presently, there are no meaningful studies to address the issue. Moreover, the concern regarding PD with oval IOLs, as discussed above, remains problematic.


Recently, however, one of us (S.M.) has been granted a United States patent for an IOL that is specifically designed to prevent ND (Fig. 41.2). The design concept was based on the effect of reverse (anterior) optic capture in reducing ND. As such, an anteriorly placed peripheral groove is featured to accept the anterior capsulotomy. In this fashion a lip of the optic overrides the anterior capsule. This facet of the design should prevent ND. Other aspects of the IOL concept would enable any preferred haptic or optic design, be it toric, multifocal, or another design.


May 13, 2018 | Posted by in OPHTHALMOLOGY | Comments Off on Understanding and Managing the Dysphotopsias

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