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Pigmentary Glaucoma and Pigment Dispersion Syndrome

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Article initiated by:
Pradeep Ramulu, M.D.
All contributors:
Sarwat Salim MD, FACS, Ahmad A. Aref, MD, MBA, Koushik Tripathy, MD (AIIMS), Dr John Davis Akkara (MBBS, MS, FAEH, FMRF), Dr. Kabir Hossain, Bharat Gurnani MBBS,DNB,FCRS,FICO(UK), FAICO (Cornea, AIIMS, AIOS), FAICO (Refractive Surgery, AIIMS, AIOS), MRCS (Ed), MNAMS, Pradeep Ramulu, M.D., Abdulaziz Khoshaim M.D
Assigned editor:
Review:
Assigned status Update Pending
 by Ahmad A. Aref, MD, MBA on December 23, 2023.


Pigmentary Glaucoma and Pigment Dispersion Syndrome
ICD-10
H40.1
OMIM
600510
MeSH
D005902


Summary

Krukenberg spindle
Image 1. Pigment is deposited on the endothelium in a vertical spindle shape

Pigment dispersion syndrome (PDS) and subsequent pigmentary glaucoma (PG) represent a spectrum of the same disease and are characterized by excessive pigment liberation throughout the anterior segment of the eye. The classic triad of indications includes dense trabecular meshwork pigmentation, mid-peripheral iris transillumination defects, and pigment deposition on the posterior surface of the central cornea. Pigment is released from the iris pigment epithelium due to rubbing of the posterior iris against the anterior lens zonules. Accumulation of pigment in the trabecular meshwork reduces aqueous outflow facility and may result in elevation of intraocular pressure (IOP), as seen in PDS, or in optic nerve damage associated with visual field loss, as seen in subsequent PG. The disease is more prevalent in males, and typically presents in the 3rd–4th decade of life. Treatment options for PG are similar to those for Primary Open Angle Glaucoma and include medical therapy, laser trabeculoplasty, and incisional surgery with either trabeculectomy or glaucoma drainage implant.

Disease Entity

Pigmentary glaucoma (PG) and pigment dispersion syndrome (PDS).

Disease

Pigmentary glaucoma is a type of secondary open-angle glaucoma characterized by heavy homogenous pigmentation of the trabecular meshwork, iris transillumination defects, and pigment along the corneal endothelium known as the Krukenberg spindle (Image 1). Pigment dispersion syndrome is used to classify individuals who exhibit these features but who have not progressed to optic nerve damage and/or visual field loss (signifiers of PG), even if the IOP is elevated.

Pigment dispersion syndrome is an autosomal dominant condition with variable penetrance and a wide variety of genetic loci, and the prevalence of PDS and PG in the general population is poorly defined. Screening of New York City employees reported that 2.5% had at least one slit lamp finding consistent with PDS,[1] while a retrospective review of charts from a glaucoma practice demonstrated that roughly 1 in 25 patients (4%) was followed for either PDS or PG.[2] In Olmstead County, Minnesota, the annual incidences of diagnosed PDS and PG were 4.8/100,000 and 1.4/100,000, respectively.[3] True incidences are likely substantially higher, as many people with PDS and PG may have undiagnosed disease.

Etiology

The underlying mechanism responsible for PDS and PG is the presence of a concave iris contour, which causes rubbing of the posterior iris surface against the anterior lens zonules bundles during physiological pupil movement. This friction leads to disruption of the iris pigment epithelial cell membrane and the release of pigment granules.[4][5] Pigment granules can produce temporary elevation of IOP by overwhelming the trabecular meshwork and reducing outflow.[6][7][8] Over time, pathological changes in the trabecular endothelial cells and collagen beams can lead to increased resistance to aqueous outflow, with chronic elevation of IOP and secondary glaucoma.[5][9] Patients with PDS or PG have a 15-fold higher concentration of aqueous pigment granules in their anterior chamber compared to normal controls.[7]

Pigment release requires irido-zonular contact and pupillary movement. Irido-zonular contact has been demonstrated to increase with blinking in eyes with PDS or PG.[10][11] Blinking has been hypothesized to burp fluid from the posterior chamber to the anterior chamber in these eyes, resulting in a higher pressure in the anterior chamber as compared to the posterior chamber.[12] The resulting pressure gradient results in a posterior-bowing (concave) iris with greater than normal iridolenticular contact, or reverse pupillary block, which has been shown to be reduced with suppression of blinking.[10][11] This is not to be confused with similar-sounding inverse pupillary block, which refers to blocking of the pupil by an abnormally shaped crystalline lens as seen in microspherophakia.

Greater iridolenticular contact also occurs with accommodation, in which the anterior lens surface moves anteriorly with contraction of the ciliary ring.[10] [13][14] Increase in iris concavity secondary to accommodation has also been reported in myopic eyes without PDS and normal eyes. This suggests that irides in eyes with PDS and PG may have inherent susceptibility to pigment liberation, and factors other than iris shape and size may be at play.[15] Pupillary movement produced by pharmacologic dilation has also been observed to produce pigment release and increased IOP in some patients with PG or PDS.[6][7][16] Likewise, physiological changes in pupil size resulting from lighting changes may produce pigment release in individuals with irido-zonular contact.[17] While significant pigment release accompanied by IOP elevation has been observed in some patients after strenuous exercise,[17][18] systematic observation of IOP in patients suggests that most patients with PDS or PG do not experience this phenomenon.[7][17] Pigment release producing elevated IOP and glaucoma has also been observed with sulcus placement of certain intraocular lens designs after cataract surgery.[19][20][21] The terms PDS and PG are not applied to this secondary form of glaucoma, despite some underlying mechanistic similarities.

Risk Factors

Pigmentary Glaucoma or Pigment Dispersion Syndrome

  • Male gender. Pigmentary glaucoma has a strong male predominance, with case series showing a male to female ratio of between 2:1 and 5:1. Much less of a male predominance is noted for PDS, with case series describing male to female ratios between 1:1 and 2:1.[2][3][16][22][23]
  • Age. Male patients with PG or PDS most often present in their 30s, whereas female patients typically present roughly a decade later in life.[3][16][22][24][25] However, cases of PDS have been identified in patients as young as 12–15 years of age.[26][27][28] Disease may be most common in middle age once the lens has enlarged and the iris is flexible enough to form a concave position.[4]
  • Myopia. Moderate myopia is the most common refractive error noted in eyes  with PDS and PG, with mean spherical equivalents typically in the range of -3 to -4 D. While a broad range of refractive errors is typically found, hyperopia is relatively rare, usually accounting for only 5–10% of patients in most case series.[2][16][22][29]
  • Race. According to case series, <5% of patients with PDS or PG are Black individuals.[2][16] However, the actual prevalence may be higher than reported, as the thick brown irides common in persons of African ancestry can make detection of iris transillumination defects more difficult.[30]
  • Concave iris and posterior iris insertion. Concave iris and more posterior iris insertion are more common in patients with PDS or PG than in the normal population and result in greater iridolenticular contact in these individuals .[11][13][31]
  • Flat corneas. Patients with PDS and PG have significantly flatter corneas than control subjects of similar age and refractive error.[29][32] A flat cornea might be more likely to result in burping of aqueous humor from the posterior chamber to the anterior chamber with blinking, resulting in increased irido-zonular contact.[32]
  • Family history. Direct examination of a small set of family members of patients with PDS showed that the disease was present in 2 out of 19 related individuals (12%).[33] In another family, signs of PDS were present in 36% of subjects’ parents and 50% of their siblings (but in no children), suggesting a possible autosomal dominant inheritance pattern with incomplete penetrance.[34] Pigmentary glaucoma or PDS has also been described in families across multiple generations, with roughly 50% of family members described as having either condition, reinforcing the idea of an autosomal dominant inheritance pattern.[35][36]

Disease Progression

  • Intraocular pressure. A retrospective study from Olmstead County Minnesota found IOP > 21 mm Hg to be the only risk factor for progression from PDS to PG. [3]
  • Degree of iridolenticular contact in patients with asymmetric disease. More iris–lens contact in one eye vs the other may be associated with greater risk of disease progression.[31]
  • Greater trabecular meshwork pigmentation. In eyes with bilateral PDS, worse disease is typically found in the eye with more severe trabecular meshwork pigmentation.[2]

General Pathology

Autopsy specimens of eyes with PG demonstrate disruption of the iris pigment epithelium cell membrane with extrusion of pigment granules.[5] The trabecular meshwork in these eyes reveals collapse of trabecular sheets, free pigment granules and cellular debris clogging the intertrabecular spaces, and macrophages and degenerated trabecular endothelial cells filled with pigment.[5][9][37]

Pathophysiology

Uveal pigment has been demonstrated to increase resistance to aqueous outflow in experimental studies[38][39] and to result in increased IOP in vivo.[6]

Primary Prevention

No methods have been definitively established for the prevention of PDS or PG. In young patients with iris concavity and active release of pigment, laser iridotomy has been suggested to be of benefit through equalization of pressures in the anterior and posterior chambers and pulling of the iris away from the zonules. Older patients with glaucoma are less likely to benefit from iridotomy due to permanent age-related changes in the trabecular meshwork architecture. One large study reported that the risk of conversion from PDS to PG is approximately 10% at 5 years and 15% at 15 years.[3] This suggests that iridotomy treatment of all patients with potential PDS or PG is not advisable and that the decision to perform a laser iridotomy should be individualized depending on the patient’s IOP and amount of pigment liberation.

Diagnosis

Image 2. Krukenberg Spindle (Photo Courtesy of Sarwat Salim, MD, University of Tennessee)

Pigment dispersion syndrome is diagnosed clinically based on the presence of iris transillumination defects in the mid-peripheral iris, pigment on the corneal endothelium (Krukenberg spindle), and heavy pigmentation of the trabecular meshwork. The presence of all three of these findings in the absence of another cause (e.g.,. history of trauma or posterior chamber IOL) suggests PDS. No formal criteria exist defining whether disease exists if only 1 or 2 of these findings are present, though disease is likely with the presence of 2 of the 3 features, particularly if other exam findings are consistent with PDS or PG. Note that PDS can be present with normal or elevated IOP.

Though commonly seen with PDS, a Krukenberg spindle (Image 2) in and of itself is not necessarily pathognomonic of the disease, as it can also be found with pseudoexfoliation syndrome. Distribution of pigmentation in the trabecular meshwork can help differentiate PDS from pseudoexfoliation syndrome, with homogenous distribution associated with PDS and patchy distribution with pseudoexfoliation syndrome. Pigmentary glaucoma is considered present when the criteria for PDS are accompanied by optic nerve cupping and/or visual field loss.[40]

History

Patients should be asked about a history of previous trauma, surgery, or eye disease as well as whether they have family members with glaucoma (including the type of glaucoma). Visual symptoms are unusual except in patients with visual field loss. Some patients may describe episodes of haloes and blurry vision resulting from intermittent IOP elevation. Patients with such symptoms should be asked if the symptoms are brought about by exercise or dark exposure, which have been described by patients with PDS or PG.

Physical examination

Careful slit lamp examination is critical to identification of PDS. Findings are typically bilateral, but they can be markedly asymmetric on occasion.

Cornea. The posterior surface of the central cornea should be carefully examined for the presence of pigment.

This pigment is often arranged in a the shape of a Krukenberg spindle, a narrow or rounded oval of brown pigment, usually 0.5–2.5 mm wide and 2–6 mm in length, vertically oriented due to convection currents. Pigment is typically densest at the center, thinning out at the edges to form a spindle-like shape.[41] Krukenberg spindles are present in roughly 90% of patients with PDS or PG. Whether dense or very fine granules of pigment are present, visual acuity is not reported to be affected. Corneas with PDS or PG are also no thicker than normal corneas and have not been reported to have decreased endothelial cell counts.[42]

Anterior chamber. The anterior chamber should be examined for the presence of pigment granules and depth. On slit-lamp examination, pigments appear brown and are smaller than anterior chamber cells seen in uveitis. Examination should be performed both prior to and after pupillary dilation.

Image 3. Iris transillumination defects in Pigmentary Glaucoma (Photo Courtesy of Sarwat Salim, MD, University of Tennessee)

Iris. The iris should be examined with retroillumination to look for iris transillumination defects (Image 3). Transillumination defects appear in a spoke-like configuration and are most common in the mid-peripheral iris, where there is maximal contact between the iris pigment epithelium and anterior lens zonules. Transillumination defects tend to be most common or prominent inferiorly or inferonasally.[12][26] Roughly 90% of PDS/PG patients demonstrate iris transillumination defects in at least 1 eye,[16] though transillumination defects may be absent in patients with thick, dark irides.[23][30] In asymmetric cases, frank iris heterochromia with increased iris pigmentation in the eye with greater pigmentation can be noted in the more affected eye.[16][23] The eye with greater pigment loss can also have a larger pupil, resulting in clinical anisocoria, possibly secondary to iris dilator hypertrophy.[43][44][45]

Lens. The lens should be examined for the presence of pigment on the anterior surface, along the zonules, and along the posterior surface. Zonular pigment is most easily noted after pupillary dilation, with the patient gazing upwards to bring the inferior zonules into view.[46] Rarely, pigment can migrate posteriorly, where it can be found trapped between the posterior lens capsule and anterior hyaloid.[47][48]

Intraocular pressure. Intraocular pressure should be measured. In a community-based retrospective study, IOP at the time of diagnosis for a population of patients with PG and PDS was 29 mm Hg and 24 mm Hg, respectively.[3] Other studies confirm that patients presenting with PG typically have elevated IOP.[22][49]

Diagnostic procedures

Image 4. Densely pigmented TM in Pigmentary Glaucoma (Photo Courtesy of Sarwat Salim, MD, University of Tennessee)

Patients with suspected PDS or PG should undergo gonioscopy prior to dilation to document the extent of trabecular pigmentation (Image 4). The angle is typically widely open, and the trabecular meshwork typically shows dense, homogenous pigmentation.[23] Pigment deposition may be noted on Schwalbe’s line. The peripheral concavity of the iris may be more prominently appreciated on gonioscopy. Pigment deposition along the zonular attachment at the posterior capsule of lens may also be noted (Schie line or Zentmayer line), which can give rise to a pigmented round line at the posterior capsule just internal to the equator of the lens.

In older patients, the only sign of PDS may be the “pigment reversal sign,” in which the trabecular meshwork is found to be darker in the superior quadrant when compared with the inferior quadrant. This finding helps to differentiate patients with “burned out” PG from other types of glaucoma. Iris concavity and the extent of iridolenticular contact can also be examined using ultrasound biomicroscopy (UBM) or anterior segment optical coherence tomography (AS-OCT). However, neither test is necessary for diagnosis.

Mydriatic provocative testing has limited utility in diagnosing or predicting the course of PDS or PG. In one case series, roughly 1/3 of patients demonstrated extensive anterior chamber pigment after phenylephrine administration, and only a fraction of these (20%) had an associated IOP rise.[17]

Differential diagnosis

Krukenberg spindles have been described in conditions other than PDS and PG, including uveitis and trauma. Trauma, previous ocular surgery, and pseudoexfoliation can also produce heavy trabecular pigmentation. Exfoliation syndrome—which presents in older individuals with signs that include peripupillary transillumination defects, exfoliative material on the anterior lens capsule, and uneven pigment distribution in the angle—is more common in patients with PDS and PG than in the general population. Patients with both conditions are described as having “overlap syndrome." Sulcus IOL placement and iris melanoma can also result in PG.

Management

General Treatment

Treatment for PG and PDS is similar to the treatment for primary open angle glaucoma (POAG). One case series found that patients with PDS or PG were more likely to require surgery than a control group with POAG. Male patients and Black individuals often present with advanced disease and may require more aggressive treatment.[49]

Medical Therapy

Pilocarpine has been demonstrated to reduce iris concavity and has been shown to block the exercise-induced elevation of IOP found in some patients.[18][27][50] However, there are important considerations. The peripheral retina should be carefully examined before the initiation of miotics, since lattice degeneration is present in up to 20% of these eyes and the incidence of retinal detachment in patients with PDS and PG is higher than in general population.[12] In addition, pilocarpine can induce additional myopia and accommodative spasms.

Newer medical agents including topical prostaglandins, beta-blockers, carbonic anhydrase inhibitors, and alpha-adrenergic agonists have largely replaced treatment with pilocarpine. Prostaglandin analogues may be preferred over aqueous suppressants, as treatment with aqueous suppressants slows down the clearance of pigment from the trabecular meshwork.

Patients treated medically should have follow-up every 3-6 months to ensure adequate control of IOP and to confirm that the glaucoma has not progressed. This follow-up should include thorough examination, visual field testing, and/or imaging of the optic nerve head and nerve fiber layer.

Surgery

Given that PDS and PG result from a pressure differential across the iris, it has been suggested that the underlying mechanism of disease might be eliminated by treatment with laser iridotomy. Some reports have demonstrated that laser iridotomy can eliminate iris concavity and reduce iridolenticular contact in eyes with PDS.[51][52][53][54] However, some eyes may retain a concave iris configuration even after laser treatment.[55] In addition, laser iridotomy may not always prevent exercise-induced pigment release and IOP elevation.[50][56] There is limited data on whether laser iridotomy is effective in controlling IOP in patients with PDS or PG. While one small randomized controlled trial of 21 patients demonstrated a lower rate of IOP elevation over 2 years of follow-up in eyes treated with laser iridotomy as compared to eyes that were not,[57] a retrospective study of 60 patients did not suggest any laser iridotomy benefit.[58] Follow-up after laser iridotomy is similar to the follow-up for iridotomy performed for angle closure.

Argon laser trabeculoplasty (ALT) may be an effective treatment option, due to the heavy trabecular pigmentation seen in PDS and PG.[59][60][61][62][63] However, long-term control of IOP is unlikely, and younger patients are more likely to have long-term IOP lowering than older individuals.[63] Some studies have suggested that one-third or more of ALT-treated eyes may require trabeculectomy.[63] Selective laser trabeculoplasty (SLT) for PDS and PG has not been well studied, but with either ALT or SLT, lower energy settings should be used to avoid the release of pigment and IOP spikes. Follow-up after ALT or SLT is similar to the follow-up schedule used when these treatments are performed for POAG.

Trabeculectomy or other incisional surgery should be considered for patients demonstrating disease progression despite treatment with medicines or trabeculoplasty, though long-term results of trabeculectomy for PG have not been reported. The use of newer surgical modalities in the treatment of PG has not been well described.

Complications

Rise in IOP after laser iridotomy is greater in PDS and PG patients than in patients with occludable angles. Ways to mitigate this concern include the use of lower energy levels for surgery, the administration of alpha-adrenergic agonists before and after the laser treatment, and the use of argon laser instead of YAG laser, as it is less disruptive in terms of pigment liberation and inflammation.[64]

Prognosis

Blindness from PG is rare. In a community-based study of 113 patients with PDS or PG who were followed for a median of 6 years, 1 patient experienced unilateral blindness and another became bilaterally blind.[3] In the same study, 10% of patients with PDS progressed to PG at 5 years, while 15% progressed at 10 years; 23% of patients were noted to have PG at diagnosis.[3] Visual fields worsened in 44% of patients with PG over a mean follow-up period of 6 years. A group of patients followed from a glaucoma clinic showed higher rates of progression (35% over a median follow-up at 15 years), and roughly 40% of patients with PG experienced worsening of optic nerve damage.[25] In some cases, trabecular meshwork pigmentation and iris transillumination defects have been observed to normalize over time, as has elevated IOP, suggesting return of normal TM function.[8][23][28][65] Some older patients with a diagnosis of normal tension glaucoma have been identified with iris transillumination defects and dense TM pigmentation, suggesting they may have had PG at some point with subsequent IOP normalization due to cessation of pigment release.[66] In such patients, the presence of “pigment reversal sign” helps to distinguish between different types of glaucoma.

Additional Resources

References

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  57. ↑ Gandolfi SA, Vecchi M. Effect of a YAG laser iridotomy on intraocular pressure in pigment dispersion syndrome. Ophthalmology. 1996;103(10):1693-5.
  58. ↑ Reistad CE et al. The influence of peripheral iridotomy on the intraocular pressure course in patients with pigmentary glaucoma. J Glaucoma. 2005;14(4):255-9.
  59. ↑ Robin AL, Pollack IP. Argon laser trabeculoplasty in secondary forms of open-angle glaucoma. Arch Ophthalmol. 1983;101(3):382-384.
  60. ↑ Lunde MW. Argon laser trabeculoplasty in pigmentary dispersion syndrome with glaucoma.Am J Ophthalmol. 1983;96(6):721-725.
  61. ↑ Horns DJ et al. Argon laser trabeculoplasty for open angle glaucoma. A retrospective study of 380 eyes. Trans Ophthalmol Soc U K. 1983;103 ( Pt 3)(Pt 3):288-296.
  62. ↑ Lehto I. Long-term follow up of argon laser trabeculoplasty in pigmentary glaucoma. Ophthalmic Surg. 1992;23(9):614-617.
  63. ↑ Jump up to: 63.0 63.1 63.2 Ritch R et al. Argon laser trabeculoplasty in pigmentary glaucoma. Ophthalmology. 1993;100(6):909-913.
  64. ↑ Birt CM. Intraocular pressure spike after YAG iridotomy in patients with pigment dispersion. Can J Ophthalmol. 2004;39(3):234-9.
  65. ↑ Speakman JS. Pigmentary dispersion. Br J Ophthalmol. 1981;65(4):249-251.
  66. ↑ Ritch R. Nonprogressive low-tension glaucoma with pigmentary dispersion.Am J Ophthalmol. 1982;94(2):190-196.
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