Definition

Pigment dispersion refers to the release of pigment granules into the anterior chamber. It results from backward bowing of the peripheral iris (reverse pupillary block) with friction between the iris pigment epithelium and the zonular fibers. Pigment is released into the aqueous and deposits in TM, leading to increased IOP and secondary open-angle glaucoma.

Mostly asymptomatic but may have blurred vision, eye pain, and colored halos around lights after exercise or pupillary dilation. More common in young  adult, myopic men (age 20 to 45 years). Usually bilateral, but asymmetric. May have lattice degeneration and increased risk of a retinal detachment.

(See Figures 9.9.1 and 9.9.2.)

Figure 9.9.1: Pigment dispersion syndrome with spoke-like iris transillumination defects.

Figure 9.9.2: Pigment dispersion syndrome with a vertical band of endothelial pigment (Krukenberg spindle).

Critical

Midperipheral, spoke-like iris TIDs corresponding to iridozonular contact; open angle with dense pigmentation of the TM for 360 degrees (seen on gonioscopy) in the absence of signs of trauma or inflammation.

Other

A vertical pigment band on the corneal endothelium typically just inferior to the visual axis (Krukenberg spindle); pigment deposition on the posterior zonular-lens attachment line (Zentmayer line or Scheie line), on the anterior hyaloid face, slightly anterior to Schwalbe line (Sampaolesi line), and sometimes on the anterior surface of the iris (which can produce iris heterochromia). The angle often shows a wide ciliary body band with 3+ to 4+ pigmentation of the posterior TM, homogenous for 360 degrees. Pigmentary glaucoma is characterized by pigment dispersion syndrome plus glaucomatous optic neuropathy. Typically, large fluctuations in IOP can occur, during which pigment cells may be seen floating in the anterior chamber.

• Exfoliative glaucoma: Iris TIDs may be present but are near the pupillary margin and are not radial. White, flaky material may be seen on the pupillary border, anterior lens capsule, and corneal endothelium. TM is highly pigmented but in a “splotchy” pattern, often with pigment anterior to Schwalbe line (also seen in PDS). See 9.10, Pseudoexfoliation Syndrome/Exfoliative Glaucoma.

• Uveitic glaucoma: White blood cells and flare in the anterior chamber; no radial iris TIDs; often PAS on gonioscopy. TM pigment concentrated inferiorly. See 9.7, Uveitic Glaucoma.

• Iris melanoma: Pigmentation of the angular structures accompanied by either a raised, pigmented lesion on the iris or a diffusely darkened iris. No iris TIDs. See 5.14, Malignant Melanoma of the Iris.

• Irradiation: Induces atrophy and depigmentation of the ciliary processes with increased TM pigment deposition.

• Postoperative pigment liberation after posterior chamber intraocular lens implantation.

• Siderosis.

• Iris chafe with sulcus intraocular lens (IOL): Iris TIDs outlining the haptics may be seen.

• Bilateral acute depigmentation of the iris: Acute-onset bilateral iris depigmentation, pigment dispersion in the anterior chamber, and heavy pigmentation of the TM. Occurs after a flu-like illness, upper respiratory tract infection, and after the use of oral moxifloxacin. Usually symmetric (pigment dispersion syndrome is typically asymmetric).

1. History: Previous episodes of decreased vision or halos? Symptoms associated with exercise? Trauma, surgery, or previous intraocular foreign body? 

2. Slit-lamp examination, particularly checking for iris TIDs. Large defects may be seen by shining a small slit beam directly into the pupil to obtain a red reflex. Look for Krukenberg spindle on the corneal endothelium. Look for pigment on the posterior zonule-lens attachment line by angling the slit beam nasally and having the patient look temporally in a pharmacologically dilated pupil (Zentmayer or Scheie line; pathognomonic for pigment dispersion). Examine the angle looking for dense, evenly dispersed TM pigmentation. Careful retinal examination because of increased incidence of lattice degeneration and retinal detachment.

3. Perform baseline glaucoma evaluation. See 9.1, Primary Open-Angle Glaucoma.

Similar to POAG. Depends on IOP, optic nerve damage, and symptom extent. Usually, patients with pigment dispersion without ocular hypertension, glaucoma, or symptoms are monitored carefully. A stepwise approach to control IOP is usually taken when glaucomatous optic nerve changes are present. Patients with advanced glaucoma may require multiple medications or filtering surgery for IOP control, similar to POAG. See 9.1, Primary Open-Angle Glaucoma.

1. Decrease mechanical iridozonular contact. Two methods have been proposed:

   • Miotic agents: A theoretical first-line therapy because they minimize iridozonular contact. However, because most patients are young and myopic, the resulting fluctuation in myopia may not be tolerated. In addition, approximately 14% of patients have lattice retinal degeneration and are thus predisposed to retinal detachment from the use of miotics. In some cases, pilocarpine 4% gel q.h.s. may be tolerated.

   • Peripheral laser iridotomy: Laser PI has been recommended to reduce pigment dispersion by decreasing iridozonular contact, but remains controversial. It may be best suited in early-stage disease among symptomatic patients and ill-advised in more advanced stages.

2. Other antiglaucoma medications. See 9.1, Primary Open-Angle Glaucoma.

3. SLT or ALT. Due to greater risk of post-laser IOP spikes, lower energy should be used and/or limitation of treatment to 180 degrees per session. Careful post-laser monitoring is needed to detect early IOP rise.

4. Consider MIGS surgery, guarded filtration procedure, or tube shunt when medical and laser therapies fail. Young myopic patients may be at greater risk for hypotony maculopathy and surgical technique should aim to avoid overfiltration.

Same as POAG. See 9.1, Primary Open-Angle Glaucoma.