Lens-Particle Glaucoma

Updated: Oct 11, 2021
Author: Donny W Suh, MD, MBA, FAAP, FACS; Chief Editor: Hampton Roy, Sr, MD 



Lens-particle glaucoma, a subclassification of lens-induced glaucoma,[1, 2, 3, 4, 5] is a type of secondary open-angle glaucoma involving intraocular retention of fragmented lens debris. Following surgery or injury, lens material may be sequestered within the capsular bag or dislocated into other areas of either the posterior eye or the anterior eye. Characteristically, large lens pieces spontaneously fragment further into small (sometimes invisible) particles that eventually migrate into the anterior chamber and obstruct aqueous outflow.[6] Lens-particle glaucoma is not associated with decentration or dislocation of an intact lens.


The mechanism involves the following 4 processes: (1) presence of a nonintact lens capsule, usually violated during trauma or intraocular surgery; (2) subsequent release of microscopic lens debris into the anterior chamber, sometimes associated with dislocation of larger lens fragments in the anterior or posterior segment; (3) obstruction of trabecular meshwork by lens particles[6] and inflammatory components[7] ; and (4) reduction of the outflow facility of an open anterior chamber angle, resulting in elevation of intraocular pressure (IOP).



United States

The frequency of penetrating eye injury in the United States has been estimated at 3.1 per 100,000 person-years,[8] with a predominance in young males. The incidence of lens-particle glaucoma in adults has not been specifically reported, but a 2019 retrospective review found an incidence of 7.1% following open globe injury in pediatric eyes.[9]


Mortality is not associated with this condition. Morbidity is rare.


No known racial predilection exists.


No known gender predilection exists for lens-particle glaucoma. However, penetrating eye trauma, a risk factor for lens-particle glaucoma, has been reported to occur more commonly in young adult males.[8] Alcohol abuse is a significant comorbidity in this population.


All ages are affected, ranging from infancy (especially when involving congenital cataract surgery) to late adulthood. Penetrating eye injuries occur most frequently in young adults. However, lens-particle glaucoma probably occurs most commonly in elderly persons as a complication of cataract surgery.




Patients are often asymptomatic.

Depending on the severity of IOP elevation and associated intraocular inflammation, symptoms of monocular eye pain, redness, and/or blurred vision may be present.

Although spontaneous rupture of the lens capsule has been described,[10, 11, 12, 13] there is typically a recent or remote history of trauma or intraocular surgery,[2, 14, 15] particularly cataract extraction.

The onset of lens-particle glaucoma has been reported to occur many years after cataract surgery[16, 17] or penetrating trauma.[18]

Lens-particle glaucoma is commonly encountered in cases of phacoemulsification that were complicated by a posteriorly dislocated lens nucleus.

Obstruction of the trabecular meshwork by lens material may have a role in the mechanism of an early postoperative IOP spike after uncomplicated phacoemulsification.

Lens-particle glaucoma also may cause elevated IOP after laser capsulotomy.[19] Obtain any history of YAG laser procedures in all pseudophakic patients under evaluation for glaucoma.

Dislocation of a posterior intraocular lens has been reported to cause late onset lens-particle glaucoma.[20]


Unilateral elevation of IOP is present.

Variable degree of inflammation, including cell and flare, corneal edema, keratic precipitates, or hypopyon, may be present.

Lens debris, sometimes seen as a fluffy pseudohypopyon layered in the inferior anterior chamber or as small free-floating fragments of cortex that circulate in the aqueous, may be visible by slit lamp examination. Lens or cellular debris also may be deposited on the corneal endothelium.

Anterior chamber angle is open by gonioscopy, although inflammatory anterior synechia may be observed later in more severe cases.

Lens fragments may be visible on dilated slit lamp examination, adherent to the lens capsule.

Large intraocular inflammatory mass has been reported in lens-induced uveitis as an exaggerated response to exposed lens fibers.[21]

Elschnig pearls may be observed in chronic cases of lens-particle glaucoma.

Particles of cortex or nucleus that are dislocated into the vitreous usually are visualized readily by indirect ophthalmoscopy. In such cases, careful scleral depression can aid in identifying occult lens particles that are positioned over the anterior retina or ora serrata. 

Lens nucleus dislocated into the inferior vitreous Lens nucleus dislocated into the inferior vitreous during cataract surgery. Reprinted from Survey of Ophthalmology, Vol 43. Monshizadeh R, Nasrollah S, Haimovici R: Management of retained intravitreal lens fragments after cataract surgery. 397-403. Copyright 1999, with permission from Elsevier Science.

In cases of glaucoma with severe associated phacoantigenic uveitis, other late findings may include posterior synechia, peripheral anterior synechia, vitreitis, and retinal detachment.


Causes include the following:

  • Penetrating eye trauma with perforation of the lens capsule

  • Blunt trauma with rupture of the lens capsule[22] or dislocation of a nonintact lens 

    Ruptured lens capsule with elevated intraocular pr Ruptured lens capsule with elevated intraocular pressure following trauma. Courtesy of KS Kooner, MD.
  • Uncomplicated cataract surgery

  • Cataract surgery with incomplete removal of the lens cortex

  • Cataract surgery complicated by posterior dislocation of the nucleus or nuclear fragments

  • Pars plana vitrectomy or other intraocular surgery involving intentional or inadvertent compromise of the lens capsule's integrity[15]

  • Atraumatic lens particle glaucoma has been reported in cases of spontaneous anterior capsular dehiscence[10, 11] and in a case of Marfan syndrome with complete lens dislocation.[13]

  • Congenital cataract with persistent fetal vasculature (PVF) was a reported cause of spontaneous lens particle glaucoma in a 4-year-old child.[12]





Laboratory Studies

Consider ruling out endophthalmitis via anterior chamber tap and vitreous tap with smears for Gram and Giemsa stains and cultures with antimicrobial sensitivities.

Culture media should include blood agar, Sabouraud media, chocolate agar, and thioglycolate broth.

Imaging Studies

In cases of ocular trauma, a 20-MHz ultrasound probe[23] and a 35-MHz ultrasound probe[24] have been reported to help facilitate the visualization of the posterior capsule's integrity. The effective use of 50-MHz ultrasound biomicroscopy has been described in the assessment of occult zonular defects in traumatic cataracts.[25]

B-scan ultrasonography may be useful in localizing and measuring posteriorly displaced lens debris, particularly large nucleus fragments.


Perform anterior chamber tap and vitreous tap if endophthalmitis is suspected.

Histologic Findings

If anterior chamber paracentesis is performed, histology may demonstrate foamy macrophages[10] and lens particles.

A coexisting phacoantigenic uveitis often exists, and the lens histology may include the classic finding of zones of granulomatous and nongranulomatous inflammation that surround degenerating lens material. Inflammatory intraocular spindle cell mass simulating a neoplasm has been reported in lens-induced uveitis,[21] with a histologic finding of a large tumefaction of histiocytes and myofibroblasts.

Anterior chamber angle histologic examination of enucleated eyes may confirm the presence of macrophages in the trabecular meshwork, perhaps contributing to decreased outflow facility.



Medical Care

The elevated IOP of lens-particle glaucoma often responds to medical management.[26]  Once infectious processes are excluded from the differential diagnoses, the most important approach to treating lens-particle glaucoma includes steroid use, cycloplegics, and ophthalmic drops to decrease intraocular pressure.

Topical beta-adrenergic antagonists are typical first-line agents.

Topical alpha-adrenergic agonists and carbonic anhydrase inhibitors are considered adjunctive agents. Be especially cautious when choosing a topical carbonic anhydrase inhibitor in cases involving compromised corneal endothelial function; irreversible corneal decompensation has been described in such scenarios.

In managing this condition, treat the associated inflammation. Initial therapy typically involves a topical corticosteroid agent in conjunction with a topical cycloplegic agent.

Therapies involving prostaglandin analogues have not been sufficiently reported, but exercise caution when using such agents in the postoperative period. Theoretical risks of increased inflammation and/or cystoid macular edema exist.

Likewise, miotic agents may exacerbate anterior segment inflammation.

In emergency management of severe acute lens-particle glaucoma, hyperosmotic agents have a useful role in controlling IOP.

Surgical Care

Fragments in Anterior Chamber

Consider surgical intervention in cases that involve large amounts of unabsorbed lens material, posteriorly dislocated lens or nuclear fragment, or uncontrolled IOP with conventional medical management. Surgical removal of lens material often leads to a substantial reduction of intraocular pressure, and further glaucoma surgery is usually not necessary.[10] Nucleus fragments in the anterior chamber should be removed surgically because of the risk of corneal decompensation. In contrast, cortical fragments in the anterior chamber often can be observed for breakdown and resorption, with appropriate medical management.

Removal of cortical debris from the posterior chamber usually requires irrigation and aspiration of lens material adherent to the lens capsule or ciliary sulcus. Intraocular lens repositioning or exchange may be necessary. Capsulectomy with anterior vitrectomy also may be indicated if the posterior capsule and/or zonules are not intact. Anterior chamber washout, achieved by irrigation and aspiration of balanced salt solution, is recommended to maximally remove the lens debris from the angle.

Fragments in Posterior Chamber

Management of posterior dislocation of lens material varies depending on the anticipated risk of complications. Large nuclear fragments are tolerated poorly in the posterior segment, even over short periods. Prompt vitreoretinal surgery is usually indicated.[27]  

However, a total lens dislocation with an intact capsule may not require immediate surgical intervention because the risks of glaucomatous, inflammatory, or retinal complications are lower in this setting.

Similarly, very small intravitreal nuclear fragments may be tolerated without specific intervention. Both the lens-particle–induced glaucoma and the inflammatory response often may appear to be proportionate to the size of the fragment. However, some data suggest that final visual outcomes may not be correlated to nucleus fragment size.[28]

Because of significant risks of further complications, the primary cataract surgeon should not attempt to retrieve intravitreal lens fragments from an anterior approach.[29, 30, 31, 32] Immediate consultation with a vitreoretinal surgeon is recommended.

Pars plana vitrectomy (with removal of lens fragments by aspiration with a fragmatome in the midanterior vitreous cavity) has become the indicated management for large intravitreal nucleus fragments.[31, 32, 33, 34, 35, 36, 37, 28] Immediate pars plana vitrectomy at the same sitting for dislocated lens fragments during cataract surgery has been described.[5, 38, 39] One study has suggested that conservative medical management may be initially undertaken in some patients without detrimental outcomes due to a delay in surgery,[40] but other data have shown major advantages to early vitrectomy within the first week.[41]

Posterior vitreolensectomy has been associated with postoperative improvement or resolution of lens-particle glaucoma. Good visual outcomes have been reported,[32, 33, 34, 36, 37, 28] particularly with prompt intervention.[41]


Immediately obtain a vitreoretinal consultation in the event of posterior lens dislocation as a complication of cataract surgery. Several studies have indicated that early vitrectomy (within 1-3 weeks postoperatively) is associated with more favorable visual results.[38, 39, 41, 42]

Also, consider a retinal consultation to assist in differentiating postoperative phacoantigenic uveitis from endophthalmitis or sympathetic ophthalmia.



Medication Summary

The goal of therapy is IOP reduction. Medications often can be used short term and then discontinued. IOP should be monitored after stopping medications, and therapy should be reinstituted when necessary.

Bimatoprost (Lumigan), travoprost (Travatan), latanoprost (Xalatan), and unoprostone (Rescula) are ophthalmic prostaglandin analogs approved in the United States. Bimatoprost is a prostamide analog with ocular hypotensive activity. It mimics the IOP-lowering activity of prostamides via the prostamide pathway. Travoprost and unoprostone are prostaglandin F2-alpha (ie, dinoprost) analogs similar to latanoprost. They are selective FP prostanoid receptor agonists believed to reduce IOP by increasing uveoscleral outflow. They are indicated for the lowering of IOP in patients with open-angle glaucoma or ocular hypertension who are intolerant of other IOP-lowering medications or insufficiently responsive (failed to achieve target IOP determined after multiple measurements over time) to another IOP-lowering medication.

Bimatoprost and travoprost are each administered once daily at bedtime (ie, 1 gtt in affected eye[s] hs); whereas, unoprostone must be administered twice daily. They have not been studied in pediatric patients. The role of prostaglandin analogs in the management of lens-particle glaucoma has not been specifically reported.

These medications are contraindicated if hypersensitivity has been documented. No drug interactions have been reported. All are classified as pregnancy category C (ie, fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus).

All ocular prostaglandin analogs demonstrate the unusual adverse effect of permanent increase in pigment of the iris (ie, increases brown pigment) and eyelid, and they may increase eyelash growth. Bacterial keratitis may occur. Use is cautioned in uveitis or macular edema. They should usually not be used if inflammation is present.


Class Summary

Topical beta-adrenergic receptor antagonists decrease aqueous humor production by the ciliary body. Adverse effects are due to systemic absorption of the drug, resulting in decreased cardiac output and bronchoconstriction. In susceptible patients, this may cause bronchospasm, bradycardia, heart block, or hypotension. Monitor the patient's pulse rate and blood pressure. Patients may be instructed to perform punctal occlusion after administering the drops. Depression or anxiety may be experienced in some patients, and sexual dysfunction may be initiated or exacerbated.

Levobunolol (AKBeta, Betagan)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increases outflow of aqueous humor.

Betaxolol ophthalmic (Betoptic, Betoptic S)

Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.

Carteolol ophthalmic (Ocupress)

Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic effects.

Timolol maleate (Timoptic, Timoptic XE) 0.25%, 0.5%

May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor or by outflow.

Adrenergic agonists

Class Summary

Topical adrenergic agonists (sympathomimetics) decrease aqueous production and reduce resistance to aqueous outflow. Adverse effects include dry mouth and allergenicity.

Brimonidine (Alphagan)

Selective alpha2-receptor that reduces aqueous humor formation and increases uveoscleral outflow.

Apraclonidine (Iopidine)

Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. Apraclonidine is a relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.

Carbonic anhydrase inhibitors

Class Summary

Reduce secretion of aqueous humor by inhibiting carbonic anhydrase (CA) in the ciliary body. These drugs are less effective, and their duration of action is shorter than many other classes of drugs. Adverse effects are relatively rare but include superficial punctate keratitis, acidosis, paresthesias, nausea, depression, and lassitude. Corneal decompensation has been reported when this class of drugs is used in patients with corneal endothelial dysfunction.

Dorzolamide (Trusopt)

Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. Reversibly inhibits CA, reducing hydrogen ion secretion at renal tubule, and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.

Brinzolamide (Azopt) 1%

Catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If more than one topical ophthalmic drug is being used, administer drugs at least 10 min apart.

Dorzolamide HCl/timolol maleate (Cosopt)

Combination drug of carbonic anhydrase inhibitor and beta-blocker.

Acetazolamide (Diamox)

Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP. Used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute angle-closure glaucoma when delay of surgery desired to lower IOP.

Methazolamide (Neptazane)

Reduces aqueous humor formation by inhibiting enzyme CA, which results in decreased IOP.

Cycloplegic agents

Class Summary

Cholinergic antagonists commonly are used in the management of anterior intraocular inflammation, and, occasionally, they may be used in eyes with lens-particle glaucoma that have an active phacoantigenic uveitis. These topical drugs exert mydriatic and cycloplegic effects on the iris and ciliary body and reduce the permeability of the blood-aqueous barrier.

Scopolamine (I-Hyoscine)

Topical antimuscarinic agent with potent mydriatic and cycloplegic action. Blocks action of acetylcholine at parasympathetic sites in the smooth muscle, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).

Homatropine (AK-Homatropine, Isopto homatropine)

Topical antimuscarinic agent with moderate cycloplegic and mydriatic effects. Homatropine is less potent than scopolamine, and the toxicity of homatropine is one fiftieth of that of atropine.


Class Summary

Corticosteroid agents commonly are used in combination with topical cycloplegics in the management of anterior uveitis. In cases of lens-particle glaucoma, the use of steroids is limited to eyes that have coexisting intraocular inflammation.

Prednisolone acetate 1% (Pred Forte)

Topical ophthalmic corticosteroid with approximately 3-5 times the potency of hydrocortisone. Topical corticosteroid therapy should be withdrawn by tapering the dosage.

Loteprednol etabonate 0.5% (Lotemax)

Topical ophthalmic corticosteroid. Although less potent, loteprednol may be associated with a lower risk of steroid-induced IOP elevation when compared to prednisolone and may be preferred in patients with glaucoma who have mild-to-moderate intraocular inflammation. Topical corticosteroid therapy should be withdrawn by tapering the dosage.



Further Outpatient Care

Any patient who develops acute glaucoma following cataract surgery, Nd:YAG capsulotomy, or trauma requires careful follow-up to monitor IOP control and medical management and/or surgery to remove residual lens particles.

Depending on the degree of IOP control and the presence of other coexisting complications, patients may require daily to weekly follow-up care early in the postoperative period.

Treat and monitor intraocular inflammation.

Further Inpatient Care

Patients with lens-particle glaucoma rarely require hospital admission. Consider admission in the following situations:

  • IOP is elevated severely.

  • Intravenous mannitol is needed to control IOP.

  • There are immediate plans for further surgical intervention.

Inpatient & Outpatient Medications

See Medication.


In addition to glaucoma, complications of retained intraocular lens particles include corneal decompensation, chronic uveitis, and cystoid macular edema.[35]

Pars plana vitrectomy for displaced nuclear fragments can be associated with complications[28, 33, 34, 35, 36, 37, 43] of persistent glaucoma, uveitis, corneal edema, bullous keratopathy, cystoid macular edema, epiretinal membrane, vitreous hemorrhage, retinal detachment, and choroidal hemorrhage.


Prognosis is generally good with appropriately timed medical and surgical intervention.[35, 41]

Visual outcome of pars plana vitrectomy is better when performed for retained cortex or epinucleus, compared with retained nucleus fragments.[28]

Studies have reported final visual acuities of 20/40 or better in approximately two thirds of cases of dropped nucleus requiring vitrectomy,[36, 37, 39, 42] but other recent data suggest a less favorable prognosis, which may be independent of the size of the retained nuclear fragment.[28]

Elevated IOP improves significantly in response to the surgical removal of intraocular lens material.

A nonsurgical approach may be equally successful in cases of small retained lens cortical fragments, if inflammation and IOP can be controlled acceptably, cellular processes in the trabecular meshwork are clearing the lens material.

Chronic open-angle glaucoma occurs in some patients following an episode of lens-particle glaucoma when lens particles have been reabsorbed.

The transient presence of lens debris in the anterior chamber angle has been theorized to possibly cause long-lasting trabecular dysfunction.

Patient Education

For patient education resources, see the Glaucoma Center, as well as Lens-Particle Glaucoma, Glaucoma FAQs, and Understanding Glaucoma Medications.


Questions & Answers


What is lens-particle glaucoma?

What is the pathophysiology of lens-particle glaucoma?

What is the US prevalence of lens-particle glaucoma?

What is the mortality and morbidity associated with lens-particle glaucoma?

What are the racial predilections of lens-particle glaucoma?

What are the sexual predilections for lens-particle glaucoma?

Which age groups have the highest prevalence of lens-particle glaucoma?


Which clinical history findings are characteristic of lens-particle glaucoma?

Which physical findings are characteristic of lens-particle glaucoma?

What causes lens-particle glaucoma?


What are the differential diagnoses for Lens-Particle Glaucoma?


What is the role of lab testing in the workup of lens-particle glaucoma?

What is the role of ultrasonography in the workup of lens-particle glaucoma?

When are anterior chamber tap and vitreous tap indicated in the workup of lens-particle glaucoma?

Which histologic findings are characteristic of lens-particle glaucoma?


How is lens-particle glaucoma treated?

What is the role of surgery in the treatment of lens-particle glaucoma?

Which specialist consultations are beneficial to patients with lens-particle glaucoma?


What is the role of medications in the treatment of lens-particle glaucoma?

Which medications in the drug class Corticosteroids are used in the treatment of Lens-Particle Glaucoma?

Which medications in the drug class Cycloplegic agents are used in the treatment of Lens-Particle Glaucoma?

Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Lens-Particle Glaucoma?

Which medications in the drug class Adrenergic agonists are used in the treatment of Lens-Particle Glaucoma?

Which medications in the drug class Beta-blockers are used in the treatment of Lens-Particle Glaucoma?


What is included in the long-term monitoring of lens-particle glaucoma?

When is inpatient care indicated for the treatment of lens-particle glaucoma?

What are the possible complications of lens-particle glaucoma?

What is the prognosis of lens-particle glaucoma?

What is included in patient education about lens-particle glaucoma?