Updated: Jan 28, 2009
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) dislocation of lens fragments into the anterior or posterior segment, with subsequent release of lens particles into the anterior chamber; (3) obstruction of trabecular meshwork by lens debris6 and inflammatory components7 ; and (4) reduction of the outflow facility of an open anterior chamber angle, resulting in elevation of intraocular pressure (IOP).
The incidence of lens-particle glaucoma has not been specifically reported. 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 of young males.
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.
| Endophthalmitis, Postoperative | Glaucoma, Malignant |
| Foreign Body, Intraocular | Glaucoma, Phacolytic |
| Glaucoma, Angle Closure, Acute | Glaucoma, Primary Open Angle |
| Glaucoma, Angle Recession | Phacoanaphylaxis |
| Glaucoma, Aphakic And Pseudophakic | |
| Glaucoma, Hyphema |
Steroid-induced glaucoma
Epithelial ingrowth
Sympathetic ophthalmia
Uveitis-glaucoma-hyphema (UGH) syndrome
If anterior chamber paracentesis is performed, histology may demonstrate foamy macrophages and lens particles.
Often, a coexisting phacoantigenic uveitis exists, and the lens histology may include the classic finding of zones of granulomatous and nongranulomatous inflammation that surround degenerating lens material.
Anterior chamber angle histologic examination of enucleated eyes may confirm the presence of macrophages in the trabecular meshwork, perhaps contributing to decreased outflow facility.
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. 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.
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 not be used if inflammation is present.
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.
Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increases outflow of aqueous humor.
1 gtt bid
Not established
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Documented hypersensitivity; COPD; CHF; asthma; cardiac conduction defects; breastfeeding
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Beta-blockade may potentiate muscle weakness that is consistent with certain myasthenic symptoms (eg, diplopia, ptosis, generalized weakness); product may have sulfites, which may cause allergic-type reactions in certain susceptible persons
Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.
1 gtt bid
Not established
May have additive systemic effects if patient is already on systemic beta-blockers
Documented hypersensitivity; CHF; cardiac conduction defects (possibly less effect on airways due to beta1 selectivity); breastfeeding
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Beta-blockade may potentiate muscle weakness consistent with myasthenic symptoms; product may have sulfites, which may cause hypersensitivity reactions in susceptible persons
Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic effects.
1 gtt bid
Not established
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Documented hypersensitivity; CHF; asthma; cardiac conduction defects; breastfeeding
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Product may have sulfites, which may cause allergic-type reactions in certain susceptible persons
May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor or by outflow.
1 gtt bid
Not established
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe COPD; overt cardiac failure; cardiogenic shock
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, COPD, and mental changes (especially in elderly persons)
Topical adrenergic agonists (sympathomimetics) decrease aqueous production and reduce resistance to aqueous outflow. Adverse effects include dry mouth and allergenicity.
Selective alpha2-receptor that reduces aqueous humor formation and increases uveoscleral outflow.
1 gtt bid (bid dosing may be as effective as tid)
Not established
Coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants, such as barbiturates, opiates, and sedatives, may potentiate effects of brimonidine
Documented hypersensitivity; patients receiving MAOIs
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack, and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy
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.
1 gtt tid
Not established
Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAOIs
Documented hypersensitivity; patients on MAOIs or have taken them in the past 14 d
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack, and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy
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.
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.
1 gtt tid
Not established
Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral CA inhibitors
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy)
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.
1 gtt tid
Not established
May have additive systemic effects if patient is already on oral CA inhibitors
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration (discontinue therapy and evaluate patient before restarting therapy)
Combination drug of carbonic anhydrase inhibitor and beta-blocker.
1 gtt bid
Not established
Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral CA inhibitors
Documented hypersensitivity; COPD; CHF; asthma; cardiac conduction defects; breastfeeding
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy); product may have sulfites, which may cause allergic-type reactions in susceptible patients
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.
125-250 mg tab PO qid or 500 mg cap PO bid; total dose not to exceed 1 g/24 h
Not established
Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine.
Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients; severe toxicities include decrease of potassium level and blood dyscrasia such as aplastic anemia
Reduces aqueous humor formation by inhibiting enzyme CA, which results in decreased IOP.
25-100 mg PO bid
Not established
May increase toxicity of salicylate, digoxin; coadministration with other diuretics may induce hypokalemia; decreases effects of lithium and alters excretion of other drugs by alkalinizing urine
Documented hypersensitivity; renal impairment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in respiratory acidosis and diabetes mellitus; impairs mental alertness and/or physical coordination; hematuria, glycosuria, polyuria, hepatic insufficiency, bone marrow suppression, thrombocytopenia/purpura, agranulocytosis, urticaria, pruritus, and rash may occur
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.
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).
1 gtt bid/tid/qid
Not established
None reported
Documented hypersensitivity; narrow-angle glaucoma; bladder outlet obstruction; ileus/GI obstruction
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid excessive systemic absorption by compressing lacrimal sac using digital pressure for 1-3 min after instillation; may produce drowsiness, blurred vision, or sensitivity to light (due to dilated pupils); observe caution while driving or performing other tasks requiring alertness, coordination, or physical dexterity
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.
1 gtt bid/tid/qid
Not established
None reported
Documented hypersensitivity; narrow-angle glaucoma
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in elderly persons where increased IOP may be present; toxic anticholinergic systemic adverse effects can occur but are rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorption
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.
Topical ophthalmic corticosteroid with approximately 3-5 times the potency of hydrocortisone. Topical corticosteroid therapy should be withdrawn by tapering the dosage.
1 gtt 1-8 times/d; dosage may be adjusted according to severity of inflammation, up to 1 gtt q1h
Not established
None reported
Documented hypersensitivity; infectious diseases of the eye, particularly those associated with herpes simplex virus, zoster, fungi, and mycobacteria
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in elderly persons where increased IOP may be present; toxic anticholinergic systemic adverse effects can occur but are rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorption
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.
1 gtt 1-6 times/d; dosage may be adjusted according to severity of inflammation, up to 1 gtt q1h
Not established
None reported
Documented hypersensitivity; infectious diseases of the eye, particularly those associated with herpes simplex virus, zoster, fungi, and mycobacteria
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Steroid-induced elevation of IOP is a particular risk in patients with glaucoma; topical corticosteroid also associated with secondary ocular infections involving bacterial, viral, and fungal pathogens; caution in cases with erosive ocular surface disease, especially in eyes with exposure or other risk factors for corneal ulceration
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lens-particle glaucoma, lens particle glaucoma, vision loss, visual deficit, lens-induced glaucoma, open-angle glaucoma, open angle glaucoma, cataract surgery, cataract surgery complications, eye trauma, eye trauma complications, pars plana lensectomy, vitreolensectomy, nucleus dislocation, intravitreal lens, intravitreal nucleus, vitreous lens fragment, intravitreal lens fragment, phacoemulsification complication, phaco complication, phacoantigenic uveitis, phacoanaphylactic uveitis
Brian R Sullivan, MD, Associate Professor, Department of Ophthalmology, University of Texas Southwestern Medical Center
Brian R Sullivan, MD is a member of the following medical societies: American Academy of Ophthalmology and American Society of Cataract and Refractive Surgery
Disclosure: Nothing to disclose.
Richard W Allinson, MD, Associate Professor, Department of Surgery, Texas A&M University Health Science Center; Senior Staff Ophthalmologist, Scott and White Clinic
Richard W Allinson, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.
Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.
Martin B Wax, MD, Clinical Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Ophthalmology Research and Development, Head, Ophthalmology Discovery Research, Alcon Labs, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Society for Neuroscience
Disclosure: Alcon Labs Salary Employment
Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.
Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.
Supported in part by an unrestricted research grant from Research to Prevent Blindness, Inc, New York, New York.
At the time of writing and subsequently updating this article, the author had no financial interests in any of the products discussed herein, nor in any of the companies that manufacture or distribute them.
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