Phacolytic Glaucoma 

Updated: Apr 06, 2017
Author: Kayoung Yi, MD, PhD; Chief Editor: Inci Irak Dersu, MD, MPH 



Phacolytic glaucoma (PG) is the sudden onset of open-angle glaucoma caused by a leaking mature or hypermature (rarely immature) cataract. It is cured by cataract extraction.[1, 2, 3]


In contrast to some forms of lens-induced glaucomas (eg, lens particle glaucoma, phacoanaphylactic glaucoma), phacolytic glaucoma occurs in cataractous lenses with intact lens capsules. The available evidence implicates direct obstruction of outflow pathways by lens protein released from microscopic defects in the lens capsule that is intact clinically. The high molecular weight proteins found in cataractous lenses produce outflow obstruction in experimental perfusion studies similar to that found in phacolytic glaucoma.[4, 5, 6] Although a macrophagic response is typically present, macrophages are believed to be a natural response to lens protein in the anterior chamber rather than the cause of the outflow obstruction.

The possibility of 2 forms of phacolytic glaucoma was proposed in a recent report: (1) a more acute presentation caused by rapid leakage of lens proteins that occlude the trabecular meshwork and (2) a more gradual presentation with macrophages resulting from an immunologic response to lens proteins in the anterior chamber.[7]



United States

Phacolytic glaucoma is infrequent in developed countries, such as the United States, because of greater access to health care and earlier cataract surgery.


Phacolytic glaucoma occurs more frequently in underdeveloped countries.


Most cases resolve after cataract extraction with excellent improvement in vision.


No racial predilection exists.


No sexual predilection exists.


Phacolytic glaucoma typically occurs in older adults. The youngest patient reported was age 35 years.




Patients with phacolytic glaucoma typically have a history of slow vision loss for months or years prior to the acute onset of pain, redness, and sometimes further decrease in vision.[8]

Vision may only be inaccurate light perception due to the density of the cataract.

Symptoms mimic acute angle-closure glaucoma (see Glaucoma, Angle Closure, Acute).

The history of slow vision loss due to advancing cataract preceding the acute onset of symptoms is a vital clue to the correct diagnosis.


Intraocular pressure (IOP) characteristically is elevated severely in phacolytic glaucoma.[9]

Slit lamp examination of phacolytic glaucoma typically reveals microcystic corneal edema, and the anterior chamber contains intense flare, large cells (macrophages), aggregates of white material, and iridescent or hyperrefringent particles. The latter represent calcium oxalate and cholesterol crystals being liberated from the degenerating cataractous lens. Unlike uveitic glaucoma (such as that seen in phacoanaphylactic glaucoma), no keratic precipitates typically are present.[10]

The anterior capsule of the lens frequently is dotted with patches of soft white material. In contrast to some forms of lens-induced glaucomas (eg, lens particle glaucoma, phacoanaphylactic glaucoma), the lens capsule is grossly intact.

Gonioscopy findings usually are normal; however, evidence of old angle recession was found in 25% of eyes in one study.


Phacolytic glaucoma may be caused by the following:

  • Mature cataract (totally opacified)

  • Hypermature cataract (liquid cortex and free-floating nucleus)

  • Focal liquefaction of immature cataract (rare)

  • Dislocated cataractous lens in vitreous[11]



Diagnostic Considerations

In addition to the above diagnoses, another lens-induced glaucoma, phacoanaphylactic glaucoma, may be confused with phacolytic glaucoma (PG). Phacoanaphylactic glaucoma is a delayed-onset granulomatous reaction to retained lens material, such as that occurring after disruption of the lens capsule from trauma or because of incomplete removal of lens material during cataract extraction (including gross loss of lens fragments into the vitreous cavity during cataract extraction). Pain, if it occurs at all, is often slow in onset and is associated with signs of granulomatous uveitis (eg, keratic precipitates) in contrast to the acute, severe pain that is typical of PG, which shows no signs of chronic inflammation.

Traumatic glaucomas, including angle-recession glaucoma and ghost cell glaucoma, also may be confused with PG.[12, 13, 14] A careful history and examination of the anterior chamber angle may reveal evidence of prior trauma. A history of long-standing vitreous hemorrhage should raise suspicion of ghost cell glaucoma.

Finally, in apparently aphakic eyes, the posterior segment must be inspected carefully for a dislocated lens that, when hypermature, may begin to leak and cause PG even when a cataract is not readily visible.

Differential Diagnoses



Histologic Findings

Although light microscopy showed an intact anterior capsule, scanning electron microscopic showed disruption of the anterior capsule in a case of phacolytic glaucoma.[15]

In questionable cases, a diagnostic paracentesis should show characteristic swollen macrophages with engulfed lens material on phase contrast microscopy.

See the images below.

Microscopy of the aspirate at the time of cataract Microscopy of the aspirate at the time of cataract extraction shows clumped, notched rectangular platelike crystals from the aqueous of a patient with phacolytic glaucoma (X160). Reproduced from J Korean Ophthalmol Soc 2000 Sep;41(9): Copyright © 2000, Korean Ophthalmological Society. All rights reserved.
Microscopy of the aspirate at the time of cataract Microscopy of the aspirate at the time of cataract extraction of a patient with phacolytic glaucoma shows round, regular cells with foamy cytoplasm consistent with macrophages (*). A leukocyte (white arrow) and an erythrocyte (black arrow) also are seen (X160). Reproduced from J Korean Ophthalmol Soc 2000 Sep;41(9): Copyright © 2000, Korean Ophthalmological Society. All rights reserved.


Medical Care

Initial treatment of phacolytic glaucoma is focused upon acute lowering of IOP using a combination of topical and systemic IOP-lowering agents. Topical steroids also may facilitate IOP lowering and decrease pain.

Medical therapy is only a temporizing measure until cataract surgery can be scheduled.

Surgical Care

The definitive treatment of phacolytic glaucoma (PG) is cataract extraction. Extracapsular cataract extraction (eg, phacoemulsification) with an intraocular lens implant has largely replaced intracapsular cataract extraction as the procedure of choice.[16, 17, 9, 18]

If PG is caused by a lens that has dislocated into the vitreous cavity, the procedure of choice is pars plana vitrectomy with removal of the lens from within the vitreous cavity.


Instruct patients not to eat or drink if emergency cataract extraction is being considered.



Medication Summary

Several applications of a topical beta-blocker, a topical alpha2-adrenergic, a topical carbonic anhydrase inhibitor, and a topical corticosteroid should be started in the office on presentation when possible. The IOP should be remeasured in 30 minutes to 1 hour. If the IOP is severely elevated or is nonresponsive to initial topical medications, a systemic carbonic anhydrase inhibitor and an osmotic agent also should be administered. The latter medications may be administered intravenously if the patient is nauseated or vomiting. Prostaglandin analogs (eg, Xalatan, Rescula, Lumigan, Travatan) may not be as useful in the treatment of phacolytic glaucoma (PG) because of their slow onset of action and their theoretical risk of exacerbating intraocular inflammation.[19] The adequacy of initial response to medical therapy helps to determine the urgency of scheduling cataract extraction.


Class Summary

The exact mechanism of ocular antihypertensive action is not established, but it appears to be a reduction of aqueous humor production.

Timolol maleate or hemihydrate (Timoptic XE, Timoptic, Betimol)

May reduce elevated and normal IOP, with or without glaucoma, by inhibiting inflow.

Levobunolol (AKBeta, Betagan)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production

Carteolol ophthalmic (Ocupress)

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

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.

Metipranolol hydrochloride (OptiPranolol)

Beta-adrenergic blocker that has little or no intrinsic sympathomimetic effects and membrane-stabilizing activity. Has little local anesthetic activity. Reduces IOP by reducing production of aqueous humor.

Topical alpha2-adrenergics agonists

Class Summary

May reduce elevated and normal IOP, with or without glaucoma, by inhibiting inflow.

Apraclonidine (Iopidine)

Reduces elevated and 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.

Brimonidine (Alphagan)

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

Carbonic anhydrase inhibitors

Class Summary

By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit carbonic anhydrase in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.

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 5 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increasing renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.

Brinzolamide (Azopt)

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 5 min apart.

Acetazolamide (Diamox, Diamox Sequels)

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 carbonic anhydrase, which results in decreased IOP.

Hyperosmotic agents

Class Summary

Create an osmotic gradient between ocular fluids and plasma. Not for long-term use.

Glycerin (50% solution prepared from Glycerin USP [450 mL, Humco, Texarkana, TX] and sterile water)

Used in glaucoma to interrupt acute attacks. Oral osmotic agent for reducing IOP. Able to increase tonicity of blood until finally metabolized and eliminated by the kidneys. Maximum reduction of IOP usually occurs 1 h after glycerin administration. Effect usually lasts approximately 5 h.

Mannitol (Osmitrol)

Reduces elevated IOP when pressure cannot be lowered by other means. Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg, given IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h. In children, assess for adequate renal function by administering a test dose of 200 mg/kg, given IV over 3-5 minutes. Should produce a urine flow of at least 1 mL/h over 1-3 h.


Class Summary

Reduce eye pain and intraocular inflammation.

Prednisolone ophthalmic (Pred Forte)

Treats acute inflammation following eye surgery or other types of insults to eye. Decreases inflammation and corneal neovascularization. Suppresses migration of polymorphonuclear leukocytes and reverses increased capillary permeability. In cases of bacterial infections, concomitant use of anti-infective agents is mandatory; if signs and symptoms do not improve after 2 days, reevaluate patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.



Further Outpatient Care

In most cases, IOP begins to rapidly normalize following cataract extraction, allowing discontinuation of ocular medications. A minority of patients will have persistent elevation of IOP requiring long-term medical therapy or filtering surgery to control the glaucoma.

Further Inpatient Care

Inpatient care is not usually necessary for phacolytic glaucoma unless the patient is briefly hospitalized following emergency cataract extraction.


Removal of mature or hypermature cataracts may be preventive.


Potential complications of phacolytic glaucoma include the following:

  • Loss of vision from uncontrolled glaucoma and/or persistent corneal edema

  • Surgical complications, including suprachoroidal hemorrhage, capsular rupture with loss of lens material into the posterior segment, corneal injury, and vitreous prolapse


Prognosis is excellent, with most patients experiencing marked improvement in vision following cataract extraction; however, delayed treatment may cause a poor outcome.

Patients with phacolytic glaucoma (PG) may have a worse prognosis than patients with phacomorphic glaucoma.

In most cases, treatment to lower intraocular pressure can be discontinued after cataract extraction. A minority of patients who have persistent intraocular pressure elevation may need long-term medical therapy or a filtering surgery to control intraocular pressure.

Patient Education

Seek a comprehensive eye examination when progressive vision loss is first noted.

For excellent patient education resources, visit eMedicineHealth's Eye and Vision Center. Also, see eMedicineHealth's patient education articles Glaucoma Overview, Glaucoma FAQs, and Glaucoma Medications.