PHACOLYTIC GLAUCOMA
Leakage of lens material through an intact lens capsule obstructs outflow channels (typically in the presence of a hypermature cataract).
Pain, decreased vision (despite poor vision from cataract, increased blurring may be noticeable), tearing, red eye, and photophobia.
Markedly increased IOP, accompanied by iridescent particles and white material in the anterior chamber or on anterior surface of lens capsule. No KP. A mature or hypermature (liquefied, Morgagnian) cataract is typical. May occur less commonly in presence of an immature cataract with liquefaction of the posterior cortex. Pain is usually severe.
Microcystic corneal edema, anterior chamber cell and flare (cells may be larger than typical uveitic white blood cells), pseudohypopyon, and severe conjunctival injection. Gonioscopy reveals open anterior chamber angles. Clumps of macrophages may be seen in the inferior angle.
All of the following can produce an acute increase in IOP to high levels, but none display iridescent particles in the anterior chamber:
Inflammatory glaucoma. See 9.7, Uveitic Glaucoma.
Acute angle-closure glaucoma. See 9.4, Acute Angle Closure Attack.
Lens particle glaucoma. See 9.11.2, Lens Particle Glaucoma.
Infectious endophthalmitis. See 12.14, Acute Postoperative Endophthalmitis and 12.15 Subacute and Chronic Postoperative Endophthalmitis.
Glaucoma secondary to intraocular tumor: May have unilateral cataract.
Others: Traumatic glaucoma, ghost cell glaucoma, phacomorphic glaucoma, phacoantigenic (formerly phacoanaphylaxis) glaucoma, neovascular glaucoma, and others.
History: Longstanding poor vision (chronic/mature cataract)? Recent trauma or ocular surgery? Recurrent episodes? Prior uveitis?
Slit-lamp examination: Look for iridescent or white particles as well as cell and flare in the anterior chamber. Measure IOP. Evaluate the cataract and lens capsule. Look for signs of trauma. Note, the lens capsule is intact in this diagnosis.
Gonioscopy of the anterior chamber angles of both eyes. Topical glycerin may be placed on the cornea, after topical anesthesia, to temporarily clear any edema.
Retinal and optic disc examination if possible. Otherwise, B-scan US before cataract extraction to rule out intraocular tumor or retinal detachment.
If the diagnosis is in doubt, an anterior chamber paracentesis can be performed to detect macrophages bloated with lens material on microscopic examination (see Appendix 13, Anterior Chamber Paracentesis).
The immediate goal of therapy is to reduce the IOP and inflammation. The cataract should be removed promptly (within several days).
Medical therapy options include:
Topical β-blocker (e.g., timolol 0.5% daily or b.i.d.), α2 agonist (e.g., brimonidine 0.1% to 0.2% b.i.d. to t.i.d.), and/or topical CAI (e.g., dorzolamide 2% t.i.d.).
Systemic CAI (e.g., acetazolamide 500 mg sequel p.o. b.i.d.). Benefit of maintaining topical CAI in addition to a systemic agent is controversial.
Topical steroid (e.g., prednisolone acetate 1% every 15 minutes for four doses then q1h).
Hyperosmotic agent if necessary and no contraindications are present (e.g., mannitol, 1 to 2 g/kg i.v. over 45 minutes).
The IOP usually does not respond adequately to medical therapy. In cases where IOP cannot be managed medically, cataract removal is usually performed within 24 to 48 hours. In patients who have noticed a sudden decrease in vision, the urgency of cataract surgery is increased, especially in those whose vision has progressed to NLP over a few hours. In such cases, lowering the IOP immediately with an anterior chamber paracentesis is necessary prior to cataract extraction (see Appendix 13, Anterior Chamber Paracentesis). Glaucoma surgery is usually not necessary at the same time as cataract surgery.
If patients are not hospitalized, they should be reexamined the day after surgery. Patients may be hospitalized for 24 hours after cataract surgery for IOP monitoring.
If the IOP returns to normal, the patient should be rechecked within 1 week.
LENS PARTICLE GLAUCOMA
Lens material liberated by trauma or surgery obstructs aqueous outflow channels.
Pain, decreased vision, red eye, tearing, and photophobia. History of recent ocular trauma or intraocular surgery.
Ruptured lens capsule. Increased IOP and white, fluffy pieces of lens cortical material in the anterior chamber. No KP.
Anterior chamber cell and flare, conjunctival injection, and corneal edema. Gonioscopy reveals open anterior chamber angles.
See 9.11.1, Phacolytic Glaucoma. In phacolytic glaucoma, the lens capsule is intact.
Infectious endophthalmitis: Usually a normal or low IOP. Unless lens cortical material can be unequivocally identified and no other atypical findings, endophthalmitis must be excluded. See 12.14, Acute Postoperative Endophthalmitis, 12.15, Subacute and Chronic Postoperative Endophthalmitis, and 12.16, Traumatic Endophthalmitis.
Phacoantigenic (formerly phacoanaphylaxis): Requires prior sensitization to lens material. Follows trauma or intraocular surgery, producing anterior chamber inflammation and sometimes a high IOP. The inflammation is often granulomatous, and fluffy lens material is not present in the anterior chamber. See 9.11.3, Phacoantigenic (formerly Phacoanaphylaxis).
Slit-lamp examination: Evaluate the lens and lens capsule. Look for ruptured lens capsule and lens cortical material in the anterior chamber. Measure IOP.
Optic nerve evaluation: Degree of optic nerve cupping helps determine how long the increased IOP can be tolerated.
See 9.11.1, Phacolytic Glaucoma, for medical treatment. If medical therapy fails to control the IOP, the residual lens material must be removed surgically.
Depending on the IOP and health of the optic nerve, patients are reexamined in 1 to 7 days.
PHACOANTIGENIC GLAUCOMA (FORMERLY PHACOANAPHYLAXIS)
Formerly known as “phacoanaphylaxis,” this rare condition presents with chronic granulomatous uveitis in response to prior sensitization of lens material liberated by trauma or intraocular surgery. It may have associated glaucomatous optic neuropathy, although this is rare at presentation. After lens material is liberated, there is a latent period where immune sensitivity develops. Inflammatory cells surround the lens material. Glaucoma may result from blockage of aqueous outflow by inflammatory cells and lens particles. KP are present. Other forms of uveitis should be considered, including sympathetic ophthalmia. Other forms of lens-induced glaucoma must be considered including lens particle and phacolytic glaucoma. Treatment is with topical steroids and antiglaucoma medications. The lens should be removed surgically, particularly if IOP or inflammation cannot be adequately controlled with medications.
PHACOMORPHIC GLAUCOMA
Phacomorphic glaucoma is caused by closure of the anterior chamber angle by a large mature cataract. A pupillary block mechanism may play a role. The initial treatment includes topical antiglaucoma medication(s) and systemic CAI; hyperosmotic agents may be necessary as well (see 9.4, Acute Angle Closure Attack). Can be mistaken for pupillary ACG, however, the anterior chamber may be more uniformly shallow compared to prominent iris bombé in a purely pupillary block mechanism. A laser iridotomy may be effective in relieving any degree of pupillary block, although this may only be a temporizing measure. Cataract extraction is the definitive treatment.
GLAUCOMA CAUSED BY LENS DISLOCATION OR SUBLUXATION
Lens dislocation/subluxation may be caused by trauma, pseudoexfoliation syndrome, or congenital zonular dysgenesis (e.g., Marfan syndrome, spherophakia). There are several ways lens dislocation can cause glaucoma. Pupillary block is the most common mechanism and can occur secondary to anterior displacement of the lens or vitreous plugging the pupil. A dislocated lens may become hypermature and cause phacolytic glaucoma (see 9.11.1, Phacolytic Glaucoma). Additionally, a dislocated/subluxed lens can lead to phacoantigenic glaucoma if associated with capsule violation (see 9.11.3, Phacoantigenic Glaucoma [Formerly Phacoanaphylaxis]). For treatment, laser iridotomy is usually indicated and necessary to relieve pupillary block. If lens is anteriorly dislocated, cycloplegics and face-up/supine head positioning are helpful to allow lens to fall back. Antiglaucoma medications are employed. Avoid miotics. Surgical lens removal is often needed, occasionally through a pars plana approach. See 13.2, Subluxed or Dislocated Crystalline Lens, for a more in-depth discussion.