264 GLAUCOMATOCYCLITIC CRISIS

364.22

(Posner–Schlossman Syndrome)

Abraham Schlossman, MD, FACS

New York, New York

ETIOLOGY/INCIDENCE

Glaucomatocyclitic crisis is unilateral glaucoma characterized by recurrent attacks of glaucoma that are usually associated with signs of mild cyclitis. The condition generally occurs in patients between 20 and 50 years old, with individual attacks of ocular hypertension lasting from a few hours to 1 month but very rarely more than 2 weeks.

Multifactorial causes have been postulated for this syndrome; the condition has been reported in association with:

●Allergies;

●Herpes simplex virus infection (but not herpes zoster);

●Immunogenetic disorders;

●Stress-related disorders such as peptic ulcer;

●Primary vascular abnormality.

The mean incidence and prevalence rates of the condition reported in one study were 0.4 and 1.9, respectively, in 100,000 population.

PROGNOSIS

The prognosis is excellent with prompt treatment, with no permanent changes detectable in the visual fields after an attack.

DIAGNOSIS

●Sudden onset.

●Mildly blurred vision, diminished visual acuity (temporary).

●Colored haloes around lights.

●Mild ocular discomfort.

●Unilateral; recurrences always in same eye (very rarely bilateral).

●Slight mydriasis (pupil of affected eye larger than that in the other eye and reactive).

● Intraocular pressure of affected eye between 40 and

60 mm Hg (fluctuates).

●Anterior chamber cells and minimal flare.

●Corneal epithelial edema, keratic precipitates (few, 25 or less; unpigmented); persist as long as 1 month after intraocular pressure has returned to normal.

●Ciliary flush.

●No posterior synechiae or iris atrophy.

●Rare glaucomatous cupping of optic nerve, after many attacks.

TREATMENT

Ocular

Treatment of the ocular hypertension should be limited to the attack and should consist of the use of mild miotics such as:

●Prostaglandin analogues;

●Ophthalmic beta blockers.

Topical ocular corticosteroids (one to four times daily) are used to control inflammation and are especially helpful during the acute phase.

Occasional pupillary dilation with:

●Phenylephrine 2.5% usually permits confirmation that no synechiae are forming.

Surgery is contraindicated; iridectomy and filtering operations do not prevent recurrences.

Supportive

To control the patient’s pain and apprehension during attacks, analgesics, tranquilizers, or both may be helpful. Follow-up examinations are important to monitor pressure elevation and inflammation.

COMPLICATIONS

Strong miotics, and perhaps strong mydriatics, are contraindicated in the treatment of glaucomatocyclitic crises because they tend to aggravate the symptoms by producing pain, congestion, and spasm of the ciliary muscle.

In view of the ineffectiveness of surgical measures and the benign and self-limited nature of the disease, there exists no indication for any surgical intervention in this syndrome; medical therapy between attacks is not indicated.

Topical corticosteroids give good results by allaying ciliary irritability; however, if such treatment is prolonged, steroidinduced glaucoma may occur.

COMMENTS

The value of recognizing this syndrome lies in the fact that surgical procedures not only are unnecessary but also are definitely contraindicated in this condition. Glaucomatocyclitic crises differ from acute narrow-angle glaucoma and glaucoma secondary to uveitis in that the angle of the anterior chamber is open, even at the height of an attack, and the eye is white with minimal pain during attacks. Also, facility of outflow is normal between attacks, and provocative tests give normal responses.

REFERENCES

De Roetth A, Jr: Glaucomatocyclitic crisis. Am J Ophthalmol 69:370–371, 1970.

Knox DL: Glaucomatocyclitic crises and systemic disease: Peptic ulcer, other gastrointestinal disorders, allergy and stress. Trans Am Ophthalmol Soc 86:473–495, 1988.

Posner A, Schlossman A: Syndrome of unilateral attacks of glaucoma with cyclitic symptoms. Arch Ophthalmol 39:517–535, 1948.

Posner A, Schlossman A: Further observations on the syndrome of glaucomatocyclitic crises. Trans Am Acad Ophthalmol Otolaryngol 57:531– 536, 1953.

264CrisisCHAPTERGlaucomatocyclitic •

Pressure Intraocular • 23 SECTION

FIGURE 265.2. Goniotomy under direct visualization after stripping oedematous epithelium with alcohol.

COMMENTS

PCG is a serious condition for which early diagnosis and treatment are vital to optimize visual prognosis. The suspicion of glaucoma in a child should always be seriously treated with urgency to avoid serious visual impairment.

REFERENCES

Anderson DR: The development of the trabecular meshwork and its abnormality in primary congenital glaucoma. Trans Am Ophthalmol Soc 79:481–485, 1981.

Budenz DL, Gedde SJ, Brandt JD, et al: Baerveldt glaucoma implant in the management of refractory childhood glaucomas. Ophthalmol 111:2204– 2210, 2004.

Cunliffe IA, Molteno ACB: Long-term follow-up of Molteno drains used in the treatment of glaucoma presenting in childhood. Eye 12:379–385, 1998.

Sidoti PA, Belmonte SJ, Liebmann JM, et al: Trabeculectomy with mitomycin-C in the treatment of pediatric glaucomas. Ophthalmology 107:422–429, 2000.

Stoilov I, Akarsu AN, Sarfarazi M: Identification of three different truncating mutations in cytochrome P4501B1 (CYP1B1) as the principle cause of primary congenital glaucoma (Buphthalmos) in families linked to the GLC3A locus on chromosome 2p21. Hum Mol Genet 6:641–647, 1997.

266 JUVENILE GLAUCOMA 365.14

Marianne E. Feitl, MD

Chicago, Illinois

Theodore Krupin, MD

Chicago, Illinois

Angelo P. Tanna, MD

Chicago, Illinois

The nonspecific term ‘juvenile glaucoma’ has traditionally been used to describe a heterogeneous group of glaucomas occurring in later childhood or early adulthood; age limits for this grouping are after the onset age of most cases of developmental (infantile) glaucoma and before the manifestation of most adult primary glaucomas.

ETIOLOGY/INCIDENCE

Juvenile-onset open-angle glaucoma, by convention, refers to chronic open-angle glaucoma diagnosed in patients between 10 and 35 years old. Unfortunately, because of a low index of suspicion on the part of the physician, the diagnosis of glaucoma in this age group is easily overlooked. In a large series of patients with glaucoma, only a small number, approximately 0.2%, were diagnosed within this age interval.

Juvenile-onset chronic open-angle glaucoma is a rare form of glaucoma that is inherited as an autosomal dominant trait with 10 to 20% of cases having mutations in the myocilin gene (MYOC). This gene was previously known as the trabecular meshwork-inducible glucocorticoid response (TIGR) gene. The 1q23-24 region of the long arm ofchromosome 1 has been identified as the location responsible for this condition (GLC1A). Mutations in MYOC are associated with only 2 to 4% of adultonset primary-open glaucoma patients. Work is currently underway to determine the role myocilin plays in the pathogenesis of glaucoma, as well as to further delineate the roles of other genes responsible for juvenile-onset glaucoma.

COURSE/PROGNOSIS

Mild cases of developmental congenital glaucoma may go unrecognized until later in childhood; these children do not have signs of ocular discomfort and have perfectly clear corneas with only:

●Mild corneal enlargement; or

●Breaks in Descemet’s membrane (Haab striae).

Intraocular pressure (IOP)-induced buphthalmos, progressive myopia, and corneal changes do not occur in children older than three years. Affected patients develop high pressure (commonly more than 50 mmHg) within the first two decades of life. The average age at diagnosis is 18 years (range, 8 to 30 years).

Juvenile open-angle glaucoma patients have a longer axial length than normal, and are more often myopic, but lack other ocular or systemic abnormalities. Visual field damage tends to be more symmetric superior-inferiorly than in adult-onset chronic open-angle glaucoma. Gonioscopy shows open iridocorneal angles without abnormal pigmentation, iris processes, or embryonic tissue. Topical medications usually are effective initially in controlling IOP, but filtration surgery may be required for long-term glaucoma control.

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smaller size, younger children face potentially higher serum drug levels than adults. Lid closure and nasolacrimal occlusion to minimize systemic absorption of topical medications are important. Children are less likely than adults to complain of drug side effects and thus must be watched and questioned more carefully.

The beta-adrenergic antagonists should be used with caution in children, although these agents can be effective. Nonselective beta blockers should be avoided in patients with asthma because of their bronchospastic effects. Asthma induced in children may be evidenced by nocturnal coughing, rather than wheezing as commonly seen in adults. Bradycardia and apneic spells may also occur. Beta-blockers also should be used cautiously in patients with heart problems, including congestive heart failure.

Betaxolol, a selective beta1-antagonist, may be better tolerated in patients with pulmonary disease. However, it can still trigger asthma in susceptible individuals.

The topical alpha-adrenergic agonists apraclonidine and brimonidine are effective IOP-lowering agents that decrease aqueous production and possibly increase uveoscleral outflow. Apraclonidine is less lipophilic than brimonidine, with reduced drug penetration of the blood-brain barrier. This property may reduce systemic and central nervous system side effects. Caution has been advised in the use of brimonidine in children, due to the risk of centrally mediated systemic hypotension and central nervous system depression. Fatigue and fainting attacks have been reported. A dry mouth may also occur. Serious potential systemic side effects demand particular caution when these agents are used in younger patients.

The prostaglandin-related drugs latanoprost, travaprost, and bimatoprost increase uveoscleral outflow, thereby lowering IOP. Once daily administration enhances compliance. Conjunctival injection, increased iris pigmentation and increased eyelash growth are ocular side effects. Systemic side effects are infrequent and mild. Although these agents can be excellent ocular hypotensives, their long-term safety profile is not yet known. IOP reduction is reported to be greater in older children than in very young patients. As with all of these agents, there is less clinical experience in children than in adults, so caution and a discussion of the possible risks with the patient and parents are warranted.

Topical carbonic anhydrase inhibitors such as dorzolamide and brinzolamide provide better tolerance and greatly reduced systemic side effects than are associated with the oral forms of these agents. While these agents decrease aqueous production, they are less effective than beta-blockers in lowering pressure. Dorzolamide and timolol are additive in their pressure-lowering effects, and a combined preparation (Cosopt) is available. Carbonic anhydrase inhibitors are sulfonamide derivatives, and the topical preparations may be contraindicated in patients with a documented sulfa allergy.

The oral carbonic anhydrase inhibitor acetazolamide, in total daily oral doses of 15 mg/kg, is administered to children in two to four divided doses. Side effects include loss of appetite, gastrointestinal disturbances, parasthesias, metabolic acidosis, and lethargy. Side effects may present differently in children, including bedwetting, failure to thrive, and disturbed hyperactive behavior. The risk of renal calculi should be borne in mind and indicated to the parents. Methazolamide is an alternative oral agent that may cause fewer side effects than acetazolamide.

Oral carbonic anhydrase inhibitors can be associated with bone marrow depression and aplastic anemia. This side effect,

while theoretically possible with topical agents because of systemic absorption, has not been reported.

Topical miotic therapy with pilocarpine, carbachol, and pphospholineiodidedecreases IOP by increasing trabecular outflow. These drugs are effective ocular hypotensive agents, particularly in children with open iridocorneal angles. Unfortunately, they induce miosis and myopia, disabling symptoms that prevent their use. Phospholine iodide also produces cataract. Systemic side effects include nausea, vomiting, diarrhea, abdominal cramping, salivation, sweating, bradycardia, hypotension, branchospasm, muscle weakness and CNS stimulation.

Phospholine iodide is an excellent miotic drug in aphakic or pseudophakic eyes. A 1/8% solution is currently available (WyethPharmaceuticals) for twice-daily administration, with some patients responding to daily delivery.

Medical

Young patients should be examined frequently until the maintenance of a satisfactory IOP level is achieved. In the absence of credible visual fields, one must rely more heavily on correlation of IOP and stability of optic disc damage.

Aggressive treatment of iritis associated with juvenile rheumatoid arthritis, using systemic cycloplegics and steroids, should be instituted to prevent peripheral anterior synechiae or neovascular membranes. In addition, topical cycloplegics increase uveoscleral outflow,which may reduce IOP. Glaucoma can be caused by either prolonged, inadequately treated intraocular inflammation or steroid treatment. Anti-glaucoma therapy should be instituted if necessary. Topical miotics are to be avoided because these agents can increase intraocular inflammation and decrease uveoscleraloutflow, resulting in a paradoxical rise in IOP.

Medical therapy usually is less effective in juvenile-onset than in adult-onset primary glaucoma. Long-term medical control of the glaucoma is often poor and surgery may be required.

Surgical

Surgery should be undertaken whenever medical therapy has not resulted in good control. Prolonged use of topical agents may adversely affect wound healing after glaucoma surgery.

Iridectomy is the procedure of choice in primary or secondary angle closure. Mechanical and technical incompatibilities of the slit-lamp-based laser and the need for general anesthesia may dictate a surgical iridectomy. The increasing availability of an operating microscope YAG laser delivery system allows performing a laser iridotomy.

Goniotomy or trabeculotomy is indicated as the initial surgery in eyes with congenital glaucoma. These procedures have a lower success rate after the age of three years. However, good results may still be obtained with trabeculotomy in infantile and juvenile glaucoma. One retrospective study showed a success rate for trabeculotomy of 60% in congenital glaucoma, 96% in infantile glaucoma, and 76% in juvenile glaucoma.

Retrospective studies of uveitic glaucoma in children have showed that one or two goniotomy procedures were often successful in obtaining pressures under 21 mmHg, although most patients continued to need glaucoma medication after surgery.

Surgical outcome is adversely affected by increased age, peripheral anterior synechiae, prior surgeries, and aphakia.

Filtration surgery is less likely to be successful in juvenile than in adult glaucomas. The lower success rate in young

266 CHAPTERGlaucoma Juvenile •

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patients may relate to increased postoperative scarring and to the types of glaucomas that tend to occur in this age group. Postoperative bleb encapsulation is more common in patients with juvenile glaucoma. Trabeculectomy has a poor prognosis in eyes that have had prior surgery and eyes with secondary glaucoma, particularly neovascular and aphakic glaucoma. The use of adjunctive antifibrotic agents (e.g. 5-fluorouracil or mitomycin C) increases the trabeculectomy success (see below).

Age as an isolated factor may have its greatest influence on surgical outcome in patients younger than 30. In one series, trabeculectomy for primary glaucoma was successful in 25 of 30 (83%) of patients 30 to 49 years old, but in only 4 of 9 patients (44%) younger than 30. In youth, Tenon’s tissue is more extensive, postoperative hypotony may be prolonged, wound healing may be more vigorous, and postoperative examination is often less than ideal.

Because limbal surgical landmarks can be obscure, transillumination at the time of surgery is recommended to avoid placing the sclerostomy incision too posteriorly. A lamellar scleral flap helps identify the limbal surgical anatomy, in particular the scleral spur. The scleral flap lowers the incidence of a postoperative flat anterior chamber and results in a thicker, more diffuse filtration bleb. However, the surgeon should remember that the sclera might be thinner in the juvenile glaucoma eye, making scleral flap dissection more difficult.

Corticosteroids should be used after filtration surgery to diminish postoperative inflammation and scarring of the bleb. A sub-Tenon’s injection of a short-acting corticosteroid, such as dexamethasone or triamcinolone, at the completion of surgery and the use of topical corticosteroid drops or ointment after surgery are recommended. Adjunctive antifibrotic agents should be used to slow wound healing and scar formation and to increase the success rate of trabeculectomy in this patient population. Intraoperative application of 5-fluorouracil or Mitomycin C is an option in these patients. Postoperative subconjunctival injections of 5-fluorouracil may be impossible for very young patients without general anesthesia or office sedation. Both of these drugs are associated with thinner, more cystic blebs and may carry a higher rate of complications, such as wound leaks, chronic hypotony, and possibly late endophthalmitis.

Releasable scleral flap sutures may be used at the time of surgery in young patients to control postoperative bleb function and to reduce the occurrence of early postoperative hypotony. These sutures are removed at the time of examination under anesthesia. Enhanced healing responses in young patients shorten the interval when removal of these sutures must be performed to increase blebfunction.

Argon laser suture lysis may be used to titrate bleb function in older, more cooperative patients.

The risks of both early and late bleb-associated ocular infection must be carefully explained to patients and parents, and they must be advised to seek medical care immediately should any signs or symptoms occur.

Cyclodestructive treatments have several useful applications in the management of juvenile glaucoma. Diode or Nd : YAG transscleral laser procedures result in less inflammation and have a lower incidence of phthisis bulbi than cyclocryotherapy. Laser cyclodestructive procedures may be used to provide IOP control in circumstances where filtration surgery has not been successful or has a low success rate, particularly aphakic glaucoma. Conjunctival hyperemia and anterior chamber reaction are the most common side effects. Multiple treatments may be needed to achieve satisfactory lowering of pressure. Results in

pediatric patients are similar to those for adults for efficacy and safety.

Endoscopic diode laser cyclophotocoagulation appears to be less effective than externally applied diode laser cyclophotocoagulation. Aphakic patients may have an increased risk of significant postoperative complications such as retinal detachment.

Cyclocryotherapyhas a higher complication rate (e.g. phthisis bulbi and loss of vision) when used to treat neovascular glaucoma.

Posterior tube drainage implants have been used to treat patients with juvenile-onset glaucoma when filtrating surgery has failed. Encouraging results have been reported with various glaucoma drainage implants. These devices place an open plastic tube into the anterior chamber that is attached to an equatorial episcleral plate, resulting in a posterior bleb over the area of the encapsulated explant. Success is related to diagnosis, number of previous glaucoma procedures, and surgeon experience.

COMPLICATIONS

Perhaps the most unfortunate error clinicians make in treating patients with juvenile-onset glaucoma is failing to recognize the condition early. The fellow eyes of patients with apparent uniocular congenital glaucoma should be followed very carefully for possible late-onset congenital glaucoma. Young patients with advancing high myopia should be regarded as potential candidates for glaucoma. Applanation tonometry is preferable to Schiotz tonometry in these patients because of their low ocular rigidity. A positive family history of glaucoma in children should suggest an examination of the patient’s relatives and siblings.

COMMENTS

With the availability of hand-held portable applanation tonometers, IOP can usually be measured in the office; this should be considered part of the complete pediatric ophthalmologic examination whenever glaucoma is suspected and should be performed in all patients who can cooperate. Gonioscopy may be performed successfully in many children, often with surprising ease. Reliable visual fields are difficult to obtain in young children. Goldmann kinetic perimetry is the preferred method. This places more responsibility on the ophthalmologist for accurate assessment of stability of glaucomatous optic nerve damage.

Routine examination of the optic disc should be performed in all patients. In children on whom tonometry cannot be performed, the disc examination may reveal suspected or definite damage from elevated IOP. In those patients, further examination with the patient under anesthesia is warranted. If possible, optic disc photography or other optic nerve and retinal nerve fiber layer measurements should be done in individuals with suspected or proven juvenile-onset glaucoma. Rapid increase and reversal of disc cupping occur more frequently in children with glaucoma than in adults.

REFERENCES

Badlani VK, Quinones R, Wilenshy JT, et al: Angle-closure glaucoma in teenagers. J Glaucoma 12:198–203, 2003.

Barsoum-Homsy M, Chevrette L: Incidence and prognosisof childhood glaucoma. Ophthalmology 93:1323–1327, 1986.

Chew E, Morin JD: Glaucoma in children. Pediatr ClinNorth Am 30:1043– 1061, 1983.

Ho CL, Wong EY, Walton DS: Goniosurgery for glaucomacomplicating chronic childhood uveitis. Arch Ophthalmol 122:838–844, 2004.

Mori M, Keech RV, Scott WE: Glaucoma and ocularhypertension in pediatric patients with cataracts. J AAPOS 1:98–101, 1997.

Neely DE, Plager DA: Endocyclophotocoagulation formanagement of difficult pediatric glaucomas. J AAPOS 5:221–229, 2001.

Rabiah PK: Frequency and predictors of glaucoma afterpediatric cataract surgery. Am J Ophthalmol 137:30–37, 2004.

Richards JE, Lichter PR, Boehnke M, et al: Mapping ofa gene for autosomal dominant juvenile-onset open-angle glaucoma to chromosomeIq. Am J Hum Genet 54:62–70, 1994.

Richter CU, Shingleton BJ, Bellows AR, et al: Thedevelopment of encapsulated filtering blebs. Ophthalmology 95:116–118, 1988.

Ritch R, Chang BM, Liebmann JM: Angle closure inyounger patients. Ophthalmology 110:1880–1889, 2003.

Rosenberg LF, Krupin T: Implants in glaucoma surgery.In: Ritch R, Shields MB, Krupin T, eds: The glaucomas. Glaucoma therapy. 2nd edn. St Louis, Mosby-Year Book, 1996:III:1783–1807.

Ritch R: Pigmentary glaucoma: a self-limited entity. Ann Ophthalmol 15:115–116, 1983.

Sheffield VC, Stone EM, Alward WL, et al: Geneticlinkage of familial open angle glaucoma to chromosome Iq21-q31. Nat Genet 4:47–50, 1993.

Talbot AWR, Russell-Eggitt: Pharmaceutical managementof the childhood glaucomas. Exp Opin Pharmacother 1(4):697–711, 2000.

Waheed S, Ritterband DC, Greenfield DS, et al: Bleb-related ocular infection in children after trabeculectomy with mitomycinC. Ophthalmology 104:2117–2120, 1997.

Walton DS: Juvenile open-angle glaucoma. In: ChandlerPA, Grant WM, eds: Glaucoma. 3rd edn. Philadelphia, Lea &Febiger, 1986:528–529.

Weisschuh N, Schiefer U: Progress in the genetics ofglaucoma. Dev Ophthalmol 37:83–93, 2003.

Wiggs JL, Lynch S, Ynagi G, et al: A genomewide scanidentifies novel earlyonset primary open-angle glaucoma loci on 9q22 and20p12. Am J Hum Genet 74:1314–1320, 2004.

Zak M, Fledelius H, Pedersen FK: Ocular complicationsand visual outcome in juvenile chronic arthritis: a 25-year follow-up study.Acta Ophthalmol Scan 81:211–215, 2003.

267LENS-INDUCED GLAUCOMA

365.51

Rober L. Stamper, MD

San Francisco, California

Stephanie M. Po, MD

Walnut Creek, California

Michelle Nee, MD

San Francisco, California

Lens-induced glaucoma may occur as three different secondary open-angle glaucomas: phacolytic, lens-particle, and phacoantigentic glaucoma. It also can occur as a pupillary block from lens intumescence (phacomorphic glaucoma) or lens dislocation (ectopia lentis).

SECONDARY OPEN ANGLE GLAUCOMAS

Phacolytic glaucoma (lens protein glaucoma)

This type of lens-induced glaucoma arises from leakage of lens protein through an intact lens capsule in the setting of a mature

or hypermature (Morgagnian) cataract. Heavy-molecular-weight proteins (greater than 150 × 106 daltons) are fourteen-fold more concentrated in mature lens cortices than in immature cataracts. In vitro experiments have demonstrated that these high molecular weight proteins can directly obstruct the aqueous outflow channels. In addition, protein-engorged macrophages, whose normal function is to phagocytose debris within the trabeculum, probably contribute to the outflow obstruction.

Clinical findings mature or hypermature cataract

●Open angle.

●Corneal edema.

●Acute rise in intraocular pressure associated with pain and redness.

●Heavy aqueous flare.

●White fluffy material on lens capsule or floating in anterior chamber.

●Diagnostic paracentesis, phase-contrast microscopy, and Milipore filter technique establish presence of macrophages (though this is not always present).

Differential diagnosis

●Uveitic glaucoma.

●Phacomorphic glaucoma.

●Pupillary block glaucoma.

●Neovascular glaucoma.

●Lens Particle glaucoma.

●Phacoanaphlactic glaucoma.

Treatment

Medical

●Topical β-adrenergic antagonist, carbonic anhydrase inhibitors, α2 agonist, prostaglandin agonists.

●Topical steroids.

●Hyperosmotic agents.

●Oral Carbonic anhydrase inhibitors.

Surgical

●Removal of cataract usually restores normal intraocular pressure.

If intraocular pressures are still high at time of surgery, gradually entering the anterior chamber with slowly decompress the globe

Lens particle glaucoma

This type of lens-induced secondary open angle glaucoma differs from phacolytic glaucoma in that actual fragments of cortical lens material are obstructing the trabecular meshwork. These fragments have been liberated into the anterior chamber from trauma, or from iatragenic causes, such as after cataract surgery or Nd-Yag capsulotomy.

The severity of the clinical course often will vary with the amount of free cortical lens material, and the onset of glaucoma can occur months to years later.

Clinical findings

●Corneal edema.

●Heavy cellular reaction and flare, possible hypopyon.

●Lens material in the angle.

Differential diagnosis

●Phacolytic glaucoma.

●Steroid-induced glaucoma.

267GlaucomaCHAPTERinduced-Lens •

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Glaucoma) tension-(Low268GlaucomaCHAPTERtension-Normal •