Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001

One study reports initial success rates for trabeculectomy in the ICE syndrome as comparable to that for primary open-angle glaucoma.38 However, others contend success rates are very poor for trabeculectomy in the ICE syndrome.38 Late failures are usually attributed to proliferation of abnormal endothelium into the filtering bleb.31 Progressive endothelialization of the blebs and the young age of the patients with the ICE syndrome are also common explanations for bleb failure. In these cases, another filtering procedure performed in a different location is appropriate. The success rates for repeated trabeculectomies are comparable to those of the initial procedure.38 The use of antimetabolites and setons may improve the results of secondary filtering procedures in recalcitrant cases.39 Vigorous control of inflammation following filtering procedures is necessary to help avoid bleb failure. Because the viral etiology of this syndrome has yet to be definitively confirmed, topical and systemic antiviral treatment may be therapeutic.40,41

Patients with corneal edema may benefit from lowering of the IOP. However, filtering surgery cannot be recommended solely in an attempt to resolve the corneal edema.42 The cornea can remain edematous even at the lowest achievable levels of IOP. Hypertonic saline drops are often helpful for mild corneal edema. If visually significant corneal edema is present after IOP has been lowered medically, then penetrating keratoplasty is usually required (Fig. 7–6). If the IOP remains controlled, the prognosis for the corneal graft is good.43 Recurrences of the endothelial abnormalities that characterize the ICE syndrome have not been noted to develop on the donor cornea.27,43

What Is the Role of Penetrating Keratoplasty

in the Management of the ICE Syndrome?

Corneal edema, even at normal intraocular pressures, predominates in Chandler’s syndrome. Early corneal edema may respond to topical hyperosmotic solutions or ointment. Lowering the IOP improves corneal clarity and visual acuity in some patients. Penetrating keratoplasty is indicated in cases in which corneal edema significantly reduces vision, precludes visualization of the optic nerve, or causes pain from bullous keratopathy, recurrent corneal erosions, or secondary infectious keratitis.43–45 The success rate for penetrating keratoplasty in the ICE syndrome has generally been favorable despite poor overall clinical prognosis for the disorder.43–45 The role of surgical pupilloplasty and lysis of peripheral anterior synechiae at the time of penetrating keratoplasty remains unclear.

What Is the Summary of Treatment of the ICE Syndrome?

The most important problem to treat in the ICE syndrome is elevated IOP. Treatment is more difficult than that of chronic open-angle glaucoma because an abnormal membrane and peripheral anterior synechiae cover the trabecular meshwork. If the IOP is controlled, corneal edema is often less severe. However, corneal edema can be visually significant and warrant penetrating keratoplasty in a small percentage of cases. Penetrating keratoplasty is usually successful in the variants with predominantly corneal disease; however, it may be less successful in those cases with extensive iris disease and glaucoma.

Table 7–6. Glaucoma Associations with Corneal Disease

1.Primary corneal endothelial disorders

•Iridocorneal endothelial syndrome

2.Anterior segment developmental abnormalities

•Peter’s anomaly

•Rieger’s syndrome

•Anterior chamber cleavage syndromes

3.Congenital

•Congenital hereditary endothelial dystrophy

•Congenital hereditary stromal dystrophy

•Posterior polymorphous dystrophy

4.Corneal and/or intraocular infectious/inflammatory processes

•Herpes simplex/herpes zoster keratitis/keratouveitis

•Any severe iritis

•Chandler’s syndrome

5.Penetrating keratoplasty performed on eyes developing glaucoma

Generally, we do not treat iris atrophy or ectopic pupils unless the pupil is significantly eccentric to interfere with visual acuity. In these cases, surgical or yttrium-aluminum-garnet (YAG) laser iridoplasty may be of value.

Future Considerations

Future considerations include morphometric characteristics of the contralateral corneal endothelium in the ICE syndrome. Luca-Glass et al37 have tried to determine whether subclinical morphologic abnormalities exist in the contralateral, clinically uninvolved eye of patients with the ICE syndrome. Their data suggest the corneal endothelium of the clinically uninvolved, contralateral eye may have increase pleomorphism, expressed as a relatively low percentage of hexagonal cells. They found that this issue is important when considering the various hypotheses proposed to explain the pathogenesis of the disease. More studies are needed to further unravel this mystery.

References

1.Scheie HG, Yanoff M: Iris nevus (Cogan-Reese) syndrome. Arch Ophthalmol 1975;93:963–970.

2.Yanoff M: Iridocorneal endothelial syndrome: unification of a disease spectrum. Surv Ophthalmol 1979;24(1):86–90.

3.Harms C: Einseitige spontane uckenbidung der Iris durch Atrophie ohne mechanische Zerrung. Kin Monatsbl Augenheilkd 1903;41:522–528.

4.Shields MB: The essential iris atrophies. Am J Ophthalmol 1978;85:749–755.

5.Shields MB: Progressive essential iris atrophy, Chandler’s syndrome and the iris-nevus (Cogan-Reese) syndrome: a spectrum of disease. Surv Ophthalmol 1979;24:3–20.

6.Cogan DG, Reese AB: A syndrome of iris nodules, ectopic Descemet’s membrane, and unilatera glaucoma. Doc Ophthalmol 1969;26:424–439.

7.Scheie HG, Yanoff M, Kellogg WT: Essential iris atrophy. Report of a case. Arch Ophthalmol 1976;94:1315–1320.

144 Glaucoma Associated with Primary Disorders of the Corneal Endothelium

8.Chandler PA: Atrophy of the stroma of the iris, endothelial dystrophy, corneal edema and glaucoma. Am J Ophthalmol 1956;41:607–615.

9.Campbell DG, Shields MB, Smith TR: The corneal endothelium and the spectrum of essential iris atrophy. Am J Ophthalmol 1986;86:317–323.

10.Eagle RC, Shields JA: Iridocorneal endothelial syndrome with contralateral guttate endothelial dystrophy: a light and electron microscopic study. Ophthalmology 1987;94:406–411.

11.Huna R, Barak A, Melamed S: Bilateral iridocorneal endothelial syndrome presented as Cogan-Reese and Chandler’s syndrome. J Glaucoma 1996;5(1):60–62.

12.Miller CA, Krachmer JH: Endothelial dystrophies. In: Kaufman HE, Barron BA, McDonald MB (eds): The Cornea, 2d Ed. Newton, MA: Butterworth-Heinemann, 1997; 470–471.

13.Sabates R, Krachmer JH, Weingeist TA: Ocular findings in Alport’s syndrome. Ophthalmologica 1983;186:204.

14.Heon E, Mathers WD, Alward WL, et al: Linkage of posterior polymorphous corneal dystrophy to 20q11. Hum Mol Genet 1995;4:485–490.

15.Kaiser-Kupfer M, Kuwabara T, Kupfer C: Progressive bilateral essential iris atrophy. Am J Ophthalmol 1977;83:340–346.

16.Hetherington J: The spectrum of Chandler’s syndrome. Ophthalmology 1978;85:240–244.

17.Rodrigues MM, Streeten BW, Spaeth GL: Chandler’s syndrome as a variant of essential iris atrophy. A clinicopathologic study. Arch Ophthalmol 1978;96:646–652.

17a. Campbell DG, Shields MB, Smith TR: The corneal endothelium and the spectrum of essential iris atrophy. Am J Ophthalmol 1978;86:317–324.

18.Leibowitz H, Waring GO: Corneal Disorders: Clinical Diagnosis and Management, 2d Ed. Philadelphia: WB Saunders, 1998;214–219.

19.Alvarado JA, Murphy CG, Juster RP, et al: Pathogenesis of Chandler’s syndrome, essential iris atrophy and the Cogan-Reese syndrome: II. Estimated age at disease onset. Invest Ophthalmol Vis Sci 1986;27:873–879.

20.Tsai CS, Ritch R, Strauss, et al: Antibodies to Epstein Barr virus in iridocorneal endothelial syndrome. Arch Ophthalmol 1990;108:1572–1579.

21.Sherrard ES, Frangoulis MA, Kerr Muir MG, et al: The posterior surface of the cornea in the iridocorneal endothelial syndrome: a specular microscopical study. Trans Ophthalmol Soc UK 1985;104:766–774.

22.Sherrard ES, Frangoulis MA, Kerr Muir MG, et al: On the morphology of cells of posterior cornea in the iridocorneal endothelial syndrome. Cornea 1991;10:233–243.

23.Snell AC, Irwin ES: Hereditary deep dystrophy of the cornea. Am J Ophthalmol 1958;45:636–674.

24.Grayson M: The nature of hereditary deep polymorphous dystrophy of the cornea: its association with iris and anterior chamber dysgenesis. Trans Am Ophthalmol Soc 1974;72:516–520.

25.Cibis GW, Tripathi RC: The differential diagnosis of Descemet’s tears and posterior polymorphous dystrophy bands. Ophthalmology 1982;89:614–617.

26.Laganowski HC, Sherrard ES, Kerr-Muir MG, et al: Distinguishing features of the iridocorneal endothelial syndrome and posterior polymorphous dystrophy: value of endothelial specular microscopy. Br J Ophthalmol 1991;75:212–216.

27.Hirst LW, Quigley HA, Stark WJ, et al: Specular microscopy of iridocorneal endothelial syndrome. Am J Ophthalmol 1980;89:11–21.

28.Rodrigues MM, Phelps CD, Krachmer JH, et al: Glaucoma due to endothelialization of the anterior chamber angle: a comparison of posterior polymorphous dystrophy of the cornea and Chandler’s syndrome. Arch Ophthalmol 1980;98:688–696.

29.Patel A, Kenyon KR, Hirst LW, et al: Chandler’s syndrome. Surv Ophthalmol 1983;27:327–344.

30.Laganowski HC, Kerr-Muir MG, Hitchings RA: Glaucoma and the iridocorneal endothelial syndrome. Arch Ophthalmol 1992;110:346–350.

31.Eagle RC, Font RL, Yanoff M, et al: The iridocorneal endothelial syndrome. Arch Ophthalmol 1979;97:2104–2110.

32.Pitts JF, Jay JL: The association of Fuchs’ corneal endothelial dystrophy with axial hypermetropia, shallow anterior chamber, and angle closure glaucoma. Br J Ophthalmol 1990;74:601–607.

33.Krachmer JH, Purcell JJ, Young CW, Buchner KD: Corneal endothelial dystrophy. A study of 64 families. Arch Ophthalmol 1978:96:2036–2044.

34.Maumenee AE: Congenital Hereditary corneal dystrophy. Am J Ophthalmol 1960;50:1114–1127.

35.Levenson JE, Chandler JW, Kaufman HE: Affected asymptomatic relatives in congenital hereditary endothelial dystrophy. AM J Ophthalmol 1973;76:967–974.

36.Sugar HS: Oculodentodigital dysplasia syndrome with angle closure glaucoma. Am J Ophthalmol 1978;86:36–39.

37.Luca-Glass TC, Baratz KH, Nelson LR, Hodge DO: Morphometric characteristics of the contralateral corneal endothelium in iridocorneal endothelial (ICE) syndrome. Invest Ophthalmol Vis Sci 1995;36(4):s600.

38.Kidd M, Hetherington J, Magee S: Surgical results in iridocorneal endothelial syndrome. Arch Ophthalmol 1988;106:199–205.

39.Wright MM, Grajewski AL, Cristol SM, et al: 5-FU after trabeculectomy and the iridocorneal endothelial syndrome. Ophthalmology 1991;98:314–319.

40.Lucas-Glass TC, Baratz KH, Nelson LR, et al: The contralateral corneal endothelium in the iridocorneal endothelial syndrome. Arch Ophthalmol 1997;115:40–47.

41.Alvarado JA, Underwood JL, Green WR, et al: Detection of herpes simplex viral DNA in the iridocorneal endothelial syndrome. Arch Ophthalmol 1994;112:1601–1607.

42.Shields MB, McCraken JS, Klintworth GK, et al: Corneal edema in essential iris atrophy. Ophthalmology 1979;86:1533–1541.

43.Buxton JN, Lash RS: Results of penetrating keratoplasty in the iridocorneal endothelial syndrome. Am J Ophthalmol 1984;98:297–301.

44.Crawford GJ, Stulting RD, Cavanagh HD, et al: Penetrating keratoplasty in the management of iridocorneal endothelial syndrome. Cornea 1989;8:34–38.

45.Gaasterland DE, Rodrigues MM, Moshell AN: Ocular involvement in xeroderma pigmentosa. Ophthalmology 1982;89:980–987.

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8

Glaucoma Associated

with Inflammation

George Shafranov and Joern B. Soltau

Definition

How Is Glaucoma Associated with Inflammation Defined?

Inflammatory ocular conditions like keratitis, episcleritis, scleritis, and uveitis may cause elevated intraocular pressure (IOP) by compromising the outflow of aqueous humor. Whether or not increased secretion of aqueous plays any role is still controversial.1,2 The anterior chamber angle may be open or occluded. The IOP may be elevated acutely and/or chronically. This chapter discusses each inflammatory condition separately.

GLAUCOMA ASSOCIATED WITH KERATITIS

Definition

How Is Glaucoma Associated with Keratitis Defined?

IOP elevation may be encountered in any active corneal inflammatory condition.3 If the elevated IOP is causing optic nerve damage and visual field loss, then the diagnosis of glaucoma secondary to corneal inflammation can be made. This implies that the elevated IOP does not necessarily lead to optic nerve damage, that is, glaucoma. This further implies that elevated IOP associated with corneal inflammation does not always need to be lowered with antiglaucoma agents. After treatment and resolution of the underlying inflammatory condition, the IOP may return to the normal level without having caused any damage to the optic nerve.

148 Glaucoma Associated with Inflammation

What Is the Cause of the Elevated IOP in Keratitis?

Anterior uveitis often accompanies keratitis. Inflammatory cells may occlude the trabecular meshwork and thus decrease aqueous outflow. Posterior synechiae may develop as a result of inflammation and cause pupillary block. Peripheral anterior synechiae may cause IOP elevation, not only acutely but also chronically, even after the inflammation subsides.3

After chemical burns, the IOP may rise rapidly initially secondary to shrinkage of the outer coats of the eye, followed by a second slow phase of IOP elevation probably mediated by an intraocular release of prostaglandins.4,5 IOP elevation usually occurs if the keratitis involves the corneal stroma, such as infectious keratitis secondary to herpes simplex,6 bacterial and fungal keratitis, and an immune response to Treponema pallidum.6–10 A shallow anterior chamber may develop in keratomycotic malignant glaucoma.11 Fungi can also penetrate the cornea and directly invade the trabecular meshwork.12

Direct involvement of the trabecular meshwork by the underlying inflammatory disease process is the main cause of elevation of the IOP.8,13 Increased corneal thickness secondary to corneal edema may lead to closure of the anterior chamber angle. Formation of anterior synechiae with secondary angle closure may also be encountered. Mechanisms of IOP elevation can also include secondary iridoschisis,14 keratouveitis,6 and open-angle glaucoma superimposed on old inflammatory changes, involving endothelialization and glassy membrane in the angle, which are refractory to medical treatment. This condition usually requires filtering surgery.8 Reversible angle-closure glaucoma associated with anatomically small anterior segments responds well to iridectomy.8,10 Sundmacher and Neumann-Haefelin15 found that secondary glaucoma was present in all herpes simplex keratitis patients with corneal endothelial disease and/or anterior uveitis who had herpes simplex virus isolated from the aqueous. Similarly, adenovirus type 10 has been associated with keratoconjunctivitis, pharyngitis, and transient increase in IOP.16

Epidemiology and Importance

How Often Is Keratitis Associated with Increased IOP?

Keratitis by itself is not commonly associated with elevated IOP. However, when herpes simplex keratitis was associated with uveitis, almost a third of the patients developed IOP elevation and 10% had glaucomatous damage.6

About 40% of patients with herpes zoster ophthalmicus can have uveitis, and more than 10% of those patients may have associated glaucoma.17 Another study showed that every third patient (five out of 14) with herpes zoster keratouveitis had IOP elevation.18 Combination of keratitis and IOP elevation may be seen in patients with acute primary angle-closure glaucoma. These patients may develop secondary keratouveitis and keratic precipitates.19 Possible mechanism of the inflammation is likely profound endothelial damage from elevated IOP. Hypopyon is also likely to be present in these eyes,19–21 secondary to ischemic iris necrosis.

Diagnosis and Differential Diagnosis

How Is Glaucoma Associated with Keratitis Diagnosed?

An accurate history is important to find the etiology and to differentiate between an acute and a chronic condition. Slit-lamp examination facilitates evaluation of possible corneal infiltration and anterior chamber reaction. Subsequent use of fluorescein helps in evaluating the corneal surface. Gonioscopy should be performed, if possible.

What Is the Differential Diagnosis of Glaucoma

Associated with Keratitis?

In a patient presenting with keratitis and IOP elevation, the following conditions should be differentiated: corneal abrasion,22 recurrent erosion syndrome,23 herpes simplex keratitis, herpes zoster keratitis, and angle-closure glaucoma causing corneal edema. Leprosy may need to be excluded when a patient presents with glaucoma, keratitis, and bilateral uveitis.24

Treatment and Management

How Is Glaucoma Associated with Keratitis Managed?

Treatment of keratitis associated with increased IOP is directed against the underlying etiology and includes administration of aqueous suppressants. One of the suggested therapeutic regimens for herpes simplex keratitis associated with glaucoma consists of antivirals, steroids, cycloplegics, and aqueous suppressants.15 The treatment can be difficult, especially if angle closure with synechiae is present. In these cases, filtering surgery8 or implantation of a drainage device might be necessary.

Future Considerations

In stromal keratitis induced by herpes simplex virus (HSV), the immune response contributes to corneal scarring and neovascularization. To analyze the efficacy of topically applied cyclosporin A (CsA) in patients with HSV keratitis, Heiligenhaus and Steuhl25 performed a prospective study in 18 patients with HSV stromal keratitis. The authors treated eyes with CsA eyedrops and acyclovir ointment. Keratitis resolved with CsA treatment in 10 of 14 patients with nonnecrotizing keratitis and in two of four with necrotizing keratitis. One-third of the patients treated with CsA developed persistent or progressive inflammation and required combined CsA and corticosteroids. The only complication from the use of CsA was toxic epitheliopathy. HSV stromal keratitis can be treated successfully with CsA eyedrops, especially in nonnecrotizing keratitis. In patients with steroid-induced glaucoma, herpetic corneal ulcers may be