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

References

1.Wand M: Neovascular glaucoma. In: Ritch RSM, Krupin T (eds): The Glaucomas, Vol 2. St. Louis: CV Mosby, 1996;1063–1110.

2.Madsen PH: Haemorrhagic glaucoma. Comparative study in diabetic and nondiabetic patients. Br J Ophthalmol 1971;55:444–450.

3.Brown GC, Magargal LE, Schachat A, et al: Neovascular glaucoma. Etiologic considerations. Ophthalmology 1984;91:315–320.

4.Tolentino MJ, Miller JW, Gragoudas ES, et al: Vascular endothelial growth factor is sufficient to produce iris neovascularization and neovascular glaucoma in a nonhuman primate. Arch Ophthalmol 1996;114:964–970.

5.Weinreb RN, Wasserstrom JP, Parker W: Neovascular glaucoma following neodymium-YAG laser posterior capsulotomy. Arch Ophthalmol 1986;104:730–731.

6.Wand M, Dueker DK, Aiello LM, et al: Effects of panretinal photocoagulation on rubeosis iridis, angle neovascularization, and neovascular glaucoma. Am J Ophthalmol 1978;86: 332–339.

7.Browning DJ, Scott AQ, Peterson CB, et al: The risk of missing angle neovascularization by omitting screening gonioscopy in acute central retinal vein occlusion. Ophthalmology 1998;105:776–784.

8.Cashwell LF, Marks WP: Panretinal photocoagulation in the management of neovascular glaucoma. South Med J 1988;81:1364–1368.

9.Tasman W, Magargal LE, Augsburger JJ: Effects of argon laser photocoagulation on rubeosis iridis and angle neovascularization. Ophthalmology 1980;87:400–402.

10.Simmons RJ, Dueker DK, Kimbrough RL, et al: Goniophotocoagulation for neovascular glaucoma. Trans Am Acad Ophthalmol Otolarygol 1977;83:80–89.

11.The Diabetic Retinopathy Study Research Group: Photocoagulation treatment of proliferative diabetic retinopathy. Clinical application of Diabetic Retinopathy Study (DRS) findings, DRS report number 8. Ophthalmology 1981;88:583–600.

12.Benson WE, Brown GC, Tasman W, et al: Complications of vitrectomy for nonclearing vitreous hemorrhage in diabetic patients. Ophthalmic Surg 1988;19:862–864.

13.The Central Vein Occlusion Study Group: A randomized clinical trial of early panretinal photocoagulation for ischemic central vein occlusion, report N (see comments). Ophthalmology 1995;102:1434–1444.

14.Hayreh SS, Klugman MR, Beri M, et al: Differentiation of ischemic from non-ischemic central retinal vein occlusion during the early acute phase. Graefes Arch Clin Exp Ophthalmol 1990;228:201–217.

15.Coppeto JR, Wand M, Bear L, et al: Neovascular glaucoma and carotid artery obstructive disease. Am J Ophthalmol 1985;99:567–570.

16.Allen RC, Bellows AR, Hutchinson BT, et al: Filtration surgery in the treatment of neovascular glaucoma. Ophthalmology 1982;89:1181–1187.

17.Tsai JC, Feuer WJ, Parrish RK, et al: 5-Fluorouracil filtering surgery and neovascular glaucoma: long term follow-up of the original pilot study. Ophthalmology 1995;102:887–893.

18.Mermoud A, Salmon JF, Alexander P, et al: Molteno tube implantation for neovascular glaucoma. Long-term results and factors influencing the outcome. Ophthalmology 1993;100: 897–902.

19.Sidoti PA, Dunphy TR, Baerveldt G, et al: Experience with the Baerveldt glaucoma implant in treating neovascular glaucoma. Ophthalmology 1995;102:1107–1108.

20.Eid TE, Katz LJ, Spaeth GL, et al: Tube-shunt surgery versus neodymium:YAG cyclophotocoagulation in the management of neovascular glaucoma. Ophthalmology 1997;104:1692–1700.

21.Tsai JC, Bloom PA, Franks WA, et al: Combined transscleral diode laser cyclophotocoagulation and transscleral retinal photocoagulation for refractory neovascular glaucoma. Retina 1996;16:164–166.

22.Threlkeld AB, Johnson MH: Contact transscleral diode cyclophotocoagulation for refractory glaucoma. J Glaucoma 1999;8:3–7.

23.Chen KH, Wu CC, Roy S, et al: Increased interkeukin-6 in aqueous humor of neovascular glaucoma. Invest Ophthalmol Vis Sci 1999;40:2627–2632.

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334 Drug-Induced Glaucoma

However, it can also be observed with an alternative form of administration of the medication to the eye, such as in the case of periocular injection to the eye. In addition, systemic administration of steroids has also been well documented to produce glaucoma in the susceptible patient. Glaucoma is also observed in Cushing’s syndrome with the production of excess endogenous steroids.

The issue of corticosteroid-induced glaucoma was first raised in the 1950s with the observation of glaucoma in association with both the systemic administration of adrenocorticotropic hormone (ACTH)1 and cortisone,2 as well as with topical administration of cortisone.3,4

Subsequently, both Becker and Chevrette5 and Armaly6 reported an association between patients with open-angle glaucoma and topical corticosteroids. An attempt was made by these authors to seek a genetic linkage between corticosteroid sensitivity and glaucoma. Subsequent authors have not shown this linkage to occur.7–10

Epidemiology and Importance

What Is the Epidemiology of Corticosteroid-Induced Glaucoma, and Which Patient Is At Risk?

Armaly11 and Becker12 have shown that within the general population 5 to 6% of healthy subjects will develop marked elevation of intraocular pressure (IOP) 4 to 6 weeks after chronic administration of topical dexamethasone or betamethasone eye drops. These studies have also shown that these numbers are directly related to the frequency of administration and duration of usage of this medication, with increasing usage related to increased risk of elevated IOP.

At higher risk are patients with primary open-angle glaucoma,13,14 their first-degree relatives,8,15,16 diabetic patients,17 highly myopic individuals,18 and patients with connective tissue disease,19 specifically rheumatoid arthritis (Table 15–1).

In addition, patients with angle recession glaucoma are more susceptible to corticosteroid-induced glaucoma.20

When Is the Risk Greatest?

Traditional thinking has been that there is a grace period of 4 to 6 weeks before an elevated IOP may be observed. This time period is dependent on the individual susceptibility of the eye at risk and may vary from 2 weeks to months to

Table 15–1. Risk Factors for Corticosteroid-Induced Glaucoma

Primary open-angle glaucoma13,14

First-degree relative of patient with primary open-angle glaucoma8,15,16 Diabetes mellitus17

High myopia18

Connective tissue disorder19 (sp. rheumatoid arthritis) Angle recession glaucoma20

Cushing’s syndrome34,35

years after the corticosteroid preparation has begun, requiring the clinician to be on constant guard and checking the patient on a regular basis.

In the patient with a history of steroid-induced glaucoma, this elevation of IOP may occur within 2 weeks of initialization of a corticosteroid preparation to the eye, whereas in an otherwise normal eye it may not occur until years later.

What Is the Risk with Differing

Corticosteroid Preparations?

Although it has been shown that any corticosteroid preparation can produce an elevated IOP, the greatest risk is observed with the most potent steroidal preparations (Table 15–2). Fluoromethalone (FML) and medrysone are less potent topical corticosteroids, but they have also been shown to produce an elevated IOP.22, 27 However, it must be noted that the risk of producing an elevated IOP with these medications is much less than with the former medications listed above.

Newer corticosteroid preparations include rimexolone (Vexol) and loteprednol etabonate (Lotemax, Alrex). The risk of producing an elevated IOP with these agents23,26 is comparable to FML.27

What Is the Route of Corticosteroid Administration?

The picture of corticosteroid-induced glaucoma is most commonly observed with topically administered corticosteroids in the form of eye drops or ointments. This condition can also be observed when corticosteroids are given periocularly in either subconjunctival,28 subtenon29 or retrobulbar injection, 30 especially in a depot preparation24 (Table 15–2).

An elevated IOP and glaucoma can also be observed to occur, though less commonly, when corticosteroid preparations are give systemically,2,25 when skin preparations in the form of lotions and creams are placed near the eye31 or applied to sites remote from the eye,32 and with inhaled steroids, such as those used in the treatment of asthma.21 It should also be noted that there appears to be an additive effect to corticosteroid usage when used both topically and systemically.33

Table 15–2. Available Steroid Preparations

336 Drug-Induced Glaucoma

Finally, in the patient producing endogenous corticosteroids, such as in the patient with adrenal hyperplasia34or Cushing’s disease,35 an elevated IOP may also be observed.

What Is the Mechanism

of Action for Corticosteroid-Induced Glaucoma?

To most authors, the mechanism of action for the increased IOP observed in these patients is felt to be due to an increased resistance to aqueous humor outflow36,37 through the trabecular meshwork rather than an increased production of aqueous humor.

Within the trabecular meshwork, an accumulation of polymerized glycos- aminoglycans38–40 can be observed in these eyes. Several authors have felt that this finding represents the stabilization of lysosomal membranes by corticosteroids.41,42 In addition, increased collagen,43 elastin,44 and fibronectin45 have been observed within the extracellular matrix in these eyes. A sialoglycoprotein has also been observed in these eyes.46

Other authors have felt that the presence of corticosteroids may produce a reorganization of the cytoskeleton within the trabecular meshwork cells, resulting in the above-mentioned changes observed in these cells.47,48

Whatever may eventually be shown to be the cause of this observed IOP rise in these eyes, it appears to reflect a change in the basic functioning of the trabecular meshwork cells49,50 which alters the resistance to outflow of aqueous humor through these cells. This change in the basic physiologic appearance and functioning of the trabecular meshwork cells is reflected in the initial clinical appearance of the patient. Indeed, the patient usually presents with white and quiet eyes with no evidence of pain or discomfort.

Diagnosis and Differential Diagnosis

What Is the Differential Diagnosis

of Corticosteroid-Induced Glaucoma?

The differential diagnosis includes open-angle glaucoma and ocular hypertension. In those patients with a prior history of steroid usage, the differential diagnosis should include normal pressure glaucoma. In those patients with occludable angles, the differential diagnosis should include chronic angleclosure glaucoma. Finally, in the pediatric patient the differential diagnosis should include congenital glaucoma (Table 15–3).

Table 15–3. Differential Diagnosis of Corticosteroid-Induced Glaucoma

Open-angle glaucoma

Ocular hypertension

Normal pressure glaucoma

Chronic angle-closure glaucoma

Congenital glaucoma

What Are the Symptoms

of Corticosteroid-Induced Glaucoma?

Occasionally, the patient may complain of intermittent blurring of vision if the IOP has risen to the point of compromising corneal function or if sufficient damage has occurred to the ocular nerve from the elevated IOP.

In addition, the patient may also complain of blurred vision from cataracts, which classically are posterior subcapsular.51 Additional findings at the time of initial presentation may include ptosis,37 mydriasis,37 atrophy of the eyelid skin,31 ocular infections,31 delayed wound healing, corneal ulcers, and conjunctival necrosis,52,53 the latter occurring following subconjunctival corticosteroid administration.

How Is the Diagnosis of Corticosteroid-Induced

Glaucoma Made by the Clinician?

The diagnosis can be made only by questioning the patient. A careful history should include any medications prescribed by the primary care physician, especially corticosteroid eye drop preparations for the treatment of red eye. Most striking is that patients may not volunteer that they are taking corticosteroids in any form.

How Is the Diagnosis of Nonsteroidal

Drug-Induced Glaucoma Made by the Clinician?

It behooves the clinician to have a healthy dose of suspicion and to carefully seek from the patient a complete list of all medications being taken, including both prescription and nonprescription agents.

Treatment and Management

How Is Corticosteroid-Induced Glaucoma Treated?

Once the diagnosis has been made, the most obvious solution is to have the patient stop using the offending corticosteroid. Although it may be possible to do this in many cases, the clinician may be forced to either substitute an alternative corticosteroid54 or to prescribe an alternative agent, such as a nonsteroid antiinflammatory drug (NSAID)55 (Fig. 15–2).

Where the offending corticosteroid can be stopped,24 this step may be enough to alleviate the problem. Unfortunately, in some cases, it is not enough, and the elevated IOP may not be relieved by the patient’s stopping the use of the corticosteroid.40 In addition, in those eyes where the corticosteroid cannot be stopped, additional treatment will be required.

If the IOP is still elevated, medical therapy may be required to lower it. In such instances, the first line of therapy appears to be the use of topical betablockers, where there is no contraindication such as pulmonary or cardiac problems or a history of allergy to beta-blockers.

338 Drug-Induced Glaucoma

Figure 15–2. Algorithm for management of corticosteroid-induced glaucoma.

Other agents, such as carbonic anhydrase inhibitors and -alpha agonists, may also be helpful in these eyes. Although miotic agents, epinephrine products, and prostaglandins are helpful in the treatment of elevated IOP, they should be used with caution in these patients, especially if there is an underlying history of ocular inflammation, which may have been the underlying reason for initially using corticosteroid agents. Also, there will be patients who are unresponsive to medical therapy. In these patients, argon laser trabeculoplasty (ALT) may be helpful, if not, filtration surgery may be required to alleviate the elevated IOP (Fig. 15–2). Although these measures may be required to save these eyes, it should also be kept in mind that many of these treatment options can be avoided by careful observation of these patients once they have been started on any corticosteroid regimen.

What Nonsteroidal Agents Are Associated with Glaucoma?

Unlike corticosteroid agents, the list of nonsteroidal agents associated with glaucoma is wide and diverse (Table 15–4). The causes of glaucoma associated with these agents are also just as varied (Fig. 15–3).

The largest single cause of glaucoma in these patients appears to be an atropine-like effect, eliciting pupillary dilatation. This class of agents includes antipsychotropics, antidepressants, the monoamine oxidase (MAO) inhibitors, antihistamines, antiparkinsonian agents, antispasmolytic agents, mydriatic agents, the sympathetic agents, and botulinum toxin.

The pupillary dilatation seen in these cases may be enough to precipitate an attack of angle-closure glaucoma in the patient with narrow angles and to raise

Table 15–4. Nonsteroidal Agents

Antipsychotropic agents

Phenothiazines

Perphenazine (Trilafon), fluphenazine decanoate (Prolixin)

Antidepressants

Tricyclic agents

Amitryptiline (Elavil), imipramine (Tofranil)

Nontricyclic agents

Fluoxetine (Prozac), mianserin HCl (Bolvidin)

Monoamine oxidase (MAO) inhibitors

Phenylzine sulfate (Nardil)

Tranylcypromine sulfate (Parnate)

Antihistamines

Ethanolamines

Orphenadrine citrate (Norgesic)

Antiparkinsonian agents

Trihexyphenidyl HCl (Artane)

Antispasmolytic agents

Propantheline bromide (Pro-Banthine)

Dicyclomine HCl (Bentyl)

Antibiotics

Sulfa, quinine

Sympathomimetic agents

Epinephrine, ephedrine

Phenylephrine

Amphetamine

Hydroxyamphetamine

Mydriatic agents

All agents

Surgical agents

Viscoelastic agents, silicone oil

Botulin toxin

Cardiac agents

Disopyramide phosphate (Norpace)