Corticosteroid-induced ocular hypertension and glaucoma: a briefreview and update of the literatureRelief Jones III and Douglas J. Rhee

Purpose of review

The purpose of this article is to briefly review the literature

of corticosteroid-induced ocular hypertension and

glaucoma, its risk factors, the pathophysiology, and

treatment options. In particular, literature pertaining to

glaucoma in response to intravitreal triamcinolone

acetonide will be reviewed.

Recent findings

Primary open-angle glaucoma, status as a glaucoma

suspect, and a family history of glaucoma are risk factors

for an ocular hypertensive response with the use of

corticosteroid therapy. Recent studies suggest that

younger age may also be a risk factor in patients treated

via the intravitreal route with corticosteroids. The

mechanism of elevated intraocular pressure is increased

aqueous outflow resistance owing to an accumulation of

extracellular matrix material in the trabecular meshwork.

Summary

Corticosteroid-induced ocular hypertension and glaucoma

has been recognized for more than 50 years. Knowing the

risk factors, prevalence, and pathophysiology can help the

clinician prevent, monitor, and treat corticosteroid-induced

ocular hypertension and glaucoma.

Keywords

intravitreal triamcinolone, ocular hypertension, review,

steroid-induced glaucoma

Curr Opin Ophthalmol 17:163–167. # 2006 Lippincott Williams & Wilkins.

Harvard Medical School, Department of Ophthalmology, Massachusetts Eye andEar Infirmary, Glaucoma Service, Boston, Massachusetts, USA

Correspondence to: Douglas J. Rhee MD, Assistant Professor of Ophthalmology,Harvard Medical School, Department of Ophthalmology, Massachusetts Eye andEar Infirmary, Glaucoma Service, 243 Charles Street, Boston, MA 02114, USATel.: +617573 3670, Fax: +617573 3707; e-mail: dougrhee@aol.com

Current Opinion in Ophthalmology 2006, 17:163–167

Abbreviations

ECM extracellular matrixIOP intraocular pressureIVTA intravitreal triamcinolone acetonidePOAG primary open-angle glaucoma

# 2006 Lippincott Williams & Wilkins1040-8738

Introduction

Increased intraocular pressure (IOP) can occur as a con-

sequence of oral, intravenous, inhaled, topical, periocu-

lar, or intravitreal corticosteroid therapy [1–6,7•,8••,

9–11]. If the ocular hypertension is of a significant mag-

nitude, not recognized, and not treated, subsequent

glaucomatous optic neuropathy can develop (that is,

steroid-induced glaucoma). Steroid-induced ocular

hypertension was first reported in 1950 when McLean

[12] reported an increase in IOP associated with the sys-

temic administration of adrenocorticotrophic hormone

(ACTH). The first report of increased IOP caused by

the local administration of cortisone occurred four years

later [13]. Since those initial reports, corticosteroid-

induced glaucoma has been studied intensively. A num-

ber of predisposing risk factors have been identified

[14–23,24••]. The intraocular potency and mode of

administration have been shown to be important in initi-

ating an ocular hypertensive response [1–6,7•,8••,9,25].

Recently, the popular use of intravitreal triamcinolone

acetonide (IVTA) for subretinal fluid, macular edema,

and adjunctive therapy in the treatment of choroidal

neovascularization has led to an increased incidence of

corticosteroid-induced ocular hypertension from IVTA

[7•,8••,9,26–28,29•]. The molecular biological factors

contributing to increased IOP are beginning to be better

understood and these findings may lead to additional

management options in the future [30–41]. We will

review selected studies with an emphasis on glaucoma

elevations associated with IVTA.

Predisposing risk factorsfor corticosteroid-induced glaucoma

When treated with topical steroids for 4–6 weeks, 5% of

the population demonstrates a rise in IOP greater

than 16 mmHg and 30% have a rise of 6–15 mmHg

[10,11]. Several variables have been identified as predis-

posing risk factors for steroid-induced ocular hyperten-

sion. Patients with predisposing risk factors should be

followed more diligently when receiving corticosteroids.

Primary open-angle glaucoma (POAG) patients and

glaucoma suspects were shown to be at an increased

risk for elevated IOP after treatment with corticoster-

oids. Studies by Armaly [14,15] revealed that approxi-

mately one-third of glaucoma suspects and more than

90% of POAG patients responded with an IOP elevation

greater than 6 mmHg after receiving a 4-week course of

163

topical dexamethasone 0.1%. The effect was noted to be

more prominent in the eyes of older adult patients com-

pared with the eyes of younger adult patients. A study

by Becker and Mills [16] also indicated that patients

with pre-existing glaucoma and glaucoma suspects

demonstrated large, highly significant increases in IOP

in 2–4 weeks with the use of topical betamethasone

0.1% and exhibited decreased outflow facility during

the treatment period. The IOP returned to baseline or

normal in approximately 1 week with discontinuation of

steroid treatment. Moreover, other studies showed that

simply having a first-degree relative with POAG could

make one susceptible to being a steroid-responder [18,

19].

Although older patients are at increased risk, the fre-

quency of steroid responsiveness with age may occur

in a bimodal distribution. Children as a group have

been shown to be greater steroid-responders as com-

pared with adults. A recent study by Lam et al. [24••]showed that 71.2 and 59.2% of children receiving topical

dexamethasone 0.1% (four times per day and two times

per day, respectively) responded with an IOP rise

greater than 21 mmHg. Additionally, 36.4 and 21.1% of

those same two groups had an IOP rise greater than 30

mmHg. Among children under 6 years old who received

dexamethasone 0.1% four times per day, the peak IOP

was greater, the net increase in IOP was greater, and the

time required to obtain the peak IOP was less. Children

greater than 6 years old (children up to age 10 were

included in the study) had a similar net increase in

IOP, but did not show a significant difference in peak

IOP or the time required to reach the peak IOP.

Gatson et al. [20] showed that patients with connective-

tissue disease tend to be steroid-responders. Men with

connective-tissue disease tended to be greater respon-

ders, although gender is not typically considered a risk

factor in people without connective-tissue disease. Addi-

tionally, patients with type-1 diabetes mellitus [20] and

high myopia [22] have also been shown to be at

increased risk to be steroid-responders.

In summary, pre-existing POAG, status as a glaucoma

suspect, or a first-degree relative with POAG are impor-

tant risk factors for corticosteroid-induced ocular hyper-

tension and glaucoma. Age may be a risk factor;

increased risk appears to occur in a bimodal distribution

peaking first at age 6. As one progresses through adult-

hood age may not be a factor until late adulthood when

the risk again rises. Finally, those with connective-tissue

disease, type-1 diabetes mellitus, and high myopia

should all be considered high risk, and prudent follow-

up should be pursued during periods of corticosteroid

use.

Types of preparations and modesof administration

Corticosteroids have been shown to exert an ocular

hypertensive response relative to the intraocular potency

of the steroid [25]. Aside from the relative ability to in-

hibit inflammation, the other main determinant of

intraocular potency is chemical structure. Acetates are

more lipophilic and penetrate through the cornea better

than phosphates, which are relatively hydrophilic.

Medrysone 1.0% caused a 1.0 mmHg rise in IOP,

while more potent steroids such as prednisolone acetate

1.0% and dexamethasone acetate 0.1% caused a 10 and

22 mmHg rise in IOP, respectively.

Corticosteroids have been shown to cause a elevation in

IOP through all modes of administration [1–6,7•,8••,9].

The rise of IOP usually occurs over a period of weeks if

used topically [15,16,25] and years if used systemically

[1]. There have been some reports of an elevation of

IOP within hours of initiating intensive topical steroid

use [42].

The mode of therapy becomes important when consid-

ering corticosteroid use in individuals with pre-existing

risk factors for an ocular hypertensive response. Some

modes of therapy can be discontinued easily, thereby

reducing or reversing any untoward effects on IOP.

Other modes of therapy, however, such as subtenon’s,

periocular, or intravitreal injections, are not as easily

reversed if problems are encountered.

Corticosteroid-induced ocular hypertensionassociated with triamcinolone acetonide

IVTA has become a useful therapy for many conditions

including uveitis, veno-occlusive disease, diabetes, and

choroidal neovascularization. When given intravenously,

triamcinolone acetonide is 35 times more potent as an

anti-inflammatory agent than cortisol. As the list of indi-

cations and use of IVTA increases, the incidence of cor-

ticosteroid-induced glaucoma associated with IVTA will

be more common and more likely to be encountered by

ophthalmologists. In a recent meta-analysis, Jonas found

that intravitreal dosages of approximately 20 mg (the

dose more commonly used in Europe) are associated

with a 41% prevalence of an IOP elevation greater

than 21 mmHg [29•]. All but one patient was managed

with topical glaucoma medications and medications

were no longer needed about 6 months after the injec-

tion. The one patient that required surgery underwent

trabeculectomy 9 months after injection and fluid aspira-

tions obtained during surgery contained soluble triamci-

nolone [43]. It was concluded that IVTA may last 9

months or longer and this fact should be considered

prior to repeating the injection.

164 Glaucoma

Another study, by Smithen and colleagues [7•], of 89

patients with a mean baseline IOP of 14.9 mmHg ana-

lyzed the prevalence of IOP elevation following IVTA

injection. All patients had received a 4 mg (the dosage

more commonly used in the United States) of IVTA and

were followed for 6 months. The mean pressure increase

was 8.0 mmHg and 40.4% experienced a pressure eleva-

tion of 24 mmHg or higher; the pressure elevation

occurred at a mean of 100.6 days. Patients were also

stratified into the categories of ‘no history of glaucoma’

and ‘glaucoma patient’. The patients in these two cate-

gories were subsequently divided into two additional

categories based on their baseline IOP. Patients without

a history of glaucoma and a baseline IOP of at least 15

mmHg had a 60% chance of developing a pressure of at

least 24 mmHg, whereas those with a baseline IOP less

than 15 mmHg had a 22.7% chance of developing an

IOP of at least 24 mmHg. Patients with a history of glau-

coma had a 50% chance of developing an IOP of at

least 24 mmHg. Of these patients, 50% had a baseline

IOP of at least 15 mmHg. In this series, patients who

received multiple IVTA injections did not experience

an increased incidence of elevated IOP, and there was

no correlation between IOP elevation and the disease

process being treated by the injection. All patients who

experienced an IOP elevation had their pressure con-

trolled with a mean of one glaucoma medication. Indivi-

duals who were already taking one glaucoma medication

required an average of one additional medication. No

patients in this study required surgical intervention to

control their elevated IOP.

Singh and colleagues [8••] reported a case series of early

and rapid increases in IOP following an IVTA injection

in three individuals. In all three cases, a significant rise

in IOP occurred within 1 week of IVTA for macular

edema. All of the individuals required subsequent surgi-

cal intervention to control the elevated IOP. A peculiar

finding was the presence of a white material in the angle

of one individual on gonioscopy, probably from the

injection. A common finding was that all three of these

patients were pseudophakic, which may have allowed

the medication to move into the anterior segment caus-

ing physical obstruction of the trabecular meshwork. To

prevent these complications, Vedantham [44] suggested

that pseudophakic patients and those with prior vitrec-

tomies be followed with greater scrutiny. In addition, he

suggested that filtering the triamcinolone and instruct-

ing patients to sleep on their backs might prevent this

complication.

Most patients with elevated IOP after IVTA are suc-

cessfully managed with topical glaucoma medications.

Traditional glaucoma surgical techniques can success-

fully control elevated IOP and are generally required

in less than 2% of cases. Filtration surgery is not the

only option. One group reported vitrectomy with

removal of the intraocular triamcinolone acetonide

from the vitreous cavity to treat the elevated IOP [45].

This procedure alone was capable of controlling the ocu-

lar hypertension and could also be considered as an

alternative if traditional glaucoma treatments are not

an option or fail to control the IOP.

IVTA appears to be increasingly popular to treat those

with visual loss from macular edema; thus the preva-

lence of its associated corticosteroid-induced ocular

hypertension will continue to rise. Clinicians should be

aware that an elevated IOP may occur in nearly half of

all cases following a single injection of IVTA. After an

injection, they should be followed with greater scrutiny.

Postinjection examinations should occur 1 day later and

approximately 1 week later for high-risk patients. Reg-

ular follow-up examinations should continue for greater

than 6 months. Weinreb et al. [42] showed that, rarely,

some patients with a prior history of glaucoma could

develop elevated IOP in a matter of hours following

topical administration. Examinations should include

monitoring of the IOP and gonioscopy for pseudophakes

and patients with prior vitrectomies to detect mechani-

cal obstruction of the trabecular meshwork by the med-

ication. If the IOP cannot be managed with the addition

of glaucoma medications, subspecialty care from a glau-

coma specialist should be sought as some patients may

go on to require surgical intervention.

The pathophysiology of corticosteroid-inducedocular hypertension and glaucoma

The mechanism of corticosteroid-induced ocular hyper-

tension is increased aqueous outflow resistance. There

are a number of observations that can be simplified into

three broad categories: corticosteroids can induce physi-

cal and mechanical changes in the microstructure of the

trabecular meshwork; cause an increase in the deposi-

tion of substances in the trabecular meshwork, thereby

causing decreased outflow facility; and inhibit proteases

and trabecular meshwork endothelial cell phagocytosis

causing a decrease in the breakdown of substances in

the trabecular meshwork.

Changes in the microstructure of the trabecular mesh-

work may cause a decrease in outflow facility and an

increase in IOP. Clark and colleagues [30] showed that

the actin stress fibers were reorganized into actin net-

works that resembled geodesic-dome-like polygonal lat-

tices in human trabecular meshwork cells cultured in the

presence of dexamethasone. Upon discontinuing dexa-

methasone, cross-linking of the actin networks was

reversible. The effect was thought to be mediated via

trabecular meshwork glucocorticoid receptors. In perfu-

Ocular hypertension and glaucoma Jones and Rhee 165

sion-cultured human eyes, Clark and colleagues [31]

found that steroid treatment had similar microstructural

changes and was associated with an increased outflow

resistance. The accumulated extracellular matrix

(ECM) has the potential to affect both the paracellular

(that is, the flow in-between trabecular meshwork

endothelial cells) and transcellular (that is, the flow

through pores created within a single and or between

two inner wall Schlemm’s canal cells) levels.

Corticosteroids also increase the deposition of ECM in

the trabecular meshwork leading to decreased outflow

facility. A study by Wilson et al. [32] found an increased

deposition of ECM material altering the ultrastructure

of the juxtacanalicular region. The corticosteroid dexa-

methasone increases glycosaminoglycan, elastin, and

fibronectin production in cultured trabecular meshwork;

the glycosaminoglycan deposition increases further with

prolonged steroid exposure [33,34]. Myocilin is a 55 kDa

protein that has also been shown to be induced in cul-

tured human trabecular meshwork cells after exposure

to dexamethasone for 2–3 weeks [35]. Mutations in

myocilin have been shown to be associated with juve-

nile-onset and adult-onset POAG [36]. Controversy

exists as to if myocilin causes an increase or a decrease

in outflow facility. In studies of perfused human trabe-

cular meshwork cell cultures, recombinant myocilin

decreased outflow facility, while studies of viral-

mediated transfer of myocilin in trabecular meshwork

cells caused an overexpression of myocilin and increased

outflow facility [37].

Finally, decreased outflow facility may be caused by

reduced degradation of substances in the trabecular

meshwork. Levels of tissue plasminogen activator, stro-

melysin [34], and metalloproteases [38,39] have been

shown to decrease in trabecular meshwork cultures trea-

ted with dexamethasone. Furthermore, dexamethasone

treatment inhibits trabecular meshwork cell arachadonic

acid metabolism [40] and reduces the phagocytic proper-

ties of the cells [38,41]. Because these cells function to

remove debris deposited in the meshwork, reduced

functional activity may lead to reduced outflow facility.

Conclusion

Corticosteroid-induced ocular hypertension and glaucoma

has been recognized for more than 50 years. A number of

risk factors have been identified for the development of

corticosteroid-induced ocular hypertension and glaucoma,

including a personal or family history of glaucoma, young

children, older adults, type-1 diabetes mellitus, connec-

tive-tissue disease, and high myopia. The intraocular

potency and mode of administration are also important

risk factors. Increasing use of IVTA will probably lead

to a greater probability that ophthalmologists will encoun-

ter steroid-induced ocular hypertension and glaucoma.

Research into the underlying mechanisms of this patho-

physiological process has improved our understanding of

the phenomenon and may lead to more efficacious treat-

ment options in the future.

References and recommended reading.

Papers of particular interest, published within the annual period of review, havebeen highlighted as:• of special interest•• of outstanding interest

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7

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8

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Ocular hypertension and glaucoma Jones and Rhee 167