Iatrogenic Glaucoma Secondary to Medications

REVIEW

Iatrogenic Glaucoma Secondary to Medications M. Reza Razeghinejad, MD,a,b Jonathan S. Myers, MD,a L. Jay Katz, MDa a

Wills Eye Institute, Jefferson Medical College, Philadelphia, Pa; bDepartment of Ophthalmology, Shiraz University of Medical Sciences, Shiraz, Iran.

ABSTRACT Glaucoma is a progressive optic neuropathy with primary and secondary forms. Iatrogenic glaucoma secondary to medications is potentially blinding but preventable. Most drug profiles listing glaucoma as a contraindication or an adverse effect are concerned with inducing acute angle-closure glaucoma. Anticholinergic or adrenergic agents are the most common for inducing “pupillary block” angle-closure glaucoma. Patients with a narrow irido-corneal angle are at high risk. Sulfa drugs induce “non-pupillary block” angle-closure glaucoma as an idiosyncratic reaction to the drug in patients with an open or narrow irido-corneal angle. Steroids and a few antineoplastic agents induce open-angle glaucoma. The risk is higher with topical rather than systemic steroids. The first step in the management is discontinuation of the drug, followed by medical, laser, and, if necessary, surgical intervention. © 2011 Elsevier Inc. All rights reserved. • The American Journal of Medicine (2011) 124, 20-25 KEYWORDS: Acute angle-closure glaucoma; Adrenergic drugs; Anticholinergic agents; Central nervous system drugs; Iatrogenic glaucoma; Steroid-induced glaucoma

Glaucoma is a progressive optic neuropathy characterized by a distinctive pattern of optic nerve and visual field loss. The optic disc exhibits increasing cupping accompanied by nerve fiber layer loss with irreversible loss of the visual field. The most useful way to classify the glaucoma is according to the anatomy and pathogenesis. Aqueous humor, produced by the ciliary body, circulates around the lens and enters the anterior chamber through the pupil. Aqueous flows out of the anterior chamber, primarily through the trabecular meshwork in an irido-corneal angle recess. When the trabecular meshwork is visible in physical examination (gonioscopy), the angle is open; when it is covered by iris tissue, the angle is closed.1 Both open- and closed-angle glaucomas can occur with no identifiable cause, making them primary glaucomas. Secondary glaucomas have identifiable causes of elevated intraocular pressure. Most but not all glaucomas are associFunding: None. Conflict of Interest: None of the authors have any conflicts of interest associated with the work presented in this manuscript. Authorship: All authors had access to the data and played a role in writing this manuscript. Requests for reprints should be addressed to L. Jay Katz, MD, Glaucoma Service at Wills Eye Institute, 840 Walnut Street, Suite 1130, Philadelphia, PA 19107. E-mail address: [email protected]

0002-9343/$ -see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.amjmed.2010.08.011

ated with elevated intraocular pressure. Elevated pressure without optic nerve damage is referred to as “ocular hypertension.” Ocular hypertension can occur as a consequence of medications administered directly to the eye or systemically. Untreated ocular hypertension may lead to glaucomatous optic neuropathy, an iatrogenic glaucoma. This review will discuss the medications that may lead to elevated intraocular pressure (Table 1).

OPEN-ANGLE GLAUCOMA Corticosteroids Armaly and Becker2 and Becker3 reported that the normal population could be divided into 3 groups according to their response to the topical administration of corticosteroid. Five percent of the population were high responders, developing an intraocular pressure increase ⬎15 mm Hg and intraocular pressures ⬎31 mm Hg after daily corticosteroid use for 4 to 6 weeks. Moderate responders, approximately one third of the population, exhibited an increase in intraocular pressure of 6 to 15 mm Hg and had intraocular pressures between 20 and 31 mm Hg. Approximately two thirds of the population were nonresponders, with pressure increases of ⬍6 mm Hg and intraocular pressures of ⬍20 mm Hg.

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21

Timing of Response. The time of onset is dependent on the corticosteroid potency and dosage. Although an acute response has been reported with intensive systemic steroid therapy, the intraocular pressure response often occurs over months or years.4 Most studies reported intraocular pressure increase 3 to 6 weeks after topical steroid use.5 Risk Factors. The possibility of a high response is more likely with certain risk factors. Patients with primary open-angle glaucoma and their first-degree relatives; elderly or young (⬍6 years) patients; and patients with type 1 diabetes or connective tissue disease (especially rheumatoid arthritis), high myopia, and angle recession glaucoma are at greater risk of steroid-induced glaucoma.6 Several genes have been shown to be unregulated in dexamethasone-treated trabecular meshwork cells. The most extensively studied is the gene that codes for the protein myocilin.7

Table 1

Mode of Administration. All methods of corticosteroid use have the potential to elevate intraocular pressure, but most are caused by drops or ointments instilled in the eye. Steroid creams, lotions, and ointments applied to the face or eyelids may also increase intraocular pressure.8,9 The likelihood of intraocular pressure elevation with systemic steroid seems to be less than the topical route. In patients who are CLINICAL SIGNIFICANCE steroid responders, pressure elevations with systemic steroid use av● Steroids may induce elevated eye pressure erage approximately 60% of those with an open angle. The risk is greatest in produced by topically applied steelderly patients; patients with primary roids. Tripathi et al10 found a sigopen-angle glaucoma and their first-denificant relationship between ingree relatives; and patients with type 1 traocular pressure and the dose of diabetes, rheumatoid arthritis, and corticosteroid administered (1.4 mm myopia. Hg increase in mean intraocular pressure for each 10 mg increase in the ● Angle-closure glaucoma occurs with anaverage daily dose of prednisolone). ticholinergic or adrenergic drugs, typiFluorometholone, medrysone, cally in hyperopes (farsighted). rimexolone, and loteprednol are ● The most common presenting sign in less potent topical corticosteroids. sulfa drug-induced glaucoma is blurred They may produce an elevated intraocular pressure, although the vision with induced myopia. risk is less.11

List of drugs involved in intraocular pressure elevation, type of induced glaucoma, clinical manifestation, and treatment Acute angle-closure glaucoma

Open-angle glaucoma

Type of glaucoma

Pupillary block

Non-pupillary block

Typical manifestation

Preexisting narrow angle Unilateral severe IOP elevation Ocular pain Red eye and swollen lid Nausea and vomiting Halo Blurred vision Antidepressants Monoamine oxidase inhibitors Antipsychotics Antihistamines Antiparkinson Sympathomimetics Parasympatholytics Parasympathomimetic agents Botulinum toxin Cardiac agents Anticoagulants Anesthetic agents Discontinue the inciting drug Topical and systemic antiglaucoma medications Laser iridotomy

Bilateral severe IOP elevation Ocular pain Red eye and swollen lid Nausea and vomiting Halo Blurred vision with induced myopia Sulfa drugs Topiramate Hydrochlorothiazide Acetazolamide Quinine Tetracycline

Usually asymptomatic

Discontinue the inciting drug Topical and systemic steroid and topical anticholinergic drug Surgical drainage of choroidal effusion if needed

Discontinue steroid or reduce the dosage of steroid or substitute with a less potent steroid If no response to antiglaucoma medication, laser trabeculoplasty or filtration surgery

Drugs

Treatment

IOP ⫽ intraocular pressure.

All forms of steroids Antineoplastic agents Docetaxel and paclitaxel Imatinib mesylate

22 Mechanism. Trabecular meshwork accounts for up to 90% of aqueous humor drainage from the human eye. Although the proposed mechanism of corticosteroid intraocular pressure elevation is increased resistance to aqueous flow via this route, the precise mechanism is still unknown.12 Changes in the microstructure of the trabecular meshwork (cross-linked actin network formation) and cell activities may lead to decreased proliferation, migration, and phagocytosis of trabecular meshwork cells. These all cause progressive accumulation of extracellular debris and increased aqueous outflow resistance. Moreover, increased production and deposition of glycosaminoglycan, elastin, fibronectin, laminin, and collagen type IV, coupled with decreased destruction because of inhibition of matrix metalloproteinase inhibitors by steroids, also lead to increased outflow resistance.12 Symptoms and Differential Diagnosis. Patients with steroid-induced glaucoma initially have relatively few symptoms. The intraocular pressure increase is generally gradual and painless, but a few patients may experience brow ache or vision changes, including the development of halos. The typical manifestation of steroid-induced glaucoma in adults is similar to primary open-angle glaucoma: high intraocular pressures with open angles on gonioscopy and glaucomatous optic nerve head cupping or visual field defects. This type of glaucoma at an early stage is generally asymptomatic and usually detected on clinical examination. Elderly patients who received corticosteroid treatment in the past may appear as having normal tension glaucoma. They have experienced intraocular pressure elevation and secondary glaucomatous optic nerve damage while taking steroids, but present later when they have stopped taking steroids and the intraocular pressure has normalized. Occasionally, the patient may have intermittent blurring of vision if the intraocular pressure has increased to the point of compromising corneal function. Corneal edema presents with blurred vision, halos around lights, red eye, pain, or tearing. In addition, the patient also may have blurred vision from steroidinduced cataracts. The clinical picture in infants treated with corticosteroid-induced glaucoma resembles congenital glaucoma.13 They present with photophobia, tearing, blepharospasm, megalocornea, and cloudy cornea. Management. The most effective treatment for corticosteroid-induced glaucoma is its prevention through judicious use of corticosteroid and close monitoring in chronic steroid use. Patients who are taking steroids, especially the topical forms, should have regular follow-up examination to prevent iatrogenic glaucomatous optic nerve damage.10 The steroid-induced intraocular pressure increase is usually short-lived and reversible by discontinuation of steroids if the drug has not been used for more than 1 year. The intraocular pressure usually returns to normal within 2 to 4 weeks after stopping the steroid, but normalization may take longer in cases of chronic steroid use.14 In cases with repository steroid injection and high intraocular pressure,

The American Journal of Medicine, Vol 124, No 1, January 2011 removal of the residual subconjunctival or intraocular steroid may15 or may not4 help. If the steroid needs to be continued, a lower dosage, lower concentration, or weaker corticosteroid may reduce the risk of glaucoma. With systemic steroids, steroid-sparing agents, such as systemic nonsteroidal anti-inflammatory agents, are a potential substitute.16 However, it may not be possible to discontinue the steroid and the elevated intraocular pressure should be managed medically or surgically. Most patients who develop iatrogenic steroid glaucoma can be controlled with topical antiglaucoma therapy.17 In those who are unresponsive to medical therapy, laser trabeculoplasty or surgical interventions (commonly trabeculectomy) are the next steps.18 Anecortave acetate is an angiostatic steroid synthesized from cortisol acetate. In a case series, a total of 8 eyes with medically uncontrolled intraocular pressure after steroid therapy, a periocular depot injection of anecortave acetate reduced the mean baseline intraocular pressure by 34.5% at 1 month.19 The mechanism underlying the anecortave effect is unclear.20

Antineoplastic Agents Docetaxel and paclitaxel produced ocular hypertension in a patient, but the mechanism is not determined.21 Imatinib mesylate induced intraocular pressure elevation in only 1 patient in a case series of 104 patients.22

CLOSED-ANGLE GLAUCOMA Most categories of drugs that list glaucoma as a contraindication or adverse effect are concerned with inducing acute angle-closure glaucoma. These medications will incite an attack only in those individuals with occludable irido-corneal angles. The risk factors for acute angle-closure glaucoma include race (Asians, Inuit Eskimos, and Hispanics), older age, female gender, hyperopia (farsightedness, wearing plus glasses that magnify objects), narrow angle, family history positive for angle closure, and previous angle closure in fellow eye.23 A simple oblique penlight illumination test can help identify the patients who are at risk. The penlight is held parallel to the plane of the iris and temporally to direct light nasally. If the entire iris appears to be illuminated, the angle of the anterior chamber is wide open (Figure 1A). In patients with a shallow anterior chamber, the iris is convex as it bows forward over the lens. In this test, the presence of a nasal shadow, or eclipse, signifies shallowness of the anterior chamber, the degree depending on the extent of the shadow (Figure 1B).23 However, this method is not fully reliable in determining the risk of angle closure. When in doubt, the patient should be referred to an ophthalmologist for definitive evaluation with gonioscopy for angle examination and grading the level of risk for angle-closure glaucoma. Medications that have a direct or secondary effect, either to stimulate sympathetic or inhibit parasympathetic activation, cause pupillary dilation, which can precipitate acute

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Figure 1 Oblique penlight illumination test to identify patients with narrow angle. A, With a deep anterior chamber, the entire iris is illuminated. B, With a shallow anterior chamber, only the proximal portion is illuminated and a shadow is seen in the distal part.

angle-closure glaucoma in patients with occludable angles (pupillary block angle-closure glaucoma). In patients with narrow angles, the dilation leads to a “ball valve” mechanism in which the lens blocks movement of aqueous fluid through the pupil, leading to fluid accumulation behind the iris, further shallowing the anterior chamber and closing the angle with resultant increase in the pressure. Acute angle-closure glaucoma presents with swollen lids, conjunctiva hyperemia, and corneal edema that results in blurred vision and intense pain experienced as a deep pain in, behind, or above the eye. The pupil is mid-dilated and non-reactive to light. Intraocular pressure is high and the main cause of pain. Some patients may have nausea and vomiting.24 The pressure may increase to more than 60 mm Hg, presenting immediate risk of sudden and permanent loss of vision. Patients experiencing these symptoms must be seen and treated emergently. Patients who have narrow angles are typically treated with laser iridotomy to break or prevent an attack of angleclosure glaucoma. Once treated, almost all of these patients may safely take medications that are associated with a risk of angle closure. Thus, warnings on medication labels may often needlessly alarm patients who have been treated for narrow angles, whereas patients at risk with undiagnosed angles will not be aware of the danger.

Sulfa Drugs Sulfa drugs have been reported to produce an idiosyncratic lens swelling, shallowing of the anterior chamber, elevated intraocular pressure, choroidal effusion, and retinal edema.25 Typically, this angle-closure glaucoma is a bilateral nonpupillary block angle-closure glaucoma that occurs within the first several doses of the medication. Patients with narrow or wide open angles are potentially susceptible to this

23 rare reaction. The most common presenting symptom is blurred vision because of forward movement of the lens (myopia).26 The acute attack has been reported with various drugs containing sulfa components, such as topiramate, hydrochlorothiazide, and acetazolamide. The same scenario has been reported with quinine and tetracycline.6 More than 100 cases of topiramate-induced angle-closure glaucoma have been reported in the literature (unilateral in only 3 patients). Glaucoma occurred between days 1 and 49 (average 7) after drug initiation. In 85%, the glaucoma developed within the first 2 weeks of drug use. Patients have sustained permanent vision loss.27 The acute attack usually resolves after stopping the suspected agent. However, a case of permanent vision loss in both eyes resulted after using sulfamethoxazole-trimethoprim even though the medication was stopped and the patient was treated for glaucoma.28 To treat these patients, the sulfa-containing drug should be discontinued and intraocular pressure should be controlled by medical management. Topical and systemic steroids, and cycloplegic and aqueous suppressants are effective agents in treating this condition. Topical miotics are contraindicated in this condition, because their use may precipitate a relative pupillary block. Laser iridotomy is of no benefit.26

Antidepressants Tricyclic agents, amitriptyline, and imipramine, and the non-tricyclic drugs mianserin hydrochloride, paroxetine, fluoxetine, fluvoxamine, citalopram, and escitalopram have been associated with acute angle-closure glaucoma.27,29 The glaucoma arises as the result of the anticholinergic action of these medications, which produces mydriasis.

Monoamine Oxidase Inhibitors These antidepressant agents have weak anti-cholinergic effects. When these agents are prescribed with other drugs with anti-cholinergic properties, the possibility of angleclosure glaucoma increases. Phenelzine sulfate and tranylcypromine sulfate have been reported to induce acute angleclosure glaucoma.27

Antipsychotics Antipsychotics have a relatively weaker anticholinergic action on the ocular smooth muscles compared with tricyclic antidepressants, and the risk of these causing glaucoma is lower. Perphenazine, trifluoperazine, and fluphenazine have been reported to induce glaucoma.6,23,30

Antihistamines The H1 and H2 receptor blockers also have anticholinergic activity that may induce glaucoma. Promethazine has been shown to produce an idiopathic swelling of the lens that could increase the risk of pupillary block angle-closure glaucoma. Cimetidine and ranitidine increased the intraoc-

24 ular pressure in a patient with glaucoma being treated for duodenal ulcer.23

Antiparkinsons Trihexyphenidyl has been shown to precipitate angle-closure glaucoma in susceptible patients.31 In addition to acute angle-closure glaucoma, trihexyphenidyl’s prolonged cumulative effect tends to cause creeping angle-closure glaucoma: glaucoma without acute symptoms of pain and redness of the eye. Because of the chronic nature of the latter scenario and cognitive impairment in some patients, the diagnosis of the glaucoma may be delayed. It is therefore advisable to have all patients who are to be treated with trihexyphenidyl undergo an ophthalmologic examination.23 Orphenadrine also has been documented to precipitate angle-closure glaucoma.6

Spasmolytics No case of angle-closure glaucoma has been reported with these anticholinergic agents. However, propantheline bromide and dicyclomine have been documented to elevate the intraocular pressure in patients with open-angle glaucoma.32

Sympathomimetics Alpha-adrenergic agents, especially those with alpha-1agonistic activity, cause mydriasis that can precipitate angleclosure glaucoma. Phenylephrine eye drops for pupillary dilation to allow ocular fundus examination, or the systemic form, used for flu management or during anesthesia and intranasally for treatment of epistaxis, may induce an acute angle-closure glaucoma.33,34 Apraclonidine, an alpha-2 agonist eye drop, used mainly after ocular laser surgeries to control intraocular pressure, may induce acute angle-closure glaucoma by its minor alpha-1 agonistic activity.23 Dipivefrin, antiglaucoma drop, is a prodrug of epinephrine that has a mild mydriatic effect and may induce angle-closure attack.23 The sympathomimetic agents are found in a wide variety of products, including inhalers used for treatment of asthma, rectal suppositories, and cold remedies.

Parasympatholytics Nebulized ipratropium bromide, used with ␤2-adrenergic agents in patients with obstructive pulmonary disease, has been associated with acute angle-closure glaucoma. Three of 5 patients who developed acute angle-closure glaucoma after receiving ipratropium and salbutamol experienced bilateral ocular involvement.35 Although tiotropium bromide has a lower incidence of anticholinergic side effects than that of ipratropium, it has been reported to induce acute angle-closure glaucoma.36 These drugs can be absorbed through the cornea and the conjunctiva after escaping from a face mask. Properly fitted and positioned masks and handheld nebulizers can minimize ocular deposition of nebulized medication, although patients may still be at some risk through the systemic circulation.

The American Journal of Medicine, Vol 124, No 1, January 2011 Topical anticholinergic agents used for pupillary dilation for ophthalmic examination and time-release discs for the treatment of motion sickness containing scopolamine should be used with caution in susceptible patients with narrow angles.37

Parasympathomimetic Agents Pilocarpine is an antiglaucoma medication; acetylcholine and carbachol are used to constrict the pupil during intraocular surgery. These agents, however, can rarely induce acute angle-closure glaucoma because of anterior movement of the iris-lens diaphragm.23

Botulinum Toxin Corridan et al38 reported a case of acute angle-closure glaucoma that occurred after a series of injections of botulinum toxin for blepharospasm. Botulinum toxins can cause pupillary dilation when injected periocularly.

Cardiac Agents Disopyramide phosphate seems to have anticholinergic activity and may induce acute angle-closure glaucoma.39,40 There are mixed reports about the effect of calcium channel blockers on the intraocular pressure.41

Anticoagulants Massive vitreous, choroidal, or subretinal hemorrhage is a rare complication of anticoagulant or thrombolytic therapy that may lead to acute angle-closure glaucoma. In addition to overtreatment with anticoagulants, some ocular issues such as age-related macular degeneration and nanophthalmos (small eye) are risk factors for this uncommon complication. Six of 17 reported patients with spontaneous posterior segment hemorrhage and angle-closure glaucoma were taking anticoagulants.42 Peripheral iridotomy is not effective because the mechanism is non-pupillary block angle closure. To prevent occurrence of hemorrhage in the contralateral eye, it may be necessary to discontinue the anticoagulant.42

Anesthetic Agents Succinylcholine and ketamine have been documented to elevate intraocular pressure. The intraocular pressure elevation is temporary and usually not associated with specific ocular complication except in patients with open globe injuries.43 Postoperative acute angle-closure glaucomas after nonocular surgeries have been reported.44 The cause of glaucoma is anticholinergic (atropine, scopolamine, and muscle relaxants) or adrenergic (ephedrine, epinephrine) drugs. The classic signs of acute angle-closure glaucoma can be masked by a patient’s more obvious surgical or anesthetic needs, and the diagnosis can be delayed for several days.

CONCLUSIONS The widespread use of steroids emphasizes the need for understanding their potential side effects, including ocular

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complications. Care should be taken when prescribing steroids for those who have risk factors for iatrogenic steroidinduced glaucoma. High-risk patients should have regular follow-up ocular examinations while taking steroids. In regard to the many drugs that may cause angle-closure glaucoma, there is no ideal solution to the problem except to warn medical practitioners to be wary of patients wearing thick plus glasses that magnify objects and to screen patients for narrow angles with the lateral penlight method to estimate the anterior chamber depth.

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