STEROIDS: Use with Caution and with Confidence
Despite their potential drawbacks, steroids are essential to eye care. Aggressive initial dosing with monitored, slow tapering is the key to success.
Corticosteroids are an integral part of topical ophthalmic therapy. When properly prescribed, topical steroids provide tremendous benefits, such as controlling inflammation and scarring, preventing vision loss, limiting lost productivity at work or school, and enabling a more rapid return to comfortable contact lens wear. However, steroids are not without risk—they can induce glaucoma, cataracts and potentiate infection, especially in longer treatment periods. This course reviews appropriate indications and prescribing steroids for a variety of pathologic ocular conditions.
William B. Potter, O.D.
COPE approval for 2 hours of CE credit is pending for this course. Check with your local state licensing board to see if this counts toward your CE requirement for relicensure.
This continuing education course is joint-sponsored by the Pennsylvania College of Optometry.
Dr. Potter is on the speakers bureau for Alcon.
Steroid medications have presented a special set of challenges to the profession of optometry as it has attained therapeutic privileges. Opponents of our expanded therapeutic drug prescribing have cited potential harm to an unwary public.
In addition, optometric education of decades past had over-emphasized the negatives of steroids, and proposed too-narrow indication for their usage.
However, when properly prescribed, topical steroids provide tremendous benefits, such as controlling inflammation and scarring, preventing vision loss, limiting lost productivity at work or school, and enabling a more rapid return to comfortable contact lens wear. Steroids are safe and effective as long as the doctor understands the risks and knows what to do in the event of a steroid induced event.
This article encourages proper topical steroid usage while minimizing the risk of adverse reactions.
Risks vs. Benefits
Topical ophthalmic steroids are categorized as synthetic glucocorticoids, meaning that they are manufactured to mimic the effects of their naturally-occurring counterpart known as cortisol. (Cortisol suppresses the release of substances in the body that cause inflammation. It also increases blood sugar through gluconeogenesis, and it aids in the metabolism of fat, protein and carbohydrate. The body increases secretion of cortisol, or “the stress hormone,” in response to physical and psychological stress.)
Steroid medications have a wide range of effects in suppressing inflammatory activity, and their use can be critical to the restoration of a patient’s well being. However, steroids are not without risk, as doctor and patient need to be acutely aware of steroid use as an etiology in glaucoma, cataracts and the potentiation of infection, especially in longer treatment periods.1
In glaucoma, 4% to 6% of patients will have significant IOP increases after a month on steroid drops.2 In fact, we have encountered patients whose pressure increases with only a week of therapy, so regular tonometry is important.
Cataract is also a concern with prolonged use of steroids. Unfortunately, this irreversible result is due to alteration of crystalline lens metabolism.
Also, because steroids are immunosuppressive, they can limit the white blood cell response that would normally fight off infection. So, herpes simplex and fungal infection are especially worrisome when steroid use is prolonged.
Thus, the key to proper steroid use is weighing the risk vs. benefit for each patient. Close monitoring in follow-up care allows for risks to be moderated with proper dosage tapering, as well as alternate therapies if adverse effects occur.
Eye care practitioners have a wide range of topical steroid choices.
The development of “soft steroids,” such as FML (fluorometholone alcohol 0.1%, Allergan) and Lotemax (loteprednol 0.5%, Bausch + Lomb), have changed how we practice. Soft steroids should have a place in any primary care optometric practice. These allow us longer tapering schedules, which are safer, as well as milder immunosuppression and fewer steroid side effects.3
While stronger topical agents—prednisolone, dexamethasone and difluprednate—are indicated for severe and acute inflammation, they lack the safety profile for most cases of chronic therapy. Diverse external diseases, ranging from herpes zoster to silicone hydrogel-associated inflammation, have an ongoing antigenicity that may require a month or more of immunosuppression. So, although the stronger agents may be required initially, the softer steroids provide a safer opportunity to taper the anti-inflammatory effect with less likelihood of inducing secondary glaucoma or cataract.
With this in mind, let’s look at how steroids are used in the following conditions.
This condition is primarily noninfectious, and can be managed confidently at the primary care level in the majority of cases. However, steroid fears can lead the practitioner to under-prescribe these agents, and actually cause a prolonged treatment period that increases the total steroid dosage.
Pred Forte (prednisolone acetate 1%, Allergan) has been the gold standard for anterior uveitis, because soft steroids may lack the needed efficacy in non-surgical uveitis.4 The AOA Clinical Practice Guideline on anterior uveitis recommends prednisolone acetate 1% every one to six hours depending on severity—the more severe the inflammation, the more frequent the dosage.5 (However, the guidelines, which were last reviewed in 2004, acknowledge that “treatment recommendations [may] change due to continuing research and clinical experience.”)
Unfortunately, sometimes patients are started on a q.i.d. prednisolone dosage, which is usually inadequate in anti-inflammatory effect. While this may be driven by the fear of steroid-induced side effects, it actually increases the likelihood that the drug will have to be used for a longer period of time. Starting the patient on hourly dosing, with tapering over the course of a month or more, seems to avoid prolonged treatment periods in most cases of anterior uveitis.
Topical Ophthalmic Corticosteroids
|Brand name||Generic name/
|FDA approved dosing|
Bausch + Lomb
|q.i.d. for 2 weeks, then b.i.d. for
1 week, and then gradual taper
|Up to q4h for first 24 to 48
hours; or b.i.d. to q.i.d., then
Bausch + Lomb
|Up to qh for first week; or q.i.d.
for 2 weeks, then gradual taper
|Up to >q.i.d. for first 24 to 48
hours; or b.i.d. to q.i.d., then
|Up to qh during the day, q2h
during the night as initial therapy;
or q4h, then t.i.d. to q.i.d.,
then gradual taper
In our practice, we seldom treat anterior uveitis at an initial dosage of less than every two hours, with an hourly dosage being most common. Severe cases are treated with an initial dosage of one drop every 15 minutes for the first hour, and hourly thereafter, for one week. We reduce the prednisolone dosage by half each week, so that the second week’s dosing is every two hours, and the third week is four times daily, and so on.
If this schedule is not maintained, we find that the patient becomes more vulnerable to a relapse of signs and symptoms, thus requiring a restarting of the treatment regimen. The result is that the total steroid use is much greater, and presents unnecessary safety risks. Aggressive initial dosing with monitored, slow tapering is the key to success.
We now have a new topical steroid option with the release of Durezol (difluprednate 0.05%, Alcon). This drug has demonstrated therapeutic equivalence to topical prednisone in treating uveitis, with a dosing schedule that is cut in half.6
Because we know that compliance decreases as prescribed dosage increases, we can likely attain better results with lesser dosing.7 As insurance formulary acceptance is increasing, Durezol should become a leading weapon in treating anterior uveitis at the primary care level.
However, this drug has not eliminated concerns of cataract and steroid-induced glaucoma (and its IOP elevation may be comparatively higher than with other steroids).8
Close follow-up is essential, and the clinician must be prepared to prescribe medications to lower intraocular pressure if ongoing steroid therapy is required. While follow-up is geared towards the severity of the underlying condition, we monitor IOP weekly if steroid use approaches a month or more.
Topical steroids should be avoided in seasonal and perennial allergic conjunctivitis, if possible, because they can dig the practitioner a deep hole in terms of chronic use. The problem with using steroids in these cases is that the patient’s relief may be so profound as to lead to demands for prescription refills. However, there are occasions when steroid use is justified. If discomfort persists to such a degree that it limits school or job performance, the practitioner is obligated to provide safe yet rapid relief.
Modern mast cell stabilizers and antihistamines are extremely effective, but may not offer symptomatic relief for the first several days of use. Work and school performance may be limited by allergy symptoms, to such an extent that a steroid prescription is indicated. Similarly, contact lens wear can be interrupted by allergy, which can be devastating to keratoconus and higher refractive error patients.
Contact lens wear can be safely restored by a conservatively short “burst” of soft steroids, such as FML, Lotemax or Alrex (loteprednol 0.2%, Bausch + Lomb).9 We typically start these agents with the instructed dosing: q.i.d. for up to one week, then reduce to b.i.d. dosing as contact lens wear is resumed.10
The duration of allergy treatment with steroid drops seldom needs to exceed two weeks.9 The patient can concurrently use mast cell stabilizer/ antihistamine drops. These drugs will provide continued relief of allergy signs and symptoms once the steroids are discontinued.11
Patient management must include discussion of the risks and benefits of steroid treatments, with emphasis on short-term treatment. The practitioner must gauge the patient’s ability to comply, and err on the side of caution if this is in doubt. It is important to limit the patient to only a 5mL quantity, and to maintain a “no refills without follow-up visit” policy.
Another reason for steroid use in allergy patients is the consideration of the eye’s cellular response. If antigens are persistent enough in their presentation, eosinophil recruitment can result. This infiltration into ocular tissue alters the inflammatory chemistry, which limits the effectiveness of mast cell stabilizers and antihistamines. Eosinophilia may contribute to scarring of lid, cornea and conjunctiva, so prevention may require steroid use. The practitioner may use conjunctival scrapings or other cytologic methods, but the clinical appearance of the eye can be the key indicator. We find that hypertrophy and dermatitis of the lid skin, paired with the chronicity of the response, can indicate that cellular elements are involved, and that steroids are indicated.
Treatment failure with mast cell stabilizer/antihistamine drugs is another clinical indication that eosinophilia has developed. This type of lid inflammation, if left uncontrolled, can lead to fibrosis and scarring, which can alter cosmetic appearance and decrease lid function. Fluorometholone and loteprednol are ideal agents if steroid treatment is required, because their propensity to elevate intraocular pressure is low.12
Contact Lens-Associated Infiltrative Keratitis
This generally non-infectious entity is a common presentation that benefits from steroid as well as antibiotic therapy. In general, lens cessation and subsequent refitting are primary treatments. However, antibiotic coverage is wise if there is suspicion of an excessive bacterial load. (See “Infectious Infiltrates vs. Sterile Infiltrates”)
It is important to differentiate inflammation
Silbert JA. Is It an Ulcer or an Infiltrate?
More problematic is the ongoing inflammatory response, which may far outlast the infectious phase, and make restarting or refitting of lens wear quite difficult. Contact lens wear itself can be an inflammatory influence, and its resumption may stimulate the eye’s immune response even in the presence of an ideal fit.13
Topical ocular steroids are often better utilized if they are not combined with antibiotic preparations. Modern antibiotics are extremely effective at stopping infection, but the patient’s inflammatory response may provide ongoing symptoms, especially in attempts to resume contact lens wear.
Combination antibiotic/steroid products can actually be problematic in infiltrative keratitis, as they commonly use tobramycin as the antibiotic agent. Tobramycin has strong antibiotic properties, especially against gram-negative bacteria, but tends to be toxic to the healing corneal epithelium.14 Clinically, this seems especially true in treatment durations of longer than one week. Fluoroquinolone antibiotics have less toxicity and are better tolerated.
Although there are asymptomatic cases of infiltrative keratitis, many patients are troubled by discomfort, blurred vision and redness. Typical treatment of infiltrative keratitis is to initiate antibiotic therapy with a fluoroquinolone, one drop in the affected eye, four times daily for one week.15 We concurrently start a soft steroid, such as fluorometholone or loteprednol 0.5%, also four times daily.
Follow-up examination in four or five days provides critical information about whether to restart contact lens wear, and when to taper the steroid drops. Significant corneal staining or persistent infiltrates can indicate that contact lens wear is a week or more away. Consultation with a cornea specialist is recommended if signs and symptoms persist.
We often see infiltrative keratitis patients who have been treated with antibiotic therapy alone. The consequence here is that ultimate resolution is delayed. Interestingly, research done in the development of Restasis (cyclosporine, Allergan) for dry eye has revealed that inflammatory white blood cells can have a life expectancy of 100 days or more.16 So, a week of antibiotic therapy does little to prevent the inflammatory cytokines that these cells release, once contact lens wear is resumed.
Contact lens wear can be an inflammatory influence under normal circumstances, but an alreadysensitized cornea can show rebound inflammation if proper steps aren’t taken. It is imperative to use the immunosuppressive benefits of steroids with a slow taper as contact lens wear is resumed, or the patient will suffer setbacks and require multiple office visits. We typically restart limited contact lens wear when the rehabilitating cornea can tolerate a limited steroid dosage of once to twice daily.
Staphylococcal Marginal Keratitis
The cornea’s immune response to Staph. infection is a familiar cause of inflammation. Both contact lens wearers and non-wearers alike can suffer from this relatively mild and treatable condition. Patients present with mild to moderate redness and discomfort, with an approximately 1mm peripheral corneal infiltrate being the significant slit lamp finding.
Antibiotic therapy is helpful, though the infectious component of this disorder is easy to eradicate. The question is whether and when steroid use is appropriate. We make two assessments: First, what is the risk of more serious infection, as indicated by the appearance of the corneal lesion? Small, non-ulcerated lesions in the corneal periphery generally have very low risk of progression to more serious and sightthreatening infection.
Second, what is the level of patient discomfort, in terms of his or her ability to function at work or school? (Though marginal keratitis does not usually cause extreme pain, it may be enough to disrupt daily routines of some patients.) Failure to initiate steroid treatment may expose the patient to unnecessary discomfort and loss of productivity.
The use of steroid via antibiotic/steroid combination, such as TobraDex (tobramycin 0.3%/ dexamethasone 0.1%, Alcon) or Zylet (tobramycin 0.3%/loteprednol 0.5%, Bausch + Lomb), on day one may be appropriate if the risk of progression is low and the patient is significantly uncomfortable.17
If there is uncertainty, prescribe an antibiotic initially and then follow up in a day or two to assess whether to add a separate steroid.
Posterior blepharitis, also known as meibomian gland dysfunction, is primarily an inflammatory disease. While antibiotic therapy is helpful in reducing lid flora, patients do not attain comfort until lid inflammation is reduced. Steroid therapy remains the best method to attain rapid patient comfort.
A classic approach has been to apply topical combination drugs, such as TobraDex or Zylet.18
The recently-launched TobraDex ST (tobramycin 0.3%/dexamethasone 0.1%, Alcon) appears highly appropriate to treat blepharitis because its retentionenhancing suspension vehicle (using xanthan gum) maintains contact with the lid and ocular surface for a longer duration. A greater therapeutic effect is often the result, though steroid concerns should limit treatment periods to one week.
Because posterior blepharitis tends to be a recurrent and chronic condition, exercise great caution in limiting steroid use, especially for dexamethasone or prednisolone. The advent of topical ophthalmic azithromycin, AzaSite (azithromycin 1%, Inspire) has provided another option, as its antibiosis is supplemented by effective anti-inflammatory activity.19
Note that the prescribing of AzaSite in posterior blepharitis remains an off-label use, as its present indication is for bacterial conjunctivitis. Azithromycin down-regulates inflammatory mediators NF-KB, cytokines and matrix metalloproteinase.20-23
Our choice for chronic blepharitis patients is to initiate AzaSite once daily for one month.24 In addition, we use a soft steroid four times daily for the first week, and one to two times daily for the second week if needed. This method provides great relief of symptoms by way of the soft steroid, and allows time for the AzaSite to begin to have its antiinflammatory and antibiotic effect.
The month of AzaSite treatment is followed by a month off in most cases, because the half-life of the drug is longer than one week. Treatment may be restarted if symptoms reappear, hopefully without the steroid accompaniment. AzaSite contains BAK as a preservative (at 0.003%), and we should always be aware of potential BAK allergy and toxicity with long-term use. However, the steroid dosage is reduced so quickly in this regimen that we have never found preservative reactions to be problematic.
AzaSite’s benefits include the possibility of limiting total steroid use in our blepharitis patients. A recent study demonstrated improved patient comfort and tear breakup time in blepharitis patients who used AzaSite once daily for a month.24 No other drug has been shown to do this to date. In addition, we use soft steroid drops for about one week in order to attain patient comfort.
Ocular Herpetic Disease
Perhaps the primary care optometrist’s most difficult decision regarding steroids involves the patient with ocular herpes. Occasional cases blur the line between simplex and zoster. Here are some guidelines for steroid use for herpetic involvement.
• Herpes simplex. Steroids are not indicated for herpes simplex cases with epithelial involvement. Yet when epithelial episodes have residual subepithelial haze, or possible evolution to a disciform involvement, then steroid use is mandatory.25 Disciform and interstitial keratitis are the immunologic results of herpetic infection, whose comanagement with a corneal specialist may be indicated.
In the case of herpes simplex keratitis, subepithelial haze can be a sight-threatening result of epithelial disease, even in the absence of true disciform inflammation. Depending on severity, we start steroid therapy once there is epithelial closure, i.e., upon resolution of the ulcer itself.25
Specifically, start fluorometholone or loteprednol 0.5% at q.i.d. dosing for the first week, then taper the dosage by half for two to four weeks. More severe cases indicate prednisolone or difluprednate treatment at similar dosages, and specialty corneal consultation is encouraged. Steroid initiation prior to epithelial closure could potentiate herpetic infection.
Meanwhile, maintain oral antiviral coverage, such as Valtrex 500mg t.i.d. (valacyclovir, GlaxoSmithKline), at least through the first week of topical steroid therapy.
• Herpes zoster. Herpes zoster ophthalmicus has a clear indication for topical steroids if there is ocular involvement, such as staining and mucoid plaques. Patients with these findings are at greater risk for uveitis, which can be severe.26
Start a soft steroid on a q.i.d. basis, with careful slit lamp monitoring on a minimum of alternate days. Tapering may take several weeks. Be prepared to increase steroid potency to Pred Forte or Durezol if corneal findings worsen or if uveitis develops.
Along with other treatments, consider steroid therapy in the disease spectrum of dry eye syndrome. As inflammatory theories have been elaborated, and optometrists gain clinical experience, steroid treatment has become standard to offer short term relief of symptoms. Restasis, AzaSite, punctal plugs and advanced lubricants are all excellent chronic treatments for dry eye. However, for acute symptoms, none of these treatments offer the rapid relief of steroid medications. If a practitioner simply increases lubricants as acute therapy, the patient will suffer a much longer course of unresolved symptoms and signs.
The soft steroids fluorometholone and loteprednol 0.5% are ideal for treatment of an acute inflammatory episode in dry eye. They should be considered mainstream therapy, even in the presence of moderate signs and symptoms.27,28 These drugs can get a patient in pain “over the hump” while the more chronic agents are given a chance to work. Steroids rapidly calm the inflammation caused by cell death in the cornea and conjunctiva, as well as calm the inflammation in the tear glands that may have contributed to the dry eye in the first place.
Dosing q.i.d. for the first week of treatment, followed by a tapering period of one to three weeks, works well and poses little risk for the acutely inflamed dry eye patient.
Many practitioners take on a philosophy of accepting no risk in terms of steroid use. Our argument is that we need to weigh risk versus benefit of symptomatic relief in a variety of inflammatory conditions. Intraocular pressure measurement is a key component at return visits, as steroid responses are fairly common.29
While we cannot practice in a risk-free environment, we can control steroid risks with close followup including tonometry, and a “no-refill without visit” policy. The rewards of patient retention and satisfaction are exponentially greater when steroid medications are used in their best indications.
Dr. Potter is chief of optometry and contact lens services at Millennium Eye Care, in Freehold, N.J. He is on the speakers bureau for Alcon.
- Jaanus SD, Cheetham JK, Lesher GA. Anti-inflammatory drugs. In: Bartlett JD, Jaanus SD, eds. Clinical Ocular Pharmacology, 4th ed. Boston: Butterworth, 2001:273-276.
- Armaly MF, Becker B. Intraocular pressure response to topical corticosteroids. Fed Proc. 1965 Nov-Dec;24(6):1274-8.
- Abelson M, Sleeper A. Insights on anti-inflammatories. Rev Ophthalmol. 2005 June; 12(6):80-4.
- Kabat AG. Uveitis. In: Bartlett JD, Jaanus SD (eds). Clinical Ocular Pharmacology, 5th ed. Boston: Butterworth-Heinemann, 2008:596.
- Optometric Clinical Practice Guideline Care of the Patient with Anterior Uveitis. St. Louis, MO: American Optometric Association; 1994, reviewed 2004:21.
- Foster CS, Davanzo R, Flynn TE, et al. Durezol (Difluprednate Ophthalmic Emulsion 0.05%) compared with Pred Forte 1% ophthalmic suspension in the treatment of endogenous anterior uveitis. J Ocul Pharmacol Ther. 2010 Oct;26(5):475-83.
- Claxton AJ, Cramer J, Pierce C. A systematic review of the associations between dose regimens and medication compliance. Clin Ther. 2001 Aug;23(8):1296-310.
- Meehan K, Vollmer L, Sowka J. Intraocular pressure elevation from topical difluprednate use. Optometry. 2010 Dec;81(12):658-62.
- Bielory L, Katelaris CH, Lightman S, Naclerio RM. Treating the ocular component of allergic rhinoconjunctivitis and related eye disorders. MedGenMed. 2007 Aug 15;9(3):35.
- Lotemax package insert. Bausch + Lomb. 2006 April. Available at: www.bausch.com/en_US/downloads/ecp/ pharma/general/lotemaxinsert.pdf (accessed January 2011).
- Khurana S, Sharma N, Agarwal T, et al. Comparison of olopatadine and fluorometholone in contact lensinduced papillary conjunctivitis. Eye Contact Lens. 2010 Jul;36(4):210-4.
- Multack RF, Genge MR, Skorin L. Immune Disease. In: Onofrey B, Skorin L, Holdeman NR (eds). Ocular Therapeutics Handbook: A Clinical Manual, 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2005:246.
- Zhivov A, Stave J, Vollmar B, Guthoff R. In vivo confocal microscopic evaluation of langerhans cell density and distribution in the corneal epithelium of healthy volunteers and contact lens wearers. Cornea. 2007 Jan;26(1):47-54.
- Matsumoto S, Stern ME. Effect of anti-infective ophthalmic solutions on corneal cells in vitro. Adv Ther. 2000 May-Jun;17(3):148-51.
- Donshik PC, Suchecki JK, Ehlers WH. Peripheral corneal infiltrates associated with contact lens wear. Trans Am Ophthalmol Soc. 1995;93:49-60.
- Jackson WB. Management of dysfunctional tear syndrome: a Canadian consensus. Can J Ophthalmol. 2009 Aug;44(4):385-94.
- Lowery RS. Blepharitis, Adult: Treatment & Medication. emedicine from WebMD. 2009 July 30. Available at: http://emedicine.medscape.com/article/1211763-treatment (accessed January 2011).
- Jackson WB. Blepharitis: current strategies for diagnosis and management. Can J Ophthalmol. 2008 Apr;43(2):170-9.
- Opitz DL, Tyler KF. Efficacy of azithromycin 1% ophthalmic solution for treatment of ocular surface disease from posterior blepharitis. Clin Exp Optom. 2010 Nov 17. [Epub ahead of print]
- D’Acquisto F, May MJ, Ghosh S. Inhibition of nuclear factor kappa B (NF- B): an emerging theme in anti-inflammatory therapies. Mol Interv. 2002;2(1):22-35.
- McDermott AM, Perez V, Huang AJW, et al. Pathways of corneal and ocular surface inflammation: a perspective from the Cullen Symposium. Ocul Surf. 2005;3(4):S131-8.
- De-Quan L, Pflugfelder SC. Matrix metalloproteinases in corneal inflammation. Ocul Surf. 2005;3(4):S198-202.
- Leonardi A, Brun P, Abatangelo G, et al. Tear levels and activity of matrix metalloproteinase (MMP)-1 and MMP-9 in vernal keratoconjunctivitis. Invest Ophthalmol Vis Sci. 2003;44(7):3052-8.
- Foulks GN, Borchman D, Yappert M, et al. Topical azithromycin therapy for meibomian gland dysfunction: clinical response and lipid alterations. Cornea. 2010 Jul;29(7):781-8.
- Wilhelmus KR, Gee L, Hauck WW, et al. Herpetic Eye Disease Study. A controlled trial of topical corticosteroids for herpes simplex stromal keratitis. Ophthalmology. 1994 Dec;101(12):1883-95.
- Foster CS. Uveitis. Lecture presented at annual meeting of American Academy of Ophthalmology, 2002; New Orleans, LA.
- Behrens A, Doyle JJ, Stern L, et al. Dysfunctional tear syndrome study group. Dysfunctional tear syndrome: a Delphi approach to treatment recommendations. Cornea. 2006;25(8):900-7.
- Pflugfelder SC, Maskin SL, Anderson B, et al. A randomized, double-masked, placebo-controlled, multicenter comparison of loteprednol etabonate ophthalmic suspension, 0.5%, and placebo for treatment of keratoconjunctivitis sicca in patients with delayed tear clearance. Am J Ophthalmol. 2004 Sep;138(3):444-57.
- Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics, II: the effect of dexamethasone in the glaucomatous eye. Arch Ophthalmol. 1963 Oct;70:492-9.