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 Iritis, or iridocyclitis, is a common form of anterior
uveitis that is frequently observed in clinical practice. It can lead to
long-term debilitation, synechiae and secondary glaucoma.1
Here, we examine research on the latest treatments for
iritis and provide six clinical pearls to help you manage this prevalent ocular
pathology.
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| Iritis, as seen in this patient, is a common form of
anterior uveitis that can cause
long-term debilitation, synechiae and secondary glaucoma, if left untreated.
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Treatment of Iritis
The goals of iritis treatment are to minimize permanent
structural alterations of aqueous outflow and prevent optic nerve damage. An
aggressive regimen is required, which may include Pred Forte (prednisolone
acetate 1%, Allergan) q1h as well as nighttime application of a topical
corticosteroid, such as Maxitrol (neomycin/polymyxin B/dexamethasone, Alcon) or
Tobradex (tobramycin/dexamethasone, Alcon).
More recently, Durezol (difluprednate 0.05%, Sirion
Therapeutics), a synthetic difluorinated prednisolone derivative, has proven
very effective for the treatment of post-cataract surgery iritis and pain.2,3
Durezol received FDA-approval for dermatological application
in June 2008. The drug derives its potency from fluorination at the C6 and C9
position.4 Durezol is also an oil-in-water emulsion (castor oil), which allows
poorly soluble drugs, such as prednisolone, to dissolve in the oil phase,
eliminating the need to shake the bottle.5 Finally, Durezol contains no
benzalkonium chloride and demonstrates higher
bioavailability than comparable ophthalmic suspensions.6
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To produce a good visual outcome, treat iritis agressively
with corticosteroids.
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6 Pearls for Iritis Management
1. Differentiate iritis from keratouveitis. First, you must
differentiate iritis from keratouveitis. Look for the presence of corneal
infiltrates and/or epithelial defects. This is critically important, because an
iritis that doesn’t involve the cornea is typically managed with
corticosteroids and cycloplegic agents.
On the other hand, the use of corticosteroids for a
keratouveitis is contraindicated in most cases due to the likelihood of
microbial keratitis development or unwanted immunosuppression.7
2. Check IOP. Next, measure the patient’s intraocular
pressure. Research suggests that a typical iritis might actually reduce IOP.8
(In some cases, however, concurrent iritis and trabeculitis can actually cause
an increase in IOP.9) Secondary glaucoma can be caused by several acute or
chronic mechanisms, and is often associated with open or closed angles,
synechiae formation, pupillary block, neovascularization and even anterior
rotation of the lens-iris diaphragm.5,10
In general, elevated IOP associated with a uveitis can be
the result of active inflammation, corticosteroid therapy, insufficient
glaucoma therapy, or permanent changes in the ocular structures that alter
aqueous humor dynamics.11 In the case of elevated IOP secondary to uveitis,
treatment with potent corticosteroids often lowers the pressure.12
Be aware, however, that steroid responders may experience an
elevation in IOP over time.5 For this reason, you should monitor patients on
corticosteroid therapy closely, prescribe concurrent pressure lowering agents,
and consider an ester-based steroid, such as Lotemax (loteprednol 0.5%, Bausch
& Lomb) if long-term management is required.13-15
3. Rule out endophthalmitis. Significant iritis following
cataract surgery, with a correspondent decrease in vision and pain, is a
hallmark sign of potential endophthalmitis. While many clinicians look for
endophthalmitis to occur immediately after cataract surgery, the mean time of
onset is actually 9.2 days post-op.16
4. Look for a systemic cause. Gauge the severity of the
iritis and order appropriate lab tests or refer to an internist to help
discover a potential systemic cause. Severe iritis is likely to be secondary to
a systemic condition, such as arthritis, lupus, sarcoidosis, Reiter’s syndrome,
Crohn’s disease, Behçet’s disease and ankylosing spondylitis.17
Indicators of uveitis secondary to one of these systemic
conditions include repeated bouts of iritis, bilateral presentation, keratic
precipitates, peripheral anterior synechiae (PAS) and granulomatous uveitis.18
One study suggested that more than 18% of patients with a uveitis associated
with a systemic condition developed secondary glaucoma, indicating that these
patients need to be monitored regularly.19
5. Treat aggressively. Once you have ruled out a
keratouveitis, begin aggressive dosing of corticosteroids at least q1h to q2h.
(However, q.i.d. dosing is recommended if using Durezol.2,3) You can always taper
the dose once a significant impact has been made on the iritis. Remember,
passively-treated, low-grade iritis is the most common cause of secondary
glaucoma in uveitis patients.20
6. Reestablish the blood-aqueous barrier. During the course
of uveitis, the blood-aqueous barrier is broken down due to an influx of
protein and inflammatory cells.5,21,22 So, in order to reestablish this
barrier, you must continue to taper corticosteroid therapy beyond elimination
of anterior chamber cell and flare.
New, potent steroids, such as Durezol, and safer, long-term
medications, such as Lotemax, will help you treat iritis with greater efficacy.
Additionally, if you differentiate keratouveitis, check IOP, rule out
endophthalmitis, look for a systemic cause, treat aggressively and reestablish
the blood-aqueous barrier, you will be in an excellent position to manage
iritis more effectively in clinical practice.
Neither Dr. Karpecki nor Dr. Shechtman have any direct
financial interest in the products mentioned.
1. Thean JH,
Hall AJ, Stawell RJ. Uveitis in herpes zoster ophthalmicus. Clin Exp
Ophthalmol. 2001 Dec;29(6):406-10.
2. Jamal KN, Callanan DG. The role of difluprednate
ophthalmic emulsion in clinical practice. Clin Ophthalmol. 2009;3:381-90.
3. Korenfeld MS, Silverstein SM, Cooke DL, et al.
Difluprednate ophthalmic emulsion 0.05% for postoperative inflammation and
pain. J Cataract Refract Surg. 2009 Jan;35(1):26-34.
4. Bikowski J, Pillai R, Shroot B. The position, not the
presence, of the halogen in corticosteroids influences potency and side
effects. J Drugs Dermatol. 2006;5(2):125-30.
5. Yamaguchi M, Yasueda S, Isowaki A, et al. Formulation of
an ophthalmic lipid emulsion containing an anti-inflammatory steroidal drug,
difluprednate. Int J Pharm. 2005 Sep 14;301
(1-2):121-8.
6. Inoue J. Preclinical pharmocokinetics of difluprednate
ophthalmic emulsion. Poster B741, program 2651. Presented at the Association
for Research in Vision and Ophthalmology’s Annual Meeting. Ft. Lauderdale,
Fla., May 2007.
7. Aasuri MK, Venkata N, Kumar VM. Differntial diagnosis of
microbial keratitis and contact lens-induced peripheral ulcer. Eye Contact
Lens. 2003 Jan;29(1 Suppl):S60-2.
8. Schubert HD, Federman JL. The role of inflammation in CW
Nd:YAG contact transscleral photocoagulation and cryopexy. Invest Ophthalmol
Vis Sci. 1989 Mar;30(3):543-9.
9. Besada E, Frauens BJ. Unilateral granulomatous
post-streptococcal uveitis with elevated tension. Optom Vis Sci. 2008
Nov;85(11):E1110-5.
10. Pleyer U, Ruokonen P, Heinz C, et al. Intraocular
pressure related to uveitis. Ophthalmologe. 2008 May;105(5):431-7.
11. Mermoud A. Physiopathology of uveitic glaucoma. Klin
Monatsbl Augenheilkd. 1997 May;210(5):269-73.
12. Panek WC, Holland GN, Lee DA, et al. Glaucoma in
patients with uveitis. Br J Ophthalmol. 1990 Apr;74(4):223-7.
13. Pavesio CE, Decory HH. Treatment of ocular inflammatory
conditions with loteprednol etabonate. Br J Ophthalmol. 2008 Apr;92(4):455-9.
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