Scleritis is an uncommon clinical entity that is frequently resistant to standard forms of topical and systemic treatment. The use of subconjunctival injections of corticosteroids for treating noninfectious, nonnecrotizing anterior scleritis has been discouraged in the literature for several decades because of a presumed risk for scleral thinning and globe perforation.1,2 The first report opposing this advice was published in 19953 and described 20 patients receiving injections during a 5-year period. Most had beneficial responses, and none developed scleral thinning or perforation.
The senior author (F.S.B.) of this report has used subconjunctival steroids as primary therapy for anterior scleritis for 28 years and has not seen significant scleral thinning or perforation as a result of an injection. We present this small case series to add supportive documentation of the safety and benefits of subconjunctival steroids for anterior nonnecrotizing scleritis. Although our experience using this mode of therapy extends beyond the 8 patients included in this series, we could not include all of our patients because some were treated before our department's use of a computerized database and thus their records were not locatable. We believe the patients included are a representative sample of our experience.
Our injection technique is as follows. Proparacaine is instilled in the patient's eye. A sterile cotton applicator soaked with proparacaine is placed on the globe over the intended injection site for 30 seconds. Most patients received triamcinolone acetonide (40 mg/mL) drawn into a 1-mm tuberculin syringe and injected through a 27-gauge needle over the involved area or next to an elevated scleral nodule. Reinjections were given usually at least 4 weeks apart.
In 1991, an 86-year-old white woman with a 13-year history of rheumatoid arthritis and chronic bilateral keratoconjunctivitis was seen for left eye pain. Both corneas had mild superior peripheral thinning. The left eye had moderate scleritis superotemporally (Figure 1, left). A subconjunctival injection of 40 mg of triamcinolone acetonide was given. Six days later, her pain had resolved and the scleral inflammation had subsided (Figure 1, right). One year later, she reported no further problems during a telephone follow-up.
Case 1. Left, Pretreatment view of left superior conjunctiva and sclera in an 86-year-old patient with rheumatoid arthritis. Note diffuse deep and superficial inflammation. Right, Same patient 6 days after a subconjunctival injection of 40 mg of triamcinolone acetonide in the upper temporal quadrant with prompt resolution of scleritis.
Three additional patients were treated with subconjunctival injections for first episodes of diffuse anterior scleritis. Each had resolution of pain and scleral inflammation within 1 week. Two of the patients had no recurrences during 18 to 45 months of follow-up. The third patient reported a recurrence 1 year later, received an injection from her local ophthalmologist, and the disease remained quiescent by her report 6 months afterward.
In August 1972, a 34-year-old white man had a 5-month history of pain and redness of the right eye, without improvement with topical steroid treatment. Visual acuity was 20/20 OU. The right eye had diffuse anterior scleritis (4+) temporally. Treatment with oral prednisone (60 mg daily) was begun. There was improvement within 5 days and the prednisone dose was reduced and discontinued over several weeks.
In November 1973, ankylosing spondylitis was diagnosed. One month later he had recurrent diffuse scleral inflammation temporally of the right eye and received his first subconjunctival injection of 35 mg of triamcinolone acetonide. Within 3 days his eye pain was diminished and the scleral inflammation was resolved superotemporally but persisted inferiorly, and he required an additional triamcinolone injection 1 month later.
The patient returned 18 months later with localized nodular scleritis in the right eye. No scleral thinning was noted. Another triamcinolone injection was given and during the next 27 months 7 additional injections for recurrences of pain and inflammation were administered at intervals ranging from 2 weeks to 9 months. In June 1976, mild scleral thinning was noted inferiorly in the right eye, with no inflammation. He then remained asymptomatic for 9 years.
In 1985, the patient developed diffuse anterior scleritis in the left eye and was given an injection that quieted the inflammation for 3 months, when he required another injection. One year later, both eyes developed recurrences and were treated with additional triamcinolone injections. In 1986, Crohn's disease was diagnosed and he began receiving oral prednisone (80 mg daily).
He was not seen again at our office for 5 years until 1992, when he had a follow-up examination. Systemic medications included diclofenac for the spondylitis and sulfasalazine and prednisone (20 mg) for the Crohn's disease. His visual acuity was 20/20 OU. He had no ocular complaints and both eyes were not inflamed. The previously noted area of slight scleral thinning inferonasally in the right eye persisted. During a 20-year period, he had received 15 subconjunctival injections of corticosteroids (12 in the right eye and 3 in the left) without complications or clinically significant scleral thinning.
In 1984, a 71-year-old white woman experienced an inflamed right eye for several months. A systemic evaluation for connective tissue disorders was negative. Her visual acuity was 20/25 OU. The right eye had inflammation (4+) with scleral thinning along the nasal limbus and with a scleral nodule posterior to the area of thinning (Figure 2, left). She was given 40 mg of triamcinolone acetonide subconjunctivally with a poor response. Two months later, the nasal bulbar conjunctiva was resected from the limbus to 8 mm posteriorly, and the eye improved for 4 years.
Case 3. Left, a 71-year-old woman with diffuse and nodular scleritis and associated keratitis recurrent for 15 years; this is a 1984 photograph showing an acute episode. Right, Same eye 10 years later after numerous interventions including subconjunctival triamcinolone, conjunctival recession, and systemic immunosuppressive treatment. Note quiet eye with a moderate band of scleral thinning nasally.
In the interim, the left eye developed recurrent episodes of nodular anterior scleritis. During the course of 2 years various treatments, including topical steroids, oral nonsteroidals (indomethacin), oral prednisone, subconjunctival steroids, conjunctival resections, and cytotoxic agents (azathioprine) were all tried with variable responses.
Ten years later, both eyes had been quiescent for more than 3 years. Visual acuity was 20/30 OD and 20/40 OS after successful cataract extractions in both eyes. Scleromalacia was apparent bilaterally (Figure 2, right).
In July 1993, a 56-year-old white woman had a 15-year history of intermittent chronic, painful nodular scleritis of the right eye. Her other medical problems included psoriasis, Hashimoto thryoiditis, irritable bowel syndrome, rheumatoid arthritis, and asthma. She was unable to tolerate oral nonsteroidal analgesics or systemic corticosteroids because of gastritis. Her systemic and ocular conditions both had improved during a 3-year period of treatment with chlorambucil, but she developed severe back pain as a complication of the medicine and it was discontinued. Her scleritis gradually returned afterward.
In 1993, the left eye developed scleritis for the first time. Visual acuity was 20/100 OD and 20/15 OS. The right eye had moderate scleral inflammation in all quadrants except a small area inferotemporally. Large, raised nodules measuring several millimeters in all dimensions were present. The left eye had a single, raised superotemporal nodule (Figure 3, left). Both corneas were clear without thinning, and the anterior chambers showed no inflammation. The right fundus had diffuse mild retinal edema throughout the posterior pole and 270° of peripheral choroidal effusion. The left fundus was normal.
Case 4. Left, Patient with a 15-year history of intermittent diffuse and nodular scleritis with failed systemic treatment. Note superonasal deep and superficial scleral inflammation. Right, Same eye 2 months after treatment with 60 mg of subconjunctival triamcinolone acetonide, much improved with residual steroid deposit beneath upper lid.
Oral indomethacin therapy (25 mg, 3 times daily) was initiated and tolerated several weeks before gastrointestinal adverse effects necessitated discontinuation. Chlorambucil therapy (2 mg daily) was then started. After several weeks, her pain had decreased but the scleral inflammation was unimproved. The dose was incrementally raised to 6 mg daily without improvement of the scleral inflammation before unacceptable leukopenia developed. Chlorambucil treatment was discontinued for 1 month and restarted at 4 mg, but the patient developed leg ulcers and the drug was discontinued entirely.
In March 1994, a total of 60 mg of triamcinolone acetonide was injected in 3 separate sites adjacent to the scleral nodules of the right eye. One month later, the eye was much improved without any scleral inflammation or pain, so the left eye was injected with triamcinolone. One month later, both eyes were pain free and without any scleral inflammation. The patient stated that it was the first time in years that her eyes had been white and painless (Figure 3, right). In the next 12 months the right eye was injected twice more and the left eye once. In June 1995 the visual acuity was 20/80 OD and 20/20 OS. The right eye had continued nodular elevation, but no associated scleritis. Neither eye had scleral thinning.
A second patient had a similar history and is included in this group.
Scleritis is an uncommon but potentially serious inflammatory condition that can accompany systemic diseases.4 Potentially useful treatments include systemic nonsteroidal anti-inflammatory drugs, systemic steroids, and systemic nonsteroidal immunosuppressive agents.2 Each of these groups of drugs can have significant systemic adverse effects.
When there is no coexisting illness requiring systemic treatment, it would be preferable to avoid the attendant problems of systemic therapies if a safe alternative existed. Subconjunctival steroids may be a preferable alternative, but until recently3 there were no published reports supporting this view.
We have had no complications of perforation, significant scleral thinning, or steroid-induced glaucoma with the use of subconjunctival steroid injections during 28 years. We have been impressed with the beneficial response that most of these 8 patients have shown. Patients in group 1 received a single injection for their episodes of scleritis, with dramatic improvement in a few days, and only 1 recurrence during follow-up periods ranging from 12 to 45 months. The 2 patients in group 2 are significant because of the length of their follow-up, 23 and 10 years, respectively. They received multiple injections that were variable in benefit, but did not cause scleral perforation or significant thinning. The patient in case 3 demonstrated scleral thinning in both eyes, but it developed gradually over many years, so it is difficult to determine whether the cause was the disease process itself or the therapeutic interventions. Group 3 represents 2 patients who were unable to tolerate systemic therapies and who responded favorably to subconjunctival steroids.
Our clinical impression is that subconjunctival steroids have a definite useful role in the treatment of noninfectious, nonnecrotizing anterior scleritis. We hope that others who have used this mode of treatment will share their experiences to add much-needed information to the literature.
This study was supported by an unrestricted grant from Research to Prevent Blindness Inc, New York, NY, and the Wisconsin Lions Foundation, Madison.
Corresponding author: Frederick S. Brightbill, MD, Department of Ophthalmology and Visual Sciences, University of Wisconsin, 2870 University Ave, Suite 102, Madison, WI 53705.
Croasdale CR, Brightbill FS. Subconjunctival Corticosteroid Injections for Nonnecrotizing Anterior Scleritis. Arch Ophthalmol. 1999;117(7):978-979. doi: