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Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA
Correspondence to:
H Nida Sen
MD, National Eye Institute, National Institutes of Health, Bldg 10, Room 10N112, Bethesda, MD 20892, USA; nidamd@yahoo.com
Accepted for publication 1 November 2004
Keywords: corticosteroids; non-necrotising anterior scleritis
Scleritis commonly is a recurrent disease that requires long term immunosuppressive treatment that can be associated with significant adverse effects.1 Although topical and periorbital steroids are accepted therapeutic options for treatment of scleritis, subconjunctival administration of depot corticosteroids has been considered unsafe owing to the risk of scleral thinning and perforation.2–4 Recently, this has been challenged by reports describing the safe and effective use of subconjunctival depot steroid injections in patients with non-necrotising scleritis.5–7 Based on these reports we reviewed our experience using subconjunctival corticosteroid injections (SCI) in the management of non-infectious, non-necrotising anterior scleritis.
Case reports
A retrospective, non-comparative review of the clinical records of patients with scleritis evaluated at the National Eye Institute was performed and four patients treated with SCI were identified. Subconjunctival triamcinolone acetonide (Kenalog 40 mg/ml, Westwood Squibb Pharmaceuticals, Buffalo, NY, USA) (2–12 mg per injection) was given to an area of active scleritis through a 30 gauge needle following topical anaesthesia in one quadrant of the eye at one time. The initial indication for SCI in all cases was unilaterally active non-necrotising scleritis with adverse effects from systemic immunosuppressive therapy in patients with no known history of ocular hypertension associated with steroids and no underlying disease requiring additional systemic immunosuppressive therapy. Patients were evaluated within 1–2 weeks after injection and, 2–4 weeks thereafter. Mean follow up time was 15.75 (SD 7.5) months (range 5–22 months).
In all cases the scleral inflammation was controlled within 2–9 days of SCI without a concurrent increase in systemic immunosuppression. Although effective, each patient subsequently required additional injections because of recurrent disease activity in the treated or the fellow eye within an average time of 7.4 months. However, with one exception, all recurrences developed in a previously untreated quadrant of the eye. Only one patient showed a recurrence of active scleritis in a previously treated quadrant 21 months following the initial SCI. The maximum number of injections given in one eye was four. Following the initiation of the SCI each patient’s prednisone dose was tapered by >50% over an average of 5 months. Complications included subconjunctival haemorrhage and transient elevations in IOP that was managed with topical antiglaucoma medications and systemic acetazolamide (table 1). No patient showed enhanced scleral thinning or progression to necrotising scleritis.
Table 1 Clinical characteristics, treatment regimens, and adverse events with subconjunctival steroid injection
Comment
Approximately 37% of patients with scleritis have associated systemic diseases.8 A seminal review of scleritis cases showed that 26.1% of patients with scleritis require systemic immunosuppressive therapy and, of these, 37.5% experience a treatment complication.1
Although associated with cataract and increased intraocular pressure, local steroid therapy offers the benefit of anti-inflammatory control without the side effects of systemic immunosuppressive drugs. However, because of the potential risk of scleral thinning and perforation subconjunctival steroid injections have been avoided for the treatment of scleritis.
Recently, two retrospective studies demonstrated rapid clinical improvement with SCI with no evidence of scleral thinning or serious side effects in non-necrotising scleritis during follow up extending to 23 years.6,7 However, recurrences occurred in both studies requiring repeated injections. In a prospective study, patients with recalcitrant scleritis were able to discontinue all immunosuppressive therapy after treatment with SCI.5
Although SCIs were effective in rapidly controlling the active scleritis in our series, two patients developed steroid response and all developed recurrent scleritis requiring repeated injections. The major benefit of the SCI in this series was that they facilitated >50% reduction in each patient’s prednisone dose which could not be achieved or sustained before their use.
This study confirms the existing literature that SCI may be an effective adjunct for the treatment of active non-necrotising anterior scleritis in appropriately selected patients and that this therapy is not unequivocally associated with the risk of scleral thinning or perforation. Local treatment with steroid injections may help reduce potential side effects from systemic therapy in patients with active scleritis in the absence of active systemic disease. As with all retrospective small case series our results should be interpreted with caution.
Figure 1 Active diffuse anterior scleritis in the temporal quadrant of the left eye (patient 4, left eye directed nasally) (A), immediately after SCI (B), and 3 months following the SCI (C) is illustrated.
References
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