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OP5.1 | Episcleritis — SDL Guide (Part 3)

Management of Episcleritis

The management of episcleritis is guided by the cardinal fact that it is a self-limiting condition that resolves spontaneously in the vast majority of patients within two to three weeks. The primary goal of treatment is symptom relief rather than cure, and the therapeutic ladder should be ascended only when symptoms are genuinely distressing.

Conservative management is the first step for most patients with simple episcleritis. This includes: (a) lubricant (artificial tear) eye drops — preservative-free drops four to six times daily to reduce ocular surface irritation; (b) cool compresses — for symptomatic relief of discomfort; and (c) reassurance — explaining the benign, self-limiting nature of the condition is therapeutically important and prevents unnecessary anxiety.

Topical NSAIDs (e.g. ketorolac tromethamine 0.5% eye drops, three to four times daily) can be used when lubricants alone provide insufficient relief. They have a modest anti-inflammatory effect on the episcleral vasculature and are generally well-tolerated.

Oral NSAIDs (e.g. flurbiprofen 100 mg three times daily or indomethacin 25-50 mg three times daily, taken with food) are used for more symptomatic cases, patients with nodular episcleritis (which tends to be more prolonged), or cases with frequent recurrences. A short course of two to three weeks is typically sufficient. Gastrointestinal precautions apply.

Topical corticosteroids (e.g. prednisolone acetate 0.5%) are sometimes used for a brief period in severe nodular episcleritis, but their role is limited and repeated courses carry risks (raised IOP, cataracts). They are NOT first-line for episcleritis.

For scleritis, the management paradigm is fundamentally different — systemic therapy is required:
1. Systemic NSAIDs (flurbiprofen 100 mg three times daily or indomethacin) are first-line for diffuse and nodular anterior scleritis.
2. Oral corticosteroids (prednisolone 1 mg/kg/day, tapering) are used when NSAIDs fail or for severe/necrotising cases.
3. Immunosuppressants (methotrexate, azathioprine, mycophenolate, cyclophosphamide for GPA-associated scleritis) are used for steroid-resistant cases or when the underlying systemic disease requires disease-modifying therapy.
4. Biological agents (rituximab for GPA, anti-TNF agents for RA-associated scleritis) are reserved for refractory cases.
5. Scleromalacia perforans (necrotising without inflammation) has no proven medical treatment — protection from trauma and management of underlying RA is the priority.

All patients with confirmed scleritis must be jointly managed with a rheumatologist.

Complications of Untreated/Severe Disease

Understanding the complication profile of these two conditions reinforces why distinguishing them accurately at the slit-lamp is clinically consequential for the patient. The difference in complication severity is stark — episcleritis is essentially benign while scleritis can be blinding.

Episcleritis has very few clinically significant complications. Occasional marginal keratitis (peripheral corneal inflammatory infiltrates) may occur in association with severe nodular episcleritis, but this is uncommon. Recurrences are the main burden — patients may have multiple episodes per year, each self-limiting. There is no risk of scleral destruction or vision loss from episcleritis itself.

Scleritis, when inadequately treated or when the underlying systemic vasculitis remains active, carries a serious and progressive complication burden that can culminate in globe perforation and permanent blindness:
1. Scleral thinning and ectasia (staphyloma) — progressive loss of scleral collagen leads to a blue-hued bulge through which the underlying uvea (choroid) is visible.
2. Corneal involvement — peripheral ulcerative keratitis (PUK) — melting of the peripheral cornea adjacent to the area of scleritis; can lead to corneal perforation.
3. Anterior uveitis — associated in approximately 30% of anterior scleritis cases, contributing to keratic precipitates, posterior synechiae, and raised IOP.
4. Cataract — from chronic inflammation or prolonged steroid use.
5. Glaucoma — from associated uveitis, steroid-induced rise in IOP, or angle involvement.
6. Globe perforation — the most feared complication of necrotising scleritis; the eye literally becomes so thin that it can perforate spontaneously or with trivial trauma.
7. Exudative retinal detachment and choroidal detachment — particularly in posterior scleritis.
8. Vision loss — the combined effect of corneal melt, macular oedema (posterior scleritis), and optic nerve involvement can lead to permanent visual impairment.

The prognosis of scleritis correlates strongly with the subtype: diffuse and nodular anterior scleritis generally respond well to treatment; necrotising scleritis and posterior scleritis carry a significant risk of visual morbidity; scleromalacia perforans has the worst anatomical prognosis.

Self-Assessment: Applying Your Clinical Reasoning

Before moving to the summary, consolidate your learning by working through these clinical reasoning challenges. Self-assessment at this stage — before review — is the single most powerful predictor of durable retention, because effortful retrieval strengthens the neural encoding of the material far more than re-reading. Use the framework you have built across the preceding arc steps: from the presenting pattern, through anatomy and pathophysiology, through examination findings, to diagnosis and management decisions.

Scenario 1. A 34-year-old woman presents with a two-day history of a red right eye. She reports mild discomfort described as 'gritty and aching' but no severe pain, no photophobia, and no change in vision. On examination, there is sectoral bright-red injection of the temporal episclera with no nodule. After instillation of phenylephrine 2.5%, the injection blanches almost completely within 90 seconds. (a) What is the diagnosis? (b) What is your immediate management? (c) What systemic associations should you ask about, and under what circumstances would you investigate?)

Scenario 2. A 55-year-old man with known rheumatoid arthritis presents with severe boring pain in the left eye, worse at night and on eye movement, with a deep violaceous injection that does NOT blanch with phenylephrine 2.5%. Visual acuity is 6/9 in the affected eye. (a) Name the condition and its most likely subtype given the RA history. (b) Which urgent investigations would you order? (c) Outline a management plan including rheumatology liaison.)

Scenario 3. A 62-year-old woman with long-standing severe RA notices grey discolouration of the sclera bilaterally. She reports NO pain and NO redness. Slit-lamp reveals avascular grey plaques in the temporal sclera with underlying uveal pigment visible through thinned tissue. (a) What specific diagnosis does this represent, and what is the paradox? (b) What is the greatest risk to this patient, and how should she be counselled?)

Reflect on your answers in light of the Watson & Hayreh classification, the phenylephrine blanching test principle, and the systemic-ocular interface — the three conceptual pillars of this SDL.