Scleritis and Episcleritis
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Direct answer
Episcleritis is a benign, recurrent, usually sectoral inflammation of the episcleral tissue — mild ache, bright redness that blanches with topical phenylephrine 2.5-10%, and spontaneous resolution within weeks without consequence. Scleritis is its serious deep counterpart: severe, boring ocular pain that classically wakes the patient at night and radiates to the brow and jaw, a blue-violet hue that does not blanch with phenylephrine, tenderness of the globe, and an association with systemic inflammatory disease — rheumatoid arthritis above all — in roughly 40-50% of cases. Scleritis is classified as anterior (diffuse, nodular, necrotising with or without inflammation) or posterior (diagnosed on B-scan ultrasonography, where the T-sign of fluid along the sclera helps), and it is treated systemically — NSAIDs, corticosteroids and immunosuppressives — because it threatens the eye through keratitis, uveitis, glaucoma and staphyloma formation.
What you must remember
- The phenylephrine test to quote: instil phenylephrine 2.5% (or 10%); episcleral vessels blanch and the redness fades, while the deep scleral plexus of scleritis remains engorged — the bedside test that separates the two entities in one step.
- Pain character: scleral pain is deep, boring and aching, worst at night, waking the patient from sleep, radiating to the eyebrow, temple or jaw, and the globe is tender to touch; episcleritis is at most a mild irritation or ache, and tenderness is absent.
- Scleritis classification: anterior — diffuse (commonest, most benign), nodular, necrotising with inflammation (destructive, associated with rheumatoid and granulomatosis with polyangiitis), and necrotising without inflammation — scleromalacia perforans, a painless thinning in elderly rheumatoid women; posterior — pain, proptosis or vision loss with the T-sign on B-scan.
- Systemic associations: about 40-50% of scleritis cases have systemic disease — rheumatoid arthritis (the largest group), granulomatosis with polyangiitis (necrotising disease should always raise it), relapsing polychondritis, lupus, inflammatory bowel disease, and tuberculosis in Indian practice; rheumatoid patients with scleritis often have extra-articular disease marking higher mortality.
- Ocular complications: sclerosing and peripheral ulcerative keratitis, uveitis, raised pressure, cataract, and staphyloma or perforation in thinned sclera — why scleritis is sight-threatening and episcleritis is not.
- Episcleritis management: reassurance, cold compresses and lubricants; a short course of topical NSAID or weak steroid only if uncomfortable; investigate only for recurrent or atypical disease.
- Scleritis treatment ladder: oral NSAIDs for mild diffuse disease, systemic corticosteroids for refractory or nodular disease, and steroid-sparing immunosuppression (methotrexate, cyclophosphamide for necrotising disease) — plus treatment of the underlying condition with the rheumatologist.
- Two examinable associations: surgically induced necrotising scleritis (SINS) after cataract or pterygium surgery, and infectious scleritis after trauma, which worsens under steroids and needs antimicrobials instead.
How to work through two red eyes that behave differently
A 34-year-old woman has her third episode in a year of a red, mildly irritated right eye: examination shows a sectoral pink-red patch, neither tender nor painful, and phenylephrine 2.5% leaves barely any injection; vision 6/6, cornea clear. This is simple episcleritis — explain its benign recurring nature, give lubricants and cold compresses, and resist starting steroids for a self-limited event. Contrast a 52-year-old with rheumatoid arthritis whose eye aches deeply, wakes him at 3 a.m., hurts on touch and shows a bluish-violet bulge of deep vessels that phenylephrine does not touch — nodular anterior scleritis. His workup includes rheumatology review and treatment that starts with a systemic NSAID but escalates early to oral corticosteroids with immunosuppression in reserve, because necrotising transformation is the pathway to globe thinning. The step that separated them took one drop and one question about sleep — the clinical economy examiners want to see.
Where students slip
The recurring mistake is merging the two diagnoses into "red sclera" — episcleritis needs no systemic workup, while scleritis earns rheumatology referral, baseline investigations and systemic therapy, so the distinction is not academic. The second slip is comfort with the eye alone: necrotising scleritis can be the presenting manifestation of granulomatosis with polyangiitis, and the candidate who treats the eye without urinalysis and chest and sinus imaging misses a diagnosis with renal and pulmonary stakes. Third, students misread scleromalacia perforans precisely because it does not hurt: a painless thinned bluish sclera in an elderly rheumatoid woman is necrotising disease without inflammation — steroids are not the answer; protection and rheumatological control are.
Frequently asked questions
How does the phenylephrine test distinguish episcleritis from scleritis?
Phenylephrine 2.5-10% constricts the superficial episcleral vessels so episcleritic redness blanches; the deep engorged scleral vessels of scleritis remain unchanged.
Which systemic disease most commonly accompanies scleritis?
Rheumatoid arthritis, followed by other systemic vasculitides and connective tissue diseases; roughly 40-50% of scleritis patients have an identifiable systemic association.
What is scleromalacia perforans?
Necrotising anterior scleritis without inflammation — painless scleral thinning with uveal show, typically in elderly women with long-standing rheumatoid arthritis, managed without steroids.
How is posterior scleritis diagnosed?
By suspicion (deep pain, proptosis, choroidal folds, exudative detachment, vision loss) confirmed on B-scan ultrasonography showing thickened sclera and the T-sign of fluid tracking along the optic nerve.
What is the treatment ladder for scleritis?
Oral NSAIDs for mild diffuse disease, systemic corticosteroids for moderate or refractory disease, and immunosuppressive agents such as methotrexate or cyclophosphamide for necrotising and vasculitic disease, alongside control of the underlying systemic condition.