Scleritis and episcleritis !

Inflammation of the white wall of the eye. Episcleritis is mild and settles alone; scleritis is very painful, often tied to autoimmune disease, and can blind.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

Two inflammatory causes of a red eye that differ in depth and severity. Episcleritis affects the thin vascular layer (episclera) between the conjunctiva and the sclera; it is benign, mildly uncomfortable and self-limiting. Scleritis affects the sclera itself, the tough collagen wall of the eyeball; it causes deep, severe pain, can thin or perforate the eye wall, and is frequently the first sign of a systemic autoimmune or vasculitic disease.

Who gets it

Episcleritis is the more common of the two and usually affects young and middle-aged adults, more often women. Scleritis is rarer, peaks in the fourth to sixth decades, is more frequent in women and is linked to a systemic disease in up to half of cases, rheumatoid arthritis being the commonest. Infectious scleritis is more frequent in men and after eye surgery. In Latin America, as elsewhere, it is seen mainly in rheumatology and ophthalmology referral services; tuberculosis and syphilis must be considered where they remain common.

Causes

Episcleritis: most cases idiopathic; some with rheumatoid arthritis, inflammatory bowel disease, gout, rosacea or herpes zoster
Scleritis, immune-mediated: rheumatoid arthritis, granulomatosis with polyangiitis, systemic lupus erythematosus, relapsing polychondritis, polyarteritis nodosa, spondyloarthritis and inflammatory bowel disease
Scleritis, infectious: herpes zoster, bacteria (for example Pseudomonas after surgery or trauma), tuberculosis, syphilis, and rarely fungi or parasites
Scleritis after eye surgery or trauma (surgically induced necrotising scleritis)
Idiopathic scleritis when no cause is found after work-up

Risk factors

Rheumatoid arthritis, especially long-standing or seropositive disease
ANCA-associated vasculitis and other systemic vasculitides
Systemic lupus erythematosus and other connective tissue diseases
Inflammatory bowel disease and seronegative spondyloarthritis
Previous pterygium surgery with antimetabolites or irradiation, or repeated eye operations
Female sex and middle age

Pathophysiology

In episcleritis, a superficial inflammatory reaction dilates the episcleral vessels without damaging the sclera, so the condition resolves without scarring. In scleritis, immune complexes and cell-mediated inflammation target the scleral collagen and the vessels that supply it, producing an obliterative vasculitis. In the necrotising form, vessel occlusion leads to ischaemia, collagen destruction and thinning, so the dark uveal tissue shows through as a bluish area and the globe may perforate. Inflammation can spread to the cornea (peripheral ulcerative keratitis), uvea and, in posterior scleritis, to the choroid and retina, causing exudative retinal detachment and choroidal folds.

Classification

Episcleritis: simple (sectoral or diffuse redness) or nodular (a mobile, tender nodule)
Anterior diffuse scleritis: the most common and most treatable form
Anterior nodular scleritis: firm, immobile, tender scleral nodules
Anterior necrotising scleritis with inflammation: the most destructive form, strongly linked to systemic vasculitis
Necrotising scleritis without inflammation (scleromalacia perforans): painless thinning, typical of long-standing rheumatoid arthritis
Posterior scleritis: behind the equator, little visible redness, risk of retinal detachment and vision loss

Symptoms and signs

Episcleritis: sectoral pink or red eye with mild discomfort or grittiness, watering and normal vision
Scleritis: severe, deep, boring eye pain that wakes the patient at night and radiates to the forehead, jaw or face
Scleritis: tenderness of the globe to touch and pain with eye movements
Scleritis: dark red or violaceous hue of the sclera, best seen in daylight
Light sensitivity and tearing, usually without purulent discharge
Blurred or reduced vision in scleritis with keratitis, uveitis or posterior involvement

Diagnosis

Clinical: Mainly clinical, with a slit-lamp examination in daylight. Episcleral vessels are superficial, move over the sclera and blanch after a drop of phenylephrine; in scleritis the deep vessels do not blanch, the eye is tender and the colour is violaceous. A full history and examination look for joint, skin, sinus, lung and kidney involvement.
Tests: Episcleritis needs no tests unless it recurs. Scleritis needs a systemic work-up: full blood count, inflammatory markers (ESR, CRP), kidney function, urinalysis, rheumatoid factor and anti-CCP, ANA, ANCA, syphilis serology, tuberculosis screening and, depending on the case, uric acid and sarcoidosis tests. Infectious scleritis needs scrapings or biopsy for culture.
Imaging: B-scan ultrasound shows thickened posterior sclera with fluid in Tenon space (the 'T sign') in posterior scleritis; orbital MRI or CT helps when the diagnosis is unclear. Chest imaging is used when tuberculosis, sarcoidosis or vasculitis is suspected.

Differential diagnosis

Conjunctivitis (discharge, diffuse redness, mobile superficial vessels)
Anterior uveitis (ciliary flush, cells in the anterior chamber, small pupil)
Acute angle-closure glaucoma (high pressure, mid-dilated pupil, cloudy cornea)
Keratitis or corneal ulcer
Subconjunctival haemorrhage
Orbital inflammation or orbital cellulitis

Goal of treatment

Relieve pain and inflammation, preserve the eye wall and vision, and find and control any underlying systemic or infectious disease.

Treatment

Conservative: Episcleritis: often settles in one to two weeks without treatment; cold compresses and lubricating drops ease symptoms, and a short course of topical corticosteroid or oral NSAID is used for persistent cases.
Medical: Non-necrotising anterior scleritis: oral NSAIDs are first line; topical treatment alone is not enough for scleritis.
Medical: Necrotising, posterior or NSAID-resistant scleritis: systemic corticosteroids, often intravenous pulses at first, plus steroid-sparing immunosuppressants (methotrexate, mycophenolate, cyclophosphamide) or biological agents such as rituximab or TNF inhibitors, coordinated with rheumatology.
Medical: Infectious scleritis: targeted antimicrobials (antivirals for herpes zoster, antibiotics, anti-tuberculosis therapy) and caution with corticosteroids.
Surgical: Scleral or corneal patch grafts for imminent or actual perforation.
Follow-up: Regular eye checks for vision, intraocular pressure and scleral thinning; monitoring of blood counts, liver and kidney function, glucose and blood pressure during systemic immunosuppression, and patient education to report new pain or visual loss quickly.

Complications

Scleral thinning and perforation of the globe
Peripheral ulcerative keratitis and corneal melting
Anterior uveitis, cataract and secondary glaucoma
Exudative retinal detachment, choroidal folds and macular oedema in posterior scleritis
Permanent visual loss
Adverse effects of long-term corticosteroids and immunosuppression

Prognosis

Episcleritis has an excellent outlook, though it may recur; it rarely progresses to scleritis. Diffuse and nodular scleritis usually respond well to treatment. Necrotising scleritis carries the greatest risk to sight and, when it reveals an untreated systemic vasculitis, a significant risk to life, which falls considerably with prompt immunosuppression. Relapses are common, so follow-up is long term.

Test yourself

Think of the answer, then tap the question to see it.

Which symptom best separates scleritis from episcleritis?

Severe, deep, boring pain that wakes the patient at night and a tender globe; episcleritis is only mildly uncomfortable.

What happens to the redness after a phenylephrine drop in episcleritis versus scleritis?

Superficial episcleral vessels blanch in episcleritis; the deep scleral vessels of scleritis do not.

Which systemic disease is most often associated with scleritis?

Rheumatoid arthritis; granulomatosis with polyangiitis is a classic cause of necrotising scleritis.

What is first-line treatment for non-necrotising anterior scleritis?

Oral NSAIDs; systemic corticosteroids and immunosuppressants are added for necrotising, posterior or resistant disease.

What is scleromalacia perforans?

A painless, non-inflammatory necrotising scleritis with scleral thinning, typically in long-standing rheumatoid arthritis.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: What Is Scleritis? (American Academy of Ophthalmology, 2025); Scleritis (EyeWiki, American Academy of Ophthalmology, 2025); Episcleritis (MedlinePlus, US National Library of Medicine, 2026).

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Representative model, for educational purposes only.

Sclera highlighted on the Durgical 3D model