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Summary Table

Category	Details
Risk Factors	Young to middle-aged adults (20-50 years), female predominance, associated with autoimmune conditions (rheumatoid arthritis, lupus, inflammatory bowel disease), though most cases are idiopathic
Etiology	Inflammation of the episcleral tissue (the thin vascular layer between the conjunctiva and sclera); most cases have no identifiable cause
Patient Presentation	Acute-onset unilateral redness, mild discomfort or foreign body sensation, notably no significant pain and no visual changes
Classic Physical Exam	Sectoral (localized) or diffuse redness that blanches with topical phenylephrine 2.5%, injected episcleral vessels with a salmon-pink hue, no tenderness on globe palpation
Key Diagnostic Results	Clinical diagnosis; no labs or imaging required in typical presentations. Phenylephrine test distinguishes it from scleritis
Management	Self-limiting; artificial tears for comfort, oral NSAIDs (e.g., ibuprofen) if symptomatic, topical corticosteroids reserved for refractory cases
Keywords	"Red eye with mild discomfort," "no vision loss," "blanches with phenylephrine," "sectoral redness," "self-limiting"

1. Pathophysiology

The episclera is a thin, highly vascular connective tissue layer situated between the overlying conjunctiva and the underlying sclera. In episcleritis, inflammation is confined to this superficial episcleral layer, which is why the disease runs a benign and self-limiting course. The episcleral vascular plexus becomes engorged and inflamed, producing the characteristic redness.

Because the inflammation does not extend into the deeper scleral tissue, there is no structural threat to the globe. This is the single most important distinction from scleritis, where inflammation penetrates the full thickness of the scleral wall and can lead to thinning, perforation, and vision loss. The superficial nature of the process explains why patients report only mild discomfort rather than the severe, boring pain seen in scleritis.

Most cases are idiopathic, but roughly one-third of patients have an underlying systemic inflammatory condition. The proposed mechanism involves a localized immune-mediated vasculitis of the episcleral vessels, triggered either by circulating immune complexes or local immune dysregulation.

A key clinical correlate of this superficial pathology is the phenylephrine blanching test. Topical phenylephrine 2.5% constricts the superficial episcleral vessels, causing the redness to fade. In scleritis, the deeper scleral plexus is inflamed and does not blanch, leaving a violaceous (blue-red) hue visible after phenylephrine application.

2. Classification and Clinical Manifestation

Classification of Episcleritis

Type	Frequency	Clinical Features
Simple (Diffuse)	More common (~70%)	Diffuse episcleral injection across a broad area, mild discomfort, rapid resolution within 7-10 days
Nodular	Less common (~30%)	Discrete, elevated, well-circumscribed nodule on the episclera; slightly more uncomfortable, takes longer to resolve (weeks), higher recurrence rate, stronger association with systemic disease

Scleritis vs. Episcleritis Comparison

This is the highest-yield table for exam purposes. The test-writer's goal is to see whether you can distinguish these two conditions, because their initial appearance overlaps.

Feature	Episcleritis	Scleritis
Layer involved	Superficial episclera	Deep sclera (full thickness)
Pain quality	Mild discomfort, foreign body sensation	Severe, deep, boring pain that radiates to the jaw, face, or periorbital area; wakes the patient from sleep
Tenderness on palpation	Absent	Present (exquisite globe tenderness)
Redness pattern	Bright red/salmon-pink, sectoral or diffuse	Deep violaceous (blue-purple) hue
Phenylephrine 2.5% test	Blanches (redness fades)	Does not blanch (deep vessels unaffected)
Vision	Normal	Can be reduced (risk of uveitis, keratitis, or posterior involvement)
Scleral thinning/necrosis	Never	Can occur (necrotizing scleritis)
Systemic disease association	~30% of cases	~50% of cases (stronger link, especially with granulomatosis with polyangiitis, rheumatoid arthritis)
Course	Self-limiting (days to weeks)	Chronic, relapsing, requires aggressive treatment
Treatment	Supportive: artificial tears, oral NSAIDs	Systemic NSAIDs, systemic corticosteroids, immunosuppressives
Complications	None	Scleromalacia, perforation, secondary glaucoma, vision loss

The quality of pain, the phenylephrine response, and the color of redness are the three pillars that separate these diagnoses.

3. Diagnostic Workup

Test	Role	Expected Finding
Clinical examination	Best initial and usually only test	Sectoral/diffuse episcleral injection, no scleral edema, mobile conjunctiva
Topical phenylephrine 2.5%	Key differentiating test	Blanching of episcleral redness confirms superficial inflammation
Slit-lamp examination	Confirms layer of inflammation	Engorged episcleral vessels without scleral involvement, no anterior chamber cells
Systemic workup (ANA, RF, ESR, CRP, ANCA)	Only in recurrent or bilateral cases	Ordered to screen for underlying autoimmune disease

Episcleritis is fundamentally a clinical diagnosis. In a straightforward first-episode presentation with unilateral sectoral redness, mild discomfort, normal vision, and a positive phenylephrine blanching test, no further workup is needed.

The phenylephrine test deserves emphasis because it is the most testable diagnostic maneuver. You instill one drop of phenylephrine 2.5% and reassess after 10-15 minutes. If the redness fades, the inflamed vessels are superficial (episcleral), confirming episcleritis. If the redness persists with a deep violaceous color showing through, the inflammation is scleral, and the diagnosis shifts to scleritis.

Slit-lamp examination should be performed to rule out concurrent anterior uveitis (which would suggest scleritis or another inflammatory process). In episcleritis, the anterior chamber is quiet with no cells or flare.

A systemic workup is not routine for a single uncomplicated episode. However, it becomes indicated when the patient presents with recurrent episodes, bilateral involvement, or the nodular subtype, as these patterns carry a higher likelihood of an underlying autoimmune condition. In that scenario, order ANA, rheumatoid factor, ESR/CRP, and consider ANCA if granulomatosis with polyangiitis is suspected.

4. Management and Treatment

Setting	Treatment	Details
Mild / first episode	Artificial tears	Lubricating drops 4-6 times daily for comfort
Moderate discomfort	Oral NSAIDs	Ibuprofen 400 mg TID or naproxen 250-500 mg BID for 1-2 weeks
Refractory to NSAIDs	Topical corticosteroid	Prednisolone acetate 1% QID, short course (1-2 weeks), with ophthalmology supervision
Recurrent episodes	Systemic workup + referral	Evaluate for underlying autoimmune disease

The cornerstone of management is reassurance and supportive care. Most episodes of episcleritis resolve spontaneously within 7-14 days without treatment. This self-limiting nature is itself a testable point: on the exam, the correct answer for a classic uncomplicated episcleritis vignette is often conservative management rather than aggressive pharmacotherapy.

Artificial tears provide symptomatic relief by reducing the foreign body sensation and mild irritation. Cold compresses can also help.

When discomfort interferes with daily activities, oral NSAIDs are the first-line pharmacologic therapy. Ibuprofen (400 mg three times daily) or naproxen (250-500 mg twice daily) for 1-2 weeks is standard. Note that the exam may test the preference for oral over topical NSAIDs, as oral agents address the episcleral inflammation more effectively than topical formulations for this condition.

Topical corticosteroids (prednisolone acetate 1%) are reserved for cases that fail to respond to oral NSAIDs. They should only be prescribed under ophthalmology supervision due to the risks of steroid-induced glaucoma and cataract formation. The exam commonly tests the principle that topical steroids are not first-line for episcleritis.

If a patient experiences three or more recurrences, a systemic autoimmune workup and rheumatology referral are warranted to investigate for conditions such as rheumatoid arthritis, lupus, or inflammatory bowel disease.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Scleritis	Both present with red eye and discomfort	Scleritis causes severe boring pain, globe tenderness, violaceous hue, does NOT blanch with phenylephrine, and threatens vision
Acute anterior uveitis	Red eye with possible photophobia	Uveitis shows ciliary flush (perilimbal injection), cells and flare on slit-lamp, and photophobia with consensual pain; vision is often affected
Bacterial conjunctivitis	Diffuse red eye	Purulent discharge, matted eyelids in the morning, bilateral involvement; no focal episcleral injection pattern
Allergic conjunctivitis	Red eye with discomfort	Bilateral, intense itching (the hallmark), chemosis, watery or stringy discharge, papillae on tarsal conjunctiva
Acute angle-closure glaucoma	Red eye with discomfort	Severe pain, mid-dilated fixed pupil, corneal edema/haze, markedly elevated IOP, halos around lights, nausea/vomiting
Subconjunctival hemorrhage	Focal redness on the eye surface	Painless, bright red, well-demarcated patch of blood that does NOT involve the episcleral vascular pattern; no injection
Pinguecula/pterygium (inflamed)	Localized redness on the nasal episclera	Visible raised yellowish (pinguecula) or fleshy triangular (pterygium) growth; chronic rather than episodic

6. Traps and High-Yield Pearls

The most common way students miss episcleritis questions is by overdiagnosing scleritis. When a vignette describes a red eye, many students default to the more dangerous-sounding diagnosis without checking for the discriminating features. The exam rewards you for recognizing that episcleritis is benign, self-limiting, and painless (or nearly so). If the patient has no severe pain, no vision change, and no globe tenderness, the answer is almost certainly episcleritis, not scleritis.

A second trap is the management question. Students who recognize episcleritis correctly may still choose topical corticosteroids as first-line therapy. The tested principle is that oral NSAIDs precede topical steroids, and many cases need nothing more than artificial tears and reassurance.

The phenylephrine blanching test is the single most testable clinical maneuver in this topic. If the vignette mentions that redness fades after instilling phenylephrine drops, the answer is episcleritis. If it does not blanch, think scleritis. This test appears frequently and should be committed to memory as an automatic trigger.

Finally, remember the association threshold: a single uncomplicated episode requires no systemic workup. Recurrent, bilateral, or nodular presentations warrant investigation for autoimmune conditions. The exam tests whether you know when to escalate the evaluation versus when to manage conservatively.

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