Painful Red Eye

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Table of Contents

This article covers the potential causes of an acutely painful red eye, including scleritis, uveitis, corneal abrasion, corneal ulcer, viral keratitis, acute angle closure glaucoma and endophthalmitis.

These serious ophthalmological conditions typically require urgent specialist evaluation and management, so early recognition and referral are essential.

Check out our article on the differential diagnosis of a painless red eye here.

You might also be interested in our medical flashcard collection which contains over 1000 flashcards that cover key medical topics.

Scleritis

Clinical presentation

Scleritis tends to present with dull boring eye pain, headaches, eye-watering and sometimes painful eye movements. Visual acuity can be affected, however, this is typically a late feature in severe scleritis. The affected area on the eye usually has a deep pinkish colour that is tender to the touch. There may also be dilated brighter red vessels superficial to these areas.

Scleritis can recur, resulting in thinning of repeatedly affected areas (as in the image below).

Causes

Scleritis is strongly associated (50% of cases) with underlying systemic rheumatological conditions (e.g. rheumatoid arthritis). Less commonly, scleritis can occur secondary to ocular surgery or infections (e.g. tuberculosis).

Management

Management involves treating the underlying cause, which may involve high-dose steroids in rheumatological disease and antibiotics for infectious causes. Urgent referral to an ophthalmologist is required for all patients presenting with possible scleritis.

Comparison of the key features of Scleritis vs Episcleritis

Episcleritis	Scleritis
May be sore, gritty, usually asymptomatic	Frankly painful, tender to touch
Linked to systemic conditions (30%)	Linked to systemic conditions (50%)
Dilated bright red vessels	Dull pinkish area, but may have overlying bright red vessels
Benign	Sight-threatening
Self-limiting	Requires systemic treatments
No investigation	Investigate
Moveable vessels that blanch with phenylephrine	Not moveable, little response to phenylephrine
Recurs – no thinning	Recurs – causes thinning
Sectoral	Diffuse and can include areas of necrosis

Uveitis

Uveitis is inflammation of the uveal tract, with or without inflammation of neighbouring structures (e.g. the retina or vitreous). Acute anterior uveitis is the most common sub-type and we will focus on this below.

Clinical Presentation

Symptoms

Typical symptoms are of a red, painful, watery eye that is photophobic. Visual acuity is also often mildly reduced. Unfortunately, these symptoms are relatively non-specific, with any insult to the cornea or uvea resulting in a similar constellation of symptoms.

Signs

Clinical findings may include:

Hypopyon – an inferior settled layer of ‘pus’ (white cells and debris)
An irregular pupil – due to posterior synechiae (attachment of the iris to the lens capsule)
Cloudy view – due to cells in the aqueous humour and corneal oedema
Circumciliary injection – injection particularly around the cornea
Some more specific signs found on slit lamp examination include ‘flare’, ‘cells’ and ‘keratic precipitates’
Uveitis can be difficult to evaluate without a slit lamp

Causes

Predominantly anterior uveitis affects young, white males and is idiopathic in a large proportion of these.

There are multiple systemic associations, including:

HLA-B27 positive autoimmune conditions, such as psoriatic arthritis and ankylosing spondylitis
Inflammatory bowel disease, sarcoidosis and Behcet’s disease
Infectious causes, such as herpes simplex, herpes zoster, TB, syphilis and hepatitides

Management

The aims of treatment are to control inflammation, prevent visual loss and minimise long-term complications of the disease and its treatment.

There is no standard treatment regimen: treatment is determined by the type of uveitis, whether it is secondary to infection and whether it is likely to threaten sight.

Treatment most commonly involves a slow tapering regime of topical steroids with cycloplegics under the care of ophthalmology, however systemic immunosuppressant or antimicrobial treatment is occasionally required for the less common causes of uveitis.

**Severe Acute Anterior Uveitis:** Note the cloudy cornea, conjunctival injection, irregularly shaped pupil and significant hypopyon. ²

Posterior synechiae visible after dilation ³

Corneal Abrasion

A corneal abrasion refers to a break in the epithelial surface of the cornea – similar to a graze on the skin.

Clinical Presentation

The extremely dense innervation of the cornea means that corneal abrasions are typically very painful. Other symptoms include redness, pain, watering and photophobia. Visual acuity may be mildly reduced if the insult is in the visual axis.

Epithelial defects can be very hard to see with the naked eye but stain brightly with fluorescein drops and a cobalt blue light.

Causes

Corneal abrasions tend to be secondary to trauma (eye pokes, gusts of wind, changing contact lenses) or foreign bodies.

Management

Most corneal abrasions will heal relatively quickly on their own, so the mainstay of management involves reduces the patient’s discomfort.

If a corneal abrasion is small and visual acuity has not been affected:

Chloramphenicol ointment – given to reduce the risk of bacterial superinfection (also acts as a lubricant)
Pain relief – ocular lubricants or oral analgesics
Avoid the use of contact lenses until the abrasion has healed

If the corneal abrasion is large (>60%), visual acuity is reduced, or if symptoms are not improving, the patient should be referred for review by an ophthalmologist.

If there is a suspicion of a penetrating injury, chemical injury or a retained foreign body, the patient needs urgent ophthalmology referral.

Central Corneal Abrasion — ^{Central corneal abrasion, after application of fluorescein ⁴}

Corneal Ulcer

Corneal ulcers can result in significant visual loss and they are therefore an ophthalmological emergency.

Corneal ulcers are usually secondary to an infected corneal abrasion, though certain pathogens may penetrate the epithelium without an initial insult (e.g. Neisseria species, Haemophilus).

In many cases, extended contact lens wear is the aetiological agent, as the lenses become colonised and infect small abrasions that result from lens insertion and removal.

Clinical Presentation

Corneal ulcers may initially present with similar symptoms to a corneal abrasion (e.g. pain, watering, photophobia). These symptoms may then escalate, involving worsening pain and visual acuity. Vision may be affected dramatically if the ulcer encroaches on the visual axis.

On examination, you may find a staining epithelial defect with associated haziness (infiltrates). The epithelial defect may appear fluffy, irregular and apparent even without a slit lamp (as below).

Causes

Identifying the infective organism is essential for effective treatment. As a result, samples need to be taken for culture (swabs, or corneal scrapes to gather infected epithelium).

Most causative organisms are similar to respiratory pathogens, with some exceptions:

Pseudomonas is common if tap water has come into contact with contact lenses
Acanthamoeba (protozoa) can be acquired from standing water (e.g. swimming pools) however this is uncommon.

Management

Severe corneal ulcers can require admission for intensive antibiotic treatment and mydriatic eye drops (a standard regime would be half-hourly in the day time, and hourly through the night). Left untreated, corneal ulcers can cause rapid deterioration in vision and permanent corneal scarring.

Viral Keratitis

Viral keratitis is a group of similar conditions which involve viral infection of the cornea.

Clinical Presentation

Symptoms are similar to those of a corneal ulcer (pain, watering, photophobia and reduced visual acuity). Some forms of viral keratitis may also affect other structures in the eye.

Most forms of viral keratitis result in a characteristic dendritic (branching) epithelial defect with associated inflammation.

Causes

The usual culprits are herpes simplex (which may come with cold sores) and varicella zoster (which may come with shingles, particularly V1 distribution).

Management

Topical antiviral medication is typically used to treat viral keratitis and all patients should be referred to ophthalmology.

Note: These conditions are the cause of the mantra ‘Do not apply steroids to the undiagnosed red eye’. This is because applying steroid to a herpes simplex keratitis will likely result in a ‘geographic ulcer’, or a very large, irregular epithelial defect (as you have impaired the body’s immune response).

Herpes Zoster Keratitis — Herpes zoster keratitis, with a pseudodendritic epithelial defect ⁶

Acute Angle Closure Glaucoma

Acute angle-closure glaucoma (AACG) is a condition of acutely raised intraocular pressure (IOP) associated with a physically obstructed anterior chamber angle. The ‘angle’ refers to that between the cornea and the iris where aqueous drainage takes place.

Clinical Presentation

In AACG, the angle becomes obstructed, resulting in aqueous accumulating and IOP rising rapidly. AACG typically presents with pain, headache, nausea, vomiting, reduced visual acuity and photophobia.

Clinical findings include a hazy cornea, reduced visual acuity and a mid-dilated unreactive pupil.

Management

The first step of management is to lie the patient flat on their back (gravity helps bring the lens away and open the anterior chamber angle).

The condition is treated acutely with:

Systemic pressure reducing agents – Acetazolamide (IV/oral)
Topical pressure reducing agents – e.g. Beta-blockers
Miotics (Pilocarpine) to constrict the pupil and open the angles
Peripheral iridotomy, or a laser hole through the iris, to allow a separate route for aqueous drainage, other than through the pupil

Acute Angle Closure Glaucoma — **AACG:** Note circumciliary injection, corneal haze, and mid-dilated ovoid pupil ⁷

Endophthalmitis

Endophthalmitis an ophthalmological emergency that can result in blindness and loss of the eye involved. It involves overwhelming infection of the internal structures of the eye.

Causes

It may be of endogenous origin, seeded from severe infections elsewhere (e.g. endocarditis). More likely though is an exogenous source (e.g. following cataract surgery or intravitreal injection).