Painful Red Eye

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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.


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).



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 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


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


Scleritis: Area of active pink inflammation superiorly. Darkened area is thinning, exposing underlying choroid from repeated episodes. 1


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


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.


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



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



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.



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.


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



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).



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.



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.

Corneal Ulcer
Corneal ulcer: Dense infiltrates (white fluffy area of inflamed corneal stroma) that will have an overlying epithelial defect. Note hypopyon and significant injection. 5

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.


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



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.



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 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.


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).

Clinical presentation

Symptoms include severe pain, photophobia and rapidly progressive visual loss. Clinical signs may include hypopyon, conjunctival injection and corneal oedema.


  • Urgent ophthalmology input
  • Systemic and intravitreal antibiotics
  • Biopsy of vitreous for culture
Endophthalmitis: Circumciliary injection, hypopyon, corneal oedema. 8

Foreign Body

Injuries sustained as a result of an ocular foreign body (FB) can vary significantly. We will discuss ‘low speed’ foreign bodies and ‘high speed’ foreign bodies separately.

Low-speed foreign body


  • Small objects that aren’t actively propelled into the eye
  • Often occur secondary to daily activities (e.g. paint, dust, gravel)



  • Some ocular irritation is common and there may be redness, watering and a ‘foreign body sensation’ (the patient is often certain the FB is still present even after it has cleared).
  • Photophobia and minor visual changes may also be present if the foreign body was close to the central cornea (a.k.a. ‘visual axis’).



Clinical examination of the affected eye should include fluorescein application to look for corneal abrasions and inspection under the upper eyelid (usually everted with a cotton bud).

Clinical findings may include:

  • No foreign body present – the patient may have already removed the FB from the eye before their arrival.
  • A FB under the upper eyelid when you evert it – this may be associated with vertical corneal abrasions due to the FB being dragged up and down by blinking (the patient may also describe pain associated with blinking)
  • A FB embedded superficially in the conjunctiva or cornea – can be seen with a simple pen torch, and may stain green
  • Corneal abrasion or irritation



  • FBs can be easily removed with some local anaesthetic eye drops, a steady hand and a cotton bud (or a green needle if superficially embedded)
  • Antibiotics drops are often used for abrasions to prevent secondary infection
  • Lubricants are used for symptomatic relief


High-speed foreign body

In most cases, high-speed FBs will behave similarly to low-speed FBs. However high-speed foreign bodies do have the potential to cause more significant damage to the eye such as corneal lacerations and penetration of the globe. If there is suspicion of a penetrating injury from a high-speed foreign body, urgent ophthalmology input should be sought.


  • Actively propelled objects
  • Industrial or hobby based – things like grinding, hammering and welding without eye protection
  • The material might be known to the patient (metal fragments are common)



  • Pain, watering, photophobia
  • Visual acuity changes are concerning (e.g. corneal laceration/retinal damage)
  • Flashes and floaters may indicate damage to the retina



  • Conjunctival injection
  • Corneal abrasion or laceration
  • Corneal oedema (increased corneal opacity as shown in the image)
  • Ferric (iron-based) foreign bodies, if embedded, will typically leave an orange rust ring within 2-4 hours


Penetrating signs

  • Hyphaema (blood in the anterior chamber, produces a fluid level)
  • Visible holes in the iris and/or a distorted iris
  • Larger wounds may leak aqueous humour, resulting in reduced intraocular pressure (hypotony)
  • Larger wounds may also be ‘plugged’ by internal structures prolapsing (often a segment of the iris will plug a corneal wound)
  • Seidel’s test can be performed to check for leaks – apply fluorescein to the surface of the eye and look for diluting rivulets on the surface coming from the site in question. This indicates a leak of aqueous humour, and hence a penetrating injury


  • Penetrating injuries may require emergency surgery to salvage the globe
  • If the foreign body cannot be found by visual inspection, ultrasound or x-ray of the orbits may need to be performed



Chemical Injury


  • Accidental (cement, plaster, household cleaners, industrial substances)
  • Deliberate (ammonia, strong acids)

Alkalis tend to cause more severe injuries than acids – they cause liquefactive necrosis as they react and so propagate themselves deeper into the eye, whereas acids cause coagulative necrosis and impede their own progress.



  • Severe eye pain and watering
  • Reduced visual acuity
  • Skin burns – erythema, blistering



  • Corneal abrasion/ large epithelial defects
  • Associated skin damage
  • Blanching of the limbus (the join between the conjunctiva and cornea) which indicates and is important prognostically



  • Test the pH for all insults if readily available
  • The most important part of management is to irrigate, irrigate, and irrigate some more.
  • Urgent ophthalmology review
  • Admission is typically required for moderate to severe injuries, for intensive eye drop regimes and oral therapies, which may include:
    • Topical steroids (e.g. prednisolone) – reduce inflammation
    • Antibiotics (e.g. chloramphenicol) – prevent secondary infection
    • Cycloplegics (e.g. cyclopentolate) – paralyse the iris and help to reduce pain
    • Citric and ascorbic acid (helps with healing)
    • Analgesia
Chemical eye injury
Corneal opacity, limbal ischaemia and symblepharon 11


  • Potential causes of a red painful eye include scleritis, uveitis, corneal abrasion, corneal ulcer, viral keratitis, acute angle closure glaucoma, endophthalmitis foreign body and chemical injury.
  • The presence of eye pain and reduced visual acuity are red flags for sinister ophthalmological diagnoses.
  • Early recognition and referral to ophthalmology have the potential to be sight-saving.



Iris and lens

Hypopyon, photophobia, circumciliary injection and reduced visual acuity


  1. Imrankabirhossain [CC BY-SA 4.0 (], via Wikimedia Commons”
  2. By EyeMD (Rakesh Ahuja, M.D.). – Own work., CC BY-SA 2.5,
  3. Manimury at English Wikipedia – Transferred from en.wikipedia to Commons., Public Domain,
  4. Ophthalmic Atlas Images by, The University of Iowa. Licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.
  5. Ophthalmic Atlas Images by, The University of Iowa. Licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.
  6. Ophthalmic Atlas Images by, The University of Iowa. Licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.
  7. Jonathan Trobe, M.D. – The Eyes Have It, CC BY 3.0,
  8. Imrankabirhossain [CC BY-SA 4.0 (], via Wikimedia Commons”
  9. Ophthalmic Atlas Images by, The University of Iowa. Licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.
  10. Ophthalmic Atlas Images by, The University of Iowa. Licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.
  11. Ophthalmic Atlas Images by, The University of Iowa. Licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.


Fiona Kirkham

Reviewed by

Dr Ashley Simpson

Ophthalmology Registrar

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