The document discusses various causes and management of acute red eye conditions, including conjunctivitis, episcleritis, scleritis, and others, emphasizing their presentations and treatments. Common causes are detailed alongside their symptoms and recommended interventions such as topical lubricants, antibiotics, and urgent referrals for severe cases. It highlights the importance of proper eye care and management to prevent complications and preserve vision.

1. Acute red eye
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2. Differential diagnosis
Common causes:
 Conjunctivitis
 Episcleritis
 Subconjunctival haemorrhage: spontaneous (e.g. coughing) or
traumatic. Self-resolves, but consider bleeding disorder if recurrent.
 Trauma: corneal abrasion (+ve fluorescein test), foreign body.

3. Site-threatening causes (often painful):
 Keratitis (corneal infection).
 Scleritis
 Anterior uveitis (iritis or iridocyclitis).
 Acute angle closure glaucoma.

4. Conjunctivitis
Inflammation of the conjunctiva, the clear moist
membrane covering the exposed sclera and inner
eyelids. Usually bilateral, but may start in one eye
before spreading.
Viral conjunctivitis
Most commonly due to adenovirus, which can come in
epidemic outbreaks.

5. Presentation:
 Acute red eye.
 Watery discharge. May dry to form yellow
crust, so don't just assume pus if you see
yellow!
 Mild foreign body sensation.
 Associated viral URTI.

6. Management:
 Supportive treatment with topical lubricant.
 Strict hand hygiene as highly contagious.
Bacterial conjunctivitis
Cause:
 Staph or strep.
 Gonorrhoea or chlamydia can be the cause in concurrent STI,
from hand transfer.

7. Presentation:
 Acute red eye.
 Mucopurulent discharge leading to crusting
and difficulty opening eyes in morning.
 Gonorrhoea may cause a severe
manifestation requiring referral.

8. Management:
Chloramphenicol eyedrops, though
usually self-resolves anyway. Apply to
both eyes, even if unilateral, to prevent
amblyopia.
Do not wear contact lenses.

9. Allergic conjunctivitis
Presentation:
 Acute red eye ± chemosis.
 Itchy, watery eyes.
 Usually seasonal (e.g. hay fever) or perennial (e.g.
dust mites).

10. Management:
Antihistamines for rapid relief and long-
term control, oral (e.g. cetirizine) or
topical (e.g. azelastine).
Topical mast cell stabilizer (e.g. sodium
cromoglicate) is an alternative for long-
term control.

11. Episcleritis
Pathophysiology
 Inflammation of the episclera, the thin vascular
sheet between the conjunctiva and sclera.
 Usually idiopathic, or secondary to RA, IBD,
polyarteritis nodosa, or sarcoidosis.

12. Presentation
 Acute red eye.
 Mild symptoms, perhaps with foreign body sensation.
 Resolves in 1-2 weeks.
Management
 Topical lubricants.
 Oral NSAIDs.

13. Scleritis
Pathophysiology
 Inflammation of the sclera.
 50% linked to connective tissue disease: RA, GPA
(Wegner's). May be the presenting complaint.
Presentation
 Severe, dull eye pain developing over days, tender to
touch.
 Bluish-red eye due to deep vascular engorgement.
 Blurred vision, photophobia.

14. Management
Rapid immunosuppression may be needed to preserve
sight.
Keratitis
Pathophysiology
 Inflammation of the cornea. Can progress to
ulceration.
 Cause can be bacterial, occurring in a contact-lens
wearer with inadequate lens care, or viral, usually
herpes simplex.

15. Presentation
 Acute red eye.
 Photophobia, severe pain, foreign body sensation.
 Purulent discharge and hypopyon – pus in anterior
chamber – may occur with Pseudomonas aeruginosa.
 Fluorescein staining may show abrasion (possible
precipitant), corneal ulcer, or dendritic lesion (herpes
simplex keratitis).

16. Management
 Urgent referral for corneal scrape and treatment, due to the
risk of sight loss from perforation.
 In contact lens wearers, culture lens, case, and cleaning
solution.
Non-infectious keratitis
 Can be caused by UV light, including in welders or sunbed
users with inadequate eye protection.
 Treat with cool compress and oral analgesia.

17. Anterior uveitis

18. Pathophysiology
Includes iritis – inflammation of the anterior chamber
and iris – and iridocyclitis – also affecting the ciliary
body.
Causes:
 Often idiopathic.
 HLA-B27 disease is the commonest identified cause: ankylosing
spondylitis, psoriatic arthritis, reactive arthritis, IBD.
 Less commonly: HSV, toxoplasma, sarcoidosis, Behcet's, juvenile
idiopathic arthritis, rheumatoid arthritis.

19. Intermediate uveitis (anterior
vitreous and ciliary body) and
posterior uveitis (choroid):
Less common than anterior uveitis.
Causes are similar to anterior uveitis.
Usually painless.

20. Presentation
Symptoms:
 Acute red eye.
 Photophobia
 Blurred vision.
 Deep aching pain.
 Floaters

21. Signs:
 Non-reactive, small pupil.
 Slit-lamp exam: cloudy aqueous humour ('flare') due
to WBCs and protein.
Management
 Topical steroids e.g. dexamethasone.
 Antimuscarinic cytoplegics e.g. cyclopentolate.

22. Endophthalmitis
Pathophysiology
Inflammation of the aqueous or vitreous humour, usually
infective.
Causes:
 Exogenous: pathogen inoculation during ophthalmic surgery
(commonly coagulase-negative staph) or trauma.
 Endogenous: infectious spread from elsewhere.

23. Presentation
Most commonly presents 3-5 days post-surgery
with:
 Red eye, hypopyon, and hazy cornea.
 Blurred vision.
 Pain (though can be painless).
 Lid swelling.

24. Investigations
 Slit-lamp exam: cells and cloudy aqueous
humour. Ultrasound if retina can't be
visualised.
 Vitreous aspiration or biopsy (vitrectomy) for
microbiology.
Management
Intravitreal antibiotics.

25. Acute angle closure glaucoma

26. Pathophysiology
 Closure of the iridocorneal angle leading to
↑intraocular pressure (IOP). A sight-threatening
emergency.
 Can also be chronic.
 Risk factors: hyperopia, female, age >60.

27. Presentation
Symptoms:
 Painful red eye, frontal headache.
 Haloes around lights, blurring, and visual loss.
Signs:
 Corneal edema or haziness.
 Non-reactive, mid-dilated pupil.
 Cupping of optic disc.

28. Investigations
Tonometry: IOP typically >30 mmHg.
Gonioscopy to examine anterior chamber
angle is the gold standard.

29. Management
 Immediate ophthalmology referral if suspected.
 Reduce IOP: topical agents (muscarinic agonist e.g.
pilocarpine +/- β-blocker e.g. timolol +/- α2-
agonist e.g. clonidine) plus acetazolamide PO/IV.
 Ophthalmology may continue medical
management, or use laser peripheral iridotomy if
refractory.

30. Thank you
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