Keratitis
Keratitis is inflammation of the corneal stroma and/or epithelium. Because untreated keratitis can progress rapidly to corneal scarring, perforation and permanent visual loss, it should be regarded as an ocular emergency that warrants same-day ophthalmology review.
A true “corneal ulcer” refers to infectious keratitis with an epithelium-stromal defect; the two terms are often (but not always) interchangeable in clinical practice.
Key risk factors
(approximate descending order of frequency)
| Contact-lens related | Ocular surface compromise | Systemic / iatrogenic |
|---|---|---|
| • Extended-wear lenses (overnight hypoxia) • Poor lens hygiene, swimming/showering with lenses | • Corneal micro-trauma (foreign body, abrasion, surgery, refractive procedures) • Neurotrophic cornea (post-herpetic, diabetes) • Exposure keratopathy (CN VII palsy, proptosis) • Severe dry-eye / meibomian gland dysfunction | • Chronic topical steroids or anaesthetics • Immunosuppression (HIV, chemotherapy, transplant) |
Aetiological classification & typical pathogens
| Type | Common pathogens / examples | Clinical clues |
|---|---|---|
| Bacterial | Pseudomonas aeruginosa (esp. contact-lens wearers) Streptococcus pneumoniae Staphylococcus aureus, incl. MRSA Klebsiella, Enterobacter, Moraxella | Rapid onset pain, purulent discharge, dense stromal infiltrate ± hypopyon |
| Fungal | Filamentous: Fusarium, Aspergillus Yeast: Candida albicans | History of vegetative corneal injury, feathery-edged infiltrate, satellite lesions |
| Viral | HSV-1: dendritic or geographic ulcers VZV ophthalmicus Adenovirus (epidemic keratoconjunctivitis) | Reduced corneal sensation (HSV), branching dendrites that stain with fluorescein |
| Protozoal | Acanthamoeba spp. | Severe “pain out of proportion”, ring-shaped stromal infiltrate; often contact-lens hygiene lapse |
| Marginal / immune | Hypersensitivity to Staph. antigens (blepharitis, rosacea) | Peripheral sterile infiltrates adjacent to limbus, minimal epithelial defect |
| Non-infectious / exposure-related | Trichiasis, entropion, foreign body, UV keratitis (welder’s flash), neurotrophic keratopathy, autoimmune (RA, GPA) | History of mechanical or UV insult; often bilateral in UV-induced cases |
Clinical presentation
- Symptoms
- Acute ocular pain or foreign-body sensation (in contrast, simple corneal abrasion pain usually improves within 24–48 h)
- Progressive photophobia, lacrimation, blepharospasm
- Blurred vision or reduced visual acuity
- Discharge: mucopurulent in bacterial, watery in viral/fungal
- Acanthamoeba: disproportionately severe pain
- Signs
- Conjunctival injection (ciliary/limbal flush)
- Focal corneal infiltrate ± overlying epithelial defect (fluorescein stains green)
- Stromal oedema, Descemet’s folds
- Hypopyon (layered leukocytes in anterior chamber)
- Raised intra-ocular pressure or irregular pupil → suggests secondary uveitis or impending perforation
Bedside assessment
| Test | Expected finding |
|---|---|
| Fluorescein staining | Epithelial defect outlines ulcer; dendritic branching in HSV |
| Slit-lamp or loupe | White-grey stromal infiltrate, endothelial plaque, keratic precipitates |
| Corneal sensation | Reduced in herpetic or neurotrophic keratitis |
| Pen-torch test | Photophobia and consensual pain indicate anterior uveitis component |
Microbiological work-up: For any ulcer >1 mm, stromal involvement, atypical organism suspicion, or symptoms not improving after 24 h empiric therapy, corneal scrapes for Gram & KOH staining, culture (bacterial, fungal) and PCR (HSV, VZV, Acanthamoeba) are mandatory prior to first antibiotic drop if possible.
Complications & red flags
- Rapid stromal melt → corneal perforation
- Destructive keratitis extending to sclera (sclerokeratitis)
- Endophthalmitis (intra-ocular spread)
- Permanent scarring/leucoma with visual axis involvement
- Secondary glaucoma from trabeculitis or synechiae
Red-flag features requiring same-day ophthalmology
- Central ulcer > 1 mm, any hypopyon or impending perforation.
- Severe pain out of proportion (think Acanthamoeba).
- Vision < 6/12 or rapidly worsening.
- Immunocompromised host or steroid-exposed eye.
- Bilateral herpetic disease in atopic or pregnant patient.
Adenoviral Keratoconjunctivitis
Key points
- Highly contagious; incubation 5–12 days.
- Begins unilaterally → typically bilateral within 2–3 days.
- Course:
- Day 0–7 conjunctivitis ± petechial subconjunctival haemorrhage.
- Day 7–10 punctate epithelial keratitis.
- Day 10–14 sub-epithelial infiltrates (“nummuli”) → photophobia, irregular astigmatism; may wax and wane for months.
- These symptoms and decreased visual acuity can persist for months or years
- ~25 % develop severe keratitis
- membranous or pseudomembranous conjunctivitis
- manifesting as punctate corneal erosions
- if not debrided they can scar the conjunctiva and symblepharon formation
- wherein the eyelid adheres to the cornea
Clinical course
| Phase | Typical timing (from day 0) | Key manifestations |
|---|---|---|
| Follicular conjunctivitis | 0 – 7 d | Unilateral red eye, watery discharge, chemosis, pre-auricular node. |
| Epithelial keratitis | 7 – 10 d | Fine punctate epithelial lesions → confluent punctate erosions. |
| Sub-epithelial infiltrates (SEIs) | 10 – 14 d | “Nummuli” in anterior stroma → photophobia, irregular astigmatism that can persist months. |
| Cicatricial phase (¼ of cases) | 2–6 w | Pseudo-/true membranes; risk symblepharon & conjunctival scarring. |
Typical ocular & systemic signs
| Ocular | Systemic |
|---|---|
| Conjunctival hyperaemia chemosis watery/mucoid discharge | Fever pharyngitis tender pre-auricular node |
| Follicular reaction of palpebral conjunctiva | |
| Punctate → nummular keratitis | |
| Photophobia Foreign body sensation Blurred vision/loss of visual acuity Eyelid swelling |
Management (eTG)
| Measure | Comment |
|---|---|
| Infection control | Work/school exclusion until tearing and redness settle (≈ 10–14 d); meticulous hand & surface hygiene. |
| Supportive | Cold compresses preservative-free lubricants q2-3 h oral analgesia. |
| Topical corticosteroid | Only if vision-threatening SEIs and after ophthalmologist review. Use low-potency agent (e.g. fluorometholone 0.1 % q.i.d.) and taper over ≥ 2–4 weeks to avoid rebound infiltrates. |
| Povidone-iodine | Single in-office 2–5 % PVP-I lavage can shorten viral shedding; evidence low-moderate and not yet routine eTG advice, but acceptable with ophthalmologist. |
No topical or oral antivirals are effective against adenovirus; prophylactic antibiotics are unnecessary.
Herpes simplex keratitis
Overview:
- Herpes simplex virus (HSV) is a highly prevalent, lifelong infection, often asymptomatic.
- Ocular HSV can cause significant, potentially vision-threatening disease, commonly unilateral but may be bilateral in rare cases.
Key Clinical Features:
- Epithelial disease: Classic dendritic lesions with terminal bulbs, staining with fluorescein and rose bengal.
- Vesicular lesions: Involving eyelids or periorbital adnexa.
- Bulbar conjunctival follicles
- Reduced corneal sensation
- Enlarged preauricular lymphadenopathy
Reactivation Pathophysiology:
Recurrent reactivation from the trigeminal ganglion may result in:
- Corneal scarring
- Stromal necrosis
- Neurotrophic keratitis (from trigeminal nerve damage)
- These can result in progressive visual impairment if untreated.
Layer-Specific Clinical Presentation:
| Layer | Hallmark Lesion | Symptoms / Signs |
|---|---|---|
| Epithelium | Branching dendrite with terminal bulbs; ± geographic ulcer | Acute pain, photophobia, watery discharge, ↓ corneal sensation |
| Stroma | Disciform stromal haze or necrotising ulcer | Blurred vision, stromal oedema, keratic precipitates, anterior chamber cells, ↑ IOP |
| Endothelium | Multifocal keratic precipitates, diffuse corneal oedema | Similar to stromal keratitis; may resemble anterior uveitis |
| Neurotrophic | Oval non-healing epithelial defect | Minimal or absent pain despite large ulcer due to loss of corneal sensation |
Risk Factors for Reactivation:
- Exposure to UV light (sunlight)
- Fever or intercurrent illness
- Trauma (ocular or periocular)
- Stress
- Thermal stimuli (e.g., heat)
- Trigeminal nerve manipulation
- Immunocompromised states (e.g., HIV, chemotherapy, systemic steroids)
Treatment:
- Primary HSV epithelial keratitis may resolve spontaneously, but topical or oral antiviral therapy (e.g., aciclovir):
- Shortens disease course
- Reduces viral replication
- May decrease risk of long-term complications
| Scenario | First-line (eTG) | Notes |
|---|---|---|
| Epithelial dendrite | Aciclovir 3 % oint. 1 cm ribbon 5 × daily until 3 d after healing (≤14 d) | Alternative: ganciclovir 0.15 % gel. |
| If ointment unavailable / bilateral / compliance concern | Valaciclovir 500 mg PO BD × 7 d or Aciclovir 400 mg PO 5 × daily | |
| Stromal / endotheliitis | Above plus prednisolone acetate 0.5 % q.i.d. (taper ≥3 w) and oral valaciclovir 500 mg BD cover | Ophthalmologist supervision essential. |
| Prophylaxis ≥ 2 episodes / year, post-keratoplasty, chronic stromal disease | Valaciclovir 500 mg PO OD for 6–12 m |
Avoid topical steroids in untreated epithelial disease — converts dendrite → geographic ulcer.
need urgent (same-day) ophthalmology referral for any HZO with eye involvement or Hutchinson’s sign:
- for Early, slit-lamp-based staging of ocular disease
- Distinguish
- epithelial dendrite vs.
- geographic ulcer vs.
- stromal/endothelial disease
- Distinguish
- Decide if/when to add steroids, establish antiviral cover – Topical steroids given without slit-lamp follow-up can convert a stromal keratitis into corneal melt or elevate IOP silently.
- Monitoring for complications
– stromal scarring
– neurotrophic keratitis
– secondary microbial super-infection
– raised IOP / herpetic trabeculitis - Long-term prophylaxis decisions
- Weigh recurrence risk, visual axis scars, patient comorbidities → decide on 6-12 months oral valaciclovir prophylaxis
Long-Term Complications:
- Corneal scarring & vascularisation
- Neurotrophic keratopathy (reduced corneal sensation)
- Severe dry eye syndrome
- Persistent epithelial defects
- Corneal thinning/perforation
- Chronic visual impairment
- acute retinal necrosis
- glaucoma from trabeculitis.
Prognosis:
- Generally favourable with timely treatment.
- However, prognosis varies based on recurrence frequency, corneal involvement depth, and immune status.
Practical GP workflow
- Confirm the dendrite
- Instil fluorescein and view under blue light; look for branching ulcer with terminal bulbs and reduced corneal sensation.
- Start topical antiviral immediately
- Aciclovir 3 % ointment 5 × daily or ganciclovir 0.15 % gel 5 × daily.
- Do not start steroids or antibiotic–steroid combinations.
- Arrange same-day ophthalmology review
- Phone the on-call registrar (or send to ED with letter) whether the patient is symptomatic or not.
- Educate & protect
- Advise no contact lenses, eye shielding at night, strict hand hygiene, and immediate return if vision drops, pain increases or photophobia worsens.
Herpes zoster ophthalmicus (HZO)
Clinical Presentation
- Dermatomal vesicular rash affecting the ophthalmic division (V1) of the trigeminal nerve
- Often preceded by pre-herpetic neuralgia
- Hutchinson’s sign (vesicles on the tip of the nose) is a strong predictor of ocular involvement due to nasociliary nerve involvement
- Ocular features (typically appear days 1–7):
- Superficial punctate keratitis
- Pseudo-dendrites (without terminal bulbs; do not stain with rose bengal)
- May be associated with anterior uveitis, episcleritis/scleritis, and elevated intraocular pressure (IOP)
Treatment (initiate within 72 hours of rash onset)
| Immunocompetent | Immunocompromised / sight-threatening |
|---|---|
| Valaciclovir 1 g PO TDS 7 d or Famciclovir 500 mg TDS 7 d or Aciclovir 800 mg 5 × daily 7 d | IV Aciclovir 10 mg/kg q8 h ≥ 7 d then PO |
Adjunctive Therapies:
- Ocular lubricants
- Cycloplegic agents (e.g., atropine) for anterior uveitis
- Topical corticosteroids for stromal keratitis or uveitis (only under ophthalmologist supervision)
need urgent (same-day) ophthalmology referral for any HZO with eye involvement or Hutchinson’s sign:
- for Early, slit-lamp-based staging of ocular disease
- for Rapid treatment escalation (Decides when to add/withhold topical steroids, antiviral ointments, IOP-lowering drops or systemic corticosteroids)
- Ongoing IOP & corneal-sensation monitoring
- Prevention & surveillance of vision-threatening complications
Potential Complications:
- Neurotrophic keratitis / corneal ulceration
- Stromal keratitis / corneal melt
- Chronic anterior uveitis
- Keratouveitic glaucoma
- Secondary cataract
- Post-herpetic neuralgia (especially in older adults)
Practical take-home for the GP
- Start oral antivirals immediately (within 72 h of rash):
- Valaciclovir 1 g TDS, or famciclovir 500 mg TDS, or aciclovir 800 mg 5-times-daily for 7 days.
- In immunocompromised or sight-threatening cases, initiate IV aciclovir 10 mg/kg q8 h and arrange hospital transfer.
- Add supportive therapy while waiting for review: preservative-free lubricants ± cycloplegic (e.g., atropine 1 % bid) for comfort.
- Refer same day (phone the on-call ophthalmology registrar) if:
- Rash in V1 distribution plus eye pain, blurred vision, photophobia, red eye, Hutchinson’s sign, or immunosuppression.
- Inability to arrange immediate review → send to ED with ophthalmology cover.
- Vaccination & PHN counselling: discuss zoster vaccine for future prevention and begin analgesic plan for neuralgia.
Microbial keratitis
Typical presentation
- Rapidly progressive pain, photophobia, mucopurulent discharge.
- Dense stromal infiltrate with overlying epithelial defect (> 1 mm), surrounding oedema, hypopyon; may progress in hours in Pseudomonas.
- Risk factors:
- contact-lens wear (esp. overnight) – the lens weakens corneal defences and supplies bacteria with a protected growth surface and warm, moist transport system, so even a small inoculum can rapidly establish infection.
- trauma, ocular surface disease
- surgery
- steroid use
- immunosuppression.
- a painful red eye in a lens wearer is Pseudomonas until proven otherwise; start hourly topical fluoroquinolone and refer same day.
Investigations
- Corneal scrape for Gram/KOH stain
- culture (bacterial, fungal)
- PCR (HSV, Acanthamoeba) before first drop where possible.
- Daily measurement of ulcer size & infiltrate.
Empiric treatment (eTG 2024 )
| Severity | Regimen | Dosing |
|---|---|---|
| Small peripheral infiltrate (< 1 mm) | Fluoroquinolone monotherapy | Ofloxacin 0.3 % or Ciprofloxacin 0.3 % 1 drop hourly × 48 h (incl. overnight), then q2 h daytime if improving. |
| Central / > 1 mm / vision-threatening | Fortified Cefazolin 5 % + Gentamicin 0.9 % 1 drop alternating every 30 min (i.e. each agent hourly) | Continue night-time dosing for first 48 h. |
| Contact-lens wearer &/or suspicion Pseudomonas | As above or Fluoroquinolone loading every 5 min × 5 then hourly | Review culture; escalate to fortified tobramycin 14 mg/mL if resistant. |
Add cycloplegic (e.g. homatropine 2 %) and oral doxycycline 100 mg BD for anti-collagenase effect if thinning.
Topical steroid may be introduced only after ≥ 48 h of documented microbial control to reduce scarring.
Sub-types & special therapy
| Organism | Additional points |
|---|---|
| Filamentous fungi (Fusarium, Aspergillus) | Natamycin 5 % 1 drop hourly ± oral voriconazole 200 mg BD. |
| Yeast (Candida) | Amphotericin-B 0.15 % hourly. |
| Acanthamoeba | Severe pain; early ring infiltrate; treat with PHMB 0.02 % + chlorhexidine 0.02 % hourly day & night for ≥ 48 h, then taper slowly over months; oral miltefosine under specialist. |
Complications
Corneal perforation, endophthalmitis, descemetocoele, secondary glaucoma, permanent central scarring with irregular astigmatism (indication for penetrating keratoplasty). EyeWiki
Practical implications for GPs & patients
- Education
- emphasise no water (shower/pool/spa) exposure
- strict case hygiene
- daily-disposable lenses for high-risk users
- Early red-eye triage – a painful red eye in a lens wearer is Pseudomonas until proven otherwise; start hourly topical fluoroquinolone and refer same day.
- Case replacement & “rub-and-rinse”
- mechanical rubbing then air-drying the case halves biofilm burden compared with soaking alone.
- Avoid overnight wear
- unless under specialist advice; it carries the single highest attributable risk.
- Review systemic factors
- diabetes
- immunosuppression
- smoking amplify infection risk
- optimise control where possible
Ultraviolet (photokeratitis / welder’s flash)
Presentation
- Bilateral intense pain, photophobia, lacrimation 6–12 h after UV exposure (snow, welding arc, tanning lamps).
- Slit-lamp: confluent punctate epithelial erosions across central cornea; conjunctival injection; normal pupil/IOP.
Treatment
- Remove contact lenses, rest in dark room.
- Preservative-free lubricants q1–2 h ± antibiotic cover chloramphenicol 0.5 % q.i.d.
- Cycloplegic (homatropine 2 %) for ciliary spasm.
- Oral NSAID / paracetamol.
- Do not dispense topical anaesthetic for home use (causes melt).
Heals within 24–48 h; review at 24 h to confirm re-epithelialisation.
Complications – rare; recurrent corneal erosion or secondary infection if epithelial healing delayed; cumulative UV damage predisposes to pterygium, cataract and macular degeneration.