What are the types of allergic conjunctivitis?
Allergic conjunctivitis is common and usually benign. The spectrum of ocular allergy includes seasonal allergic conjunctivitis (SAC), perennial allergic conjunctivitis (PAC), vernal keratoconjunctivitis (VKC), atopic keratoconjunctivitis (AKC) and giant papillary conjunctivitis (GPC). SAC and PAC account for most cases and cause no permanent damage; VKC and AKC are chronic and can threaten vision, with shield ulcers and limbal stem cell deficiency.
| Type | Who and when | Key signs | Mechanism |
|---|---|---|---|
| SAC | Seasonal pollen exposure; any age | Itching, hyperaemia, watery discharge, chemosis, lid oedema; mild papillary reaction | Type I IgE-mediated |
| PAC | Year round (dust mite, dander) | Same as SAC but milder and persistent | Type I IgE-mediated |
| VKC | Young boys, warm dry climates, spring and summer | Giant (cobblestone) papillae, Horner-Trantas dots, thick ropy mucus, shield ulcer | IgE plus cell-mediated (type IV, Th2), eosinophils |
| AKC | Adults aged 20 to 50 with atopic dermatitis | Perennial; inferior tarsal involvement, cicatrisation, lid eczema | IgE plus cell-mediated |
| GPC | Contact lens wearers, prosthesis, sutures | Giant papillae on the upper tarsal conjunctiva, mucus, lens intolerance | Mechanical plus immune; not classically IgE-mediated |
How does simple allergic conjunctivitis (SAC and PAC) present?
The hallmark symptom is itching, with diffuse bulbar and tarsal conjunctival injection. Discharge is clear and watery, the condition is typically bilateral, and minimal morning crusting may occur. Eyelid oedema and chemosis can be marked, and episodes often come with sneezing and rhinitis. Pain and reduced visual acuity are uncommon and should make you consider another diagnosis.
- Triggers: pollen (tree, grass, weed), house dust mites, mould, animal dander; risk factors are atopy, air pollution and pet contact.
- Diagnosis is clinical. Skin-prick tests or serum specific IgE can identify allergens; conjunctival scraping may show eosinophils.
- Fluorescein staining is done if a corneal abrasion is suspected.
- Papillary hypertrophy of the tarsal conjunctiva is the usual sign in allergic disease.
What is vernal keratoconjunctivitis (VKC)?
VKC is a recurrent, bilateral allergic inflammation, more common in males, starting usually after age five, with seasonal peaks in spring and summer (hence 'spring catarrh') and a tendency to become perennial. It is commoner in warm, dry climates and in tropical and sub-tropical countries. There is often a history of atopy; a family history of atopy is present in close to 49%. Most cases remit by puberty, although a few progress to AKC.
Mechanism: both IgE-mediated and cell-mediated (type IV, CD4 Th2) immunity, with activated eosinophils and cytokines (IL-4, IL-5, IL-13) in the conjunctiva. The adenoid layer is densely infiltrated with eosinophils, plasma cells, lymphocytes and histiocytes, and epithelial hyperplasia and fibroblast proliferation produce the giant papillae. Conjunctival scraping shows eosinophils.
| Form | Site | Hallmark |
|---|---|---|
| Palpebral | Upper tarsal conjunctiva | Velvety papillae, then flat-topped cobblestone macropapillae (under 1 mm); giant papillae (over 1 mm) when septa rupture; mucus between papillae; more corneal disease |
| Limbal (bulbar) | Peri-limbal bulbar conjunctiva; commoner in Black and Asian patients and severe in the tropics | Gelatinous thickened limbus with Horner-Trantas dots |
| Mixed | Both | Features of both forms |
What are the corneal complications of VKC?
VKC is a sight-threatening disease because of corneal involvement, mostly in the palpebral and mixed forms. The cornea is damaged by inflammatory cytokines and by mechanical trauma from the papillae.
| Complication | Description |
|---|---|
| Punctate epithelial erosions | Superior corneal punctate keratopathy, with mucus deposits; macroerosions in more severe disease |
| Shield ulcer | Oval, superior, sterile ulcer with plaque; calcium phosphate and mucus coat exposed Bowman's membrane, delaying wetting and re-epithelialisation; needs prompt treatment to avoid bacterial infection |
| Subepithelial scar | Oval, grey scar that reduces vision |
| Pseudogerontoxon | Paralimbal band of superficial scarring in limbal disease, mimicking arcus senilis |
| Keratoconus | From chronic eye rubbing |
| Limbal stem cell deficiency, vascularisation | Severe chronic disease |
Severity staging: the Bonini system (symptoms, hyperaemia, papillae, limbal involvement, Horner-Trantas dots and corneal disease, from quiescent to very severe) and the Gokhale system (limbal inflammation, papillae, epithelial disease, shield ulcers, limbal stem cell deficiency and fibrosis) guide treatment intensity. Corneal topography is advised to detect subclinical keratoconus.
What are AKC and giant papillary conjunctivitis (GPC)?
Atopic keratoconjunctivitis (AKC) affects adults aged 20 to 50 and is strongly linked to atopic dermatitis (over 90%), asthma and rhinitis. It is perennial, more chronic and less intense than VKC, but more cicatrising. Giant papillary conjunctivitis (GPC) is papillary inflammation of the upper tarsal conjunctiva caused by a foreign body on the ocular surface: contact lenses, ocular prostheses, sutures or cyanoacrylate glue.
| Feature | VKC | AKC | GPC |
|---|---|---|---|
| Age and sex | Young boys, remits at puberty | Adults 20 to 50 | Contact lens or suture exposure |
| Conjunctiva involved | Superior tarsal (palpebral), limbus | Inferior palpebral more than superior | Upper tarsal |
| Discharge | Thick, stringy, mucoid | Watery | Thick mucus, worse after lens removal |
| Papillae | Giant, cobblestone | Smaller; macropapillae can occur | Fine to medium; large ones may ulcerate at the apex |
| Skin and lids | Mild blepharitis | Eczema, Hertoghe sign (lateral eyebrow loss), Dennie-Morgan folds, madarosis | Mucus, deposits on lens |
| Cornea | Superior keratopathy, shield ulcer | Inferior erosions, scarring, vascularisation, keratoconus, herpes keratitis | Keratopathy uncommon; ptosis may occur |
| Cicatrisation | Not usual | Symblepharon, fornix shortening | No |
| Goblet cells | Increased | Decreased | - |
- AKC complications: anterior or posterior subcapsular cataract (partly from steroids), keratoconus, herpes simplex keratitis, higher risk of endophthalmitis from lid margin Staphylococcus aureus colonisation, and retinal detachment risk after cataract surgery.
- GPC symptoms: worsening itching, thick mucus, contact lens intolerance, blurred vision and a foreign-body sensation; signs include proteinaceous deposits on the lens, excessive lens movement and upper tarsal papillae. Review lens cleaning and maintenance.
- GPC, unlike SAC, PAC, VKC and AKC, is not IgE-mediated, but treatment and some pathways overlap with atopic disease.
How is allergic conjunctivitis treated?
The first step is allergen avoidance and non-drug measures: cold compresses, lid hygiene (preventing staphylococcal blepharitis) and lubricants. Dark goggles help photophobia in VKC; a bandage contact lens protects persistent epithelial defects. Then step up through drugs.
| Step | Drugs | Notes |
|---|---|---|
| Mild (SAC/PAC) | Topical dual-action antihistamine and mast-cell stabiliser (olopatadine, ketotifen); lubricants | Rapid onset and long-term disease-modifying effect; antihistamines act on H1 receptors |
| Mast cell stabilisers | Sodium cromoglicate (2%), nedocromil (2%), lodoxamide | Slow onset (weeks); better as maintenance and prophylaxis; less effective alone |
| NSAIDs | Ketorolac, diclofenac, nepafenac | Symptomatic relief |
| Topical steroids | Fluorometholone, loteprednol, rimexolone; stronger for severe disease | Short intensive course then taper; monitor IOP (steroid glaucoma, cataract) |
| Steroid-sparing | Cyclosporine (0.05% to 2%), tacrolimus (0.03% to 0.1%) | For recurrent or severe VKC/AKC; cyclosporine needs about 6 weeks, rebound on stopping |
| Severe palpebral VKC | Supratarsal steroid injection (betamethasone, dexamethasone or triamcinolone) | Everted lid; for patients unresponsive to drops |
| Systemic | Oral antihistamines, montelukast, dupilumab, omalizumab (off-label); doxycycline or azithromycin for blepharitis in AKC | Refractory disease or associated atopy |
Related reading: eyelid disorders, lacrimal apparatus and dacryocystitis and primary glaucoma (steroid-induced rise of IOP). Practise in NEET PG Ophthalmology PYQs, the INI-CET PYQs and the most repeated topics.
What are the common exam traps?
- VKC: young boys, spring and summer, upper tarsal cobblestone papillae, Horner-Trantas dots, shield ulcer, eosinophils in scraping, resolves at puberty.
- AKC: adults with atopic dermatitis, inferior conjunctiva, cicatrisation; goblet cells decreased (VKC increased).
- GPC: contact lens or suture; upper tarsal giant papillae; the only one not IgE-mediated.
- Shield ulcer is sterile and heals poorly because of Bowman's membrane exposure and calcium phosphate and mucus deposits.
- Pseudogerontoxon mimics arcus senilis in limbal VKC.
- Steroids must be monitored for IOP; use steroid-sparing cyclosporine or tacrolimus for chronic disease.