Allergic eye disease, trachoma and phlyctenules

3. Allergic Eye Diseases: SAC, PAC, VKC & AKC

Seasonal (SAC) & Perennial Allergic Conjunctivitis (PAC)

Type I IgE-mediated hypersensitivity reactions triggered by environmental airborne allergens (tree/grass pollens in SAC; dust mites and animal dander in PAC). Hallmark symptom is intense ocular pruritus (itching) accompanied by bilateral chemosis, eyelid oedema, and a fine papillary conjunctival reaction. Managed with dual-action topical antihistamine/mast-cell stabilisers (olopatadine 0.1%–0.2%, ketotifen 0.025%).

Vernal Keratoconjunctivitis (VKC)

A severe, bilateral, chronic external ocular inflammation predominantly affecting young boys (male-to-female ratio 3:1 to 4:1) between the ages of 4 and 12 residing in warm, dry, Mediterranean or subtropical climates. It often improves after puberty, but persistent adult disease occurs.

• Immunopathogenesis: Mixed Type I (IgE) and Type IV (cell-mediated Th2) hypersensitivity, characterized by massive local eosinophil infiltration and overproduction of IL-4, IL-5, and IL-13.
• Clinical Subtypes:
  1. Palpebral VKC: Features giant, flat-topped, polygonal cobblestone papillae ($> 1\text{ mm}$) covering the superior tarsal conjunctiva, associated with thick, ropy, stringy mucin discharge.
  2. Limbal VKC: Features thickened, gelatinous opacification of the limbus studded with Horner-Trantas dots—focal white chalky aggregates of degenerated eosinophils and epithelial debris.
• Corneal Complications: Punctate keratitis may coalesce into a vernal shield ulcer—a sterile, shallow, oval superior corneal stromal ulcer coated with a dense plaque of dried mucus and major basic protein that mechanically arrests epithelial migration.
• Stepwise Management:
  • Prophylaxis: Topical mast-cell stabilisers and cold compresses.
  • Acute flares: Short pulses of topical corticosteroids (fluorometholone or loteprednol; dexamethasone for severe inflammation).
  • Steroid-sparing maintenance: Use an appropriate ophthalmic formulation and local prescribing pathway. Ciclosporin 0.1% Verkazia has a European severe-VKC indication from age four in children and adolescents; tacrolimus use and formulation require specialist review. EMA Verkazia.
  • Shield ulcer: Debridement of the inflammatory plaque, bandage contact lens, or amniotic membrane transplantation.

Atopic Keratoconjunctivitis (AKC)

A chronic, debilitating ocular surface disease occurring in young to middle-aged adults (peaks between 20 and 50 years) with a personal history of severe atopic dermatitis (eczema) and asthma:

• Eyelid Signs: Erythematous, indurated, scaly, lichenified eyelids; blepharitis; lateral madarosis; and Hertoghe's sign (loss of lateral eyebrows).
• Conjunctival Signs: Hyperaemia with papillae predominantly affecting the inferior tarsal conjunctiva (distinguishing it from palpebral VKC where superior papillae dominate); progression to conjunctival cicatrisation, fornix foreshortening, and symblepharon.
• Corneal Signs: Corneal neovascularisation and scarring can occur, persistent epithelial defects, high risk of secondary microbial and herpetic keratitis, and anterior/posterior subcapsular "atopic shield" cataracts.
• Therapy: Periocular and topical Tacrolimus 0.03%–0.1% ointment, topical ciclosporin, specialist-selected systemic therapy for refractory disease. Dupilumab used for atopic dermatitis can itself cause ocular surface disease and should not be listed as routine ocular treatment.

Trachoma and Phlyctenular Disease

Trachoma follows repeated ocular Chlamydia trachomatis infection and can cause conjunctival scarring, inward lashes and corneal opacity. Examine the upper tarsus and distinguish active inflammation from old damage. The WHO simplified signs are follicular inflammation (TF), intense inflammation (TI), scarring (TS), trichiasis (TT) and corneal opacity (CO). TF requires at least five follicles of at least 0.5 mm in the central upper tarsus; TI obscures more than half the normal deep tarsal vessels. These are defined observations, not a guarantee that every patient progresses through a fixed sequence.

The SAFE strategy combines surgery for trichiasis, antibiotics, facial cleanliness and environmental improvement. Clearing infection does not correct established lid scarring or restore an opaque cornea. A person with inward lashes needs assessment for lid treatment as well as community infection control. Population antibiotic programmes use local public-health criteria, not an instruction to give every red-eye patient mass-treatment medication. See WHO trachoma guidance.

Phlyctenular keratoconjunctivitis is an antigen-related delayed hypersensitivity pattern, often with a small limbal or conjunctival nodule and surrounding injection. Corneal extension can cause photophobia, ulceration, vascularization and scarring. Lid bacterial antigen exposure is a common context; TB or other causes require consideration according to geography, exposure and systemic findings. A nodule does not by itself demonstrate active tuberculosis.

Treat the inflammatory lesion under supervision after excluding microbial keratitis, and address the associated lid or systemic cause. A brief topical steroid course may be appropriate with monitoring; steroid monotherapy on an unrecognized infectious ulcer can worsen disease. Recurrent episodes require reassessment of blepharitis, treatment adherence and the systemic differential rather than repeated unreviewed steroid prescriptions.

In a child with a shield ulcer, assess plaque, infection, vision and steroid risk. In a patient with an inflamed limbal nodule, distinguish phlyctenular disease from infection. In a scarred tarsus with inward lashes, assess trachoma and competing cicatrising causes. Detailed MMP and SJS management is covered separately; a shortened fornix should not automatically be attributed to allergy.