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Notes on Vernal Keratoconjunctivitis (VKC) or Spring Catarrh

November 9, 2025
Vernal Keratoconjunctivitis
Index

    Notes on Vernal Keratoconjunctivitis (VKC) or Spring Catarrh

    Vernal Keratoconjunctivitis (VKC) is a chronic, recurrent, bilateral, interstitial, allergic inflammation of the conjunctiva that shows seasonal recurrence—most often during warm months.
    It is self-limiting, but can lead to corneal complications that may threaten vision if untreated.

    Synonyms

    • Spring Catarrh
    • Warm-Weather Conjunctivitis
    • Vernal Conjunctivitis

    Nature of the Disease

    • Recurrent and bilateral.
    • Non-infectious (allergic in origin).
    • Has a distinct seasonal pattern, particularly in spring and summer.
    • Involves both conjunctiva and cornea in varying degrees.
    • Self-limiting, generally subsides after puberty.

    Etiopathogenesis

    1. Immunological Mechanism

    VKC represents a complex allergic disorder involving both:

    • Type I Hypersensitivity (IgE-mediated): Immediate hypersensitivity to airborne allergens such as pollen, dust, and animal dander.
    • Type IV Delayed Hypersensitivity: Chronic cellular infiltration and tissue remodeling mediated by Th2 lymphocytes and cytokines (IL-4, IL-5, IL-13).

    2. Cellular Pathways

    • Mast Cells → Degranulate to release histamine, leukotrienes, prostaglandins → acute itching, redness, chemosis.
    • Eosinophils and Basophils → Release toxic proteins (e.g., major basic protein) → epithelial damage → shield ulcer.
    • Th2 Lymphocytes → Produce IL-4 and IL-13 promoting IgE synthesis; IL-5 stimulates eosinophil activation.
    • Fibroblasts and vascular changes → papillary hypertrophy and scarring.

    3. Immunoglobulin E (IgE) and Histamine Role

    • Elevated tear IgE levels in active VKC.
    • Histamine causes itching, hyperemia, and vascular permeability.

    Predisposing Factors

    1. Age: Commonly between 4 – 20 years.
    2. Sex: Markedly more common in boys (ratio ≈ 3 – 4 : 1).
    3. Season: Peaks in spring and summer; rare in winter.
    4. Climate: More prevalent in tropical and subtropical areas; rare in cold climates.
    5. Atopy: Often associated with eczema, asthma, allergic rhinitis or family history of atopy.
    6. Socio-environmental: Dusty, windy, sun-exposed environments increase recurrence.

    Pathology

    Conjunctival Changes

    1. Epithelial hyperplasia with downward projections into the subepithelial tissue.
    2. Adenoid layer infiltration with eosinophils, plasma cells, lymphocytes, and histiocytes.
    3. Fibrous layer proliferation → hyaline degeneration → papilla formation.
    4. Blood vessels: Dilated, permeable, and proliferated → chemosis and congestion.

    Corneal Changes

    • Punctate epithelial erosions.
    • Shield ulcer formation.
    • Plaque formation.
    • Limbal infiltration and pseudogerontoxon.

    Clinical Features

    Symptoms

    • Intense itching: hallmark symptom, aggravated by heat and wind.
    • Burning and foreign-body sensation.
    • Photophobia and lacrimation.
    • Thick ropy (mucoid) discharge.
    • Heaviness of eyelids and drooping appearance.

    Signs

    VKC manifests in three main clinical forms:


    1. Palpebral (Form)

    • Involves upper tarsal conjunctiva bilaterally.
    • Typical lesion: Large, flat-topped papillae arranged in a cobblestone or pavement-stone pattern.
    • Color: Grayish-pink elevations.
    • Severe cases: Papillae may become hypertrophic → “Giant Papillae”.
    • Discharge: Thick, ropy, whitish mucus.
    • Associated: Hyperemia, lid oedema, ptosis.

    2. Bulbar (Limbal) Form

    • Dusky-red triangular injection near the limbus.
    • Gelatinous thickened mass around the limbus.
    • Tranta’s spots: Small white raised dots — accumulations of eosinophils and epithelial debris at limbus.
    • More common in dark-skinned individuals (e.g., African, Indian populations).

    3. Mixed Form

    • Features of both palpebral and bulbar types.
    • Common in moderate to severe VKC.

    Corneal Involvement (Vernal Keratopathy)

    Corneal changes occur in ~6–30 % of patients.

    TypeDescription / Features
    1. Punctate Epithelial KeratitisFine superficial epithelial erosions in upper cornea that stain with fluorescein and rose bengal. Results from mechanical friction of papillae.
    2. Shield UlcerShallow transverse ulcer in upper cornea due to macro-erosions and eosinophil toxicity. Serious complication; predisposes to secondary bacterial infection.
    3. Vernal Corneal PlaqueWhite coating of fibrin and degenerating epithelium over healing ulcer — seen as an opaque plaque.
    4. Subepithelial ScarringRing-shaped opacity after repeated inflammation.
    5. PseudogerontoxonPeripheral lipid deposition near limbus forming a “cupid’s bow” appearance.

    Course and Prognosis

    • Chronic and recurrent, lasting 5–10 years.
    • Peaks in late childhood and early teens.
    • Spontaneous resolution after puberty in most cases.
    • Vision-threatening complications possible if corneal ulcer occurs.
    • Not contagious.

    Differential Diagnosis

    ConditionDifferentiating Features
    TrachomaFollicles present on upper tarsal conjunctiva; scarring and Herbert’s pits common.
    Atopic KeratoconjunctivitisOccurs in older patients (> 20 yrs); associated with eczema of eyelids.
    Giant Papillary ConjunctivitisRelated to contact lens use or foreign body; no seasonal pattern.
    Phlyctenular KeratoconjunctivitisLocalized phlycten lesions with ulceration and photophobia; delayed hypersensitivity to tubercular protein.

    Investigations

    1. Eosinophilia in tears or conjunctival scrape.
    2. Elevated serum IgE levels.
    3. Conjunctival smear: Eosinophils and mast cells.
    4. Tear film tests: Often show reduced stability.
    5. In vivo confocal microscopy: Demonstrates inflammatory cell infiltrate.

    Complications

    • Corneal shield ulcer → scarring → vision loss.
    • Steroid-induced glaucoma or cataract if steroids misused.
    • Keratoconus association (chronic eye rubbing).
    • Secondary bacterial keratitis.

    Treatment

    A. Topical Anti-inflammatory Therapy

    1. Corticosteroids: (Fluorometholone, Medrysone, Dexamethasone)
      • Rapid control of inflammation.
      • Short course under IOP monitoring.
    2. Mast Cell Stabilizers: (Sodium Cromoglycate 2%, Lodoxamide 0.1%)
      • Prevent mast cell degranulation; use prophylactically.
    3. Dual-Action Agents: (Azelastine, Olopatadine, Ketotifen)
      • Antihistaminic + mast cell stabilizing effect; excellent for long-term control.
    4. NSAID Drops: (Ketorolac, Diclofenac)
      • Symptomatic relief of pain and inflammation.
    5. Immunomodulators: (Cyclosporine 0.5–1%, Tacrolimus 0.03%)
      • Used in severe or steroid-resistant cases as steroid-sparing agents.

    B. Lubricating and Mucolytic Therapy

    • Artificial tears (carboxymethyl cellulose or hydroxypropyl methylcellulose) → comfort and tear film stability.
    • Acetyl Cysteine 0.5 % → breaks down mucoid plaque and ropy discharge.

    C. Systemic Therapy

    • Oral Antihistamines: (Cetirizine, Loratadine) for itching relief.
    • Short course of oral steroids: only for very severe unresponsive cases.

    D. Management of Giant Papillae

    • Supratarsal injection of long-acting steroid (e.g., triamcinolone).
    • Cryotherapy or Surgical excision if mechanically irritating cornea.

    E. General Measures

    • Avoid rubbing eyes.
    • Use cold compresses and dark goggles for symptom relief.
    • Maintain clean, dust-free environment.
    • Relocation to cooler climate in severe chronic cases can help.

    F. Treatment of Vernal Keratopathy

    LesionManagement
    Punctate KeratitisIncrease frequency of topical steroids and lubricants.
    Shield UlcerDebridement of necrotic epithelium ± bandage contact lens or amniotic membrane transplant.
    Corneal PlaqueSuperficial keratectomy to remove plaque.
    Non-healing ulcerExcimer laser therapeutic keratectomy (PTK) may be needed.

    G. Desensitization and Allergen Control

    • Allergen avoidance is key.
    • Immunotherapy has shown limited benefit but may be tried in refractory atopic patients.

    Follow-Up and Optometrist’s Role

    1. Monitor IOP during steroid therapy.
    2. Educate patients about avoiding eye rubbing.
    3. Recommend UV-protective sunglasses.
    4. Identify early signs of keratoconus and refer promptly.
    5. Reinforce compliance with maintenance therapy to prevent exacerbations.

    Prognosis

    • Usually self-limiting; resolves after puberty.
    • Chronic cases require long-term maintenance therapy.
    • With proper management, visual prognosis is good; however, untreated shield ulcers can lead to permanent corneal scarring.

    Summary Table

    AspectKey Points
    TypeAllergic (Keratoconjunctivitis)
    OnsetChildhood (4–20 yrs)
    LateralityBilateral
    SeasonWarm months / spring
    SymptomsItching, burning, ropy discharge, photophobia
    SignsCobblestone papillae, Tranta’s spots, shield ulcer
    TreatmentSteroids, mast cell stabilizers, antihistamines, immunomodulators
    ComplicationsCorneal ulcer, scarring, secondary infection, glaucoma (due to steroids)