Vernal keratoconjunctivitis (VKC) is a recurrent eye disorder affecting young males in hot, dry climates seasonally. It involves inflammation of the conjunctiva and cornea. Symptoms include itching, tearing, photophobia, and thick mucus discharge. Signs include papillae on the conjunctiva, plaques or ulcers on the cornea, and subepithelial scarring. Treatment involves mast cell stabilizers, antihistamines, steroids, antibiotics, and immunosuppressants applied topically or taken orally. Surgery may be needed for severe cases to remove plaques or grafts the cornea.

1. Vernal Keratoconjunctivitis
Presentor:Disaleni

2. Presentation title 2
Vernal keratoconjunctivitis (VKC) is
recurrent bilateral disorder in which
both IgE- and cell-mediated
immune mechanisms play
important roles. . It
characteristically affects young
males in hot dry climates in a
seasonal manner; however this is
not always the rule.

3. • Palpebral VKC primarily involves the upper tarsal conjunctiva. It may be
associated with significant corneal disease as a result of the close
apposition between the inflamed conjunctiva and the corneal epithelium
.• Limbal disease typically affects black and Asian patients.
• Mixed VKC has features of both palpebral and limbaldisease.
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Classification

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5. Diagnosis
Symptoms
• intense itching, which may beassociated with lacrimation
• photophobia
• a foreign body sensation
• burning and thick mucoid discharge
• Increased blinking is common
• Heaviness in eyelid

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Signs
A)Palpebral disease
1. Early-mild disease is characterized by conjunctivalhyperaemia and diffuse velvety
papillary hypertrophy onthe superior tarsal plate
2. Macropapillae (<1 mm) have a flat-topped polygonalappearance reminiscent of
cobblestone
3. Focal or diffuse whitish inflammatory infiltrates may be seen in intense disease
4. Progression to giant papillae (>1 mm) can occur, as adjacent smaller lesions
amalgamate when dividing septa rupture
5. Mucus deposition between giant papillae
6. Decreased disease activity is characterized by milderconjunctival injection and
decreased mucus production

8. B) Limbal disease
○ Gelatinous limbal
conjunctival papillae
that may be
associated with
transient apically
located white cellular
collections (Horner–
Trantas dots )
○ In tropical regions,
limbal disease may be
severe
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C) Mixed :Combined features of both forms

10. Vernal keratopathy
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Occours in about 50% patients of VKC frequent in palpebral disease and may take the
following forms:
• Superior punctate epithelial erosions associatedwith layers of mucus on the superior
cornea
• Epithelial macroerosions caused by a combination ofepithelial toxicity from
inflammatory mediators and adirect mechanical effect from papillae
• Plaques and ‘shield’ ulcers may developin palpebral or mixed disease when the
exposed Bowman membrane becomes coated with mucus and calcium phosphate,
leading to inadequate wetting and delayed re-epithelialization. This development is
serious and warrants urgent attention to prevent secondary bacterial infection.○
• Subepithelial scars that are typically grey and oval and may affect vision.

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○ Pseudogerontoxon can develop in recurrent
limbal disease. It is characterized by a paralimbal
band of superficial scarring resembling arcus
senilis , adjacent to a previously inflamed segment
of the limbus.
○ Vascularization does not tend to be prominent,
though some peripheral superficial vessel
ingrowth is common, especially superiorly.
○ Keratoconus and other forms of corneal ectasia
are more common in VKC and are thought to be at
least partly due to persistent eye rubbing.
○ Herpes simplex keratitis is more common than
average, though less so than in atopic
keratoconjunctivitis. It can be aggressive and is
occasionally bilateral.

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Treatment
General measures
• Allergen avoidance, if possible. An allergy specialist opinion may be requested; allergen
(e.g. patch) testing is sometimes useful, but often gives non-specific results.
• Cool compresses may be helpful.
• Lid hygiene should be used for associated staphylococcalblepharitis.
• Moisturizing cream such as E45 can be applied to dry, fissured skin
• .Bandage contact lens wear to aid healing of persistent epithelial defects.

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Local treatment
Mast cell stabilizers (e.g. sodium cromoglicate, nedocromil sodium, lodoxamide) reduce the
frequency of acute exacerbations and the need for steroids and so form the basis of many
regimens, but are seldom effective in isolation. Several days to weeks of treatment are
needed for a reasonable response and long-term therapy may be needed (lodoxamide is not
licensed for long-term use).
Topical antihistamines (e.g. emedastine, epinastine, levocabastine, bepotastine) when used
in isolation are about as effective as mast cell stabilizers. They are suitable for acute
exacerbations but generally not for continuous long-term use, and courses of several
preparations are licensed for use only in courses of limited duration. A trial of several
different agents may be worthwhile.
Combined antihistamine and vasoconstrictor (e.g. antazoline with xylometazoline) may offer
relief in some cases.
Combined action antihistamine/mast cell stabilizers (e.g. azelastine, ketotifen, olopatadine)
are helpful in many patients and have a relatively rapid onset of action.
Non-steroidal anti-inflammatory preparations (e.g. ketorolac, diclofenac) may improve
comfort by blocking non-histamine mediators. Combining one of these with a mast cell
stabilizer is an effective regimen in some patients

16. • Topical steroids (e.g. fluorometholone 0.1%, rimexolone 1%, prednisolone 0.5%, loteprednol etabonate 0.2% or 0.5%) are used for
(a) severe exacerbations of conjunctivitis and (b) significant keratopathy; reducing conjunctival activity generally leads to corneal
improvement. They are usually prescribed in short but intensive (e.g. 2-hourly initially) courses, aiming for very prompt tapering.
Although the risk of elevation of intraocular pressure is low, monitoring is advisable if long-term treatment is necessary. Stronger
preparations such as prednisolone 1% can be used but carry a higher risk of steroid-induced glaucoma.
• Steroid ointment (e.g. hydrocortisone 0.5%) may be used to treat the eyelids in AKC, though as with eye drops, the duration of
treatment should be minimized and the intraocular pressure (IOP) monitore
.• Antibiotics may be used in conjunction with steroids in severe keratopathy to prevent or treat bacterial infection
.• Acetylcysteine is a mucolytic agent that is useful in VKC for dissolving mucus filaments and deposits, and addressing early plaque
formation
.• Immune modulators○ Ciclosporin (0.05–2% between two and six times daily)may be indicated if steroids are ineffective, inadequate
or poorly tolerated, or as a steroid-sparing agent in patients with severe disease. The effects typically take some weeks to be exerted,
and relapses may occur if treatment is CHAPTERConjunctiva 5 151stopped suddenly. Irritation and blurred vision arecommon.○
Calcineurin inhibitors show increasing promise as analternative to steroids in the treatment of allergic eye disease. Tacrolimus 0.03%
ointment can be effective in AKC for severe eyelid disease. Instillation into the fornices has been effective in modulating conjunctival
inflammation in refractory cases.
• Supratarsal steroid injection may be considered in severe palpebral disease or for non-compliant patients. The injection is given into
the conjunctival surface of the anaesthetized everted upper eyelid; 0.1 ml of betamethasone sodium phosphate 4 mg/ml,
dexamethasone 4 mg/ml or triamcinolone 40 mg/ml is given.
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17. Systemic treatment
• Oral antihistamines help itching, promote sleep and reduce nocturnal eye rubbing.
Because other inflammatory mediators are involved besides histamines, effectiveness
is not assured. Some antihistamines (e.g. loratadine) cause relatively little drowsiness
.• Antibiotics (e.g. doxycycline 50–100 mg daily for 6 weeks, azithromycin 500 mg once
daily for 3 days) may be given to reduce blepharitis-aggravated inflammation, usually in
AKC
.• Immunosuppressive agents (e.g. steroids, ciclosporin, tacrolimus, azathioprine) may
be effective at relatively low doses in AKC unresponsive to other measures. Short
courses of high-dose steroids may be necessary to achieve rapid control in severe
disease. Monoclonal antibodies against T cells have shown some promise in refractory
cases
.• Other treatments that may be effective in some patients include aspirin in VKC
(avoided in children and adolescents due to Reye syndrome risk), allergen
desensitization, and plasmapheresis in patients with high serum IgE levels.
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18. Surgery
• Superficial keratectomy may be required to remove plaques or debride
shield ulcers and allow epithelialization. Medical treatment must be
maintained until the cornea has re-epithelialized in order to prevent
recurrences. Excimer laser phototherapeutic keratectomy is an alternative
.• Surface maintenance/restoration surgery such asamniotic membrane
overlay grafting or lamellar keratoplasty, or eyelid procedures such as
botulinum toxin-induced ptosis or lateral tarsorrhaphy, may be required
for severe persistent epithelial defects or ulceration. Gluing may be
appropriate for focal (‘punched-out’) corneal perforations
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19. Thank you