It is a recurrent, bilateral, interstitial, self-limiting,
allergic inflammation of the conjunctiva having a
periodic seasonal incidence.
It is considered a hypersensitivity reaction to some
exogenous allergen, such as grass pollens. VKC is
thought to be an atopic allergic disorder in many
cases, in which IgE-mediated mechanisms play an
important role. Such patients may give personal or
family history of other atopic diseases such as hay
fever, asthma, or eczema and their peripheral blood
shows eosinophilia and inceased serum IgE levels.
Predisposing factors
1. Age and sex. 4-20 years; more common in boys
than girls.
2. Season. More common in summer; hence the
name spring catarrh looks a misnomer. Recently
it is being labelled as 'Warm weather
3. Climate. More prevalent in tropics, less in
temperate zones and almost non-existent in cold
1. Conjunctival epithelium undergoes hyperplasia
and sends downward projections into the
subepithelial tissue.
2. Adenoid layer shows marked cellular infiltration
by eosinophils, plasma cells, lymphocytes and
3. Fibrous layer shows proliferation which later on
undergoes hyaline changes.
4. Conjunctival vessels also show proliferation,
increased permeability and vasodilation.
All these pathological changes lead to formation of
multiple papillae in the upper tarsal conjunctiva.
Clinical picture
Symptoms. Spring catarrh is characterised by marked
burning and itching sensation which is usually
intolerable and accentuated when patient comes in a
warm humid atmosphere. Itching is more marked with
palpebral form of disease.
Other associated symptoms include: mild
photophobia, lacrimation, stringy (ropy) discharge
and heaviness of lids.
Signs of vernal keratoconjunctivitis can be described
in following three clinical forms:
1. Palpebral form. Usually upper tarsal conjunctiva
of both eyes is involved. The typical lesion is
characterized by the presence of hard, flat topped,
papillae arranged in a 'cobble-stone' or 'pavement
stone', fashion (Fig. 4.20). In severe cases, papillae
may hypertrophy to produce cauliflower like
excrescences of 'giant papillae'. Conjunctival
changes are associated with white ropy discharge.
Fig. 4.20. Palpebral form of vernal keratoconjunctivitis.
2. Bulbar form. It is characterised by: (i) dusky red
triangular congestion of bulbar conjunctiva in
palpebral area; (ii) gelatinous thickened
accumulation of tissue around the limbus; and
(iii) presence of discrete whitish raised dots along
the limbus (Tranta's spots) (Fig. 4.21).
3. Mixed form. It shows combined features of both
palpebral and bulbar forms (Fig. 4.22).
Vernal keratopathy. Corneal involvement in VKC may
be primary or secondary due to extension of limbal
lesions. Vernal keratopathy includes following 5 types
of lesions:
1. Punctate epithelial keratitis involving upper
cornea is usually associated with palpebral form
of disease. The lesions always stain with rose
bengal and invariably with fluorescein dye.
2. Ulcerative vernal keratitis (shield ulceration)
presents as a shallow transverse ulcer in upper
part of cornea. The ulceration results due to
epithelial macroerosions. It is a serious problem
which may be complicated by bacterial keratitis.
3. Vernal corneal plaques result due to coating of
bare areas of epithelial macroerosions with a
layer of altered exudates (Fig. 4.23).
4. Subepithelial scarring occurs in the form of a
ring scar.
5. Pseudogerontoxon is characterised by a classical
‘cupid’s bow’ outline.
Fig. 4.21. Bulbar form of vernal keratoconjunctivitis.
Fig. 4.23. Vernal corneal plaque.
Fig. 4.22. Artist's diagram of mixed form of vernal
76 Comprehensive OPHTHALMOLOGY
Clinical course of disease is often self-limiting and
usually burns out spontaneously after 5-10 years.
Differential diagnosis. Palpebral form of VKC needs
to be differentiated from trachoma with pre-dominant
papillary hypertrophy (see page 67).
A. Local therapy
1. Topical steroids. These are effective in all forms
of spring catarrh. However, their use should be
minimised, as they frequently cause steroid
induced glaucoma. Therefore, monitoring of
intraocular pressure is very important during
steroid therapy. Frequent instillation (4 hourly) to
start with (2 days) should be followed by
maintenance therapy for 3-4 times a day for 2
Commonly used steroid solutions are of
fluorometholone medrysone, betamethasone or
dexamethasone. Medrysone and fluorometholone
are safest of all these.
2. Mast cell stabilizers such as sodium cromoglycate
(2%) drops 4-5 times a day are quite effective in
controlling VKC, especially atopic cases. It is
mast cell stabilizer. Azelastine eye drops are also
effective in controlling VKC.
3. Topical antihistaminics are also effective.
4. Acetyl cysteine (0.5%) used topically has
mucolytic properties and is useful in the treatment
of early plaque formation.
5. Topical cyclosporine (1%) drops have been
recently reported to be effective in severe
unresponsive cases.
B. Systemic therapy
1. Oral antihistaminics may provide some relief
from itching in severe cases.
2. Oral steroids for a short duration have been
recommended for advanced, very severe, nonresponsive
C. Treatment of large papillae. Very large (giant)
papillae can be tackled either by :
Supratarsal injection of long acting steroid or
Cryo application
Surgical excision is recommended for extraordinarily
large papillae.
D. General measures include :
Dark goggles to prevent photophobia.
Cold compresses and ice packs have soothing
Change of place from hot to cold area is recommended
for recalcitrant cases.
E. Desensitization has also been tried without much
rewarding results.
F. Treatment of vernal keratopathy
Punctate epithelial keratitis requires no extra
treatment except that instillation of steroids should
be increased.
A large vernal plaque requires surgical excision
by superficial keratectomy.
Severe shield ulcer resistant to medical therapy
may need surgical treatment in the form of
debridment, superficial keratectomy, excimer laser
therapeutic kerateotomy as well as amniotic
membrane transplantation to enhance reepithelialization.

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