VERNAL KERATOCONJUNCTIVITIS

• BY:

• DR. ZULFIQAR ALI

• ASSISTANT PROFESSOR
• DEPARTMENT OF OPHTHALMOLOGY
• QAMC, BVH, BAHAWALPUR
VERNAL KERATOCONJUNCTIVITIS
• Pathogenesis
• Vernal keratoconjunctivitis (VKC) is a recurrent bilateral disorder
• IgE- and cell-mediated immune response.
• VKC is typically recognized as a type I hypersensitivity reaction,
• Evidence has been found that supports some involvement
of type IV hypersensitivity reaction.
• primarily affects boys
• Mean age of onset is 7 years
• common in warm dry climates
• over 90% of patients associated with asthma , eczema and hay fever
• two-thirds of cases have a family history of atopy.
• often occurs on a seasonal basis, with a peak incidence over late spring and summer,
although there may be mild perennial symptoms.
CLASSIFICATION
•    1    Palpebral VKC primary involves the upper tarsal conjunctiva.

   2    Limbal disease typically affects black and Asian patients.

   3    Mixed VKC has features of both palpebral and limbal disease.
SYMPTOMS
• consist of intense itching,
• lacrimation,
• photophobia,
• a foreign body sensation,
• burning and thick mucoid discharge.
• Increased blinking is common.
  
SIGNS
• Palpebral disease       
• conjunctival hyperaemia
• Different types of papallea
• Diffuse papillary hypertrophy on the superior tarsus
• Macropapillae (<1 mm) have a flat-topped polygonal appearance lead to cobblestones
• Giant papillae (>1 mm) can occur, as adjacent smaller lesions amalgamate when
dividing septa rupture.
   •    Mucus deposition between giant papillae shows active disease
   •    Decreased disease activity is characterized by milder conjunctival injection and
decreased mucus production
LIMBAL DISEASE OR LIMBITIS   
• •    Limbal papillae having white top lesions called Horner-Trantas dots
   •    Histologically they are collection of Eosinophils on the top of pappillae
• MIXED Signs of both limbal and palpebral variety
 COMPLICATIONS
• Keratopathy is more frequent in palpebral disease and may take the
following forms:   
• a    Superior punctate epithelial erosions associated with sheets of mucus
on the superior cornea
   b    Epithelial macroerosions caused by a combination of epithelial
toxicity from inflammatory mediators and a direct mechanical effect from
papillae.
   c    Plaques and ‘shield’ ulcers may develop in 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.
  
• d    Subepithelial scars that are typically grey and oval, and may affect
vision .
   e    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.
   f    Peripheral Superficial vasculrization   
•    Vascularization does not tend to be prominent, though some
peripheral superficial vessel ingrowth is common, especially
superiorly.
• ASSOCIATION
   •    Keratoconus and other forms of corneal ectasia are more
common in VKC.
   •    Herpes simplex keratitis is more common than average, though
less so than in atopic keratoconjunctivitis (AKC). It can be aggressive
and is occasionally bilateral.
LOCAL TREATMENT
•    1    Mast cell stabilizers (lodoxamide
   2    Antihistamines
   3    Combined preparations
•    4    Steroids (fluorometholone 0.1%, rimexolone 1%, prednisolone 0.5% or loteprednol
etabonate 0.2% or 0.5%) are usually prescribed in short but intensive courses, aiming for
prompt tapering. Although the risk of elevation of intraocular pressure is low, monitoring
is advisable if long-term medication is necessary, particularly in AKC.
   •    Stronger preparations such as prednisolone 1% can be used but carry a higher risk
of steroid-induced glaucoma.
   •    Supratarsal steroid injection may be considered in severe palpebral disease, for
non-compliance or for patients resistant to conventional therapy. The injection is given
into the conjunctival surface of the anaesthetized everted upper eyelid; 0.1 mL of
betamethasone sodium phosphate 4 mg/mL (Betnesol), dexamethasone 4 mg/mL or
triamcinolone 40 mg/mL is given.
•   IMMUNE MODULATORS   
• a    Ciclosporin 0.05% b.d. may be indicated if steroids are ineffective,
inadequate or poorly tolerated, or as a steroid-sparing agent in patients with
severe disease. The drug may cause ocular irritation and blurred vision when
used for several weeks and relapses may occur if it is stopped suddenly. Its
efficacy as a first line agent for long-term therapy requires further study.
   b    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.

   6    OTHER MEASURES   

• a    Antibiotics are used in conjunction with steroids in severe keratopathy to
prevent or treat bacterial infection.
   b    Acetylcysteine is a mucolytic agent that is useful in VKC for dissolving
mucus filaments and deposits, and addressing early plaque formation.
• SYSTEMIC TREATMENT
•    1    Antihistamines help itching, promote sleep and reduce nocturnal eye rubbing.
   2    Antibiotics (doxycycline 50–100 mg daily for 6 weeks or azithromycin 500 mg once daily
for 3 days) to reduce blepharitis-aggravated inflammation, usually in AKC.
   3    Immunosuppressive agents (e.g. steroids, ciclosporin, tacrolimus, azathioprine)
   4    Aspirin may be useful in VKC, although the risk of Reye's syndrome means it should be
avoided in children and adolescents (the group predominantly affected by VKC).

• SURGERY
•    1    Bandage contact lens wear may be appropriate to aid the healing of persistent epithelial
defects.
   2    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.
   3    Surface maintenance-restoration surgery such as amniotic 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.
 Adenoviral conjunctivitis
• Viral conjunctivitis is most frequently caused by an adenovirus (a non-
enveloped double-stranded DNA virus).
• MODE OF TRANSMISSION
• Transmission is generally by contact with respiratory or ocular
secretions, including via fomites such as contaminated towels.
• RISK OF SPREAD OF INFECTION
• Risk of spread is more in hospitals, schools and swimming pools.
• The spread of this highly contagious disease is facilitated by the ability
of viral particles to survive on dry surfaces for weeks, and by the fact
that viral shedding may occur for many days before clinical features
are apparent.
 TYPES
• 1    PHARYNGOCONJUNCTIVAL FEVER (PCF)
• Conjunctivitis associated with pharyngitis and fever
• Caused by adenovirus serovars 3, 4 and 7.
• MODE OF SPREAD
• It is spread by droplets within families with upper respiratory tract infection.
• COMPLICATION
• Keratitis develops in about 30% of cases but is seldom severe.
• 2. EPIDEMIC KERATOCONJUNCTIVITIS (EKC)
• It is keratoconjunctivits occus in epidemics
• caused by adenovirus serovars 8, 19 and 37.
• MODE OF SPREAD
• Direct contact with ocular secretions through fomites, tonometers etc.
• PRECAUTION
• Disinfection of instruments and clinical surfaces after examination of an infected patient (e.g. sodium
hypochlorite, povidone-iodine).
• COMPLICATON
• It is the most severe type and is associated with keratitis in about 80% of cases.
3. NON-SPECIFIC ACUTE FOLLICULAR CONJUNCTIVITIS
is the most common and is caused by a range of adenoviral
serological variants. Ocular involvement is generally milder than in
other forms of adenoviral infection although accompanying (usually
mild) systemic symptoms such as a sore throat or cold are frequent.
4  CHRONIC/RELAPSING ADENOVIRAL CONJUNCTIVITIS,
characterized by chronic non-specific follicular/papillary lesions, is
rare but can persist for years.
CLINICAL FEATURES
SYMPTOMS
• Foreign body sensation
• Redness
• Watering
• Eye Lid Swelling
• Sore Throat
• Fever
Signs
•    1    Eyelid oedema
• 2. pre-auricular lymphadenopathy.
   3    conjunctival hyperaemia and follicles .
   4    Pin dot heamorrhages and chemosis
   5    Pseudomembranes or membranes may
   6    Corneal infilterates may be present
• 7. Pharyngitis and fever
•
 DIFFERENTIAL DIAGNOSIS

•    1    Acute haemorrhagic conjunctivitis typically occurs in tropical areas and

usually caused by enterovirus and coxsackievirus. It has a rapid onset and
resolves within 1–2 weeks; conjunctival haemorrhages are characteristic.
   2    Herpes simplex virus (HSV) can cause a follicular conjunctivitis,
particularly in primary infection, which is usually unilateral and often
associated with skin vesicles
   3    Systemic viral infections such as those common in childhood, e.g.
varicella, measles and mumps, can be associated with follicular
conjunctivitis.Varicella-zoster virus causes a conjunctivitis as part of
ophthalmic shingles. An HIV conjunctivitis is also recognized.
INVESTIGATION

• Spontaneous resolution usually occurs within 2–3 weeks.   

1. Giemsa stain shows predominantly mononuclear cells in adenoviral
conjunctivitis and multinucleated giant cells in herpetic infection.
   2. PCR are sensitive and specific for viral DNA.
   3. Viral culture with isolation is the reference standard but is
expensive and fairly slow (days–weeks), and requires specific transport
media. Sensitivity is variable but specificity around 100%.
   4. A ‘point-of-care’ immunochromatography test takes 10 minutes to
detect adenoviral antigen in tears; sensitivity and specificity are
excellent.
TRETMENT
1. Topical steroids such as prednisolone 0.5% q.i.d. may be required

INDICATION:
• Severe membranous or pseudomembranous adenoviral
conjunctivitis.
• Symptomatic keratitis
2. Topical antibiotics if secondary bacterial infection is suspected.
3. Cold (or warm) compresses for symptomatic relief.
4. Artificial tears q.i.d. may be useful for symptomatic relief.
5. Povidone-iodine is very effective against free (although less so
against intracellular) adenovirus, and has been proposed as a
means of decreasing infectivity.
6. Removal of symptomatic pseudomembranes or membranes.
7. Discontinuation of contact lens wear until resolution of symptoms.
COMPLICATIONS
• Epithelial microcysts (non-staining) are common during the early
stage.
• Punctate epithelial keratitis may develop within 7–10 days of the
onset of symptoms and resolves within 2 weeks.
• Focal white subepithelial/anterior stromal infiltrates may develop
beneath the fading epithelial lesions, probably as an immune
response to the virus, and may persist or recur over months or years .
TREATMENT OF COMPLICATIONS
• TOPICAL STERIODS Lotepred or FML Eye drops can be given TDS
• TOPICAL CICLOSPORIN Eye drops TDS
• FOLLOW UP
• Check IOP if using topical steriods
• COUNCELLING
• Hand hygiene,
• Avoiding eye rubbing and towel sharing.
THANK U