Dr Abdul basit

PGR EYE UNIT 2

AMC/PGMI/LGH
 Common and self limiting
 Caused by
 Streptococcus pneumoniae
 Staphylococcus aureus
 Haemophilus influenzae
 Moraxella catarrhalis
 Symptoms
 Acute onset of redness,grittiness,burning and
discharge
 Involvement is usually bilateral
 On waking eyelids are frequently stuck
together and may be difficult to open
 Systemic symptoms may occur in patients
with severe conjunctivitis associated with
gonococcus,meningococcus,chlamydia,
H.influenzae
Signs
Eyelid odema and erythema in severe
infection
Conjunctival injection
Hyperacute purulent discharge
Superficial corneal punctate epithelial
erosions
Peripheral corneal ulceration
lymphadenopathy
Binocular conjunctival swabs and scrapings for
urgent gram staining to exclude gonococcla
and meningococcal infection
Culture should include enriched media such as
chocolate agar or thayer martin for
N.gonorrhoea
PCR may be required for cases that fail to
respond to treatment
 60 percent of case resolve within 5 days without
treatment
 Topical antibiotics
 usually 4 times daily for upta a week
 Ointments and gels provide a higher
concentration for longer periods than drops
 Following antibiotics are available
 Chloramphenicol,
aminoglycosides(tobramycin,gentamicin,
 neomycin),quinolones(ciprofloxacin,ofloxacin,
 Moxifoloxacin,levofloxacin)
 quinolones(ciprofloxacin,ofloxacin,
Moxifoloxacin,levofloxacin)
 Polymyxin B
 Fusidic acid
 bacitracin
 Gonococcal and meningococcal meningitis
should be treated with a
quinolone,gentamicin,chloranphenicol 1-2
hourly as well as systemic therapy
 Systemic antibiotics
 Gonococcal infection is treated with third
generation cephalosporin such as
ceftriaxone, quinolones and some macrolides
are alternative. Essential to seek advice from
genitourinary specialist.
 H.influenxae infexction particularly in
children are treated with oral amoxicillin with
clauvanic acid
 Meningococcal conjunctivitis with
intramuscular benzylpenicillin,ceftriaxone,or
oral ciprofloxacin should not be delayed
 Topical steroids may reduce scarring in
membranes and pseudomebranous
conjunctivtis
 Irrigation
 Contact lens wear
 Risk of transmission should be reduced with
hand washing and avoidance of towel sharing
 Chlamydial conjunctivitis is oculogenital
infection caused by serological variants D-K
of
C.trachoamatis and affects 5-20 percent of
sexually active young active adults in western
countries
 Transmission is by autoinoculation from
genital secretions. Incubation period is about
a week.
 Chlamydia trachomatis
 Exists in two principal forms
(a) infective extracellular ‘elementary body’
(b) intracellular replicating ‘reticular body’
 In males chlamydial infection is the most
common cause of non gonococcal urethritis.
 In females chlaydial urethriris typically causes
dysuria, discharge. It may progress to pelvic
inflammatory disease carrying a risk of
infertility 5-10 percent.
 Symptoms
 Consist of subacute onset of unilateral or
bilateral redness watering and discharge
 If untreated the conjunctivitis become chronic
 Watery or mucopurulent discharge
 Tender periauricular lymphadenopathy
 Large follicles
 Superficial puctate keratitis is common
 Perilimibal subepithelial corneal infiltrtes may
appear after 2-3 weeks
 Mild conjunctival scarring and superior
corneal pannus are not uncommon.
 Tarsal conjunctival scrapings
 Nucleic acid amplification tests such as PCR
are likely to be the investigation of choice in
time
 Geimsa staining of basophilic
intracytoplasmic bodies is performed by
applying scrappings on to a glass side
 Direct immunofloresence detects free
elementary bodies with about 90% sensitivity
and specifity
 Enzyme immunoassay for direct antigen
detection is also useful
 McCoy cell culture is highly specific
 Swabs can be taken for bacterial culture and
serology
 Systemic therapy involves
 Azithromycin 1g repeated after one week is
generally the treatment of choice
 Doxycycline 100mg twice daily for 10 days
 Topical antibiotics
such as erythromycin or tetracycline
ointment are sometimes used to acheive
rapid relief of ocular symptoms but are
insufficient alone
 Refferal to genitourinary specialist is
mandatory in confirmed cases
 Reduction of transmission risk
 Re testing
 Trachoma Pathogenesis
Trachoma is the leading cause of preventable
irreversible blindness in the world. It is
related to poverty, overcrowding and poor
hygiene, the morbidity being a consequence
of the establishment of re-infection cycles
within communities
 Elicits a chronic immune response consisting
of a cell-mediated delayed hypersensitivity
(Type IV) reaction to the intermittent
presence of chlamydial antigen and can lead
to loss of sight. Prior contact with the
organism confers short-term partial
immunity but also leads to a heightened
inflammatory reaction upon reinfection.
Vaccination has an effect similar to primary
infection in sensitizing the individual,
 Trachoma is associated principally with
infection by serovars A, B, Ba and C of
Chlamydia trachomatis, but the serovars D–K
conventionally associated with adult inclusion
conjunctivitis, and other species of the
Chlamydiaceae family such as Chlamydophila
psittaci and Chlamydophila pneumoniae have
also been implicated.
Features of trachoma are divided into an
‘active’ inflammatory stage and a ‘cicatricial’
chronic stage, with considerable overlap.
Active trachoma is most common in pre-
school children and is characterized by the
following:
○ Mixed follicular/papillary conjunctivitis
associated with a mucopurulent discharge. In
children under the age of 2 years the
papillary component may predominate.
○ Superior epithelial keratitis and pannus
formation
.
 ○ Linear or stellate conjunctival scars in mild
cases, or broad confluent scars (Arlt line) in
severe disease
 ○ Although the entire conjunctiva is involved, the
effects are most prominent on the upper tarsal
plate.
 ○ Superior limbal follicles may resolve to leave a
row of shallow depressions (Herbert pits ).
 ○ Trichiasis, distichiasis, corneal vascularization
and cicatricial entropion
 ○ Severe corneal opacification.
 ○ Dry eye caused by destruction of goblet cells
and the ductules of the lacrimal gland
Diagnosis being made on clinical features in
most cases. Various field techniques (e.g.
dipstick enzyme immunoassay) are available.
 Management The SAFE strategy for trachoma
management supported by the WHO and
other agencies encompasses Surgery for
trichiasis, Antibiotics for active disease, Facial
hygiene and Environmental improvement. •
Antibiotics should be administered to those
affected and to all family members. A single
antibiotic course is not always effective in
eliminating infection in an individual, and
communities may need to receive annual
treatment to suppress infection
 A single dose of azithromycin (20 mg/kg up to
1 g) is the treatment of choice.
 ○ Erythromycin 500 mg twice daily for 14 days
or doxycycline 100 mg twice daily for 10 days
(tetracyclines are relatively contraindicated in
pregnancy/breastfeeding and in children under
12).
 ○ Topical 1% tetracycline ointment is less
effective than oral treatment. • Facial
cleanliness is a critical preventative measure. •
Environmental improvement, such as access to
adequate water and sanitation, as well as
control of flies, is important.
 • Surgery is aimed at relieving entropion and
trichiasis and maintaining complete lid closure,
principally with bilamellar tarsal rotation
 Causes
 Organisms acquired during vaginal delievery
C.trachomatis, N.gonorrhoeae
HSV
Staphylococci are usually responsible for mild
conjunctivitis, other causes are streptococci,
H.influenzae and various gram negative
organisms
Topical preparations
Congenital nasolacrimal duct obstruction
 Timing of onset
 chemical irritation; first few weeks
 Gonococcal ; first week
 Staphylococci and other bacteria; end of first
week
 HSV; 1-2 weeks
 Chlamydia 1-3 weeks
 History
 Signs
 Mild sticky eyes may occur in stapylococcal
infection or with delayed nasolacrimal duct
canalization
 Discharge is watery in chemical preparations
and HSV infection
 Mucopurulent in chlamydial infection
 Purulent in bacterial infection
 Severe eyelid edema occurs in gonococcal
infection
 Eyelid and periocular vesicles may occur in
HSV infection and can aid early diagnosis and
treatment
 Corneal examination is mandatory and is
particularly important if gonococcal infection
is suspected as ulceration with rapid
progression is common
 Pseudomembranes are not uncommon in
chlamydial conjunctivitis
 Congenital glaucoma may masquerade as
neonantal conjunctivitis and should always be
considered particularly in monocular cases
 The results pf any parental testing for STI should
be obtained
 Conjunctival scrappings are taken for nucleic acid
amplification (PCR) particularly for chlamydia and
HSV
 Conjunctival swabs are taken with a calcium
alginate swab or sterile cotton tipped aplicator
for standard bacterial culture and chocolate agar
 Epithelial cella infected with HSV may show
eosinophilic intranuclear inclusions on Pap smear
 Conjunctival scrapings or fluid from skin vesicles
can be sent for viral culture for HSV
 Prophylaxis with
 povidone iodine 2-5% solution
 Erythromycin 0.5% or tetracycline 1%
ointment
 Silver nitrate 1% solutioin
 Chemical conjunctivitis does not require
treatment apart from artificial tears
 Mild conjuctivitis is treated with topical
antibiotics such as chloramphenicol,
erythromycin or fusidic acid ointment
 Moderate to severe conjunctivitis
 microscopy with gram staining alone is
highly sensitive and will often provide a
working diagnosis
 If diagnosi is uncertain but chlamydial
infection is a reasonable possibility; oral
erythromycin can be commenced on empirical
basis after samples have been collected
 If bacteria are evident on gram staining a
broad spectrum topical antibiotic
(choramphenicol, erythromycin,or bacitracin
for gram positive organisms, neomycin,
ofoxacin or gentamicin for gram negative)
should be used untill senstivities are
available.
 Severe conjunctivitis or when systemic illness
is suspected , requires hospital admission.
 Samples should be taken and broad spectrum
antibiotis erythromycin commenced
 Chlamydial infection is treated with oral
erythromycin for 2 weeks
 Gonococcal conjunctivitis is treated
systemically with 3rd generation
cephalosporin. Saline irrigation for removing
excess discharge should be considered
 Herpes simplex infection should always be
considered as a systemic condition and is treated
with high dose intravenous aciclovir under
pediatric specialist care. Toipcal aciclovir may be
considered in addition
 Microbiological advice should be sought in severe
cases
 Pediatric specialist involvement is mandatory
when systemic disease is present.
 Genitourinary refferal for mother and her sexual
contact is important when STI is diagnosed
 Viral conjunctivitis is a common external
ocular infection, adenovirus (a non-
enveloped double-stranded DNA virus) being
the most frequent (90%) causative agent. It
may be sporadic, or occur in epidemics in
environments such as workplaces (including
hospitals), schools and swimming pools. The
spread of this highly contagious infection is
facilitated by the ability of viral particles to
survive on dry surfaces for weeks
 The spread of this highly contagious infection
is facilitated by the ability of viral particles to
survive on dry surfaces for weeks
 Transmission
 is generally by contact with respiratory or
ocular secretions, including via fomites such
as contaminated towels.
 Presentation The spectrum of viral conjunctivitis
varies from mild subclinical disease to severe
inflammation with significant morbidity•
 Non specific acute follicular conjunctivitis
 most common clinical form of viral
conjunctivitis,
 Unilateral watering, redness, irritation and/or
itching, and mild photophobia occur, the
contralateral eye generally being affected 1–2
days later, often less severely. The condition is
usually milder than the other clinical forms of
adenoviral conjunctivitis; patients may have
accompanying (usually mild) systemic symptoms,
such as a sore throat or common cold.
 Pharyngoconjunctival fever (PCF)
 is caused mainly by adenovirus serovars 3, 4 and 7.
It is spread by droplets within families with upper
respiratory tract infection. Keratitis develops in about
30% of cases but is seldom severe. Sore throat is
typically prominent. •
Epidemic keratoconjunctivitis (EKC)
 is caused mainly by adenovirus serovars 8, 19 and
37.
 The most severe ocular adenoviral infection. Keratitis,
which may be marked, develops in about 80%;
photophobia may be correspondingly prominent
 Acute haemorrhagic conjunctivitis
 usually occurs in tropical areas. It is typically
caused by enterovirus and coxsackievirus,
though other microorganisms may present
similarly. It has a rapid onset, and resolves
within 1–2 weeks.
Conjunctival haemorrhage is generally
marked. •
 Chronic/relapsing adenoviral conjunctivitis
giving a chronic non-specific
follicular/papillary clinical picture can persist
over years, but is rare and eventually self-
limiting. •
 Herpes simplex virus (HSV)
can cause a follicular conjunctivitis,
particularly in primary infection; this is
usually unilateral and there are often
associated skin vesicles.
 Systemic viral infections
such as those common in childhood, e.g.
varicella, measles and mumps, can feature an
associated follicular conjunctivitis; varicella-
zoster virus secondary infection commonly
causes a conjunctivitis as part of ophthalmic
shingles.
 Molluscum contagiosum is a skin infection
caused by a human specific double-stranded
DNA poxvirus that typically affects otherwise
healthy children, with a peak incidence
between the ages of 2 and 4 years.
 Transmission is by contact, A chronic
follicular conjunctivitis can be associated, and
is due to skin lesion shedding of viral
particles. Chronic unilateral ocular irritation
and mild discharge is typical. The eyelash line
should be examined carefully in patients with
chronic conjunctivitis so as not to overlook a
molluscum lesion
 Signs • Eyelid oedema ranges from negligible
to severe. • Lymphadenopathy is common:
tender pre-auricular. • Conjunctival
hyperaemia and follicles are typically
prominent; papillae may also be seen,
particularly in the superior tarsal conjunctiva. •
Severe inflammation may be associated with
conjunctival haemorrhages, chemosis,
membranes (rare) and pseudomembranes,
sometimes with conjunctival scarring after
resolution
Keratitis (adenoviral):
○ Epithelial microcysts (non-staining) are
common at an early stage.
○ Punctate epithelial keratitis (staining) may occur,
usually within 7–10 days of the onset of
symptoms, typically resolving within 2 weeks.
○ Focal white subepithelial/anterior stromal
infiltrates often develop beneath the fading
epithelial lesions, probably as an immune
response to the virus; they may persist or recur
over months or years.
○ Small pseudodendritic epithelial formations
sometimes occur
 • Anterior uveitis is sometimes present, but
is mild. •
 Molluscum contagiosum.
○ A pale, waxy, umbilicated nodule on the lid
margin associated with follicular
conjunctivitis and mild watery and mucoid
discharge.
○ Bulbar nodules and confluent cutaneous
lesions may occur in immunocompromised
patients.
 Investigation
 • Giemsa stain shows predominantly
mononuclear cells in adenoviral conjunctivitis
and multinucleated giant cells in herpetic
infection. •
 Nucleic acid amplification techniques such as
PCR are sensitive and specific for viral DNA. •
 Viral culture with isolation is the reference
standard but is expensive and fairly slow (days
to weeks), and requires specific transport
media. Sensitivity is variable but specificity is
around 100%. •
 ‘
 Point-of-care’ immunochromatography test
takes 10 minutes to detect adenoviral antigen
in tears; sensitivity and specificity are
excellent. • Serology for IgM or rising IgG
antibody titres to adenovirus
 Treatment
 Spontaneous resolution of adenoviral infection
usually occurs within 2–3 weeks, so specific
treatment is typically unnecessary. No antiviral
agent with clinically useful activity against
adenovirus has yet been produced. •
 Reduction of transmission risk by meticulous
hand hygiene, avoiding eye rubbing and towel
sharing. There should be scrupulous disinfection
of instruments and clinical surfaces after
examination of an infected patient (e.g. sodium
hypochlorite, povidone-iodine).
 • Molluscum contagiosum. Although lesions
are self-limiting in immunocompetent
patients, removal is often necessary to
address secondary conjunctivitis or for
cosmetic reasons. Expression is facilitated by
making a small nick in the skin at the margin
of the lesion with the tip of a needle.
 Topical steroids
 such as prednisolone 0.5% four times daily may
be required for severe membranous or
pseudomembranous adenoviral conjunctivitis.
Symptomatic keratitis may require weak topical
steroids but these should be used with caution as
they do not speed resolution but only suppress
inflammation, and lesions commonly recur after
premature discontinuation. Steroids may enhance
viral replication and extend the period during
which the patient remains infectious. Intraocular
pressure should be monitored if treatment is
prolonged.
 Other mesures
 ○ Discontinuation of contact lens wear until
resolution of symptoms.
 ○ Artificial tears four times daily may be
useful for symptomatic relief. Preservative-
free preparations may give superior comfort,
and if supplied in single-dose units may
reduce transmission risk.
 ○ Cold (or warm) compresses for
symptomatic relief.
 ○ Topical antihistamines and
vasoconstrictors may improve symptoms,
particularly itching.
 .
 ○ Removal of symptomatic
pseudomembranes or membranes.
 ○ Topical antibiotics if secondary bacterial
infection is suspected.
 ○ Povidone-iodine is very effective and has
been proposed as a means of decreasing
infectivity
 Allergic conjunctivitis is a Type I (immediate)
hypersensitivity reaction, mediated by
degranulation of mast cells in response to the
action of IgE; there is evidence of an element
of Type IV hypersensitivity in at least some
forms
 Clinical manifestations include the various
forms of allergic conjunctivitis, as well as hay
fever (seasonal allergic rhinitis), asthma and
eczema.
 Acute allergic conjunctivitis
Acute allergic conjunctivitis is a common
condition caused by an acute conjunctival
reaction to an environmental allergen, usually
pollen.
Acute itching and watering are common, but
the hallmark is chemosis
Treatment is not usually required. Cool
compresses can be used and a single drop of
adrenaline 0.1% may reduce extreme
chemosis
. Seasonal allergic conjunctivitis (‘hay
fever eyes’)
It is worse during the spring and summer, is
the more common.
The most frequent allergens are tree and grass
pollens, although the specific allergen varies
with geographic location.
 • Perennial allergic conjunctivitis
causes symptoms throughout the year
worse in the autumn when exposure to
house dust mites, animal dander and fungal
allergens is greatest. It is less common and
tends to be milder than the seasonal form
Diagnosis
• Symptoms. Transient acute or subacute attacks
of redness, watering and itching, associated
with sneezing and nasal discharge.
• Signs. Conjunctival hyperaemia with a
relatively mild papillary reaction, variable
chemosis and lid oedema.
• Investigations are generally not performed
although conjunctival scraping in more active
cases may demonstrate the presence of
eosinophils. Skin testing for particular
allergens is rarely required.
Treatment
• Artificial tears for mild symptoms.
• Mast cell stabilizers (e.g. sodium cromoglicate,
nedocromil sodium, lodoxamide) must be used
for a few days before exerting maximal effect,
but are suitable (except lodoxamide) for long-
term use if required.
• Antihistamines (e.g. emedastine, epinastine,
levocabastine, bepotastine) can be used for
symptomatic exacerbations and are as effective
as mast cell stabilizers.
• Dual action antihistamine and mast cell
stabilizers (e.g. azelastine, ketotifen,
olopatadine) act rapidly and are often very
effective for exacerbations
 Combined preparation of an antihistamine and
a vasoconstrictor (e.g. antazoline with
xylometazoline).
 • Non-steroidal anti-inflammatory
preparations (e.g. diclofenac) can provide
symptomatic relief but are rarely used. •
Topical steroids are effective but rarely
necessary.
 • Oral antihistamines may be indicated for
severe symptoms. Some, such as
diphenhydramine, cause significant drowsiness
and may be useful in aiding sleep; others, such
as loratadine, have a far less marked sedative
action
 Pathogenesis
 Vernal keratoconjunctivitis (VKC)
 is a recurrent bilateral disorder in which both
IgE- and cell-mediated immune mechanisms
play important roles. It primarily affects boys
and onset is generally from about the age of
5 years onwards. There is remission by the
late teens in 95% of cases, although many of
the remainder develop atopic
keratoconjunctivitis
 VKC often occurs on a seasonal basis, with a
peak incidence over late spring and summer.
 Classification
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
limbal disease.
 Diagnosis
 The diagnosis is clinical; investigations are
generally not indicated. Eosinophils may be
abundant in conjunctival scrapings. •
Symptoms
consist of intense itching, which may be
associated with lacrimation, photophobia, a
foreign body sensation, burning and thick
mucoid discharge. Increased blinking is
common.
 Palpebral disease
 ○ Early-mild disease is characterized by
conjunctival hyperaemia and diffuse velvety
papillary hypertrophy on the superior tarsal
plate
 ○ Macropapillae (1 mm) can occur, as
adjacent smaller lesions amalgamate when
dividing septa rupture
 ○ Mucus deposition between giant papillae.
 ○ Decreased disease activity is characterized
by milder conjunctival injection and
decreased mucus production
 Limbal disease
 ○ Gelatinous limbal conjunctival papillae that
may be associated with transient apically
located white cellular collections (Horner–
Trantas dots)
 Keratopathy
 is more frequent in palpebral disease and may
take the following forms
 ○ Superior punctate epithelial erosions associated
with layers of mucus on the superior cornea.
 ○ Epithelial macroerosions caused by a
combination of epithelial toxicity from
inflammatory mediators and a direct mechanical
effect from papillae
 ○ 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
Keratopathy
Subepithelial scars that are typically grey and oval
and may affect vision.
○ 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.
 Eyelid disease is usually mild, in contrast to
atopic keratoconjunctivitis.
 Pathogenesis
 Atopic keratoconjunctivitis (AKC) is a rare
bilateral disease that typically develops in
adulthood (peak incidence 30–50 years) following
a long history of atopic dermatitis (eczema);
asthma is also extremely common in these
patients. About 5% have suffered from childhood
VKC.
 There is little or no gender preponderance. AKC
tends to be chronic and unremitting, with a
relatively low expectation of eventual resolution,
and is associated with significant visual
morbidity.
 The distinction between AKC and VKC is
essentially clinical; eosinophils tend to be less
common in conjunctival scrapings than with
VKC. •
 Symptoms
 are similar to those of VKC, but are
frequently more severe and unremitting. •
Eyelids
 ○ Skin changes are more prominent than in
VKC, and are typically eczematoid: erythema,
dryness,
 scaliness and thickening, sometimes with
disruption to epidermal integrity such as
fissuring and scratches (excoriation), the
latter due to intense itching.
 ○ Associated chronic staphylococcal
blepharitis and madarosis are common.
 ○ There may be keratinization of the lid
margin.
 ○ Hertoghe sign: absence of the lateral
portion of the eyebrows.
 ○ Dennie–Morgan folds: lid skin folds caused
by persistent rubbing.
 ○ Tightening of the facial skin may cause
lower lid ectropion and epiphora.
 ○ Ptosis is not uncommon.
 Conjunctival involvement
 is preferentially inferior palpebral, whereas in
VKC it is worse superiorly.
 ○ Discharge is generally more watery than the
stringy mucoid discharge in VKC
 . ○ Hyperaemia; chemosis is not uncommon
during active inflammation.
 ○ Papillae are initially smaller than in VKC
although larger lesions may develop later
 Diffuse conjunctival infiltration and scarring
may give a whitish, featureless appearance
 ○ Cicatricial changes can lead to moderate
symblepharon formation, forniceal shortening
and keratinization of the caruncle.
 ○ Limbal involvement similar to that of limbal
VKC can be seen, including Horner–Trantas
dots
 Keratopathy
 ○ Punctate epithelial erosions over the inferior
third of the cornea are common and can be marked
 ○ Persistent epithelial defects sometimes with
associated focal thinning, can occasionally
progress to perforation with descemetocoele
formation.
 ○ Plaque formation may occur
 ○ Peripheral vascularization and stromal scarring
are more common than in VKC.
 ○ Predisposition to secondary bacterial and fungal
infection, and to aggressive herpes simplex
keratitis.
 ○ Keratoconus is common (about 15%) and as with
VKC may be secondary to chronic ocular rubbing
 • Cataract
○ Presenile shield-like anterior or posterior
subcapsular cataracts are common and may
be exacerbated by long-term steroid therapy.
○ Because of the high lid margin carriage of
S. aureus, cataract surgery carries an
increased risk of endophthalmitis. • Retinal
detachment is more common than in the
general population, and is a particular risk
following cataract surgery
 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
staphylococcal blepharitis. Moisturizing
cream such as E45 can be applied to dry,
fissured skin.
Bandage contact lens wear to aid healing of
persistent epithelial defects.
 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
 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.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.
 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.
 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) monitored. •
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 stopped suddenly
 Calcineurin inhibitors show increasing promise
as an alternative 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
 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
 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
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.