VERNAL KERATOCONJUNCTIVITIS

VERNAL KERATOCONJUNCTIVITIS (VKC) OR
SPRING CATARRH
It is a recurrent, bilateral, interstitial, self-limiting,
allergic inflammation of the conjunctiva having a
periodic seasonal incidence.
Etiology
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
conjunctivitis'.
3. Climate. More prevalent in tropics, less in
temperate zones and almost non-existent in cold
climate.
Pathology
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
histiocytes.
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
DISEASES OF THE CONJUNCTIVA 75
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
keratoconjunctivitis.c
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).
Treatment
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
weeks.
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
cases.
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
effects.
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.

TRACHOMA

Trachoma (previously known as Egyptian
ophthalmia) is a chronic keratoconjunctivitis,
primarily affecting the superficial epithelium of
conjunctiva and cornea simultaneously. It is
characterised by a mixed follicular and papillary
response of conjunctival tissue. It is still one of the
leading causes of preventable blindness in the world.
The word 'trachoma' comes from the Greek word for
'rough' which describes the surface appearance of
the conjunctiva in chronic trachoma.
Table 4.2. Summary of ocular infections caused by chlamydia
Genus Chlamydia
Species C. trachomatis C. lymphogranulomatis C. psittacosis
(TRIC agent) (Humans) (Humans) (Animals)
Serotype A, B, Ba, C D to K L1, L2, L3
Ocular Hyperendemic Paratrachoma Lymphogranuloma
disease trachoma (– neonatal venereum
and adult inclusion conjunctivitis
conjunctivitis)
Transmission Eye to eye Genitals to eye Genitals to eye
DISEASES OF THE CONJUNCTIVA 63
Etiology
A. Causative organism. Trachoma is caused by a
Bedsonian organism, the Chlamydia trachomatis
belonging to the Psittacosis-lymphogranulomatrachoma
(PLT) group. The organism is epitheliotropic
and produces intracytoplasmic inclusion bodies
called H.P. bodies (Halberstaedter Prowazeke
bodies). Presently, 11 serotypes of chlamydia, (A, B,
Ba, C, D, E, F, G, H, J and K) have been identified
using microimmunofluorescence techniques.
Serotypes A, B, Ba and C are associated with
hyperendemic (blinding) trachoma, while serotypes
D-K are associated with paratrachoma (oculogenital
chlamydial disease).
B. Predisposing factors. These include age, sex, race,
climate, socioeconomic status and environmental
factors.
1. Age. The infection is usually contracted during
infancy and early childhood. Otherwise, there is
no age bar.
2. Sex. As far as sex is concerned, there is general
agreement that preponderance exists in the
females both in number and in severity of disease.
3. Race. No race is immune to trachoma, but the
disease is very common in Jews and comparatively
less common among Negroes.
4. Climate. Trachoma is more common in areas with
dry and dusty weather.
5. Socioeconomic status. The disease is more
common in poor classes owing to unhygienic
living conditions, overcrowding, unsanitary
conditions, abundant fly population, paucity of
water, lack of materials like separate towels and
handkerchiefs, and lack of education and
understanding about spread of contagious
diseases.
6. Environmental factors like exposure to dust,
smoke, irritants, sunlight etc. increase the risk of
contracting disease. Therefore, outdoor workers
are more affected in comparison to office workers.
C. Source of infection. In trachoma endemic zones
the main source of infection is the conjunctival
discharge of the affected person. Therefore,
superimposed bacterial infections help in
transmission of the disease by increasing the
conjunctival secretions.
D. Modes of infection. Infection may spread from
eye to eye by any of the following modes:
1. Direct spread of infection may occur through
contact by air-borne or water-borne modes.
2. Vector transmission of trachoma is common
through flies.
3. Material transfer plays an important role in the
spread of trachoma. Material transfer can occur
through contaminated fingers of doctors, nurses
and contaminated tonometers. Other sources of
material transfer of infection are use of common
towel, handkerchief, bedding and surma-rods.
Prevalence
Trachoma is a worldwide disease but it is highly
prevalent in North Africa, Middle East and certain
regions of Sourth-East Asia. It is believed to affect
some 500 million people in the world. There are about
150 million cases with active trachoma and about 30
million having trichiasis, needing lid surgery.
Trachoma is responsible for 15-20 percent of the
world's blindness, being second only to cataract.
Clinical profile of trachoma
Incubation period of trachoma varies from 5-21 days.
Onset of disease is usually insidious (subacute),
however, rarely it may present in acute form.
Clinical course of trachoma is determined by the
presence or absence of secondary infection. In the
absence of such an infection, a pure trachoma is so
mild and symptomless that the disease is usually
neglected. But, mostly the picture is complicated by
secondary infection and may start with typical
symptoms of acute conjunctivitis. In the early
stages it is clinically indistinguishable from the
bacterial conjunctivitis and the term 'trachomadubium'
(doubtful trachoma) is sometimes used for
this stage.
Natural history. In an endemic area natural history
of trachoma is characterized by the development of
acute disease in the first decade of life which
continues with slow progression, until the disease
becomes inactive in the second decade of life. The
sequelae occur at least after 20 years of the disease.
Thus, the peak incidence of blinding sequelae is seen
in the fourth and fifth decade of life.
64 Comprehensive OPHTHALMOLOGY
Symptoms
In the absence of secondary infection, symptoms
are minimal and include mild foreign body
sensation in the eyes, occasional lacrimation,
slight stickiness of the lids and scanty mucoid
discharge.
In the presence of secondary infection, typical
symptoms of acute mucopurulent conjunctivitis
develop.
Signs
A. Conjunctival signs
1. Congestion of upper tarsal and forniceal
conjunctiva.
2. Conjunctival follicles. Follicles (Fig. 4.9 and
Fig.4.10) look like boiled sagograins and are
commonly seen on upper tarsal conjunctiva and
fornix; but may also be present in the lower
fornix, plica semilunaris and caruncle. Sometimes,
(follicles may be seen on the bulbar conjunctiva
(pathognomic of trachoma).
follicular conjunctivitis.
3. Papillary hyperplasia. Papillae are reddish, flat
topped raised areas which give red and velvety
appearance to the tarsal conjunctiva (Fig. 4.11).
Each papilla consists of central core of numerous
dilated blood vessels surrounded by lymphocytes
and covered by hypertrophic epithelium.
Fig. 4.10. Trachomatous inflammation follicular (TF)
Structure of follicle. Follicles are formed due to
scattered aggregation of lymphocytes and other
cells in the adenoid layer. Central part of each follicle
is made up of mononuclear histiocytes, few
lymphocytes and large multinucleated cells called
Leber cells. The cortical part is made up of a zone
of lymphocytes showing active proliferation. Blood
vessels are present in the most peripheral part. In
later stages signs of necrosis are also seen. Presence
of Leber cells and signs of necrosis differentiate
trachoma follicles from follicles of other forms of
Fig. 4.9. Signs of active traochoma (diagramatic).
Fig. 4.11. Trachomatous inflammation intense (TI)
4. Conjunctival scarring (Fig. 4.12), which may be
irregular, star-shaped or linear. Linear scar present
in the sulcus subtarsalis is called Arlt's line.
5. Concretions may be formed due to accumulation
of dead epithelial cells and inspissated mucus in
the depressions called glands of Henle.
DISEASES OF THE CONJUNCTIVA 65
Fig. 4.12. Trachomatous scarring (TS)
Fig. 4.13. Trachomatous pannus : (A) progressive,
(B) regressive (diagramatic) and (C) clinical photograph
B. Corneal signs
1. Superficial keratitis may be present in the upper
part.
2. Herbert follicles refer to typical follicles present
in the limbal area. These are histologically similar
to conjunctival follicles.
C
3. Pannus i.e., infiltration of the cornea associated
with vascularization is seen in upper part (Fig.
4.13). The vessels are superficial and lie between
epithelium and Bowman's membrane. Later on
Bowman's membrane is also destroyed. Pannus
may be progressive or regressive.
In progressive pannus, infiltration of cornea is
ahead of vascularization.
In regressive pannus (pannus siccus) vessels
extend a short distance beyond the area of
infiltration.
4. Corneal ulcer may sometime develop at the
advancing edge of pannus. Such ulcers are usually
shallow which may become chronic and indolent.
5. Herbert pits are the oval or circular pitted
scars, left after healing of Herbert follicles in the
limbal area (Fig. 4.14).
6. Corneal opacity may be present in the upper
part. It may even extend down and involve the
pupillary area. It is the end result of trachomatous
corneal lesions.
Grading of trachoma
McCallan's classification
McCallan in 1908, divided the clinical course of the
trachoma into following four stages:
Stage I (Incipient trachoma or stage of infiltration).
It is characterized by hyperaemia of palpebral
conjunctiva and immature follicles.
Stage II (Established trachoma or stage of florid
infiltration). It is characterized by appearance of
mature follicles, papillae and progressive corneal
pannus.
Fig. 4.14. Trachomatous Herbert's pits.
A
B
66 Comprehensive OPHTHALMOLOGY
Stage III (Cicatrising trachoma or stage of
scarring). It includes obvious scarring of palpebral
conjunctiva.
Stage IV (Healed trachoma or stage of sequelae).
The disease is quite and cured but sequelae due
to cicatrisation give rise to symptoms.
WHO classification
Trachoma has always been an important blinding
disease under consideration of WHO and thus many
attempts have been made to streamline its clinical
profile. The latest classification suggested by WHO
in 1987 (to replace all the previous ones) is as follows
(FISTO):
1. TF: Trachomatous inflammation-follicular. It is
the stage of active trachoma with predominantly
follicular inflammation. To diagnose this stage at
least five or more follicles (each 0.5 mm or more
in diameter) must be present on the upper tarsal
conjunctiva (Fig. 4.10). Further, the deep tarsal
vessels should be visible through the follicles
and papillae.
2. TI : Trachomatous inflammation intense. This
stage is diagnosed when pronounced
inflammatory thickening of the upper tarsal
conjunctiva obscures more than half of the normal
deep tarsal vessels (Fig. 4.11).
3. TS: Trachomatous scarring. This stage is
diagnosed by the presence of scarring in the
tarsal conjunctiva. These scars are easily visible
as white, bands or sheets (fibrosis) in the tarsal
conjunctiva (Fig. 4.12).
4. TT: Trachomatous trichiasis. TT is labelled when
at least one eyelash rubs the eyeball. Evidence of
recent removal of inturned eyelashes should also
be graded as trachomatous trichiasis (Fig. 4.15).
5. CO: Corneal opacity. This stage is labelled when
easily visible corneal opacity is present over the
pupil. This sign refers to corneal scarring that is
so dense that at least part of pupil margin is
blurred when seen through the opacity. The
definition is intended to detect corneal opacities
that cause significant visual impairment (less than
6/18).
Sequelae of trachoma
1. Sequelae in the lids may be trichiasis (Fig. 4.15),
entropion, tylosis (thickening of lid margin), ptosis,
madarosis and ankyloblepharon.
Fig. 4.15. Trachomatous trichiasis (TT).
2. Conjunctival sequelae include concretions,
pseudocyst, xerosis and symblepharon.
3. Corneal sequelae may be corneal opacity, ectasia,
corneal xerosis and total corneal pannus (blinding
sequelae).
4. Other sequelae may be chronic dacryocystitis,
and chronic dacryoadenitis.
Complications
The only complication of trachoma is corneal ulcer
which may occur due to rubbing by concretions, or
trichiasis with superimposed bacterial infection.
Diagnosis
A. The clinical diagnosis of trachoma is made from
its typical signs; at least two sets of signs should be
present out of the following:
1. Conjunctival follicles and papillae
2. Pannus progressive or regressive
3. Epithelial keratitis near superior limbus
4. Signs of cicatrisation or its sequelae
Clinical grading of each case should be done as
per WHO classfication into TF, TI, TS, TT or CO.
B. Laboratory diagnosis. Advanced laboratory tests
are employed for research purposes only. Laboratory
diagnosis of trachoma includes :
1. Conjunctival cytology. Giemsa stained smears
showing a predominantly polymorphonuclear
reaction with presence of plasma cells and Leber
cells is suggestive of trachoma.
2. Detection of inclusion bodies in conjunctival
smear may be possible by Giemsa stain, iodine
DISEASES OF THE CONJUNCTIVA 67
stain or immunofluorescent staining, specially in
cases with active trachoma.
3. Enzyme-linked immunosorbent assay (ELISA) for
chlamydial antigens.
4. Polymerase chain reaction (PCR) is also useful.
5. Isolation of chlamydia is possible by yolk-sac
inoculation method and tissue culture technique.
Standard single-passage McCoy cell culture
requires at least 3 days.
6. Serotyping of TRIC agents is done by detecting
specific antibodies using microimmunofluorescence
(micro-IF) method. Direct
monoclonal fluorescent antibody microscopy of
conjunctival smear is rapid and inexpensive.
Differential diagnosis
1. Trachoma with follicular hypertrophy must be
differentiated from acute adenoviral follicular
conjunctivitis (epidemic keratoconjunctivitis) as
follows :
Distribution of follicles in trachoma is mainly on
upper palpebral conjunctiva and fornix, while in
EKC lower palpebral conjunctiva and fornix is
predominantly involved.
Associated signs such as papillae and pannus
are characteristic of trachoma.
In clinically indistinguishable cases, laboratory
diagnosis of trachoma helps in differentiation.
2. Trachoma with predominant papillary
hypertrophy needs to be differentiated from palpebral
form of spring catarrh as follows:
Papillae are large in size and usually there is
typical cobble-stone arrangement in spring catarrh.
pH of tears is usually alkaline in spring catarrh,
while in trachoma it is acidic,
Discharge is ropy in spring catarrh.
In trachoma, there may be associated follicles
and pannus.
In clinically indistinguishable cases, conjunctival
cytology and other laboratory tests for trachoma
usually help in diagnosis.
Management
Management of trachoma should involve curative as
well as control measures.
A. Treatment of active trachoma
Antibiotics for treatment of active trachoma may be
given locally or systemically, but topical treatment is
preferred because:
It is cheaper,
There is no risk of systemic side-effects, and
Local antibiotics are also effective against
bacterial conjunctivitis which may be associated
with trachoma.
The following topical and systemic therapy
regimes have been recommended:
1. Topical therapy regimes. It is best for individual
cases. It consists of 1 percent tetracycline or 1
percent erythromycin eye ointment 4 times a day
for 6 weeks or 20 percent sulfacetamide eye
drops three times a day along with 1 percent
tetracycline eye ointment at bed time for 6 weeks.
The continuous treatment for active trachoma
should be followed by an intermittent treatment
especially in endemic or hyperendemic area.
2. Systemic therapy regimes. Tetracycline or
erythromycin 250 mg orally, four times a day for
3-4 weeks or doxycycline 100 mg orally twice
daily for 3-4 weeks or single dose of 1 gm
azithromycin has also been reported to be equally
effective in treating trachoma.
3. Combined topical and systemic therapy regime.
It is preferred when the ocular infection is severe
(TI) or when there is associated genital infection.
It includes: (i) 1 per cent tetracycline or
erythromycin eye ointment 4 times a day for 6
weeks; and (ii) tetracycline or erythromycin 250
mg orally 4 times a day for 2 weeks.
B. Treatment of trachoma sequelae
1. Concretions should be removed with a
hypodermic needle.
2. Trichiasis may be treated by epilation, electrolysis
or cryolysis (see page 348).
3. Entropion should be corrected surgically (see
page 349).
4. Xerosis should be treated by artificial tears.
C. Prophylaxis
Since, immunity is very poor and short lived, so
reinfections and recurrences are likely to occur.
Following prophylactic measures may be helpful
against reinfection of trachoma.
1. Hygienic measures. These help a great deal in
decreasing the transmission of disease, as
trachoma is closely associated with personal
68 Comprehensive OPHTHALMOLOGY
hygiene and environmental sanitation. Therefore,
health education on trachoma should be given to
public. The use of common towel, handkerchief,
surma rods etc. should be discouraged. A good
environmental sanitation will reduce the flies. A
good water supply would improve washing habits.
2. Early treatment of conjunctivitis. Every case of
conjunctivitis should be treated as early as
possible to reduce transmission of disease.
3. Blanket antibiotic therapy (intermittent
treatment). WHO has recommended this regime
to be carried out in endemic areas to minimise the
intensity and severity of disease. The regime is
to apply 1 percent tetracycline eye ointment twice
daily for 5 days in a month for 6 months.
D. Prevention of trachoma blindness
See page 447.

PHLYCTENULAR KERATOCONJUNCTIVITIS

Phlyctenular keratoconjunctivitis is a characteristic
nodular affection occurring as an allergic response
78 Comprehensive OPHTHALMOLOGY
watering. However, usually there is associated
mucopurulent conjunctivitis due to secondary
bacterial infection.
Signs. The phlyctenular conjunctivitis can present in
three forms: simple, necrotizing and miliary.
1. Simple phylctenular conjunctivitis. It is the most
commonly seen variety. It is characterised by the
presence of a typical pinkish white nodule
surrounded by hyperaemia on the bulbar
conjunctiva, usually near the limbus. Most of the
times there is solitary nodule but at times there
may be two nodules (Fig. 4.25). In a few days the
nodule ulcerates at apex which later on gets
epithelised. Rest of the conjunctiva is normal.
2. Necrotizing phlyctenular conjunctivitis is
characterised by the presence of a very large
phlycten with necrosis and ulceration leading to
a severe pustular conjunctivitis.
3. Miliary phlyctenular conjunctivitis is characterised
by the presence of multiple phlyctens
which may be arranged haphazardly or in the
form of a ring around the limbus and may even
form a ring ulcer.
Phlyctenular keratitis. Corneal involvement may
occur secondarily from extension of conjunctival
phlycten; or rarely as a primary disease. It may present
in two forms: the 'ulcerative phlyctenular keratitis' or
'diffuse infiltrative keratitis'.
A. Ulcerative phlyctenular keratitis may occur in
the following three forms:
1. Sacrofulous ulcer is a shallow marginal ulcer
formed due to breakdown of small limbal phlycten.
It differs from the catarrhal ulcer in that there is
no clear space between the ulcer and the limbus
and its long axis is frequently perpendicular to
limbus. Such an ulcer usually clears up without
leaving any opacity.
2. Fascicular ulcer has a prominent parallel leash
of blood vessels (Fig. 4.26). This ulcer usually
remains superficial but leaves behind a bandshaped
superficial opacity after healing.
Fig. 4.25. Phylctenular conjunctivitis.
Fig. 4.26. Fascicular corneal ulcer.
3. Miliary ulcer. In this form multiple small ulcers
are scattered over a portion of or whole of the
cornea.
B. Diffuse infiltrative phlyctenular keratitis may
appear in the form of central infiltration of cornea
with characteristic rich vascularization from the
periphery, all around the limbus. It may be superficial
or deep.
Clinical course is usually self-limiting and phlycten
disappears in 8-10 days leaving no trace. However,
recurrences are very common.
Differential diagnosis
Phlyctenular conjunctivitis needs to be differentiated
from the episcleritis, scleritis, and conjunctival
foreign body granuloma.
Presence of one or more whitish raised nodules on
the bulbar conjunctiva near the limbus, with
hyperaemia usually of the surrounding conjunctiva,
in a child living in bad hygienic conditions (most of
DISEASES OF THE CONJUNCTIVA 79
the times) are the diagnostic features of the
phlyctenular conjunctivitis.
Management
It includes treatment of phlyctenular conjunctivitis
by local therapy, investigations and specific therapy
aimed at eliminating the causative allergen and general
measures to improve the health of the child.
1. Local therapy.
i. Topical steroids, in the form of eye drops or
ointment (dexamethasone or betamethasone)
produce dramatic effect in phlyctenular
keratoconjunctivitis.
ii. Antibiotic drops and ointment should be added
to take care of the associated secondary infection
(mucopurulent conjunctivitis).
iii. Atropine (1%) eye ointment should be applied
once daily when cornea is involved.
2. Specific therapy. Attempts must be made to search
and eradicate the following causative conditions:
i. Tuberculous infection should be excluded by Xrays
chest, Mantoux test, TLC, DLC and ESR. In
case, a tubercular focus is discovered,
antitubercular treatment should be started to
combat the infection.
ii. Septic focus, in the form of tonsillitis, adenoiditis,
or caries teeth, when present should be
adequately treated by systemic antibotics and
necessary surgical measures.
iii. Parasitic infestation should be ruled out by
repeated stool examination and when discovered
should be adequately treated for complete
eradication.
3. General measures aimed to improve the health of
child are equally important. Attempts should be made
to provide high protein diet supplemented with
vitamins A, C and D.

OPHTHALMIA NEONATORUM

Ophthalmia neonatorum is the name given to bilateral
inflammation of the conjunctiva occurring in an infant,
less than 30 days old. It is a preventable disease
usually occurring as a result of carelessness at the
time of birth. As a matter of fact any discharge or
even watering from the eyes in the first week of life
should arouse suspicion of ophthalmia neonatorum,
as tears are not formed till then.
Etiology
Source and mode of infection
Infection may occur in three ways: before birth, during
birth or after birth.
1. Before birth infection is very rare through infected
liquor amnii in mothers with ruptured membrances.
Fig. 4.18. Benign folliculosis.
72 Comprehensive OPHTHALMOLOGY
2. During birth. It is the most common mode of
infection from the infected birth canal especially
when the child is born with face presentation or
with forceps.
3. After birth. Infection may occur during first bath
of newborn or from soiled clothes or fingers with
infected lochia.
Causative agents
1. Chemical conjunctivitis It is caused by silver
nitrate or antibiotics used for prophylaxis.
2. Gonococcal infection was considered a serious
disease in the past, as it used to be responsible
for 50 per cent of blindness in children. But,
recently the decline in the incidence of gonorrhoea
as well as effective methods of prophylaxis and
treatment have almost eliminated it in developed
countries. However, in many developing countries
it still continues to be a problem.
3. Other bacterial infections, responsible for
ophthalmia neonatorum are Staphylococcus
aureus, Streptococcus haemolyticus, and
Streptococcus pneumoniae.
4. Neonatal inclusion conjunctivitis caused by
serotypes D to K of Chlamydia trachomatis is
the commonest cause of ophthalmia neonatorum
in developed countries.
5. Herpes simplex ophthalmia neonatorum is a rare
condition caused by herpes simplex-II virus.
Clinical features
Incubation period
It varies depending on the type of the causative agent
as shown below:
Causative agent Incubation period
1. Chemical 4-6 hours
2. Gonococcal 2-4 days
3. Other bacterial 4-5 days
4. Neonatal inclusion
conjunctivitis 5-14 days
5. Herpes simplex 5-7 days
Symptoms and signs (Fig. 4.19)
1. Pain and tenderness in the eyeball.
2. Conjunctival discharge. It is purulent in
gonococcal ophthalmia neonatorum and mucoid
or mucopurulent in other bacterial cases and
neonatal inclusion conjunctivitis.
3. Lids are usually swollen.
4. Conjunctiva may show hyperaemia and chemosis.
There might be mild papillary response in neonatal
inclusion conjunctivitis and herpes simplex
ophthalmia neonatorum.
5. Corneal involvement, though rare, may occur in
the form of superficial punctate keratitis especially
in herpes simplex ophthalmia neonatorum.
Complications
Untreated cases, especially of gonococcal ophthalmia
neonatorum, may develop corneal ulceration, which
may perforate rapidly resulting in corneal
opacification or staphyloma formation.
Treatment
Prophylactic treatment is always better than curative.
A. Prophylaxis needs antenatal, natal and postnatal
care.
1. Antenatal measures include thorough care of
mother and treatment of genital infections when
suspected.
2. Natal measures are of utmost importance, as
mostly infection occurs during childbirth.
Deliveries should be conducted under hygienic
conditions taking all aseptic measures.
The newborn baby's closed lids should be
thoroughly cleansed and dried.
3. Postnatal measures include :
Use of either 1 percent tetracycline ointment
or 0.5 percent erythromycin ointment or 1
percent silver nitrate solution (Crede's method)
into the eyes of the babies immediately after
birth.
Single injection of ceftriaxone 50 mg/kg IM or
IV (not to exceed 125 mg) should be given to
Fig. 4.19. Ophthalmia neonatorum.
DISEASES OF THE CONJUNCTIVA 73
infants born to mothers with untreated
gonococcal infection.
B. Curative treatment. As a rule, conjunctival
cytology samples and culture sensitivity swabs
should be taken before starting the treatment.
1. Chemical ophthalmia neonatorum is a self-limiting
condition, and does not require any treatment.
2. Gonococcal ophthalmia neonatorum needs
prompt treatment to prevent complications.
i. Topical therapy should include :
Saline lavage hourly till the discharge is
eliminated.
Bacitracin eye ointment 4 times/day. Because
of resistant strains topical penicillin therapy is
not reliable. However in cases with proved
penicillin susceptibility, penicillin drops 5000
to 10000 units per ml should be instilled every
minute for half an hour, every five minutes for
next half an hour and then half hourly till the
infection is controlled.
If cornea is involved then atropine sulphate
ointment should be applied.
ii. Systemic therapy. Neonates with gonococcal
ophthalmia should be treated for 7 days with one
of the following regimes:
Ceftriaxone 75-100 mg/kg/day IV or IM, QID.
Cefotaxime 100-150 mg/kg/day IV or IM, 12
hourly.
Ciprofloxacin 10-20 mg/kg/day or Norfloxacin
10 mg/kg/day.
If the gonococcal isolate is proved to be
susceptible to penicillin, crystalline benzyl
penicillin G 50,000 units to full term, normal
weight babies and 20,000 units to premature or
low weight babies should be given
intramuscularly twice daily for 3 days.
3. Other bacterial ophthalmia neonatorum should
be treated by broad spectrum antibiotic drops and
ointments for 2 weeks.
4. Neonatal inclusion conjunctivitis responds well
to topical tetracycline 1 per cent or erythromycin 0.5
per cent eye ointment QID for 3 weeks. However,
systemic erythromycin (125 mg orally, QID for 3 weeks
should also be given since the presence of chlamydia
agents in the conjunctiva implies colonization of
upper respiratory tract as well. Both parents should
also be treated with systemic erythromycin.
5. Herpes simplex conjunctivitis is usually a selflimiting
disease. However, topical antiviral drugs
control the infection more effectively and may prevent
the recurrence.

GIANT PAPILLARY CONJUNCTIVITIS (GPC)

GIANT PAPILLARY CONJUNCTIVITIS (GPC)
It is the inflammation of conjunctiva with formation
of very large sized papillae.
Etiology. It is a localised allergic response to a
physically rough or deposited surface (contact lens,
prosthesis, left out nylon sutures). Probably it is a
sensitivity reaction to components of the plastic
leached out by the action of tears.
Symptoms. Itching, stringy discharge and reduced
wearing time of contact lens or prosthetic shell.
Signs. Papillary hypertrophy (1 mm in diameter) of
the upper tarsal conjunctiva, similar to that seen in
palpebral form of VKC with hyperaemia are the main
signs (Fig. 4.24).
of the conjunctival and corneal epithelium to some
endogenous allergens to which they have become
sensitized. Phlyctenular conjunctivitis is of worldwide
distribution. However, its incidence is higher in
developing countries.
Etiology
It is believed to be a delayed hypersensitivity (Type
IV-cell mediated) response to endogenous microbial
proteins.
I. Causative allergens
1. Tuberculous proteins were considered,
previously, as the most common cause.
2. Staphylococcus proteins are now thought to
account for most of the cases.
3. Other allergens may be proteins of Moraxella
Axenfeld bacillius and certain parasites (worm
infestation).
II. Predisposing factors
1. Age. Peak age group is 3-15 years.
2. Sex. Incidence is higher in girls than boys.
3. Undernourishment. Disease is more common in
undernourished children.
4. Living conditions. Overcrowded and unhygienic.
5. Season. It occurs in all climates but incidence is
high in spring and summer seasons.
Pathology
1. Stage of nodule formation. In this stage there
occurs exudation and infiltration of leucocytes
into the deeper layers of conjunctiva leading to
a nodule formation. The central cells are polymorphonuclear
and peripheral cells are lymphocytes.
The neighbouring blood vessels dilate and their
endothelium proliferates.
2. Stage of ulceration. Later on necrosis occurs at
the apex of the nodule and an ulcer is formed.
Leucocytic infiltration increases with plasma cells
and mast cells.
3. Stage of granulation. Eventually floor of the
ulcer becomes covered by granulation tissue.
4. Stage of healing. Healing occurs usually with
minimal scarring.
Clinical picture
Symptoms in simple phlyctenular conjunctivitis are
few, like mild discomfort in the eye, irritation and reflex
Fig. 4.24. Giant papillary conjunctivities (GPC).
Treatment
1. The offending cause should be removed. After
discontinuation of contact lens or artificial eye or
removal of nylon sutures, the papillae resolve
over a period of one month.
2. Disodium cromoglycate is known to relieve the
symptoms and enhance the rate of resolution.
3. Steroids are not of much use in this condition.

CLASSIFICATION OF CONJUNCTIVITIS

INFLAMMATIONS OF
CONJUNCTIVA
Inflammation of the conjunctiva (conjunctivitis) is
classically defined as conjunctival hyperaemia
associated with a discharge which may be watery,
mucoid, mucopurulent or purulent.
Etiological classification
1. Infective conjunctivitis: bacterial, chlamydial, viral,
fungal, rickettsial, spirochaetal, protozoal, parasitic
etc.
2. Allergic conjunctivitis.
3. Irritative conjunctivitis.
4. Keratoconjunctivitis associated with diseases of
skin and mucous membrane.
5. Traumatic conjunctivitis.
6. Keratoconjunctivitis of unknown etiology.
Clinical classification
Depending upon clinical presentation, conjunctivitis
can be classified as follows:
1. Acute catarrhal or mucopurulent conjunctivitis.
2. Acute purulent conjunctivitis
3. Serous conjunctivitis
4. Chronic simple conjunctivitis
5. Angular conjunctivitis
6. Membranous conjunctivitis
7. Pseudomembranous conjunctivitis
8. Papillary conjunctivitis
9. Follicular conjunctivitis
10. Ophthalmia neonatorum
11. Granulomatous conjunctivitis
12. Ulcerative conjunctivitis
13. Cicatrising conjunctivitis

BACTERIAL CONJUNCTIVITIS

BACTERIAL CONJUNCTIVITIS
There has occurred a relative decrease in the
incidence of bacterial conjunctivitis in general and
those caused by gonococcus and corynebacterium
diphtheriae in particular. However, in developing
countries it still continues to be the commonest type
of conjunctivitis. It can occur as sporadic cases and
as epidemics. Outbreaks of bacterial conjunctivitis
epidemics are quite frequent during monsoon season.
Etiology
A. Predisposing factors for bacterial conjunctivitis,
especially epidemic forms, are flies, poor hygienic
conditions, hot dry climate, poor sanitation and dirty
habits. These factors help the infection to establish,
as the disease is highly contagious.
B. Causative organisms. It may be caused by a wide
range of organisms in the following approximate order
of frequency :
Staphylococcus aureus is the most common cause
of bacterial conjunctivitis and blepharoconjunctivitis.
Staphylococcus epidermidis is an innocuous flora
of lid and conjunctiva. It can also produce
blepharoconjunctivitis.
Streptococcus pneumoniae (pneumococcus)
produces acute conjunctivitis usually associated
with petechial subconjunctival haemorrhages. The
disease has a self-limiting course of 9-10 days.
Streptococcus pyogenes (haemolyticus) is virulent
and usually produces pseudomembranous
conjunctivitis.
Haemophilus influenzae (aegyptius, Koch- Weeks
bacillus). It classically causes epidemics of
mucopurulent conjunctivitis, known as ‘red-eye’
especially in semitropical countries.
Moraxella lacunate (Moraxella Axenfeld bacillus)
is most common cause of angular conjunctivitis
and angular blepharoconjunctivitis.
Pseudomonas pyocyanea is a virulent organism.
It readily invades the cornea.
Neisseria gonorrhoeae typically produces acute
purulent conjunctivitis in adults and ophthalmia
neonatorum in new born. It is capable of invading
intact corneal epithelium.
Neisseria meningitidis (meningococcus) may
produce mucopurulent conjunctivitis.
Corynebacterium diphtheriae causes acute
membranous conjunctivitis. Such infections are
rare now-a-days.
C. Mode of infection. Conjunctiva may get infected
from three sources, viz, exogenous, local surrounding
structures and endogenous, by following modes :
1. Exogenous infections may spread: (i) directly
through close contact, as air-borne infections or
as water-borne infections; (ii) through vector
transmission (e.g., flies); or (iii) through material
transfer such as infected fingers of doctors,
nurses, common towels, handkerchiefs, and
infected tonometers.
2. Local spread may occur from neighbouring
structures such as infected lacrimal sac, lids, and
nasopharynx. In addition to these, a change in
the character of relatively innocuous organisms
present in the conjunctival sac itself may cause
infections.
3. Endogenous infections may occur very rarely
through blood e.g., gonococcal and meningococcal
infections.
Pathology
Pathological changes of bacterial conjunctivitis
consist of :
1. Vascular response. It is characterised by
congestion and increased permeability of the
conjunctival vessels associated with proliferation
of capillaries.
2. Cellular response. It is in the form of exudation
of polymorphonuclear cells and other
inflammatory cells into the substantia propria of
conjunctiva as well as in the conjunctival sac.
3. Conjunctival tissue repsonse. Conjunctiva
becomes oedematous. The superficial epithelial
cells degenerate, become loose and even
56 Comprehensive OPHTHALMOLOGY
desquamate. There occurs proliferation of basal
layers of conjunctival epithelium and increase in
the number of mucin secreting goblet cells.
4. Conjunctival discharge. It consists of tears,
mucus, inflammatory cells, desquamated epithelial
cells, fibrin and bacteria. If the inflammation is
very severe, diapedesis of red blood cells may
occur and discharge may become blood stained.
Severity of pathological changes varies depending
upon the severity of inflammation and the causative
organism. The changes are thus more marked in
purulent conjunctivitis than mucopurulent
conjunctivitis.