Pterygium

Pterygium (L. Pterygion = a wing) is a wing-shaped
fold of conjunctiva encroaching upon the cornea from
either side within the interpalpebral fissure.
Etiology. Etiology of pterygium is not definitely
known. But the disease is more common in people
living in hot climates. Therefore, the most accepted
view is that it is a response to prolonged effect of
environmental factors such as exposure to sun
(ultraviolet rays), dry heat, high wind and abundance
of dust.
Pathology. Pathologically pterygium is a
degenerative and hyperplastic condition of
conjunctiva. The subconjunctival tissue undergoes
elastotic degeneration and proliferates as
vascularised granulation tissue under the epithelium,
which ultimately encroaches the cornea. The corneal
epithelium, Bowman's layer and superficial stroma are
destroyed.
Clinical features. Pterygium is more common in
elderly males doing outdoor work. It may be unilateral
or bilateral. It presents as a triangular fold of
conjunctiva encroaching the cornea in the area of
palpebral aperture, usually on the nasal side (Fig.4.28),
but may also occur on the temporal side. Deposition of
iron seen sometimes in corneal epithelium anterior to
advancing head of pterygium is called stocker's line.
Parts. A fully developed pterygium consists of three
parts (Fig.4.28):
i. Head (apical part present on the cornea),
ii. Neck (limbal part), and
iii. Body (scleral part) extending between limbus and
the canthus.

Types. Depending upon the progression it may be
progressive or regressive pterygium.
Progressive pterygium is thick, fleshy and
vascular with a few infiltrates in the cornea, in
front of the head of the pterygium (called cap of
pterygium).
Regressive pterygium is thin, atrophic, attenuated
with very little vascularity. There is no cap.
Ultimately it becomes membranous but never
disappears.
Symptoms. Pterygium is an asymptomatic condition
in the early stages, except for cosmetic intolerance.
Visual disturbances occur when it encroaches the
pupillary area or due to corneal astigmatism induced
due to fibrosis in the regressive stage. Occasionally
diplopia may occur due to limitation of ocular
movements.
Complications like cystic degeneration and infection
are infrequent. Rarely, neoplastic change to
epithelioma, fibrosarcoma or malignant melanoma,
may occur.
Differential diagnosis. Pterygium must be
differentiated from pseudopterygium. Pseudopterygium
is a fold of bulbar conjunctiva attached to
the cornea. It is formed due to adhesions of chemosed
bulbar conjunctiva to the marginal corneal ulcer. It
usually occurs following chemical burns of the eye.
Differences between pterygium and pseudopterygium
are given in Table 4.3.
Table 4.3. Differences between pterygium and
pseudopterygium
Pterygium Pseudopterygium
1. Etiology Degenerative Inflammatory
process process
2. Age Usually occurs Can occur at any
in elderly age
persons
3. Site Always situated Can occur at any
in the palpebral site
aperture
4. Stages Either progressive, Always stationary
ssive,
regressive or
stationary
5. Probe Probe cannot A probe can be
test be passed passed under the
underneath neck
Treatment. Surgical excision is the only satisfactory
treatment, which may be indicated for: (1) cosmetic
reasons, (2) continued progression threatening to
encroach onto the pupillary area (once the pterygium
has encroached pupillary area, wait till it crosses on
the other side), (3) diplopia due to interference in
ocular movements.
Recurrence of the pterygium after surgical excision
is the main problem (30-50%). However, it can be
reduced by any of the following measures:
1. Transplantation of pterygium in the lower fornix
(McReynold's operation) is not performed now.
2. Postoperative beta irradiations (not used now).
3. Postoperative use of antimitotic drugs such as
mitomycin-C or thiotepa.
4. Surgical excision with bare sclera.
5. Surgical excision with free conjunctival graft taken
from the same eye or other eye is presently the
preferred technique.
6. In recurrent recalcitrant pterygium, surgical
excision should be coupled with lamellar
keratectomy and lamellar keratoplasty.
Surgical technique of pterygium excision
1. After topical anaesthesia, eye is cleansed, draped
and exposed using universal eye speculum.
2. Head of the pterygium is lifted and dissected off
the cornea very meticulously (Fig. 4.29A).

3. The main mass of pterygium is then separated
from the sclera underneath and the conjunctiva
superficially.
4. Pterygium tissue is then excised taking care not
to damage the underlying medial rectus muscle
(Fig. 4.29B).
5. Haemostasis is achieved and the episcleral tissue
exposed is cauterised thoroughly.
6. Next step differs depending upon the technique
adopted as follows:
i. In simple excision the conjunctiva is sutured
back to cover the sclera (Fig. 4.29C).
ii. In bare sclera technique, some part of
conjunctiva is excised and its edges are
sutured to the underlying episcleral tissue
leaving some bare part of sclera near the
limbus (Fig. 4.29D).
iii. Free conjunctival membrane graft may be
used to cover the bare sclera (Fig. 4.29E).
This procedure is more effective in reducing
recurrence. Free conjunctiva from the same
or opposite eye may be used as a graft.
iv. Limbal conjunctival autograft transplantation
(LLAT) to cover the defet after
pterygium excision is the latest and most
effective technique in the management of
pterygium.

Pinguecula

Pinguecula is an extremely common degenerative
condition of the conjunctiva. It is characterized by
formation of a yellowish white patch on the bulbar
conjunctiva near the limbus. This condition is termed
pinguecula, because of its resemblance to fat, which
means pinguis.
Etiology of pinguecula is not known exactly. It has
been considered as an age-change, occurring more
commonly in persons exposed to strong sunlight, dust
and wind. It is also considered a precursor of
pterygium.
Pathology. There is an elastotic degeneration of
collagen fibres of the substantia propria of
conjunctiva, coupled with deposition of amorphous
hyaline material in the substance of conjunctiva.
Clinical features. Pinguecula (Fig. 4.27) is a bilateral,
usually stationary condition, presenting as yellowishwhite
triangular patch near the limbus. Apex of the
triangle is away from the cornea. It affects the nasal
side first and then the temporal side. When
conjunctiva is congested, it stands out as an
avascular prominence.
Complications of pinguecula include its
inflammation, intraepithelial abscess formation and
rarely conversion into pterygium.
Treatment. In routine no treatment is required for
pinguecula. However, if so desired, it may be excised.

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

may hypertrophy to produce cauliflower like
excrescences of 'giant papillae'. Conjunctival
changes are associated with white ropy discharge.

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.

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.

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.

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

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.

Acute Mucopurulent Conjunctivitis

Acute mucopurulent conjunctivitis is the most
common type of acute bacterial conjunctivitis. It is
characterised by marked conjunctival hyperaemia and
mucopurulent discharge from the eye.
Common causative bacteria are: Staphylococcus
aureus, Koch-Weeks bacillus, Pneumococcus and
Streptococcus. Mucopurulent conjunctivitis
generally accompanies exanthemata such as measles
and scarlet fever.
Clinical picture
Symptoms
Discomfort and foreign body sensation due to
engorgement of vessels.
Mild photophobia, i.e., difficulty to tolerate light.
Mucopurulent discharge from the eyes.
Sticking together of lid margins with discharge
during sleep.
Slight blurring of vision due to mucous flakes in
front of cornea.
Sometimes patient may complain of coloured
halos due to prismatic effect of mucus present on
cornea.
Signs (Fig. 4.4)
Conjunctival congestion, which is more marked
in palpebral conjunctiva, fornices and peripheral
part of bulbar conjunctiva, giving the appearance
of ‘fiery red eye’. The congestion is typically less
marked in circumcorneal zone.
Chemosis i.e., swelling of conjunctiva.
Petechial haemorrhages are seen when the
causative organism is pneumococcus.
Flakes of mucopus are seen in the fornices,
canthi and lid margins.
Cilia are usually matted together with yellow
crusts.
Clinical course. Mucopurulent conjunctivitis
reaches its height in three to four days. If untreated,
in mild cases the infection may be overcome and the
condition is cured in 10-15 days; or it may pass to
less intense form, the ‘chronic catarrhal
conjunctivitis’.
Complications. Occasionally the disease may be
complicated by marginal corneal ulcer, superficial
keratitis, blepharitis or dacryocystitis.
Differential diagnosis
1. From other causes of acute red eye (see page
147).
2. From other types of conjunctivitis. It is made out
from the typical clinical picture of disease and is
confirmed by conjunctival cytology and
bacteriological examination of secretions and
scrapings

Treatment
1. Topical antibiotics to control the infection
constitute the main treatment of acute
mucopurulent conjunctivitis. Ideally, the antibiotic
should be selected after culture and sensitivity
tests but in practice, it is difficult. However, in
routine, most of the patients respond well to
broad specturm antibiotics. Therefore, treatment
may be started with chloramphenicol (1%),
gentamycin (0.3%) or framycetin eye drops 3-4
hourly in day and ointment used at night will not
only provide antibiotic cover but also help to
reduce the early morning stickiness. If the patient
does not respond to these antibiotics, then the
newer antibiotic drops such as ciprofloxacin
(0.3%), ofloxacin (0.3%) or gatifloxacin (0.3%)
may be used.
2. Irrigation of conjunctival sac with sterile warm
saline once or twice a day will help by removing
the deleterious material. Frequent eyewash (as

advocated earlier) is however contraindicated as
it will wash away the lysozyme and other
protective proteins present in tears.
3. Dark goggles may be used to prevent photophobia.
4. No bandage should be applied in patients with
mucopurulent conjunctivitis. Exposure to air keeps
the temperature of conjunctival cul-de-sac low
which inhibits the bacterial growth; while after
bandaging, conjunctival sac is converted into an
incubator, and thus infection flares to a severe
degree within 24 hours. Further, bandaging of
eye will also prevent the escape of discharge.
5. No steroids should be applied, otherwise infection
will flare up and bacterial corneal ulcer may
develop.
6. Anti-inflammatory and analgesic drugs (e.g.
ibuprofen and paracetamol) may be given orally
for 2-3 days to provide symptomatic relief from
mild pain especially in sensitive patients.