XEROPHTHALMIA

They term xerophthalmia is now reserved (by a joint
WHO and USAID Committee, 1976) to cover all the
ocular manifestations of vitamin A deficiency,
including not only the structural changes affecting
the conjunctiva, cornea and occasionally retina, but
also the biophysical disorders of retinal rods and
cones functions.
Etiology
It occurs either due to dietary deficiency of vitamin
A or its defective absorption from the gut. It has long
been recognised that vitamin A deficiency does not
occur as an isolated problem but is almost invariably
accompanied by protein-energy malnutrition (PEM)
and infections.
WHO classification (1982)
The new xerophthalmia classification (modification
of original 1976 classification) is as follows:
XN Night blindness
X1A Conjunctival xerosis
X1B Bitot’s spots
X2 Corneal xerosis
X3A Corneal ulceration/keratomalacia affecting
less than one-third corneal surface
X3B Corneal ulceration/keratomalacia affecting
more than one-third corneal surface.
XS Corneal scar due to xerophthalmia
XF Xerophthalmic fundus.
Clinical features
1. X N (night blindness). It is the earliest symptom of
xerophthalmia in children. It has to be elicited by
taking detailed history from the guardian or relative.
2. X1A (conjunctival xerosis). It consists of one or
more patches of dry, lustreless, nonwettable
conjunctiva (Fig. 19.1), which has been well described
as ‘emerging like sand banks at receding tide’ when
the child ceases to cry. These patches almost always
involve the inter-palpebral area of the temporal
quadrants and often the nasal quadrants as well. In
more advanced cases, the entire bulbar conjunctiva
may be affected. Typical xerosis may be associated
with conjunctival thickening, wrinkling and
pigmentation.
3. X1B (Bitot’s spots). It is an extension of the xerotic
process seen in stage X1A. The Bitot’s spot is a
raised, silvery white, foamy, triangular patch of
keratinised epithelium, situated on the bulbar
conjunctiva in the inter-palpebral area (Fig. 19.2). It is
usually bilateral and temporal, and less frequently
nasal.
4. X2 (corneal xerosis). The earliest change in the
cornea is punctate keratopathy which begins in the
lower nasal quadrant, followed by haziness and/or
granular pebbly dryness (Fig. 19.3). Involved cornea
lacks lustre.
5. X3A and X3B (corneal ulceration/keratomalacia),
Stromal defects occur in the late stage due to
colliquative necrosis and take several forms. Small
ulcers (1-3 mm) occur peripherally; they are
characteristically circular, with steep margins and are
sharply demarcated (Fig. 19.4). Large ulcers and areas
of necrosis may extend centrally or involve the entire
cornea. If appropriate therapy is instituted immediately,
stromal defects involving less than one-third of
corneal surface (X3A) usually heal, leaving some
useful vision. However, larger stromal defects (X3B)
(Fig. 19.5) commonly result in blindness.
6. XS (corneal scars). Healing of stromal defects
results in corneal scars of different densities and sizes
which may or may not cover the pupillary area (Fig.
19.6). A detailed history is required to ascertain the
cause of corneal opacity.
7. XFC (Xerophthalmic fundus). It is characterized
by typical seed-like, raised, whitish lesions scattered
uniformly over the part of the fundus at the level of
optic disc (Fig. 19.7).
Treatment
It includes local ocular therapy, vitamin A therapy
and treatment of underlying general disease.
1. Local ocular therapy. For conjunctival xerosis
artificial tears (0.7 percent hydroxypropyl methyl
cellulose or 0.3 percent hypromellose) should be
instilled every 3-4 hours. In the stage of keratomalacia,
full-fledged treatment of bacterial corneal ulcer
should be instituted (see pages 120-123).
2. Vitamin A therapy. Treatment schedules apply to
all stages of active xerophthalmia viz. XN, X1A, X1B,
X2, X3A and X3B. Oral administration is the
recommended method of treatment. However, in the
presence of repeated vomiting and severe diarrhoea,
intramuscular injections of water-miscible preparation
should be preferred. The WHO recommended
schedule is as given below:
i. All patients above the age of 1 year (except
women of reproductive age): 200,000 IU of vitamin
A orally or 100,000 IU by intramuscular injection
should be given immediately on diagnosis and
repeated the following day and 4 weeks later.
ii. Children under the age of 1 year and children
of any age who weigh less than 8 kg should be
treated with half the doses for patients of more
than 1 year of age.
iii. Women of reproductive age, pregnant or not: (a)
Those having night blindness (XN), conjunctival
xerosis (X1A) and Bitot’s spots (X1B) should be
treated with a daily dose of 10,000 IU of vitamin
A orally (1 sugar coated tablet) for 2 weeks.
(b) For corneal xerophthalmia, administration of
full dosage schedule (described for patients above
1 year of age) is recommended.
3. Treatment of underlying conditions such as PEM
and other nutritional disorders, diarrhoea,
dehydration and electrolyte imbalance, infections and
parasitic conditions should be considered
simultaneously.
Prophylaxis against xerophthalmia
The three major known intervention strategies for the
prevention and control of vitamin A deficiency are:
1. Short-term approach. It comprises periodic
administration of vitamin A supplements. WHO
recommended, universal distribution schedule of
vitamin A for prevention is as follows:
i. Infants 6-12 100,000 IU orally every
months old and 3-6 months.
any older children
who weigh less
than 8 kg.
ii. Children over 200,000 IU orally every
1 year and under 6 months.
6 years of age
iii. Lactating 20,000 IU orally once at
mothers delivery or during the next
2 months. This will raise
the concentration of vitamin
A in the breast milk and
therefore, help to protect
the breastfed infant.
iv. Infants less 50,000 IU orally should
than 6 months be given before they
old, not being attain the age of 6
breastfed. months.
A revised schedule of vitamin A supplements being
followed in India since August 1992, under the
programme named as ‘Child Survival and Safe
Motherhood (CSSM)’ is as follows:
First dose (1 lakh I.U.)—at 9 months of age along
with measles vaccine.
Second dose (2 lakh I.U.)—at 18 months of age
along with booster dose of DPT/OPV.
Third dose (2 lakh I.U.)—at 2 years of age.
2. Medium-term approach. It includes food
fortification with vitamin A.
3. Long-term approach. It should be the ultimate
aim. It implies promotion of adequate intake of vitamin
A rich foods such as green leafy vegetables, papaya
and drum- sticks (Fig. 19.8). Nutritional health
education should be included in the curriculum of
school children.

Keratoplasty

Keratoplasty, also called corneal grafting or corneal
transplantation, is an operation in which the patient's
diseased cornea is replaced by the donor's healthy
clear cornea.
Types
1. Penetrating keratoplasty (full-thickness grafting)
2. Lamellar keratoplasty (partial-thickness grafting).
Indications
1. Optical, i.e., to improve vision. Important indications
are: corneal opacity, bullous keratopathy, corneal
dystrophies, advanced keratoconus.
2. Therapeutic, i.e., to replace inflamed cornea not
responding to conventional therapy.
3. Tectonic graft, i.e., to restore integrity of eyeball
e.g. after corneal perforation and in marked corneal
thinning.

4. Cosmetic, i.e., to improve the appearance of the eye.
Donor tissue
The donor eye should be removed as early as
possible (within 6 hours of death). It should be stored
under sterile conditions.
Evaluation of donor cornea. Biomicroscopic
examination of the whole globe, before processing
the tissue for media stroage, is very important. The
donor corneal tissue is graded into excellent, very
good, good, fair, and poor depending upon the
condition of corneal epithelium, stroma, Descemet's
membrane and endothelium (Table 5.1).
Methods of corneal preservation
1. Short-term storage (up to 48 hours). The whole
globe is preserved at 4oC in a moist chamber.
2. Intermediate storage (up to 2 weeks) of donor
cornea can be done in McCarey-Kaufman (MK)
medium and various chondroitin sulfate enriched
media such as optisol medium.
3. Long-term storage up to 35 days is done by
organ culture method.
Surgical technique
1. Excision of donor corneal button (Fig. 5.23A).
The donor corneal button should be cut 0.25 mm
larger than the recipient, taking care not to damage
the endothelium.
2. Excision of recipient corneal button. With the
help of a corneal trephine (7.5 mm to 8 mm in size)
a partial thickness incision is made in the host
cornea (Fig. 5.23B). Then, anterior chamber is
entered with the help of a razor blade knife and
excision is completed using corneo-scleral scissors
(Fig. 5.23C).
3. Suturing of corneal graft into the host bed (Fig.
5.23D) is done with either continuous (Fig. 5.23E)
or interrupted (Fig. 5.23F) 10-0 nylon sutures.
Complications
1. Early complications. These include flat anterior
chamber, iris prolapse, infection, secondary
glaucoma, epithelial defects and primary graft
failure.
2. Late complications. These include graft rejection,
recurrence of disease and astigmatism.

CORNEAL OEDEMA

The water content of normal cornea is 78 percent. It
is kept constant by a balance of factors which draw
water in the cornea (e.g., intraocular pressure and
swelling pressure of the stromal matrix = 60 mm of
Hg) and the factors which draw water out of cornea
(viz. the active pumping action of corneal
endothelium, and the mechanical barrier action of
epithelium and endothelium).
Disturbance of any of the above factors leads to
corneal oedema, wherein its hydration becomes above
78 percent, central thickness increases and
transparency reduces.
Causes of corneal oedema
1. Raised intraocular pressure
2. Endothelial damage
i. Due to injuries, such as birth trauma (forceps
delivery), surgical trauma during intraocular
operation, contusion injuries and penetrating
injuries.
ii. Endothelial damage associated with corneal
dystrophies such as, Fuchs dystrophy,
congenital hereditary endothelial dystrophy
and posterior polymorphous dystrophy.
iii. Endothelial damage secondary to inflammations
such as uveitis, endophthalmitis and corneal
graft infection.
3. Epithelial damage due to :
i. mechanical injuries
ii. chemical burns
iii. radiational injuries
Clinical features
Initially there occurs stromal haze with reduced vision.
In long-standing cases with chronic endothelial
failure (e.g., in Fuch's dystrophy) there occurs
permanent oedema with epithelial vesicles and bullae
formation (bullous keratopathy). This is associated
with marked loss of vision, pain, discomfort and
photophobia, due to periodic rupture of bullae.
Treatment
1. Treat the cause wherever possible, e.g., raised
IOP and ocular inflammations.
2. Dehydration of cornea may be tried by use of:
i. Hypertonic agents e.g., 5 percent sodium
chloride drops or ointments or anhydrous
glycerine may provide sufficient dehydrating
effect.
ii. Hot forced air from hair dryer may be useful.
3. Therapeutic soft contact lenses may be used to
get relief from discomfort of bullous keratopathy.
4. Penetrating keratoplasty is required for longstanding
cases of corneal oedema, non-responsive
to conservative therapy.

Keratoconus

Keratoconus (conical cornea) (Fig. 5.18) is a noninflammatory
bilateral (85%) ectatic condition of
cornea in its axial part. It usually starts at puberty
and progresses slowly.
Etiopathogenesis. It is still not clear. Various theories
proposed so far label it as developmental condition,
degenerative condition, hereditary dystrophy and
endocrine anomaly. Essential pathological changes
are thinning and ectasia which occur as a result of
defective synthesis of mucopolysaccharide and
collagen tissue.
Clinical features. Symptoms. Patient presents with a
defective vision due to progressive myopia and
irregular astigmatism, which does not improve fully
despite full correction with glasses.
Signs. Following signs may be elicited:
1. Window reflex is distorted.
2. Placido disc examination shows irregularity of
the circles (Fig. 5.18B).
3. Keratometry depicts extreme malalignment of
mires.
4. Photokeratoscopy reveals distortion of circles.
5. Slit lamp examination (Fig. 5.18C) may show
thinning and ectasia of central cornea, opacity at
the apex and Fleischer's ring at the base of cone,
folds in Descemet's and Bowman's membranes.
Very fine, vertical, deep stromal striae (Vogt lines)
which disappear with external pressure on the
globe are peculiar feature.
6. On retinoscopy a yawning reflex (scissor reflex)
and high oblique or irregular astigmatism is
obtained.
7. On distant direct ophthalmoscopy an annular
dark shadow (due to total internal reflection of
light) is seen which separates the central and
peripheral areas of cornea (oil droplet reflex).
8. Munson's sign, i.e. localised bulging of lower lid
when patient looks down is positive in late stages.
Morphological classification. Depending upon the
size and shape of the cone. the keratoconus is of
three types:
Nipple cone has a small size (<5mm) and steep
curvature.
Oval cone is larger (5-6 mm) and ellipsoid in
shape.

Complications. Keratoconus may be complicated by
development of acute hydrops due to rupture of
Descemet's membrane. The condition is characterised
by sudden development of corneal oedema associated
with marked defective vision, pain, photophobia and
lacrimation.
Associations. Keratoconus may be associated with :
Ocular conditions e.g. ectopia lentis, congenital
cataract, aniridia, retinitis pigmentosa, and vernal
keratoconjunctivitis (VKC).
Systemic conditions e.g., Marfan's sysndrome,
atopy, Down's syndrome, Ehlers-Danlos
syndrome, osteogenesis imperfecta and mitral
valve prolapse.
Treatment. Falling vision may not be corrected by
glasses due to irregular astigmatism.
Contact lenses (rigid gas permiable) usually
improve the vision in early cases.
In later stages penetrating keratoplasty may be
required.
Intacs, the intracorneal ring segments, are
reported to be useful in early cases.

Arcus Senilis

Arcus senilis refers to an annular lipid infiltration of
corneal periphery. This is an age-related change
occurring bilaterally in 60 percent of patients between
40 and 60 years of age and in nearly all patients over
the age of 80. Sometimes, similar changes occur in
young persons (arcus juvenilis) which may or may
not be associated with hyperlipidemia.
The arcus starts in the superior and inferior
quadrants and then progresses circumferentially to
form a ring which is about 1 mm wide. This ring of
opacity is separated from the limbus by a clear zone
(the lucid interval of Vogt) (Fig. 5.16). Sometimes
there may be double ring of arcus.

HERPES ZOSTER OPHTHALMICUS

Herpes zoster ophthalmicus is an acute infection of
Gasserian ganglion of the fifth cranial nerve by the
varicella-zoster virus (VZV). It constitutes
approximately 10 percent of all cases of herpes zoster.
Etiology
Varicella -zoster virus. It is a DNA virus and produces
acidophilic intranuclear inclusion bodies. It is
neurotropic in nature.

Mode of infection. The infection is contracted in
childhood, which manifests as chickenpox and the
child develops immunity. The virus then remains
dormant in the sensory ganglion of trigeminal nerve.
It is thought that, usually in elderly people (can occur
at any age) with depressed cellular immunity, the virus
reactivates, replicates and travels down along one or
more of the branches of the ophthalmic division of
the fifth nerve.
Clinical features
In herpes zoster ophthalmicus, frontal nerve is
more frequently affected than the lacrimal and
nasociliary nerves.
About 50 percent cases of herpes zoster
ophthalmicus get ocular complications.
The Hutchinson's rule, which implies that ocular
involvement is frequent if the side or tip of nose
presents vesicles (cutaneous involvement of
nasociliary nerve), is useful but not infallible.
Lesions of herpes zoster are strictly limited to
one side of the midline of head.
Clinical phases of H. zoster ophthalmicus are :
i. Acute, which may totally resolve.
ii. Chronic, which may persist for years.
iii. Relapsing, where the acute or chronic lesions
reappear sometimes years later.
Clinical features of herpes zoster ophthalmicus
include general features, cutaneous lesions and
ocular lesions. In addition, there may be associated
other neurological complications as described below:
A. General features. The onset of illness is sudden
with fever, malaise and severe neuralgic pain along
the course of the affected nerve. The distribution of
pain is so characteristic of zoster that it usually
arouses suspicion of the nature of the disease before
appearance of vesicles.
B. Cutaneous lesions. Cutaneous lesions (Fig. 5.10)
in the area of distribution of the involved nerve appear
usually after 3-4 days of onset of the disease. To
begin with, the skin of lids and other affected areas
become red and oedematous (mimicking erysipelas),
followed by vesicle formation. In due course of time
vesicles are converted into pustules, which
subsequently burst to become crusting ulcers. When
crusts are shed, permanent pitted scars are left. The
active eruptive phase lasts for about 3 weeks. Main
symptom is severe neuralgic pain which usually
diminishes with the subsidence of eruptive phase;
but sometimes it may persist for years with little
diminution of intensity. There occurs some anaesthesia
of the affected skin which when associated with
continued post-herpetic neuralgia is called
anaesthesia dolorosa.
C. Ocular lesions. Ocular complications usually
appear at the subsidence of skin eruptions and may
present as a combination of two or more of the
following lesions:
1. Conjunctivitis is one of the most common
complication of herpes zoster. It may occur as
mucopurulent conjunctivitis with petechial
haemorrhages or acute follicular conjunctivitis with
regional lymphadenopathy. Sometimes, severe
necrotizing membranous inflammation may be seen.
2. Zoster keratitis occurs in 40 percent of all patients
and sometimes may precede the neuralgia or skin
lesions. It may occur in several forms, which in order
of chronological clinical occurrence are (Fig. 5.11) :
Fine or coarse punctate epithelial keratitis.
Microdendritic epithelial ulcers. These unlike
dendritic ulcers of herpes simplex are usually
peripheral and stellate rather than exactly dendritic
in shape. It contrast to Herpes simplex dendrites,
they have tapered ends which lack bulbs.
Nummular keratitis is seen in about one-third
number of total cases. It typically occurs as
multiple tiny granular deposits surrounded by a
halo of stromal haze.
Disciform keratitis occurs in about 50 percent of
cases and is always preceded by nummular keratitis.

Neuroparalytic ulceration may occur as a
sequelae of acute infection and Gasserian ganglion
destruction.
Exposure keratitis may supervene in some cases
due to associated facial palsy.
Mucous plaque keratitis develops in 5% of cases
between 3rd and 5th months characterised by
sudden development of elevated mucous plaque
with stain brilliantly with rose bengal.

3. Episcleritis and scleritis occur in about one-half
of the cases. These usually appear at the onset of the
rash but are frequently concealed by the overlying
conjunctivitis.
4. Iridocyclitis is of a frequent occurrence and may
or may not be associated with keratitis. There may be
associated hypopyon and hyphaema (acute
haemorrhagic uveitis).
5. Acute retinal necrosis may occurs in some cases.
6. Anterior segment necrosis and phthisis bulbi. It
may also result from zoster vasculitis and ischemia.
7. Secondary glaucoma. It may occur due to
trabeculitis in early stages and synechial angle
closure in late stages.

D. Associated neurological complications. Herpes
zoster ophthalmicus may also be associated with
other neurological complications such as :
1. Motor nerve palsies especially third, fourth, sixth
and seventh.
2. Optic neuritis occurs in about 1 percent of cases.
3. Encephalitis occurs rarely with severe infection.
Treatment
Therapeutic approach to herpes zoster ophthalmicus
should be vigorous and aimed at preventing severe
devastating ocular complications and promoting rapid
healing of the skin lesions without the formation of
massive crusts which result in scarring of the nerves
and postherpetic neuralgia. The following regime may
be followed:
I. Systemic therapy for herpes zoster
1. Oral antiviral drugs. These significantly decrease
pain, curtail vesiculation, stop viral progression
and reduce the incidence as well as severity of
keratitis and iritis. In order to be effective, the
treatment should be started immediately after the
onset of rash. It has no effect on post herpetic
neuralgia.
Acyclovir in a dose of 800 mg 5 times a day
for 10 days, or
Valaciclovir in a dose of 500mg TDS
2. Analgesics. Pain during the first 2 weeks of an
attack is very severe and should be treated by
analgesics such as combination of mephenamic
acid and paracetamol or pentazocin or even
pethidine (when very severe).
3. Systemic steroids. They appear to inhibit
development of post-herpetic neuralgia when
given in high doses. However, the risk of high
doses of steroids in elderly should always be
taken into consideration. Steroids are commonly
recommended in cases developing neurological
complications such as third nerve palsy and
optic neuritis.
4. Cimetidine in a dose of 300 mg QID for 2-3 weeks
starting within 48-72 hours of onset has also
been shown to reduce pain and pruritis in acute
zoster - presumably by histamine blockade.
5. Amitriptyline should be used to relieve the
accompanying depression in acute phase.

II. Local therapy for skin lesions
1. Antibiotic-corticosteroid skin ointment or lotions.
These should be used three times a day till skin
lesions heal.
2. No calamine lotion. Cool zinc calamine
application, as advocated earlier, is better avoided,
as it promotes crust formation.
III. Local therapy for ocular lesions
1. For zoster keratitis, iridocyctitis and scleritis
i. Topical steroid eye drops 4 times a day.
ii. Cycloplegics such as cyclopentolate eyedrops
BD or atropine eye ointment OD.
iii. Topical acyclovir 3 percent eye ointment
should be instilled 5 times a day for about 2
weeks.
2. To prevent secondary infections topical antibiotics
are used.
3. For secondary glaucoma
i. 0.5 percent timolol or 0.5% betaxolol drops BD.
ii. Acetazolamide 250 mg QID.
4. For neuroparalytic corneal ulcer caused by
herpes zoster, lateral tarsorrhaphy should be
performed.
5. For persistent epithelial defects use :
i. Lubricating artificial tear drops, and
ii. Bandage soft contact lens.
6. Keratoplasty. It may be required for visual
rehabilitation of zoster-patients with dense
scarring. However, these are poor risk patients.

HERPES SIMPLEX KERATITIS

Ocular infections with herpes simplex virus (HSV) are
extremely common and constitute herpetic
keratoconjunctivitis and iritis.
Etiology
Herpes simplex virus (HSV). It is a DNA virus. Its
only natural host is man. Basically HSV is
epitheliotropic but may become neurotropic.
According to different clinical and immunological
properties, HSV is of two types: HSV type I typically
causes infection above the waist and HSV type II
below the waist (herpes genitalis). HSV-II has also
been reported to cause ocular lesions.
Mode of Infection
HSV-1 infection. It is acquired by kissing or
coming in close contact with a patient suffering
from herpes labialis.
HSV-II infection. It is transmitted to eyes of
neonates through infected genitalia of the mother.
Ocular lesions of herpes simplex
Ocular involvement by HSV occurs in two forms,
primary and recurrent; with following lesions:
[A] Primary herpes
1. Skin lesions
2. Conjunctiva-acute follicular conjunctivitis
3. Cornea
i. Fine epithelial punctate keratitis
ii. Coarse epithelial punctate keratitis
iii. Dendritic ulcer
[B] Recurrent herpes
1. Active epithelial keratitis
i. Punctate epthelial keratitis
ii. Dendritic ulcer
iii. Geographical ulcer
2. Stromal keratitis
i. Disciform keratitis
ii. Diffuse stromal necrotic keratitis
3. Trophic keratitis (meta-herpetic)
4. Herpetic iridocyclitis

[A] Primary ocular herpes
Primary infection (first attack) involves a nonimmune
person. It typically occurs in children between 6
months and 5 years of age and in teenagers.
Clinical features
1. Skin lesions. Vesicular lesions may occur
involving skin of lids, periorbital region and the
lid margin (vesicular blepharitis).
2. Acute follicular conjunctivitis with regional
lymphadenitis is the usual and sometimes the
only manifestation of the primary infection.
3. Keratitis. Cornea is involved in about 50 percent
of the cases. The keratitis can occur as a coarse
punctate or diffuse branching epithelial keratitis
that does not usually involve the stroma.
Primary infection is usually self-limiting but the
virus travels up to the trigeminal ganglion and
establishes the latent infection.
[B] Recurrent ocular herpes
The virus which lies dormant in the trigeminal
ganglion, periodically reactivates and causes
recurrent infection.
Predisposing stress stimuli which trigger an attack
of herpetic keratitis include: fever such as malaria,
flu, exposure to ultraviolet rays, general ill- health,
emotional or physical exhaustion, mild trauma,
menstrual stress, following administration of topical
or systemic steroids and immunosuppressive agents.
1. Epithelial keratitis
i. Punctate epithelial keratitis (Fig. 5.9A). The
initial epithelial lesions of recurrent herpes resemble
those seen in primary herpes and may be either in
the form of fine or coarse superficial punctate
lesions.
ii. Dendritic ulcer (Figs. 5.9B and C). Dendritic ulcer
is a typical lesion of recurrent epithelial keratitis.
The ulcer is of an irregular, zigzag linear branching
shape. The branches are generally knobbed at the
ends. Floor of the ulcer stains with fluorescein and
the virus-laden cells at the margin take up rose
bengal. There is an associated marked diminution of
corneal sensations.
iii. Geographical ulcer (Fig. 5.9D). Sometimes, the
branches of dendritic ulcer enlarge and coalesce to
form a large epithelial ulcer with a 'geographical' or
'amoeboid' configuration, hence the name. The use
of steroids in dendritic ulcer hastens the formation
of geographical ulcer.
Symptoms of epithelial keratitis are: photophobia
lacrimation, pain.
Treatment of epithelial keratitis
I. Specific treatment
1. Antiviral drugs are the first choice presently.
Always start with one drug first and see the response.
Usually after 4 days the lesion starts healing which is
completed by 10 days. After healing, taper the drug
and withdraw in 5 days. If after 7 days of initial therapy,
there is no response, it means the virus is resistant to
this drug. So change the drug and/or do mechanical
debridement. Commonly used antiviral drugs with
their dose regime is given below (for details see page
420).
i. Acycloguanosine (Aciclovir) 3 percent ointment:
5 times a day until ulcer heals and then 3 times
a day for 5 days. It is least toxic and most
commonly used antiviral drug. It penetrates intact
corneal epithelium and stroma, achieving
therapeutic levels in aqueous humour, and can
therefore be used to treat herpetic keratitis.

ii. Ganciclovir (0.15% gel), 5 times a day until ulcer
heals and then 3 times a day for 5 days. It is more
toxic than aciclovir.
iii. Triflurothymidine 1 percent drops : Two hourly
until ulcer heals and then 4 times a day for 5
days.
iv. Adenine arabinoside (Vidarabine) 3 percent
ointment: 5 times a day until ulcer heals and then
3 times a day for 5 days.
2. Mechanical debridement of the involved area along
with a rim of surrounding healthy epithelium with the
help of sterile cotton applicator under magnification
helps by removing the virus-laden cells.
Before the advent of antiviral drugs, it used to be
the treatment of choice. Now it is reserved for:
resistant cases, cases with non-compliance and those
allergic to antiviral drugs.
II. Non-specific supportive therapy and physical and
general measures are same as for bacterial corneal
ulcer (see page 98).
2. Stromal keratitis
(a) Disciform keratitis
Pathogenesis. It is due to delayed hypersensitivity
reaction to the HSV antigen. There occurs low grade
stromal inflammation and damage to the underlying
endothelium. Endothelial damage results in corneal
oedema due to imbibation of aqueous humour.
Signs. Disciform keratitis is characterized by (Fig.
5.9E):
Focal disc-shaped patch of stromal oedema
without necrosis,
Folds in Descemet's membrane,
Keratic precipitates,
Ring of stromal infilterate (Wessley immune ring)
may be present surrounding the stromal oedema.
It signifies the junction between viral antigen and
host antibody.
Corneal sensations are diminished.
Intraocular pressure (IOP) may be raised despite
only mild anterior uveitis. In severe cases, anterior
uveitis may be marked.
Sometimes epithelial lesions may be associated
with disciform keratitis.
Important note. During active stage diminished
corneal sensations and keratic precipitates are the
differentiating points from other causes of stromal
oedema.
Treatment consists of diluted steroid eye drops
instilled 4-5 times a day with an antiviral cover
(aciclovir 3%) twice a day. Steroids should be tapered
over a period of several weeks. When disciform
keratitis is present with an infected epithelial ulcer,
antiviral drugs should be started 5-7 days before the
steroids.
(b) Diffuse stromal necrotic keratitis. It is a type of
interstitial keratitis caused by active viral invasion
and tissue destruction.
Symptoms : Pain, photophobia and redness are
common symptom.
Signs. It presents as necrotic, blotchy, cheesy white
infiltrates that may lie under the epithelial ulcer or
may present independently under the intact
epithelium. It may be associated with mild iritis and
keratic precipitates. After several weeks of
smouldering inflammation, stromal vascularization
may occur.
Treatment is similar to disciform keratitis but
frequently the results are unsatisfactory.
Keratoplasty should be deferred until the eye has
been quiet with little or no steroidal treatment for
several months; because viral interstitial keratitis is
the form of herpes which is most likely to recur in a
new graft.
3. Metaherpetic keratitis
Metaherpetic keratitis (Epithelial sterile trophic
ulceration) is not an active viral disease, but is a
mechanical healing problem (similar to recurrent
traumatic erosions) which occurs at the site of a
previous herpetic ulcer.
Clinically it presents as an indolent linear or
ovoid epithelial defect.
Treatment is aimed at promoting healing by use
of lubricants (artificial tears), bandage soft

Fungal Corneal Ulcer

MYCOTIC CORNEAL ULCER
The incidence of suppurative corneal ulcers caused
by fungi has increased in the recent years due to
injudicious use of antibiotics and steroids.
Etiology
1. Causative fungi. The fungi which may cause
corneal infections are :
i. Filamentous fungi e.g., Aspergillus, Fusarium,
Alternaria, Cephalosporium, Curvularia and
Penicillium.
ii. Yeasts e.g., Candida and Cryptococcus.
(The fungi more commonly responsible for mycotic
corneal ulcers are Aspergillus (most common),
Candida and Fusarium).
2. Modes of infection
i. Injury by vegetative material such as crop
leaf, branch of a tree, straw, hay or decaying
vegetable matter. Common sufferers are field
workers especially during harvesting season.
ii. Injury by animal tail is another mode of
infection.
iii. Secondary fungal ulcers are common in
patients who are immunosuppressed
systemically or locally such as patients
suffering from dry eye, herpetic keratitis,
bullous keratopathy or postoperative cases of
keratoplasty.
3. Role of antibiotics and steroids. Antibiotics
disturb the symbiosis between bacteria and fungi;
and the steroids make the fungi facultative pathogens
which are otherwise symbiotic saprophytes.
Therefore, excessive use of these drugs predisposes
the patients to fungal infections.
Clinical features
Symptoms are similar to the central bacterial corneal
ulcer (see page 95), but in general they are less marked
than the equal-sized bacterial ulcer and the overall
course is slow and torpid.
Signs. A typical fungal corneal ulcer has following
salient features (Fig. 5.8):
Corneal ulcer is dry-looking, greyish white, with
elevated rolled out margins.
Delicate feathery finger-like extensions are present
into the surrounding stroma under the intact
epithelium.
A sterile immune ring (yellow line of demarcation)
may be present where fungal antigen and host
antibodies meet.
Multiple, small satellite lesions may be present
around the ulcer.

Usually a big hypopyon is present even if the
ulcer is very small. Unlike bacterial ulcer, the
hypopyon may not be sterile as the fungi can
penetrate into the anterior chamber without
perforation.
Perforation in mycotic ulcer is rare but can occur.
Corneal vascularization is conspicuously absent.
Diagnosis
1. Typical clinical manifestations associated with
history of injury by vegetative material are
diagnostic of a mycotic corneal ulcer.
2. Chronic ulcer worsening in spite of most efficient
treatment should arouse suspicion of mycotic
involvement.
3. Laboratory investigations required for
confirmation, include examination of wet KOH,
Calcofluor white, Gram's and Giemsa- stained films
for fungal hyphae and culture on Sabouraud's
agar medium.
Treatment
I. Specific treatment includes antifungal drugs:
1. Topical antifungal eye drops should be used
for a long period (6 to 8 weeks). These
include :
Natamycin (5%) eye drops
Fluconazol (0.2%) eye drops
Nystatin (3.5%) eye ointment.
For details see page 422.
2. Systemic antifungal drugs may be required for
severe cases of fungal keratitis. Tablet
fluconazole or ketoconazole may be given for
2-3 weeks.
II. Non specific treatment. Non-specific treatment
and general measures are similar to that of bacterial
corneal ulcer (see page 98).
III. Therapeutic penetrating keratoplasty may be
required for unresponsive cases.

Corneal Ulcer

Corneal ulcer may be defined as discontinuation in
normal epithelial surface of cornea associated with
necrosis of the surrounding corneal tissue.
Pathologically it is characterised by oedema and
cellular infiltration. Common types of corneal ulcers
are described below.
INFECTIVE KERATITIS
BACTERIAL CORNEAL ULCER
Being the most anterior part of eyeball, the cornea is
exposed to atmosphere and hence prone to get
infected easily. At the same time cornea is protected
from the day-to-day minor infections by the normal
defence mechanisms present in tears in the form of
lysozyme, betalysin, and other protective proteins.
Therefore, infective corneal ulcer may develop when:
either the local ocular defence mechanism is
jeopardised, or
there is some local ocular predisposing disease,
or host's immunity is compromised, or
the causative organism is very virulent.
Etiology
There are two main factors in the production of
purulent corneal ulcer:
Damage to corneal epithelium; and
Infection of the eroded area.
However, following three pathogens can invade
the intact corneal epithelium and produce ulceration:
Neisseria gonorrhoeae, Corynebacterium
diphtheriae and Neisseria meningitidis.
1. Corneal epithelial damage. It is a prerequisite for
most of the infecting organisms to produce corneal
ulceration. It may occur in following conditions:
i. Corneal abrasion due to small foreign body,
misdirected cilia, concretions and trivial trauma
in contact lens wearers or otherwise.
ii. Epithelial drying as in xerosis and exposure
keratitis.
iii. Necrosis of epithelium as in keratomalacia.
iv. Desquamation of epithelial cells as a result of
corneal oedema as in bullous keratopathy.
v. Epithelial damage due to trophic changes as
in neuroparalytic keratitis.
2. Source of infection include:
i. Exogenous infection. Most of the times corneal
infection arises from exogenous source like
conjunctival sac, lacrimal sac (dacryocystitis),
infected foreign bodies, infected vegetative
material and water-borne or air-borne infections.
ii. From the ocular tissue. Owing to direct

anatomical continuity, diseases of the
conjunctiva readily spread to corneal epithelium,
those of sclera to stroma, and of the uveal tract
to the endothelium of cornea.
iii. Endogenous infection. Owing to avascular
nature of the cornea, endogenous infections
are of rare occurrence.
3. Causative organisms. Common bacteria associated
with corneal ulceration are: Staphylococcus aureus,
Pseudomonas pyocyanea, Streptococcus
pneumoniae, E. coli, Proteus, Klebsiella, N.
gonorrhoea, N. meningitidis and C. diphtheriae.
Pathogenesis and pathology of corneal ulcer
Once the damaged corneal epithelium is invaded by
the offending agents the sequence of pathological
changes which occur during development of corneal
ulcer can be described under four stages, viz.,
infiltration, active ulceration, regression and
cicatrization. The terminal course of corneal ulcer
depends upon the virulence of infecting agent, host
defence mechanism and the treatment received.
Depending upon the prevalent circumstances the
course of corneal ulcer may take one of the three
forms:
(A) Ulcer may become localised and heal;
(B) Penetrate deep leading to corneal perforation;
or
(C) Spread fast in the whole cornea as sloughing
corneal ulcer.
The salient pathological features of these are as
under:
[A] Pathology of localised corneal ulcer
1. Stage of progressive infiltration (Fig. 5.2A). It is
characterised by the infiltration of polymorphonuclear
and/or lymphocytes into the epithelium
from the peripheral circulation supplemented by
similar cells from the underlying stroma if this tissue
is also affected. Subsequently necrosis of the
involved tissue may occur, depending upon the
virulence of offending agent and the strength of host
defence mechanism.
2. Stage of active ulceration (Fig. 5.2B). Active
ulceration results from necrosis and sloughing of the
epithelium, Bowman's membrane and the involved
stroma. The walls of the active ulcer project owing to
swelling of the lamellae by the imbibition of fluid and
the packing of masses of leucocytes between them.
This zone of infiltration may extend to a considerable
distance both around and beneath the ulcer. At this
stage, sides and floor of the ulcer may show grey
infiltration and sloughing.
During this stage of active ulceration, there occurs
hyperaemia of circumcorneal network of vessels which
results into accumulation of purulent exudates on the
cornea. There also occurs vascular congestion of the
iris and ciliary body and some degree of iritis due to
absorption of toxins from the ulcer. Exudation into
the anterior chamber from the vessels of iris and ciliary
body may lead to formation of hypopyon.

Ulceration may further progress by lateral extension
resulting in diffuse superficial ulceration or it may
progress by deeper penetration of the infection
leading to Descemetocele formation and possible
corneal perforation. When the offending organism is
highly virulent and/or host defence mechanism is
jeopardised there occurs deeper penetration during
stage of active ulceration.
3. Stage of regression (Fig. 5.2C). Regression is
induced by the natural host defence mechanisms
(humoral antibody production and cellular immune
defences) and the treatment which augments the
normal host response. A line of demarcation develops
around the ulcer, which consists of leucocytes that
neutralize and eventually phagocytose the offending
organisms and necrotic cellular debris. The digestion
of necrotic material may result in initial enlargement
of the ulcer. This process may be accompanied by
superficial vascularization that increases the humoral
and cellular immune response. The ulcer now begins
to heal and epithelium starts growing over the edges.
4. Stage of cicatrization (Fig. 5.2D). In this stage
healing continues by progressive epithelization which
forms a permanent covering. Beneath the epithelium,
fibrous tissue is laid down partly by the corneal
fibroblasts and partly by the endothelial cells of the
new vessels. The stroma thus thickens and fills in
under the epithelium, pushing the epithelial surface
anteriorly.
The degree of scarring from healing varies. If the
ulcer is very superficial and involves the epithelium
only, it heals without leaving any opacity behind.
When ulcer involves Bowman's membrane and few
superficial stromal lamellae, the resultant scar is called
a 'nebula'. Macula and leucoma result after healing of
ulcers involving up to one-third and more than that
of corneal stroma, respectively.
[B] Pathology of perforated corneal ulcer
Perforation of corneal ulcer occurs when the ulcerative
process deepens and reaches up to Descemet's
membrane. This membrane is tough and bulges out
as Descemetocele (Fig. 5.3). At this stage, any
exertion on the part of patient, such as coughing,
sneezing, straining for stool etc. will perforate the
corneal ulcer. Immediately after perforation, the
aqueous escapes, intraocular pressure falls and the

iris-lens diaphragm moves forward. The effects of
perforation depend upon the position and size of
perforation. When the perforation is small and
opposite to iris tissue, it is usually plugged and healing
by cicatrization proceeds rapidly (Fig. 5.4). Adherent
leucoma is the commonest end result after such a
catastrophe.
[C] Pathology of sloughing corneal ulcer and
formation of anterior staphyloma
When the infecting agent is highly virulent and/or
body resistance is very low, the whole cornea sloughs
with the exception of a narrow rim at the margin and
total prolapse of iris occurs. The iris becomes inflamed

and exudates block the pupil and cover the iris
surface; thus a false cornea is formed. Ultimately
these exudates organize and form a thin fibrous layer
over which the conjunctival or corneal epithelium
rapidly grows and thus a pseudocornea is formed.
Since the pseudocornea is thin and cannot withstand
the intraocular pressure, so it usually bulges forward
along with the plastered iris tissue. This ectatic cicatrix
is called anterior staphyloma which, depending upon
its extent, may be either partial or total. The bands of
scar tissue on the staphyloma vary in breadth and
thickness, producing a lobulated surface often
blackened with iris tissue which resembles a bunch
of black grapes (hence the name staphyloma).
Clinical picture
In bacterial infections the outcome depends upon
the virulence of organism, its toxins and enzymes,
and the response of host tissue.
Broadly bacterial corneal ulcers may manifest as:
i. Purulent corneal ulcer without hypopyon; or
ii. Hypopyon corneal ulcer.
In general, following symptoms and signs may be
present :
Symptoms
1. Pain and foreign body sensation occurs due to
mechanical effects of lids and chemical effects of
toxins on the exposed nerve endings.
2. Watering from the eye occurs due to reflex
hyperlacrimation.
3. Photophobia, i.e., intolerance to light results from
stimulation of nerve endings.
4. Blurred vision results from corneal haze.
5. Redness of eyes occurs due to congestion of
circumcorneal vessels.
Signs
1. Lids are swollen.
2. Marked blepharospasm may be there.
3. Conjunctiva is chemosed and shows conjunctival
hyperaemia and ciliary congestion.
4. Corneal ulcer usually starts as an epithelial defect
associated with greyish-white circumscribed
infiltrate (seen in early stage). Soon the epithelial
defect and infiltrate enlarges and stromal oedema
develops. A well established bacterial ulcer is
characterized by (Fig. 5.5):
Yellowish-white area of ulcer which may be oval
or irregular in shape.

Margins of the ulcer are swollen and over hanging.
Floor of the ulcer is covered by necrotic material.
Stromal oedema is present surrounding the ulcer
area.
Characteristic features produced by some of the
causative bacteria are as follows:
Staphylococal aureus and streptococcus
pneumoniae usually produce an oval, yellowish
white densely opaque ulcer which is surrounded
by relatively clear cornea.
Pseudomonas species usually produce an irregular
sharp ulcer with thick greenish mucopurulent
exudate, diffuse liquefactive necrosis and
semiopaque (ground glass) surrounding cornea.
Such ulcers spread very rapidly and may even
perforate within 48 to 72 hours.
Enterobacteriae (E. coli, Proteus sp., and Klebsiella
sp.) usually produce a shallow ulcer with
greyish white pleomorphic suppuration and
diffuse stromal opalescence. The endotoxins
produced by these Gram –ve bacilli may produce
ring-shaped corneal infilterate.
5. Anterior chamber may or may not show pus
(hypopyon). In bacterial corneal ulcers the
hypopyon remains sterile so long as the
Descemet's membrane is intact.
6. Iris may be slightly muddy in colour.
7. Pupil may be small due to associated toxin–
induced iritis.
8. Intraocular pressure may some times be raised
(inflammatory glaucoma).

Complications of corneal ulcer
1. Toxic iridocyclitis. It is usually associated with
cases of purulent corneal ulcer due to absorption of
toxins in the anterior chamber.
2. Secondary glaucoma. It occurs due to fibrinous
exudates blocking the angle of anterior chamber
(inflammatory glaucoma).
3. Descemetocele. Some ulcers caused by virulent
organisms extend rapidly up to Descemet's membrane,
which gives a great resistance, but due to the effect
of intraocular pressure it herniates as a transparent
vesicle called the descemetocele or keratocele
(Fig.5.3). This is a sign of impending perforation and
is usually associated with severe pain.
4. Perforation of corneal ulcer. Sudden strain due
to cough, sneeze or spasm of orbicularis muscle may
convert impending perforation into actual perforation
(Fig. 5.4). Following perforation, immediately pain is
decreased and the patient feels some hot fluid
(aqueous) coming out of eyes.
Sequelae of corneal perforation include :
i. Prolapse of iris. It occurs immediately following
perforation in a bid to plug it.
ii. Subluxation or anterior dislocation of lens
may occur due to sudden stretching and rupture
of zonules.
iii. Anterior capsular cataract. It is formed when
the lens comes in contact with the ulcer following
a perforation in the pupillary area.
iv. Corneal fistula. It is formed when the perforation
in the pupillary area is not plugged by iris and
is lined by epithelium which gives way
repeatedly. There occurs continuous leak of
aqueous through the fistula.
v. Purulent uveitis, endophthalmitis or even
panophthalmitis may develop due to spread of
intraocular infection.
vi. Intraocular haemorrhage in the form of either
vitreous haemorrhage or expulsive choroidal
haemorrhage may occur in some patients due to
sudden lowering of intraocular pressure.
5. Corneal scarring. It is the usual end result of
healed corneal ulcer. Corneal scarring leads to
permanent visual impairment ranging from slight
blurring to total blindness. Depending upon the
clinical course of ulcer, corneal scar noted may be
nebula, macula, leucoma, ectatic cicatrix or kerectasia,
adherent leucoma or anterior staphyloma (for details
see pages 122).
Management of a case of corneal ulcer
[A] Clinical evaluation
Each case with corneal ulcer should be subjected to:
1. Thorough history taking to elicit mode of onset,
duration of disease and severity of symptoms.

2. General physical examination, especially for
built, nourishment, anaemia and any immunocompromising
disease.
3. Ocular examination should include:
i. Diffuse light examination for gross lesions of
the lids, conjunctiva and cornea including
testing for sensations.
ii. Regurgitation test and syringing to rule out
lacrimal sac infection.
iii. Biomicroscopic examination after staining of
corneal ulcer with 2 per cent freshlyprepared
aqueous solution of fluorescein dye or sterilised
fluorescein impregnated filter paper strip to note
site, size, shape, depth, margin, floor and
vascularization of corneal ulcer. On
biomicroscopy also note presence of keratic
precipitates at the back of cornea, depth and
contents of anterior chamber, colour and pattern
of iris and condition of crystalline lens.
[B] Laboratory investigations
(a) Routine laboratory investigations such as
haemoglobin, TLC, DLC, ESR, blood sugar, complete
urine and stool examination should be carried out in
each case.
(b) Microbiological investigations. These studies
are essential to identify causative organism, confirm
the diagnosis and guide the treatment to be instituted.
Material for such investigations is obtained by
scraping the base and margins of the corneal ulcer
(under local anaesthesia, using 2 percent xylocaine)
with the help of a modified Kimura spatula or by
simply using the bent tip of a 20 gauge hypodermic
needle. The material obtained is used for the following
investigations:
i. Gram and Giemsa stained smears for possible
identification of infecting organisms.
ii. 10 per cent KOH wet preparation for
identification of fungal hyphae.
iii. Calcofluor white (CFW) stain preparation is
viewed under fluorescence microscope for
fungal filaments, the walls of which appear
bright apple green.
iv. Culture on blood agar medium for aerobic
organisms.
v. Culture on Sabouraud's dextrose agar medium
for fungi.
[C] Treatment
I. Treatment of uncomplicated corneal ulcer
Bacterial corneal ulcer is a vision threatening
condition and demands urgent treatment by
identification and eradication of causative bacteria.
Treatment of corneal ulcer can be discussed under
three headings:
1. Specific treatment for the cause.
2. Non-specific supportive therapy.
3. Physical and general measures.
1. The specific treatment
(a) Topical antibiotics. Initial therapy (before
results of culture and sensitivity are available)
should be with combination therapy to cover
both gram-negative and gram-positive
organisms.
It is preferable to start fortified gentamycin (14
mg/ml) or fortified tobramycin (14mg/ml)
eyedrops along with fortified cephazoline (50mg/
ml), every ½ to one hour for first few days and
then reduced to 2 hourly. Once the favourable
response is obtained, the fortified drops can be
substituted by more diluted commercially
available eye-drops, e.g. :
Ciprofloxacin (0.3%) eye drops, or
Ofloxacin (0.3%) eye drops, or
Gatifloxacin (0.3%) eye drops.
(b) Systemic antibiotics are usually not required.
However, a cephalosporine and an aminoglycoside
or oral ciprofloxacin (750 mg twice daily)
may be given in fulminating cases with
perforation and when sclera is also involved.
2. Non-specific treatment
(a) Cycloplegic drugs. Preferably 1 percent atropine
eye ointment or drops should be used to reduce
pain from ciliary spasm and to prevent the
formation of posterior synechiae from secondary
iridocyclitis. Atropine also increases the blood
supply to anterior uvea by relieving pressure
on the anterior ciliary arteries and so brings
more antibodies in the aqueous humour. It also
reduces exudation by decreasing hyperaemia
and vascular permeability. Other cycloplegic
which can be used is 2 per cent homatropine
eye drops.

(b) Systemic analgesics and anti-inflammatory
drugs such as paracetamol and ibuprofen relieve
the pain and decrease oedema.
(c) Vitamins (A, B-complex and C) help in early
healing of ulcer.
3. Physical and general measures
(a) Hot fomentation. Local application of heat
(preferably dry) gives comfort, reduces pain
and causes vasodilatation.
(b) Dark goggles may be used to prevent
photophobia.
(c) Rest, good diet and fresh air may have a
soothing effect.
II. Treatment of non-healing corneal ulcer
If the ulcer progresses despite the above therapy the
following additional measures should be taken:
1. Removal of any known cause of non-healing
ulcer. A thorough search for any already missed
cause not allowing healing should be made and
when found, such factors should be eliminated.
Common causes of non-healing ulcers are as
under:
i. Local causes. Associated raised intraocular
pressure, concretions, misdirected cilia,
impacted foreign body, dacryocystitis,
inadequate therapy, wrong diagnosis,
lagophthalmos and excessive vascularization
of ulcer.
ii. Systemic causes: Diabetes mellitus, severe
anaemia, malnutrition, chronic debilitating
diseases and patients on systemic steroids.
2. Mechanical debridement of ulcer to remove
necrosed material by scraping floor of the ulcer
with a spatula under local anaesthesia may hasten
the healing.
3. Cauterisation of the ulcer may also be considered
in non-responding cases. Cauterisation may be
performed with pure carbolic acid or 10-20 per
cent trichloracetic acid.
4. Bandage soft contact lens may also help in
healing.
5. Peritomy, i.e., severing of perilimbal conjunctival
vessels may be performed when excessive corneal
vascularization is hindering healing.
III. Treatment of impending perforation
When ulcer progresses and perforation seems
imminent, the following additional measures may help
to prevent perforation and its complications:
1. No strain. The patient should be advised to
avoid sneezing, coughing and straining during
stool etc. He should be advised strict bed rest.
2. Pressure bandage should be applied to give
some external support.
3. Lowering of intraocular pressure by
simultaneous use of acetazolamide 250 mg QID
orally, intravenous mannitol (20%) drip stat, oral
glycerol twice a day, 0.5% timolol eyedrops twice
a day, and even paracentesis with slow evacuation
of aqueous from the anterior chamber may be
performed if required.
4. Tissue adhesive glue such as cynoacrylate is
helpful in preventing perforation.
5. Conjunctival flap. The cornea may be covered
completely or partly by a conjunctival flap to
give support to the weak tissue.
6. Bandage soft contact lens may also be used.
7. Penetrating therapeutic keratoplasty (tectonic
graft) may be undertaken in suitable cases, when
available.
IV. Treatment of perforated corneal ulcer
Best is to prevent perforation. However, if perforation
has occurred, immediate measures should be taken
to restore the integrity of perforated cornea.
Depending upon the size of perforation and
availability, measures like use of tissue adhesive glues,
covering with conjunctival flap, use of bandage soft
contact lens or therapeutic keratoplasty should be
undertaken. Best is an urgent therapeutic
keratoplasty.

Cornea: Anatomy, Transparency

The cornea is a transparent, avascular, watch-glass
like structure. It forms anterior one-sixth of the outer
fibrous coat of the eyeball.
Dimensions
The anterior surface of cornea is elliptical with
an average horizontal diameter of 11.7 mm and
vertical diameter of 11 mm.
The posterior surface of cornea is circular with
an average diameter of 11.5 mm.
Thickness of cornea in the centre is about 0.52
mm while at the periphery it is 0.7 mm.
Radius of curvature. The central 5 mm area of the
cornea forms the powerful refracting surface of
the eye. The anterior and posterior radii of
curvature of this central part of cornea are 7.8 mm
and 6.5 mm, respectively.
Refractive power of the cornea is about 45
dioptres, which is roughly three-fourth of the
total refractive power of the eye (60 dioptres).
Histology
Histologically, the cornea consists of five distinct
layers. From anterior to posterior these are: epithelium,
Bowman’s membrane, substantia propria (corneal
stroma), Descemet’s membrane and endothelium
(Fig. 5.1).
1. Epithelium. It is of stratified squamous type and
becomes continuous with the epithelium of bulbar
conjunctiva at the limbus. It consists of 5-6 layers of
cells. The deepest (basal) layer is made up of columnar
cells, next 2-3 layers of wing or umbrella cells and the
most superficial two layers are of flattened cells.
2. Bowman's membrane. This layer consists of
acellular mass of condensed collagen fibrils. It is
about 12μm in thickness and binds the corneal stroma
anteriorly with basement membrane of the epithelium.
It is not a true elastic membrane but simply a
condensed superficial part of the stroma. It shows

considerable resistance to infection. But once
destroyed, it does not regenerate.
3. Stroma (substantia propria). This layer is about
0.5 mm in thickness and constitutes most of the
cornea (90% of total thickness). It consists of collagen
fibrils (lamellae) embedded in hydrated matrix of
proteoglycans. The lamellae are arranged in many
layers. In each layer they are not only parallel to each
other but also to the corneal plane and become
continuous with scleral lamellae at the limbus. The
alternating layers of lamellae are at right angle to each
other. Among the lamellae are present keratocytes,
wandering macrophages, histiocytes and a few
leucocytes.
4. Descemet's membrane (posterior elastic lamina).
The Descemet's membrane is a strong homogenous
layer which bounds the stroma posteriorly. It is very
resistant to chemical agents, trauma and pathological
processes. Therefore, 'Descemetocele' can maintain
the integrity of eyeball for long. Descemet's membrane
consists of collagen and glycoproteins. Unlike
Bowman's membrane it can regenerate. Normally it
remains in a state of tension and when torn it curls
inwards on itself. In the periphery it appears to end at
the anterior limit of trabecular meshwork as
Schwalbe's line (ring).
5. Endothelium. It consists of a single layer of flat
polygonal (mainly hexagonal) cells which on slit lamp
biomicroscopy appear as a mosaic. The cell density
of endothelium is around 3000 cells/mm2 in young
adults, which decreases with the advancing age.
There is a considerable functional reserve for the
endothelium. Therefore, corneal decompensation
occurs only after more than 75 percent of the cells are
lost. The endothelial cells contain 'active-pump'
mechanism.
Blood supply
Cornea is an avascular structure. Small loops derived
from the anterior ciliary vessels invade its periphery
for about 1 mm. Actually these loops are not in the
cornea but in the subconjunctival tissue which
overlaps the cornea.
Nerve supply
Cornea is supplied by anterior ciliary nerves which
are branches of ophthalmic division of the 5th cranial
nerve. After going about 2 mm in cornea the nerves
lose their myelin sheath and divide dichotomously
and form three plexuses — the stromal, subepithelial
and intraepithelial.
APPLIED PHYSIOLOGY
The two primary physiological functions of the
cornea are (i) to act as a major refracting medium; and
(ii) to protect the intraocular contents. Cornea fulfills
these duties by maintaining its transparency and
replacement of its tissues.
Corneal transparency
The transparency is the result of :
Peculiar arrangement of corneal lamellae (lattice
theory of Maurice),
Avascularity, and
Relative state of dehydration, which is maintained
by barrier effects of epithelium and endothelium
and the active bicarbonate pump of the
endothelium.
For these processes, cornea needs some energy.