Keratitis 09

Keratitis
Cornea.
 The cornea is the
eye’s optical window
that makes it possible
for humans to see.
 The cornea tissue
consist of five layers.
1. The surfase of the
cornea is formed by
stratified
nonkeratinized
squamous
epithelium.
The cornea tissue consist of five layers.
2. A thin basement
membrane anchors the
basal cells of the
stratified squamous
epithelium to
Bowman’s layer.
3. The stroma is a highly
bradytrophic tissue
The cornea tissue consist of five layers.
4. Descemet’s
membrane is a
relatively strong
membrane
5. The corneal
endothelium is
responsible for the
transparency of the
cornea. The corneal
endothelium does not
regenerate.
Infectious Keratitis (purulent ulcer of the
cornea)
Protective Mechanisms of the Cornea
 * Reflexive eye closing.
 * Flushing effect of tear fluid (lysozyme).
 * Its hydrophobic epithelium forms a diffusion barrier.
 * Epithelium can regenerate quickly and completely.
Pathogens causing corneal infections may
include:
 Viruses.
 Bacteria.
 Acanthamoeba.
 Fungi.
Pathogenesis:
Once these pathogens have invaded the
bradytrophic tissue through a superficial
corneal lesion, a typical chain of events will
ensue:
 Corneal lesion.
 Pathogens invade and colonize the corneal
stroma (red eye).
 Antibodies will infiltrate the site.
 As a result, the cornea will opacity and the
point of entry will open further, revealing the
cornea infiltrate.
Pathogenesis:
 Irritation of the anterior
chamber with hypopyon
(typically pus will accumulate
on the floor of the anterior
chamber).
 The pathogens will infest the
entire cornea.
 As a result the stroma will
melt down to Descemet's
membrane, which is
relatively strong This is
known as a descemetocele;
only Descemet’s membrane
is still intact.
Pathogenesis:
 As the disorder
progresses, perforation of
Descemet’s membrane
occurs and the aqueous
humor will be seen to
leak. This is referred to as
a perforated corneal
ulcer and is an indication
for immediate surgical
intervention (emergency
keratoplasty).
Pathogenesis:
 Prolapse of the iris (the iris
will prolapse into the newly
created defect) closing the
corneal perforation posteriorly.
 This rapidly progressing form
of infectious corneal ulcer
(usually bacterial) is referred to
as a serpiginous corneal ulcer.
It penetrates the cornea
particularly rapidly
A serpiginous corneal ulcer is
one of the most dangerous
clinical syndromes as it can
rapidly lead to loss of the eye.
General Notes on Diagnosing
Infectious Forms of Keratitis
 Symptoms:
 Patients report a foreign body sensation,
moderate pain in the eye,
 photophobia,
 impaired vision,
 tearing,
 and purulent discharge
Treatment: Conservative therapy.
Treatment is initiated with topical antibiotics :
 Eye drops: 0,25% Laevomycetin, 0,5%
Gentamycin, 1% Erythromycin, 0,5% Neomycin,
0,3% Ciprolet, 0,3% Ciromed, 0,3% Ocacin, 0,3%
Tobramycin, 0,3%Floxal
 Ointments:0,3% Tobramycin, 0,3%Floxal
 Mydriatics: 1% Atropin, 0,1%-0,25% Scopolamin,
0,5% Homotropin, 0,1% Platyphyllin, 0,1%
Adrenalin,0,5% Mydriacyl, 1% Tropicamide, 1%
Ciclomed, 2,5% Eryphrin
Treatment:
 Non-steroid drags: diclofenac, naclof, diclof

 Actovegin gele 20%, solcoseril gele.
 Subconjunctival application of antibiotics
may be required to increase the
effectiveness of the treatment
Surgical treatment.
Emergency keratoplasty is
indicated to treat a
descemetocele or a
perforated corneal ulcer
(see emergency
keratoplasty). Broad areas
of superficial necrosis may
require a conjunctival flap to
accelerate healing. Stenosis
or blockage of the lower
lacrimal system that may
impair healing of the ulcer
should be surgically
corrected.
Viral Keratitis
Viral keratitis is frequently caused by:
1. Herpes simplex virus.
2. Varicella-zoster virus.
3. Adenovirus.
Herpes Simplex Keratitis

Epidemiology and pathogenesis: Herpes
simplex keratitis is among the more
common causes of corneal ulcer.
Herpes Simplex Keratitis
Symptoms: Herpes
simplex keratitis is
usually very painful and
associated with
photophobia,
lacrimation, and
swelling of the eyelids.
Vision may be impaired
depending on the
location of findings
Forms and diagnosis of herpes
simplex keratitis:
 The following forms of herpes simplex

keratitis are differentiated according to
the specific layer of the cornea in which
the lesion is located.
Dendritic keratitis.
 This is characterized by
branching epithelial lesions
(necrotic and vesicular
swollen epithelial cells).
These findings will be visible
with the unaided eye after
application of fluorescein
dye and are characteristic of
dendritic keratitis. Corneal
sensitivity is usually
reduced. Dendritic keratitis
may progress to stromal
keratitis.
Stromal Keratitis.
 Slit lamp examination
will reveal central
diskiform corneal
infiltrates (diskiform
keratitis) with or without
a whitish stromal
infiltrate. Depending on
the frequency of
recurrence, superficial
or deep vascularization
may be present.
Treatment of the Viral Keratitis :
 Viral static agents can be used for

treatment, such as acyclovir, which is
available for topical use (in ointment form)
and systemic use.
Corticosteroids are contraindicated in
epithelial herpes simplex infections.
Endogenous keratitis
I. Tuberculous keratitis
 Tuberculo-allergic keratitis
 Hematogenic tuberculous keratitis
а) Deep diffused keratitis.
в) Deep corneal infiltrate.
с) Sclerosing keratitis
II. Parenchymatous syphilitic keratitis
Tuberculo-allergic keratitis
 Small phlyctenas (miliary) that are smaller than
millet in size are more often numerous. Solitary
phlyctenas look like grayish-yellow nodes up to 3
or 4 mm in diameter. Phlyctenas are always
situated in the superficial layers of the cornea, but
they also may involve deep stromal layers. Right
after phlyctena appears superficial vessels
reaching out to the focus in the form of bundles
are seen on the cornea. Appearance of
phlyctenas is accompanied by severe
photophobia
Tuberculo-allergic keratitis
 Rarely phlyctenas get absorbed without leaving
any signs such as ulceration. More commonly
they disintegrate. Disintegration is accompanied
by crater-shaped ulcers, which bases are quickly
covered with epithelium (facet stage). After that
they are gradually replaced by the connective
tissue and a circumscribed scar forms. Seldom
disintegration of phlyctemas ends with complete
destruction of the stroma and appearance of
descemetocele and perforation.
Hematogenic tuberculous keratitis
 Deep diffused keratitis. The disease is
characterized by lacrimation, photophobia
and pericorneal injection. The cornea
becomes cloudy fast. Against such a
background separate big yellowish-gray foci
are apparently seen in deep and medium
layers. There is a moderate vascularization of
the cornea. As a rule only one eye becomes
affected. Remissions go together with an
acute stage. Forecast is unfavorable.
Hematogenic tuberculous keratitis
 Deep corneal infiltrate. The focus is
situated in the deepest corneal layers.
Vascularization is insignificant. In
unfavorable course infiltrates get absorbed,
more seldom necrosis with ulceration
appears.
Sclerosing keratitis develops when deep
keratitis is present. Infiltration of deep layers
appears first on a limited area at the limb and
then spreads toward the center. Infiltrated
areas have the shape of a tongue or
demilune. Vascularization is not evident.
Treatment
Treatment includes administration of

specific antituberculous agents such as
Streptomycin, Phthivazide, Metazide,
Tubazide, Saluzide etc. Medicines used for
treatment for purulent ulcer of the cornea
are also prescribed:
 antibiotics (Ciprolet, Cipromed, Tobrex),
 mydriatics (Atropine, Cyclomed, Mesaton,
Mydriacyl, Irifrin and others),
Treatment
 keratoplastic agents (Actovegin, Solcoseryl,

vitamins A and E),
 nonsteroid anti-inflammatory drugs (Dycdoph,
Nacloph).
 If epithelial defect is absent application of
glucocorticosteroids is possible (Acetolomide,
Dexamethasone, Prednisolone).
 Inhibitors of proteolytic enzymes can also be
administered (Cortical, Gordox, Tracylol).
Parenchymatous syphilitic keratitis
 Clinical features. The disease is characterized
by cyclic course, bilateral lesion, involvement of the
uveal tract, absence of recurrence and relatively
favorable outcome. The course of parenchymatous
syphilitic keratitis has three stages: infiltration,
vascularization and absorption. At the first stage a
patient has slight photophobia and lacrimation.
Insignificant pericorneal injection is present on the
fundus. There is diffused gray-white infiltration at the
limb in the corneal stroma. The infiltrate consists of
separate dots, lines and strokes. The surface above
the infiltrate is rough. The infiltrate gradually spreads
over the whole cornea. Infiltration period takes 3 to 4
weeks.
 At the first stage a patient has slight
photophobia and lacrimation. Insignificant
pericorneal injection is present on the
fundus. There is diffused gray-white
infiltration at the limb in the corneal stroma.
The infiltrate consists of separate dots, lines
and strokes. The surface above the infiltrate
is rough. The infiltrate gradually spreads
over the whole cornea. Infiltration period
takes 3 to 4 weeks.
 In the 5th weeks the vessels begin to appear on
the cornea. Vascularization is deep. The limb gets
edematous. Vessel injection is mixed.
Vascularization period lasts from 6 to 8 weeks.
The vessels run through the whole cornea making
it look like non-fresh meat. Absorption period lasts
from 1 to 2 years. Irritation of the eye becomes
less. Infiltrates get absorbed starting from the limb
and ending with the center of the cornea. The
cornea becomes transparent again. The vessels
get empty and are seen in the form of thin threads
(vascular pannus).
 Treatment. Specific therapy with penicillin drugs
and treatment like in usual keratitis.

Keratitis 09

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Keratitis 09

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Keratitis

 Non-steroid drags: diclofenac, naclof, diclof

Herpes Simplex Keratitis

 The following forms of herpes simplex

 Viral static agents can be used for

Treatment includes administration of

 keratoplastic agents (Actovegin, Solcoseryl,

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