Corneal disorders

CORNEAL DISORDERS
By
Prof./ Ahmad Mostafa Abdallah
Professor of Ophthalmology
Sohag Faculty of Medicine, Egypt
Prof. Ahmad Mostafa Abdallah

The following will be discussed
in order:
 Anatomy of the cornea
 Physiology of the cornea
 Congenital anomalies of the cornea
 General signs of corneal diseases
 Inflammations of the cornea (Keratitis)
 Ectatic conditions of the cornea
 Corneal Degenerations

ANATOMY OF THE CORNEA

(A) Gross Anatomy
 It is a transparent clear, smooth structure forms
the anterior 1/6 of the outer coat of the eye.
 It has the following dimentions:
● Diameter: 11 mm vertically and 12 mm horizontally.
● Thickness: 0.6 mm at the centre and about 0.7-1mm. at
the periphery.
● Refractive index: 1.37.
● Refractive power 42 D.
● Radius of curvature: About 7.8 mm anteriorly and
6.6. mm posteriorly.

B. Minute Anatomy
● Histologically, the cornea is divided into
two zones:
 The cornea proper
 The limbus.

(1) The Cornea Proper
 It is composed of 5 layers:
1. Epithelium
2. Bowman’s membrane
3. Substantia Propria (Stroma)
4. Descemet’s membrane
5. Endothelium

1. The epithelium
 It is a stratified squamous, non keratinized
epithelium continuous at the limbus with the
conjunctival epithelium.
 It is about 5 – 6 layers of cells, with
superficial microvilli.

a) Basal cells:
- Resting on a basement membrane,
formed of a single layer of columnar
cells with a flat bases and rounded
heads
- The basal cells are firmly connected
with the basement membrane by
hemi-desmosomes.

B) Polyhedral or Wing cells (Umbrella cells):
- Of polyhedral shape, arranged in 2-3 layers.
- Their anterior surface is convex, the posterior
surface is concave fitting onto the heads of the
basal cells.
C) Surface cells:
- Two layers of flattened cells with flattened nuclei,
and microvilli.

2. Bowman's Membrane
 It is formed of collagenous fibers being
considered as the superficial condensed
layers of the stroma.
 It terminates one mm from the limbus.
 Numerous pores for corneal nerves are
present.
 If it is destroyed, it does not regenerate but
it will be replaced by fibrous tissue.

3. Stroma
 Constitute 90% of the corneal thickness
 it is formed of:
a. Lamellae and
b. Cells

 A. Lamellae:
 100-150 in number run parallel to each other and
to the surface.
 Criss cross each others in alternate lamellae at
90°.
 Composed of collagenous fibres and their
surrounding matrix which is rich in
mucopolysaccharides.
 In between the lamellae interlamellar spaces
exist which contain cells.

Corneal stroma

 B. Cells:
i. Fixed corneal corpuscles or keratocytes:
Are flattened cells parallel to the surface forming a
syncytium with flattened nuclei.They are important for
metabolic processes of the cornea and repair.
ii. Wandering cells: They are histocytes, flattened
cells, near the limbus, derived from the limbal blood
vessels.

4. Descemet’s Membrane
 It is a thin lamellated highly elastic membrane
formed of collagen fibrils embbeded in
glycoprotein matrix.
 It serves as a basement membrane for the
endothelium.
 It is resistant to pathological processes but
reforms after destruction from the endothelium.

Bowman's membrane Descemet's membrane
1.Offers little resistance
to any pathological
process
2.Easily destroyed
3.Never regenerates
4.A modified lamella of
the stroma
1.Highly resistant
2.Resistant
3.regenerates
4.A cuticular product of
endothelial cells
Differences between Bowman's & Descemet's
Membranes

5. Endothelium
 It is formed of a single layer of flat hexagonal
cells continuous around the angle of anterior
chamber with the endothelium of the iris.
 The cells are attached to D.M. by
hemidesmosomes.
 The endothelial cells show interdigitations
and microvilli.

Corneal Endothelium
 These cells play a major role in controlling the normal
hydration of the cornea both by:
a. A barrier function, limiting the access of water from the
aqueous humor to the corneal stroma &
b. Active transport mechanism (active metabolic
endothelial pump). Prof. Ahmad Mostafa Abdallah

(2) The limbus (Corneoscleral
Junction)
 At the limbus , the following changes occur:
1- Corneal epithelium becomes continuous with
conjunctival epithelium and becomes thicker (10
layers), and the cells are more irregularly
arranged.
2- Bowman's membrane ends in a rounded border,
short distance from the limbus.

3- The fibers of substantia propria become
irregular and continuous with the sclera.
4- D.M becomes continuous with the trabecular
meshwork.
5- Endothelium is continuous with the
endothelium at the angle and on iris.
6- Characterized by the presence of blood vessels
and lymphatics.

Importance of the limbus
 1- Contains the exit channels of aqueous.
 2- Landmark for eye surgery especially for
glaucoma and cataract operations.
 3- Contains the basal stem cells essential for
corneal epithelium regeneration after damage.

Nerve Supply of the Cornea
 Is from the 2 long ciliary nerves (of the
nasociliary branch of ophthalmic division of
trigeminal nerve).
 The cornea is only sensitive to pain, cold and
touch.
 The D.M and endothelium are not innervated.

PHYSIOLOGY OFTHE CORNEA

Physiology of the Cornea
 I. Nutrition of the Cornea
 II. Corneal transparancy
 III. Functions of the Cornea
 IV. PrecornealTear Film

I. Nutrition of the Cornea
 The cornea being avascular with no lymph
drainage, it derives its nutrition from the
following sources:
1- Diffusion from limbal capillaries.
2- Diffusion from the aqueous posteriorly and the
tears anteriorly.
3- Oxygen mainly from the atmosphere and
limbal capillaries.

II. Corneal transparancy
● The factors responsible for corneal transparency
are:
A. Anatomical Factors
B. Physiological Factors

A. Anatomical Factors:
1) Non-Keratinized epithelium.
2) The stromal lamellae are regular & parallel.
3) Non-myelinated nerve fibres.
4) Absence of blood Vs and lymphatics.

B. Physiological Factors:
1) Dehydrated state of the cornea (Active
metabolic endothelial pump)
2) Constant refractive index.

III. Functions of the Cornea
1.Optical:
 The cornea is the most powerful refractive
medium of the eye.
 The refractive power of the cornea =+ 42
Dioptres (the lens is + 18D).
 The clarity of the objects seen by the eye
largely depends on the integrity and
transparency of the cornea.

 2. Protective:
 The extreme sensitivity of the cornea is an
efficient protective mechanism producing a very
quick lid reflex, which rapidly closes the
palpebral fissure.

IV. The Precorneal Tear Film
● It is composed of 3 layers:
 1) Outer lipid layer
 2) Middle aqueous layer
 3) Inner mucin layer

(1) Outer lipid layer
● secreted by Meibomian glands
● Functions:
 1) Retard evaporation of tears.
 2) Reduce surface tension of the tear film and
draws more water to the aqueous layer.
 3) Lubricate the movement of the eyelids.

(2) Middle aqueous layer
● Secreted by lacrimal glands
● Functions:
 1) Supplies atmospheric oxygen to the cornea.
 2) Antibacterial function due to its content of
tear proteins (IgA, lysosome SJactoferrin).
 3) Refractive(abolish minute irregularities of the
anterior corneal surface).
 4) Washes away debris & allows passage of
leukocytes.

(3) Inner mucin layer
● Secreted by conjunctival goblet cells
● Functions:
 1)Wetting of the cornea by converting the
corneal epithelim from a hydrophobic to a
hydrophilic surface.
 2) Lubrication

CONGENITAL ANOMALIES OFTHE CORNEA

Congenital Anomalies of the
Cornea
 Microcornea
 Megalocornea
 Cornea plana
 Keratoconus
 Sclerocornea

1. Microcornea
 - Unilateral or bilateral.
 - Adult horizontal corneal diameter is 10 mm
or less.
 - AC is shallow, other dimensions are normal,
 - Associations: glaucoma, hypermetropia,
congenital cataract.

2. Megalocornea
 - Bilateral non progressive enlargement of
the cornea.
 - Corneal diameter 13 mm or more.
 -Very deep AC, high myopia.
 - Lens subluxation may occur due to zonular
stretching.

3. Cornea Plana
 Bilateral condition.
 Associated with: Hypermetropia, shallow AC,
angle closure glaucoma.

4. Keratoconus
 Congenital bilateral weakness of the cornea with
protrusion of its central part (cone).
 Onset: at puberty (10 – 20 ys)
 Diminution of vision occurs because of:
curvature myopia, irregular astigmatism, central
corneal opacity (late).

4. Sclerocornea
 Usually bilateral.
 Opacification & vascularization of the
peripheral part or the entire cornea.

GENERAL SIGNS OF CORNEAL DISEASES

General signs of Corneal Inflammation
1) Punctate epithelial erosions (PEE)
2) Punctate epithelial keratitis (PEK)
3) Mucus Filaments
2) Corneal edema (epithelial & stromal)
3)Vascularization of the cornea
4) Pannus
5) Breaks in DM

1) Punctate epithelial erosions (PEE):
 Are tiny epithelial defects which stained with
fluorescein
 They are non-specific but their location may
help to indicate the cause:-
● Superior PEEs: occur in spring catarrh &chlamydial infections.
● Interpalpebral PEEs: in dry eye & neurotrophic keratitis.
● Inferior PEEs: in lid margin disease, exposure keratitis & eye drops
toxicity.
Sup
I.P
Inf

Punctate epithelial erosions [PEE]

2) Punctate epithelial keratitis (PEK):
 Are swollen opaque epithelial cells which
stain with rose bengal
 Causes: Occur in viral keratitis

3) Mucus Filaments:
 Are mucus strands attached at one end to the
corneal surface & the other end moves with
each blink.
 Causes:
 1. Dry eye syndrome (most common cause)
 2. Neurotrophic keratitis
 3. Superior limbic keratoconjunctivitis
 4. Corneal epithelial instability

4) Corneal Edema
a) Epithelial Edema
 Is characterized by loss of normal corneal lustre
and may be vesicle and bullae formation.
 It is a sign of endothelial decompensation or
severe acute rise of IOP.

b) Stromal Edema
 Occurs in disciform keratitis & surgical
damage to the corneal endothelium.
 Is associated with increased corneal thickness
and decrease in corneal transparency

Corneal Edema

5) Vascularization of the cornea
 May be superficial or deep
Superficial vascularization . Deep vascularization.
1-Vessels derived from conj.Vs
2-Vs.are seen crossing limbus
3-Bright red, well-defined
4-Branch dichotomously
5-The surface of the cornea is
irregular (raised by the B.Vs.)
6-Vessels run in the superficial
layers of the stroma
7-Occur in: pannus, corneal
ulcers, trichiasis & pterygium.
1-From anterior ciliary Vs
2-End abruptly at the limbus
3-Dark red, ill-defined
4-Run parallel
5-Surface is smooth
6-Run in the posterior2/3
7-Occur in:
interstitial keratitis & deep ulcers

Superficial C.V. Deep C.V.

6) Pannus
 Is an inflammatory or degenerative sub-
epithelial ingrowth of fibrovascular tissue
from the limbus.
 It is called progressive if the infiltration
extends beyond the blood vessels; and
regressive if the blood vessels extend beyond
the infiltration.

PannusProf. Ahmad Mostafa Abdallah

7) Breaks In DM
 Breaks in DM may occur as a result of corneal
enlargement, trauma & keratoconus.
 Result in acute influx of aqueous into the
corneal stroma.
 Ex. Haab’s Striae in congenital glaucoma

Special Investigations of Corneal Diseases

A. Optical
 1) Pachymetry : Involves measurement of corneal thickness
which is an indirect indication of the corneal endothelial
function. It is also used for pre-LASIK evaluation.
 2) Specular microscopy: is a noninvasive photographic
technique that allows you to visualize and analyze
the cellular characteristics of corneal endothelium.
 3) Keratometry: Measures the curvature of the axial 3 mm
zone of the anterior corneal surface .
 4) Corneal topography & Pentacam: Gives a color-coded
map of the corneal surface according to dioptric power.

Corneal Pachymetry
Corneal Pachymetry map

Corneal endothelium shown by specular microscopy

Mannual (Classic) Keratometer Automatic Keratometer

Pentacam map

B. Microbiological
 Corneal scrapings & Corneal biopsy.

INFLAMMATIONS OF THE CORNEA
(Keratitis)

Classification of Keratitis
► In broad terms, inflammations of the cornea may be divided
into two types:
I. Ulcerative Keratitis (Corneal Ulcer)
Ulcerative keratitis is a condition in which there is
destruction of some portion of both the epithelium
and the stroma of the cornea.
II. Non-UIcerative Keratitis
Non-suppurative keratitis is a condition in which the
stroma of the cornea is affected by the
inflammatory process while the epithelium remains
intact.

(I) Classification of
Ulcerative Keratitis
A. Primary
Corneal
Ulcers
B. Secondary
Corneal
Ulcers

(I) Classification of Ulcerative Keratitis
A. Primary Corneal Ulcers:
Ulcers occuring primarily in the cornea without conjunctivitis.
They are classified into two main categories, namely :—
1. Infective:
(a) Hypopyon ulcer (b) Dendritic ulcer
(c) Fungal (mycotic) ulcer (d) Parasitic (Acanthameba ) ulcer
2. Non-Infective:
(a) Traumatic ulcer (b) Exposure keratitis.
(c) Neuroparalytic keratitis. (d) Nutritional ulcer
(e) Keratomalacia. (f) Atheromatous ulcer.
(g) Mooren's ulcer.

B. Secondary Corneal Ulcers, i.e. ulcers occurring
as a complication of acute or chronic
conjunctivitis, e.g. :—
1. Gonococcal conjunctivitis.
2. Phlyctenular conjunctivitis.
3. Trachomatous conjunctivitis.

(II) Classification of
Non-UIcerative Keratitis
A. Superficial Keratitis
B. Interstitial
(Parenchymatous) Keratitis
C. Deep Keratitis (Keratitis
profunda).

(II) Classification of Non-UIcerative Keratitis
A. Superficial Keratitis :
1. Superficial punctate keratitis (SPK).
2. Pannus, e.g. trachomatous, phlyctenular & leprotic.
B. Interstitial (Parenchymatous) Keratitis :
1. Interstitial keratitis.
2. Discifonn keratitis.
C. Deep Keratitis (Keratitis profunda).

► According to etiology, corneal ulcers
may be classified into:
1. Infective ulcers: e.g.
(a) Hypopyon ulcer (Bacterial)
(b) Dendritic ulcer (Viral)
(c) Mycotic ulcer (Fungal)
(d) Acanthameba keratitis (Parasitic)
2. Non-Infective ulcers e.g.
(a) Traumatic ulcer (b) Exposure keratitis
(c) Neuroparalytic keratitis. (d) Nutritional ulcer
(e) Keratomalacia (f) Atheromatous ulcer
(g) Mooren's ulcer.

● Causes of Peripheral Corneal ulcers
1. Catarrhal (Staphylococcal) ulcer
2.Trachomatous ulcer
3. Phlyctenular ulcer
4. Mooren's ulcer

Peripheral Catarrhal (Staphylococcal) ulcer

Mooren’s ulcer

● Causes of Central corneal ulcers
1. Hypopyon ulcer
2. Gonococcal ulcer
3. Herpetic keratitis
4. Neuroparalytic keratitis
5. Nutritional ulcer (e.g. atheromatous ulcer
and keratomalacia

Hypopyon ulcer Herpetic (dendritic) ulcer

● Commonest Corneal Ulcers in Egypt
1. Trachomatous ulcer
2. Phlyctenular ulcer
3. Hypopyon ulcer
4. Gonococcal ulcer
5. Corneal Ulcer due to Koch-Weeks bacilli

CORNEAL ULCERS
Predisposing Factors
Pathology
Clinical Picture
Complications
Treatment

● Predisposing Factors (For corneal ulcers)
1- General:
a) Old age.
b) Debilitating diseases, e.g. Diabetes.
c) Malnutrition and vitamin deficiency.
d) Septic foci.

2- Local:
1. Trauma, e.g. F.B. abrasion, trichiasis.
2. Exposure. e.g. lagophthalmos or proptosis.
3. Dryness (xerosis) e.g. with vitamin A
deficiency
4. Dacryocystitis leading to hypopyon ulcer.
5. Necrosis: from malnutrition, e.g.
keratomalacia.
6. Loss of sensation: Neuroparalytic
Keratitis.
7. Scar: with poor vitality leading to
atheromatous ulcer.Prof. Ahmad Mostafa Abdallah

Pathology of Corneal Ulcer
1. Stage of infiltration
2. Ulcerative stage
3. Healing stage

1. Stage of infiltration
In which there is a localized disc of
polymorph cellular infiltration, with
edema of the overlying epithelium
and ciliary injection.

2. Ulcerative stage
 Which is classified into:
a. Progressive stage
b. Regressive stage

a. Progressive stage
 Unclean ulcer, in which the ulcer is saucer shaped
with necrotic material, organisms and inflammatory
cells in its floor, with a swollen edge.
 A line of demarcation of polymorphonuclear
leucocytes forms a second line of defence where the
leucocytes exert their digestive functions,
macerating and dissolving the necrotic tissues.,
which is thrown off.
 Diffusion of toxins leads to irritis ± hypopyon.

b) Regressive stage
 Clean ulcer. Here the ulcer is larger with no
necrotic material, with minimal inflammatory
cells, with a proliferating epithelium and
superficial vascularization, which bring
antibodies and substances necessary for the
healing process.

3. Healing Stage
 Shows:
1) Epithelium migration and proliferation .
2) Fibrosis:
- Sources of fibroblasts:
1- Vessels
2- Keratocytes.
3- Macrophages.
● Vessels obliteration  GHOST vessels

 ● If Bowman's membrane is destroyed corneal
scarring (opacity) results which may be:
faint (Nebula) or
dense white (Leucoma) or
of medium density (Macula).

Clinical Picture of Corneal Ulcer
A. Symptoms:
1. Pain
2. Photophobia.
3. Lacrimation [From reflex irritation of the nerve
endings].
4. Blepharospasm [Spasm of orbicularis oculi].
5. Diminution of vision: due to loss of transparency of
the cornea (oedema, cellular infiltration, irregularity of
the surface).

B. Signs:
1 . Lid: Oedema and redness + Blepharospasm.
2. Lacrimation.
3. Ciliary injection
4. Loss of lustre and transparency of the cornea (due to
oedema, cellular infiltration & ulceration ).
5.The ulcer stains green with fluorescein.
6.Variable degree of iridocyclitis ± hypopyon.

Corneal ulcers stained with fluorescein

Corneal ulcer with hypopyon

Complications of corneal
Ulcer
► Complications of corneal ulcers
are divided into:
1. Complications of non-perforated
corneal ulcer
2. Complications of perforated
corneal ulcer

(A) Cmplications of non-perforating
corneal ulcers:
 a) Early Complications
 b) Late complications

a)EarlyComplications
1) Iridocyclitis ± hypopyon:
due to diffusion of toxins through the
cornea to the AC.

2) 2ry Glaucoma:
- Early: due to plasmoid aqueous or hypopyon.
- Late: due to PAS with angle block.

3) Descematocele (Keratocele).
- Cause: Bulging of DM due to destruction of the
whole thickness of the cornea except DM which
can not withstand the IOP.
- Clinically:
transparent bulging vesicle from the cornea.
- Fate:
- Rupture with perforation.
- Healing with cicatrization.

NB. (important)
 Descematocele doesn’t occur in:
1) Children, due to thin DM.
2) Typical hypopyon ulcer, due to destruction of DM by
the posterior abscess

b)LateComplications
1. Corneal opacities
2. Defective corneal scarring
3. Corneal vascularization

1. Corneal opacities:
a-Nebula: Faint superficial corneal opacity; the
iris is partially seen through it.
b-Macula: Corneal opacity of medium density;
the iris is seen with difficulty through it.
c-Leucoma non adherent: Dense deep-white
opacity; the iris cannot be seen through it.

2. Defective corneal scarring:
1) Corneal facet: depressed area in the cornea.
Due to insufficient scarring in which the epithelium is
not raised to its original level.
2) Keratectasia: (Ex-ulcero) the scar is weak &
bulges in front of IOP.
3) Pseudo-pterygium: adherent fold of the
conjunctiva to the base of the ulcer (in peripheral
ulcers with severe conjunctivitis).

3. Corneal vascularization
Corneal vascularization is late and may be:
1- Superficial (from conjunctival vessels.)
2- Deep (from episcleral vessels.)
Superficial C.V. Deep C.V.

(B) Cmplications of Perforating
corneal ulcers:
► Complications of perforation: depend on the site
and size of the perforation:
1. Peripheral perforation may be:
a. Small perforation
b. Large perforation
2. Central perforation:
a. Small perforation
b. Large perforation

1) Peripheral perforation:
a) Small peripheral perforation:  Ant. Synechiae.
b) Large peripheral perforation:  Iris prolapse
which leads to:
i- Leucoma adherent.
ii- Corneal (anterior) staphyloma (partial or total).

2) Central perforation
a) Small central perforation: 
i- Corneal fistula
ii- Anterior polar cataract
b) Large central perforation: 
i-Intra-ocular infections:
- Suppurative iridocyclitis
- Endophthalmitis
ii-Intra-ocular hemorrhage:
-Vitreous, retinal, or choroidal hemorrhage
- Expulsive hemorrhage
iii-Subluxation, anterior dislocation or extrusion of the lens.

Treatment of Corneal Ulcers
(In General)
► The treatment of corneal ulcers include:
1) AetiologicalTreatment
2)Treatment of the ulcer itself
3)Treatment of complications

1- Aetiological Treatment:
a. Removal of the predisposing factors
b.Treatment of the source of infection e.g.
conjunctivitis

2- Treatment of the ulcer itself:
A. LocalTreatment
1. Non-specific measures
2. Specific treatment:
a. Medical treatment
b. Surgical treatment
B. GeneralTreatment

A. Local Treatment
1. Non-specific measures
 Eye wash: if there is discharge.
 Worm compresses :decrease pain due to the
counter-irritant effect and dilate the blood vessels
thus toxins are removed and antibodies increased.
 Protection of the eye: eye patch (if there is no
discharge) or, dark Glasses (if there is discharge).
 Therapeutic (Bandage) soft contact lens for resistant
corneal ulcers.

2-Specific treatment
 Which may be:
A. Medical Treatment
B. SurgicalTreatment

A. Medical Treatment
 (1) Identification of the organism: Ideally, a
smear is taken to diagnose the causative
organism, stained by Gram and Giemsa stain
and culture and sensitivity test is carried out
but treatment must be started immediately
(before the result of the culture).

 (2) Start with a broad-spectrum topical
antibiotics
drops during the day and ointment at
bedtime
Then, modify the dose of eye drops
according to the condition of the eye.
 (3) In severe (vision-threatening) cases 
use fortified eye drops

 (4) Consider subconjunctival injection of antibiotics
In severe cases with AC reaction and hypopyon
or if no improvement with fortified eye drops.
 (5) Mydriatic-Cycloplegic drugs:
Atropine or cyclopentolate, to prevent the
formation of post. Synechiae & reduce pain from
ciliary spasm.

Causes of failure of antibiotic treatment:
a) Incorrect diagnosis: due to unrecognized
infection with HSV, Fungi, or acanthameba
b) Incorrect treatment. Due to inappropriate
choice of Antibiotics.
c) Drug toxicity.

B. Surgical Treatment
 Surgical treatment of corneal ulcers may
include the following options:
1-Tarsorrhaphy.
2- Conjunctival flap
3-Theapentic keratopasty

Surgical Treatment
 Tarsorrhaphy
 Indications:
 Lateral tarsorrhaphy for treatment of ulcers with
lagophthalmos as in facial palsy.
 Median or paramedian tarsorrhaphy in
neuroparalytic keratitis
 Conjunctival Flap : helps healing by improving
the nutrition of resistant corneal ulcers.
 Therapeutic keratoplasty: For descematocele
& resistant ulcers.

3. Treatment of complications
 e.g.
1. Irirtis
2. 2ry glaucoma
3. Descematocele
4. Perforation
5. Large leucoma adherent
6. Corneal fistula
7. Anterior staphyloma
8. Endophthalmitis

Specific Clinical
Types of Primary
Corneal Ulcers

A. Primary Infective
Corneal Ulcers

Specific Clinical Types of Primary
Infective Corneal Ulcers
keratitis (Hypopyon ulcer)
keratitis (HS & HZ)
(mycotic) keratitis
(acanthamoeba) keratitis

I. BACTERIAL CORNEAL
ULCERS

Hypopyon Ulcer
(Ulcus Serpens = Acute Serpiginous ulcer)
 Definition:
- A severe form of corneal ulcer which is usually
associated with hypopyon.
- It creeps over the cornea because it has a healing
edge and an advancing edge and has a great
tendency to perforate.

● Aetiology:
1) Predisposing factors:
(organism + abrasion + poor general resistance).
a) Chronic dacryocystitis provides the pneumococci (50% or more
of typical hypopyon ulcer is associated with ch.dacryocystitis).
b) An abrasion is necessary because the organism cannot invade the
normal epithelium.The abrasion is produced by a F.B.,a finger
nail, a lash...etc.
c) Poor general resistance: It is common in old debilitated people
and following fevers.

2) Causative organisms:
a) Pneumococci: cause 80% of cases (Typical
hypopyon ulcer)
b) Atypical hypopyon ulcer (20 %):
- Bacteria: Morax-Axenfeld diplobacilli,
other pyogenic organisms.
- Fungi: aspergillus fumigatus.
-Viruses and protozoa (rare).

 N.B. The pneumococcal type is called the
typical hypopyon ulcer.
 Hypopyon ulcers caused by other organisms
are called atypical hypopyon ulcers.

Chacters Typical
hypopyon ulcer
Atypical
hypopyon ulcer
-Cause
-Site
-Character
-Descematocele
-Perforation
-pneumococci .
-Starts near the center.
-Serpiginous .
-Never occur.
-Perforation is common.
-other organisms.
-Starts anywhere.
-Spreads in all directions
.
-May occur.
-Perforation less
common.

● Clinical picture:
a) Symptoms: as in corneal ulcer but severer.

b) Signs: as in corneal ulcer
but:
1)The ulcer is disc shaped, usually near the center
of the cornea, serpiginous (creeps over the
cornea) and has an advancing and a healing
edge:
-Central advancing edge: crescentic, undermined
and densly infilterated.
- peripheral healing edge: flat, epithelialized,
vascularized and cicatrizing.

 2) Deep ulceration, posterior abscess formation
and perforation are common.
 Perforation occurs commonly because:
a-The ulcer tends to go deep.
b- A posterior abscess commonly forms.This occurs
opposite the ulcer just anterior to DM in the form of
cellular infiltration which might ulcerate posteriorly
(posterior ulcer).
This will weaken the cornea and make perforation
very common. Also for the same reason
descematocele is very rare.

3) Hypopyon:
 It is a sterile pus which is yellow in color and
tends to settle at the bottom of the AC.
 It has an upper straight level.
 It originates from the inflamed iris and is
composed of polymorphs-fibrin-iris pigment
(no organism).

II. VIRAL KERATITIS

VIRAL KERATITIS
Herpes Simplex
keratitis
Herpes Zoster
ophthalmicus

1. Herpes Simplex keratitis
 Introduction:
 Herpes simplex virus (HSV) is a DNA virus
with humans as the only host.
 HSV is divided into 2 types:
1. HSV-1: causes infection above the waist (face,
lips, and eyes)
2. HSV-2: causes infection below the waist (genital
herpes)

Clinical Features
 HSV infection can be classified into 3 stages:
1. Primary ocular infection
■ Blepharoconjunctivitis
■ Keratitis
2. Recurrent keratitis
■ Epithelial
■ Stromal
3.Trophic Keratitis (metaherpetic keratitis)

(I) Primary ocular infection
● Cause
● Clinical Features
●Treatment

● Cause: direct transmission of virus
through infected secretions to a
non-immune subject.

● Clinical features
A. Presentation (Symptoms):
-Typically occurs in children between the age
of 6 months and 5 years, with unilateral
ocular irritation and redness, and may be
associated with generalized symptoms of
viral illness.
- it is rare during the first 6 months of life
because of the protection given by the
maternal antibodies).

B.Signs:
1. Mild, self-limited blepharoconjunctivitis.
2.The skin lesions (vesicles, then crusts, then heal
without scarring) involve the lids and periorbital
area.
3. Keratitis (fine epithelial punctate keratitis) may
develop in 50% of cases.

Skin lesions in primary HS infection

● Treatment
 Most cases are subclinical or have mild fever.
 Blepharoconjunctivitis is usually self-limited
 If Keratitis present (rare in 1ry infection) 
Acycloguanosine 3% ointment (Acyclovir,
Zovirax), 5 times/day, for 3 weeks.

(II) Recurrent Keratitis
(A) Epithelial
keratitis
(B) Stromal
necrotic
keratitis
(C) Disciform
keratitis

(A) Recurrent epithelial keratitis
 Cause
 Clinical Features
 Treatment

Cause
 Reactivation of latent virus and invasion of
the corneal epithelium.

Clinical Features
 A. Presentation (Symptoms)
With an acute onset of unilateral irritation,
redness, photophobia, and blurring of vision.

B. Signs
1. Dendritic
ulcer
● Starts with coarse stellate
PEK and develops into a
 branching (dendritic)
ulcer
● Fluorescein stains bed of
the ulcer
● Corneal sensation is
reduced.

2. Geographical ulcer
starts as a dendritic ulcer and enlarges to
assume a geographical shape
Dendritic ulcer
Geographical ulcer

● Treatment:
With antiviral drugs
Acycloguanosine 3% ointment (Acyclovir,
Zovirax), 5 times/day, for 3 weeks.

(B) Stromal necrotic keratitis
 Cause
 Clinical Picture
 Treatment

● Cause
 Direct viral invasion and destruction of the
corneal stroma.

● Presentation (Symptoms):
with a gradual onset of unilateral pain,
redness, and severe visual impairment.

● Signs: are cheesy and necrotic stroma similar to
bacterial or fungal infection.
There may be an associated anterior uveitis with KPs
underlying the area of active stromal infiltration.
Stromal necrotic keratitis in recurrent HS infection

Stromal necrotic keratitisProf. Ahmad Mostafa Abdallah

● Complications
 1.Vascularization and scarring (common)
 2. Perforation (rare)
Vascularization and scarring Perforation

● Treatment:
 The first aim is to heal any associated active
epithelial lesions with antiviral drugs and non-
preserved tear substitutes (Lubricants)
 In severe, resistant cases, the cautious use of
topical steroids under cover of antiviral and
antibiotic drops, may be necessary to relieve
symptoms and prevent severe corneal scarring.

(C) Disciform keratitis
 Cause
 Clinical Picture
 Treatment

(C) Disciform keratitis
● Cause: the exact aetiology of disciform keratitis is
controversial. It may be:
1. HSV infection of keratocytes or endothelium
(endotheliitis) or
2. Exaggerated hypersensitivity reaction to the virus
antigen.

 Presentation: with subacute onset of unilateral blurred
vision.
 Signs:
1. Central (occasionally eccentric) zone of stromal
and epithelial edema
2. KPs underlying the involved area
3. Small stromal infiltrates with a surrounding
ring (Wessely ring) around the lesion.

Central epithelial & stromal
edema with
Underlying KPs
Wessely ring
Disciform keratitisProf. Ahmad Mostafa Abdallah

●Treatment:
1. Initially, topical steroids under cover of antivirals
(drops), are given 4 times daily.
2. As improvement occurs, topical steroids should be
tapered gradually over a period of several weeks.

(III) Trophic Keratitis
" metaherpetic keratitis"
 Cause: it is not caused by active viral disease,
but by failure of re-epithelialization
(persistent defects in the basement membrane),
plus stromal devitalization, drug toxicity, and
elements of denervation

 Treatment consists of:
1. Withdrawal of potentially toxic topical drugs
2. Frequent topical Lubricants to promote epithelial
healing (non-preserved drops)
3.Topical antibiotics to prevent secondary bacterial
infection.

(2) Herpes Zoster
Ophthalmicus (HZO)

(2) Herpes Zoster Ophthalmicus (HZO)
● Introduction
■ About 15% of all cases of HZ affect the ophthalmic division
of trigeminal nerve and referred to as HZO.
■ Involvement of the nasociliary nerve which supplies the side
of the nose correlates significantly with subsequent
development of ocular complications (Hutchinson's sign).

(Hutchinson's sign)

 Clinically, HZO can be divided into the following:
3 stages
1. Acute stage
(stage 1)
2. Chronic
stage (stage
2)
3. Recurrent
stage (stage 3)

Acute stage (stage 1)
 1. Skin lesions
 2. Ocular lesions
 3. Neurological lesions

(1) Skin lesions
 Signs in chronological order (Fig. next slide )
1. Unilateral maculopapular rash involving one or all
3 branches of the ophthalmic nerve: (1) frontal, (2)
lacrimal, and (3) nasociliary.Then 
2. Maculopapules become pustules which burst to form 
3. Crusting ulcers which heal 
4. Scarring

Figure : Skin lesions in HZ. top left: Hutchinson's sign; top right:
involvement of maxillary division; bottom left: crusting changes; bottom
right: extremely severe crusting stage.

■ Treatment
(1) Systemic therapy: oral acyclovir (Zovirax),
800 mg tablets, 5 times/day for 7 days
(2)Topical therapy: consists of antiviral creams
(Zovirax), and a steroid-antibiotic ointment
applied 3 times/day

(2) Ocular lesions
 Signs include:
1. MP conjunctivitis
2. Episcleritis
3. Keratitis
4. Anterior uveitis
5. Scleritis (rare)

Treatment
 Treatment with combined topical steroids
and acyclovir oint. (zovirax) for keratitis and
uveitis

(3) Neurological complications
 Cranial nerve palsies affecting the 3rd , 4th & 6th CNs.
 Optic neuritis
 Encephalitis

Chronic Stage (Stage 2)
 1. Skin lesions
 2. Ocular lesions
 3. Post-herpetic neuralgia

(1) Skin lesions are typical "punched-out"
scars.
(2) Ocular lesions
1. Mucus-secreting conjunctivitis (common)
2. Scleritis: when becomes chronic  patches
of scleral atrophy
3. Keratitis (Non dendritic)
4. chronic anterior uveitis
(3) Post-herpetic neuralgia: is severe and
chronic

(3) Recurrent stage (Stage 3)
 Recurrent lesions may re-appear as long as 10
years after acute lesions.
 They are frequently precipitated by sudden
withdrawal or reduction of topical steroids
 The most common lesions are:
1. episcleritis 2. Scleritis 3. Keratitis
4. Anterior uveitis 5. Glaucoma.

Character
Herpes simlex Herpes Zoster
(1) Aetiology
-Virus
(2) lateteralety
(3) Distribution
(4) Pain
(5) Recurrence
(6) corneal signs
a. Shape of ulcer
b. Sensitivity
c. Level of corneal
affection
Eptheliotropic
May be bilateral
Non specific
No preceding
neuralgia
Common
usually dendrilic
Diminished
(hyposthesia)
Affects superficial
layers
Neurotropic
Always unilateral
Follow the affected nerves
Precedes the eruption
Solid immunity (No Rec.).
Variable (Never dendritic)
Abscent
Deep layers
Differential Diagnosis (HS Vs HZ)

III. Fungal Keratitis

Fungal Keratitis
● Predisposing factors:
 - Filamentous fungal keratitis (caused by
Aspergillus and Fusarium spp.) typically is
preceded by ocular trauma with vegetable
matter.
 - Yeast (Candida keratitis) usually occurs in
association with chronic corneal disease or
immunocompromised and debilitated patients.

Clinical Features
● Signs
 Filamentous fungal keratitis: grayish-white
lesion with feathery projections into the stroma
with an intact overlying epithelium.
 Candida keratitis: dense, white-yellow
suppuration similar to bacterial keratitis & may
be associated with hypopyon.

Filamentous fungal keratitis

Candida keratitis

●Treatment:
 1. Culture +/- corneal biopsy to establish the
diagnosis
 2. Antifungal drugs:Topical and systemic (oral)
e.g. Ketoconazole.

IV. Parasitic Ulcer
(Acanthamoeba Keratitis)

Parasitic Ulcer
(Acanthamoeba Keratitis)
● Predisposing factors
 -This disease typically affects contact lens
wearers who use distilled water for contact
lens care instead of the commercially available
solutions.

■ Presentation is with blurred vision and pain
which is characteristically severe and
disproportionate to the extent of ocular
involvement.

■ Signs
a. Early: multifocal anterior stromal infiltrates
b. Then, these infiltrates gradually enlarge and
coalesce to form a ring abscess.
c. In severe cases, there may scleritis and
hypopyon.

Central Ring abscess in Acanthamoeba keratitis

●Treatment
 1. Stained corneal +/- Corneal biopsy to
confirm the diagnosis.
 2. Topical Specific anti-Acanthameba eye
drops
 3. Penetrating keratoplasty may be indicated
if medical ttt fails (in resistant cases ).

B. Primary Non-Infective
Corneal Ulcers

Primary Non-infective Corneal
Ulcers
1. Mooren's ulcer
2. Neurotrophic keratitis
3.Traumatic ulcers
4. Exposure keratopathy
5. Atheromatous ulcer
6. Keratomalacia

1. Mooren's Ulcer
(Chronic Serpiginous Ulcer)
● Definition:
- It is a rare, idiopathic disease characterized by
progressive circumferential, peripheral,
stromal ulceration with later central spread.
- Diagnosis depends on clinical features &
exclusion of other causes of peripheral
ulcerative keratitis.

● Aetiology:The exact aetiology is Unknown,.
Recently: it is considered as an autoimmune
reaction against a specific antigen in the
corneal stroma.

a. Symptoms: as any ulcer with marked lacrimation
and severe persistent neuralgic pain &
photophobia.
b. Signs:
 A chronic serpiginous ulcer which starts near the
limbus as grey infiltrates in the interpalpebral
space then creeps over the cornea with a white
advancing edge.
 It spreads centrally as well as circumferentially.
 Healing  thin vascularized scar.
 Recurrence is common

Mooren's Ulcer

●Treatment:.
- There is no single effective ttt for Mooren’s
ulcer.
- A wide range of therapies have been
reported.
 1.Topical Steroids
 2. Systemic immunosuppressive drugs
 3. Excision of the perilimbal conjunctiva
 4. Conjunctival cryotherapy
 5.Therapeutic penetrating keratoplasty

2. NEUROPARALYTIC KERATITIS
(Neurotrophic Keratitis)
(Ulcer without Pain)
● Definition:
 The term "neuroparalytic keratitis“ is a
misnomer because the keratitis develops as a
sequel to a trigeminal nerve lesion and lesions
of sensory nerves do not lead to paralysis.
 Its appropriate term is neurotrophic
keratitis.

 1. Pain is absent: due to loss of corneal
sensations
 2. Epithelial desquamation: starts at the center
of cornea
 3. Corneal ulceration with 2ry infection 
 4. Dense scar or perforation

●Treatment:
 A. Medical treatment:
i.The usual treatment of corneal ulcer (Topical antibiotics)
+
ii. Lubricants (Artificial tears eye drops )
iii. Cycloplegic eye drops
iv. Bandage is essential (bandage soft contact lens)
v. lid taping at bed time
 B. SurgicalTreatment (Tarsorrhaphy):
 Tarsorrhaphy is essential line of treatment
(Median or paramedian)

3. TRAUMATIC ULCERS
● Definition:The cornea is traumatized followed by
secondary infection occurs.
● Aetiology: the traumatizing agent may be:
1. From outside e.g. wound, burn, chemical, F.B,
finger nail. .
2. Local e.g. eye lash, PTD.
● Treatment: Remove the cause + usual treatment.

4. KERATITIS WITH LAGOPHTHALMOS
(Exposure Keratopathy)
● Aetiology: Occurs in eyes insufficiently
covered by the lids (lagophthalmos) due to
corneal exposure. e.g. due to: facial palsy,
proptosis ...etc.

● Clinical features:
 - Dryness of corneal epithelium occurs (usually
the lower third) due to rotation of the globe
upwards during sleep (Bell's phenomenon),
followed by epithelial cell desquamation and
secondary infection.
 -The defective closure of lids during sleep and
absence of blinking reflex are important factors.

●Treatment:
 Treatment of the cause of lagophthalmos
 The usual treatment of corneal ulcer.
 Lid taping at bed time.
 Tarsorrhaphy if medical treatment fails

5. Keratomalacia
(Malnutritional Ulcer)
● Aetiology: Affecting badly nourished
children, usually occurs in the first year of life,
many of them are suffering from severe
starvation, parasitic infestation or malnutrition
with vitamin A deficiency.

 -The disease starts by night blindness, and may
be bilateral.
 Signs:
1. Conjunctiva: dry with Bitot's spots.
2. Cornea:
a. Dry (Xerosis) loss of lustre, hazy & insensitive.
b. yellowish infiltrates start at the center of the cornea &
increase until 
c. Corneal melting  perforation occurs with iris prolapse
and panophthalmitis.
d. No or minimal inflammatory reaction (No ciliary
injection)

●Treatment:
(General treatment is more important than local treatment) .
a. General treatment
1. Improve the general health
2. Vitamin A
b. Local treatment: as usual treatment of corneal
ulcer

Ectatic conditions of the cornea

ECTATIC CONDITIONS OF THE
CORNEA
A. Post-Inflammatory B. Degenerative (Non-inflammatory)
1. Keratectasia 1. Keratoconus
2. Anterior (corneal) 2. Keratoglobus
staphyloma.

1. Keratectasia
● Definition: Is protrusion of the corneal scar
without iris incarceration.
● Causes:
1) Weakness of the cornea following healing of a
corneal ulcer (Keratectasia ex ulcero).
2) Corneal weakness following interstitial keratitis
(k. ex pano).
●Treatment:
• Penetrating Keratoplasty is often needed in
most cases as an opacity is present.

2. Anterior Staphyloma
● Definition: It is an ectatic scar of the cornea in which the iris is
incarcerated.
 It may be:
 Partial: If it involves part of the cornea
 Total : If it involves the whole cornea
● Complications: 2ry glaucoma may occur with partial anterior
staphyloma, but it always present in total staphyloma (angle block by
PAS)
● Treatment:
1. Partial type: by combined penetrating keratoplasty +
trabeculectomy
2.Total type: Usually glaucoma is absolute.
a. Enucleation of the blind painful eye + artifial globe
b. Retrobulbar injection of alcohol if the patient refuses enucleation
c. Cyclodestructive procedure

3. KERATOCONUS (Conical Cornea)
● Definition:
- Is a congenital non inflammatory ectatic disorder of the
cornea due to weakness of the cornea mostly affecting
its center.
 It is a bilateral, asymmetric disorder.
 The onset characteristically occurs in the mid to late
teens (especially around puberty).
 It progress for 5-15 years, then becomes stable.
 Sex: more common in females.

● Aetiology:
The exact cause of keratoconus is unknown.
However, it is caused by weakness of the
corneal stroma probably due to a defect in the
structure of collagen.

● Associated conditions:
 Systemic disorders:
i. Down's syndrome (Mongolism)
ii.Turner syndrome
iii. Marfan syndrome
iv. Atopic conditions
 Ocular disorders:
i. Vernal keratoconjunctivitis (Spring catarrh)
ii. Blue sclera
iii. Aniridia
iv. Ectopia lentis
v. Retinitis pigmentosa

● Gross Pathological changes:
1.Thickness: The center of the cornea is
markedly thin.
2. Shape: conical with apex usually below and
nasal to the corneal center. Later, the apex
becomes opacified (Acute hydrops).
3. A brown ring surrounds the base of the cone
due to iron deposition in the epithelial cells
(Fleischer's ring)

 A. Symptoms:
1) Gradual painless progressive diminution of
vision due to:
i. Progressive curvature myopia (steepening of cornea
 Myopia)
ii. Later, irregular astigmatism
2) Glare, halos around lights, light sensitivity and
ocular irritation.
3) Acute loss of vision may occur due to rupture of
DM  corneal edema (Acute hydrops)

 B. Signs: in chronological order:
(1) Early signs:
1. Conical shape of the cornea
2. Retinoscopy shows irregular "scissor" reflex
3. Placido's disc shows irregular rings .
4. Keratometry shows irregular astigmatism
5. Slitlamp examination shows fine vertical
folds in the deep stroma (Vogt's striae) .
Conical shape of the cornea

Placido's disc shows irregular
rings
Vogt’s striae in keratoconus

(2) Late signs
 1. Progressive central or paracentral corneal
thinning
 2. Bulging of the lower lid on down-gaze
(Munson's sign)
 3. Epithelial iron deposits (Fleischer's ring) may
be around the base of the cone
 4. Acute hydrops results from ruptures in
Descemet's membrane and acute leakage of fluid
into the corneal stroma and epithelium.This
causes a sudden severe diminution of vision
associated with discomfort and lacrimation.

Munson's sign in KC
central corneal thinning

Fleischer's ring in KC
(iron deposition)

Acute hydrops in KC
Acute hydrops & Corneal opacity

● Diagnosis:
 The hallmark of keratoconus includes:
a- Central or paracentral corneal thinning
b- Apical protrusion
c- Irregular astigmatism
 It can be graded by keratometry into:
a. Mild KC: < 48 D
b. Moderate KC: 48 - 58 D
c. Severe KC: > 54 D

 Diagnosis basically depends upon:
a. Clinical signs (Previously mentioned)
including slitlamp biomicroscopy,
ophthalmoscopy, retinoscopy &
keratometry.
b. Corneal topography (& pentacam):
Is the most sensitive method of detecting early
KC & monitoring its progression.

Pentacam in diagnosis of keratoconus

● Treatment:
 Rigid gas permeable contact lenses are helpful to
correct the irregular Astigmatism (Early cases).
 Recent treatment modalities:
(1) Crosslinking :
 Principle: Corneal Collagen crosslinking depends on
the use of the photosensitzer riboflavin and
ultraviolet A-light as an effective method for
increasing the stiffness of corneal stroma which
helps in stabilizing the cornea and delay the
progression of keratoconus.
(2) Intrastromal Corneal Rings implantation
(3) Penetrating keratoplasty for advanced cases
associated with corneal scarring.

 For Acute hydrops:
i. cycloplegic eye drops + Hyperosmotic eye
drops (NaCl 5% ).
ii. Topical steroids eye drops may minimize
scarring, and new vessel formation.

Corneal Degenerations

1. Arcus Senilis
● Definition: Bilateral peripheral annular infiltration of
the corneal stroma which occurs in old people
● Aetiology: Degenerative condition with lipoidal
infiltration.

 Symptoms: No symptoms as it never affects
vision.
 Signs:
1.The infiltration at first appears down then up but soon
surrounds the whole cornea.
2. A ring shaped opacity one mm in breadth, being
separated from the limbus by a clear interval (lucid
interval ofVogt).

●Treatment: No treatment is needed as it is
symptomless & peripheral.
 N.B. Arcus Juvenilis (Juvenile Arcus):
 Occurs in young age (< 30 yrs).
 May be associated with Hyper
cholestrolaemia

2. Band Shaped Keratopathy
● Definition: Band shaped horizontal corneal opacity
across the middle 1/3 of the cornea. (Hyaline + calcareous
degeneration)
● Causes:
1. Metastatic calcification: in conditions of hypercalcaemia.
2. Dystrophic calcification: in degenerated blind eyes e.g.
absolute glaucoma, old standing uveitis.

● Clinical picture
 Signs:
i- band shaped horizontal opacity which starts
peripherally and spreads centrally involving the
middle 3rd of the cornea with clear cornea
separating the band from the limbus.
ii- Clear areas are present within the opacity giving
Swiss-Cheese appearance (represent holes in BM).
.
● Treatment: Can be removed if cosmetically
bad or if affecting the vision by:
 .Scraping of the corneal epithelium or
 Lamellar keratoplasy

With Best Wishes

Corneal disorders

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