الدكتور محمد عبد هللا منصور
كلية الطب
-
جامعة تكريت
2018- 2019
“The cornea is a transparent structure in the
anterior segment of eye ...
”
Anatomy of the cornea
Gross anatomy
General dimensions
☸ 12.0 mm horizontal diameter
☸ 11.5 mm vertical diameter
☸ l mm thick peripherally
☸ 0.5mm thick centrally
☸ Anterior surface radius 7.7mm
☸ Posterior surface radius 6.8mm
Disorders of the Cornea
The cornea consists of the following
five layers:
1. The epithelium.
2. Bowman's layer.
3. The stroma.
4. Descemet's membrane.
5. The endothelium.
Microscopic anatomy
Physiology of cornea
Main functions
1. Light transmission (400-700nm light)
2. Light refraction
Total refractive power of cornea 43 D
(70% of eye
’s
refractive power)
Refractive index of cornea 1.376
3. Protection
“The cornea is innervated by the V CN.”
Nerve supply of cornea
☸ V CN
☸ Ophthalmic division
☸ Long posterior ciliary nerves gives off
Annular plexus at limbus
lntraepithelial plexus
Subepithelial plexus just below Bowman
’s
Disorders of the Cornea
The three main techniques are:
1. Direct illumination
with diffuse light
is used to detect gross abnormalities.
2. Scleral scatter: -
This technique is
especially useful in the detection of
subtle
opacities
and
mild
corneal
oedema.
3. Retroillumination
uses the reflection
of light from the iris to illuminate the
cornea from behind. This allows the
detection
of
fine
epithelial
and
endothelial changes, keratic precipitates
and small blood vessels.
BY SLITLAMPBIOMICROSCOPY
Punctate epitheliopathy or
punctate epithelial erosions (PEE)
Epithelial oedema
Corneal filaments
Punctate epithelial keratitis (PEK)
A pannus
Disorders of the Cornea
Superficial (epithelial) signs
Signs involving the stroma and Descemet's membrane
Stromal infiltrates
Stromal oedema
Stromal vascularization
Breaks in Descemet's membrane
Folds in Descemet's membrane
Pachometry
Keratometry measures corneal curvature
Keratoscopy
Specular microscopy photographs
1. Hand-held Placido's disc
2. Photokeratoscopes
3.Computer-assisted
photokeratoscopes (corneo- scopes)
Scrapings
Corneal biopsy
Disorders of the Cornea
Disorders of the Cornea
Bacterial keratitis
Fungal keratitis
Acanthamoeba keratitis
Interstitial keratitis
Viral keratitis
Disorders of the Cornea
Bacterial keratitis
1. Contact lens wear.
2. Ocular surface disease.
3. Trauma
4. Other factors include local or systemic
immunosuppression, diabetes and vit. A defi.
PREDISPOSING FACTORS
MANAGEMENT
Methods of administration of the medicine: -
• Topical
• Subconjunctival injections of antibiotics
• Systemic antibiotics
• Hospitalization, and Scrapings.
• Antibiotics choices depend on the result of C/S.
• The initial therapy should be with a combination
of a fortified aminoglycoside and fluoroquinolones gp.
• Topical cycloplegics
Disorders of the Cornea
Fungal keratitis
Although
Rare
, fungal corneal infection (keratomycosis)
should always be considered if the differential diagnosis of
suppurative bacterial keratitis and herpetic stromal necrotic
keratitis is suspected.
1. Filamentous fungal keratitis
2. Candida keratitis
Type of infectious agent: -
Disorders of the Cornea
Topical and broad-spectrum antifungal agent
such as
Econazole 1%
.
Systemic antifungal agent
such as
Itraconazole
or
Ketoconazole
may also be helpful in severe cases.
Antifungal treatment should be continued for 6 weeks.
Therapeutic penetrating keratoplasty
may be
required in unresponsive cases.
Steroids are absolute contraindication.
TREATMENT
Fungal keratitis
Disorders of the Cornea
It may occur following a minor corneal abrasion.
Contact lens wearers who use non commercially saline
risk.
Misdiagnosed
Important clues to the diagnosis includes:-
1. history of soft contact lens wear,
2. negative cultures for bacteria, fungi and viruses.
3. lack of response to conventional antimicrobial therapy.
Acanthamoeba keratitis
The initial treatment is with a combination of
Dipropamidine
and
Polyhexamethylene biguanide
drops.
Penetrating keratoplasty
may be required if medical therapy fails.
TREATMENT
Herpes
simplex
keratitis
PRIMARY OCULAR INFECTION
DENDRITIC ULCER
STROMAL NECROTIC KERATITIS
DISCIFORM KERATITIS
TROPHIC KERATITIS
Herpes zoster
ophthalmicus
ACUTE PHASE
CHRONIC PHASE
RELAPSING PHASE
Disorders of the Cornea
Herpes simplex keratitis
It (HSV) is a DNA virus with humans as the only host.
PRIMARY OCULAR INFECTION
It is occurs at the ages of 6 months
and 5 years, +/- generalized
symptoms of a viral illness.
Clinical features
Blepharoconjunctivitis
The conjunctivitis is unilateral
preauricular LAP
.
canalicular obstruction
.
Keratitis
. may occurs.
Treatment
Topical antiviral ointment 5X a day for 21 days to prevent keratitis.
Clinical features
Blepharoconjunctivitis
is usually benign and self-limited. The
skin lesions typically involve the lids and periorbital area. heal without
scarring.
The conjunctivitis is unilateral
, acute, follicular, and with a
watery discharge and
preauricular LAP
. It may cause secondary
canalicular obstruction
.
Keratitis
(fine epithelial punctate keratitis). may occurs.
Treatment
Topical antiviral ointment 5X a day for 21 days to prevent keratitis.
Single or multiple ulcer.
Arranged in a dendritic pattern.
Central desquamation & a linear-branching
ulcer.
Diminished corneal sensitivity.
Geographical ulcer shape
(enhanced by injudicious use of
topical steroids).
Herpes simplex keratitis
DENDRITIC ULCER
Disorders of the Cornea
1. Acycloguanosine
(3%
oint.)
(acyclovir,
Zovirax).
2. Trifluorothymidine (1% drops).
Herpes simplex keratitis
DENDRITIC ULCER
TREATMENT
Antiviral drugs
Débridement is an effective way of treating
dendritic ulcers, especially when combined with
antivirals.
Not appropriate for geographical ulcers.
Débridement
Clinical features
Stromal necrotic (infiltrative) keratitis is caused by active viral invasion
and destruction. It may be associated with an intact epithelium or it may
follow epithelial disease.
O/E
The stroma shows a cheesy, necrotic appearance, like that of active and
severe bacterial keratitis.
There may be an associated anterior uveitis with keratic precipitates
underlying the area of active stromal infiltration, vascularization, scarring
and perforation.
Treatment
Combined use of steroids, with topical antiviral and antibiotic cover.
If corneal perforation occur, emergency penetrating keratoplasty (PKP).
Herpes simplex keratitis
STROMAL NECROTIC KERATITIS
Disorders of the Cornea
The aetiology
is either caused by a
reactivated viral infection of keratocytes
and endothelium or an exaggerated
hypersensitivity reaction to antigen.
(+/ -)
past history of dendritic ulceration.
O/E: -
Central zone of epithelial oedema and stromal thickening.
The lesion is centric or eccentric.
Other features include folds in Descemet's membrane, a mild-to-
moderate anterior uveitis, and small keratic precipitates.
The IOP may be elevated.
Treatment
Topical steroids combined with antiviral cover are required.
Cycloplegics agents (atropine).
DISCIFORM KERATITIS
Herpes simplex keratitis
Disorders of the Cornea
It is not caused by active viral disease alone but
also by elements of denervation, drug toxicity and
persistent defects in the basement membrane.
When trying to differentiate a geographical from a
trophic ulcer.
Treatment
consists of withdrawal of potentially toxic
topical therapy and measures to promote epithelial
healing.
Herpes simplex keratitis
TROPHIC KERATITIS
Herpes Zoster Ophthalmicus
It is a common infection
caused by
human herpes virus 3
(HHV3)
HZO = 15% of all cases.
Chickenpox
Viraemia
Dorsal root ganglion
Reactivates
migrates back
down the
sensory nerves
Skin & Eye
characteristic
lesions
HZO
ACUTE PHASE
CHRONIC PHASE
1/3
nasociliary nerve
(Hutchinson's sign)=
ocular complications.
RELAPSING PHASE
Herpes Zoster Ophthalmicus
Disorders of the Cornea
ACUTE PHASE
Features of skin lesions
Initially it is maculopapular and then becomes pustular. The pustules subsequently burst to
form crusting ulcers. Initially, the rash is accompanied by periorbital oedema.
Treatment of skin lesions
Systemic antiviral therapy
is with
Acyclovir
(Zovirax), 800 mg tablets administered five
times daily for 7 days. (Other antiviral agents: -
Valaciclovir
1gm three times daily or
Famciclovir
250mg three times daily).
This significantly diminishes vesiculation, accelerates healing and reduces pain during the
eruptive phase, especially in immunosuppressed patients.
Systemic steroid therapy
has a beneficial effect on the severity of chronic postherpetic
neuralgia.
Topical therapy
consists of:-
Antiviral creams and paints (acyclovir, idoxuridine) and a
Steroid-antibiotic preparation (Neo-Cortef ointment or Terra-Cortril spray).
Calamine and starch powder promote crust formation and should be avoided.
An influenza like illness, heralds the neuralgia which precedes
the cutaneous lesions of HZO.
Extremely severe crusting following inappropriate use of starch powder
1. Punctate epithelial keratitis.
2. Microdendritic ulcers.
3. Nummular keratitis.
4. Disciform keratitis.
5. Anterior uveitis.
6. Acute retinal necrosis.
7. Neurological complications: - CN palsies affecting the III, IV
and VI. Optic neuritis, Encephalitis, Contralateral hemiplegia.
Disorders of the Cornea
Herpes Zoster Ophthalmicus
ACUTE PHASE
1. Conjunctivitis, is associated with vesicles on the lid margin.
2. Episcleritis.
3. Scleritis, it may involves the cornea (sclerokeratitis).
Corneal lesions include the following:
Clinical features of ocular lesions
Disorders of the Cornea
Herpes zoster ophthalmicus
Topical steroids.
Topical and systemic acyclovir.
Topical cycloplegics
ACUTE PHASE
Treatment of ocular lesions
Herpes zoster ophthalmicus
CHRONIC PHASE
1. Typical
'punched-out'
scars
associated
with
varying
degrees
of
hyperpigmentation
and
hypopigmentation.
2. Ptosis may occur as a result of scarring of the lids.
3. Trichiasis,
4. Loss of lashes,
5. Ectropion,
6. Entropion.
7. Lid-notching.
Skin lesions
Herpes zoster ophthalmicus
CHRONIC PHASE
Ocular lesions
1. Mucus-secreting conjunctivitis.
2. Scleritis and sclerokeratitis may lead to a progressive scarring of
the cornea.
3. Corneal vascularized and infiltrated by lipid.
4. Neutrophic and exposure keratitis may lead to
severe ulceration,
secondary infection and even perforation.
5. Mucous plaque keratitis.
6. Post-herpetic neuralgia: -It may be constant or intermittently severe
and stabbing as in tic douloureux. The pain may be worse at night and
aggravated by touch and heat.
Disorders of the Cornea
Herpes zoster ophthalmicus
RELAPSING PHASE
Episcleritis,
Scleritis,
Iritis,
Glaucoma
Nummular, disciform and
mucous plaque keratitis.
Relapsing or recurrent lesions may reappear as long as 10 years
after the acute lesions. They are frequently precipitated by the
sudden withdrawal or reduction of topical corticosteroids.
The most commonly occurring lesions are:
Marginal keratitis
Rosacea keratitis
Phlyctenulosis
Caused by a hypersensitivity reaction
to staphylococcal exotoxins.
It is in patients suffering from chronic staphylococcal blepharitis.
O/E: -
A subepithelial infiltrate. The 10, 2, 4 or 8 o'clock
positions are affected first.
Treatment
with a short course of topical steroids is extremely
effective
in
promoting
resolution.
To
prevent
recurrence
associated chronic staphylococcal blepharitis, should also be
treated.
Marginal keratitis
O/E chronic hyperaemia of the face, usually involving the nose, central
forehead and upper cheeks. Other features include variable degrees of
telangiectasia, papules, pustules and Rhinophyma is the most advanced
form of the disease.
Rosacea keratitis
1. Punctate epitheliopathy (inferior two thirds).
2. Peripheral vascularization (inferotemporal and inferonasal quadrants).
3. Thinning (either by resolution of the infiltrates or by gross ulceration).
4. Perforation (caused by the excessive use of topical steroids).
5. Chronic posterior blepharitis and recurrent chalazia.
KERATITIS
Topical therapy with steroid drops is a very effective short-term measure.
Systemic therapy is with one of the following antibiotics:
1. Tetracycline 250 mg 4X daily.
2. Doxycycline 100mg once daily.
Treatment
Skin lesions in acne rosacea
Hypertrophy of sebaceous glands
Rhinophyma
Severe thinning
Rosacea keratitis
pannus formation
and scarring
Rosacea keratitis
peripheral
vascularization
O/E:-
Conjunctival phlycten shows a small pinkish-white nodule near the
limbus, surrounded by hyperaemia.
A corneal phlycten starts astride the limbus and it may either resolve
spontaneously or extend radially on to the cornea.
Treatment
1. Short course of topical steroids is effective in promoting resolution.
2. Systemic tetracycline may be necessary.
It is caused by a non-specific delayed hypersensitivity reaction to
staphylococci or other bacterial antigens.
Presentation: -
Photophobia,
Lacrimation and
Blepharospasm.
Phlyctenulosis
Various stages of
phlyctenulosis
Healed corneal phlycten
Limbal phlycten
Conjunctival phlycten
Phlyctenulosis
Disorders of the Cornea
Dellen
Marginal corneal degeneration
Mooren's ulcer
Disorders of the Cornea
Dellen
Consist of localized areas of corneal thinning which occur as a
result of localized tear film instability. The three main causes are:
(1) raised limbal lesions, (2) hard contact lenses and (3) idiopathic
in the elderly.
O/E
shows saucer-like thinning of the peripheral cornea.
Treatment
Involves
elimination of
the cause, and
promoting corneal
rehydration by
patching and
the use of
lubricants.
Disorders of the Cornea
It is a thinning of the peripheral cornea. It is usually bilateral and
asymmetrical.
O/E
Early cases show fine, yellow-white, punctate stromal opacities which are
frequently associated with mild superficial vascularization.
Vision gradually deteriorates as a result of
increasing corneal astigmatism.
Treatment for
Severe astigmatism can be treated by
a crescent-shaped excision of the gutter
with suturing of the 'healthier' margins
.
Marginal corneal degeneration
Disorders of the Cornea
Mooren's ulcer
It is a
rare
peripheral ulcerative keratitis thought to be caused by an
ischaemic necrosis resulting from vasculitis of limbal vessels.
O/E
of early cases shows patches of grey infiltrate near the margin of
the cornea. This spreads by slowly undermining the corneal epithelium
and superficial corneal lamellae at its advancing border, forming an
overhanging edge.
Treatment
1. Topical therapy with steroids used at hourly intervals.
2. Systemic therapy with cyclosporin, steroids and cytotoxic drugs
(cyclophosphamide, azathioprine or methotrexate).
3. Conjunctival excision, may be effective in some cases resistant to
systemic therapy.
Early Mooren's ulcer
Advanced
Mooren's ulcer
with
circumferential involvement
Mooren's ulcer with central spread
Healing Mooren's ulcer with
corneal vascularization
and opacification
Disorders of the Cornea
The presence of severe, persistent, peripheral, corneal
infiltration,
ulceration
or
thinning
unexplained
by
coexistent ocular disease should prompt a search for an
associated systemic collagen vascular disease.
The ocular lesions may occasionally precede the
clinical manifestation of the systemic disease.
The four main diseases that should be
considered are:
1. Rheumatoid arthritis.
2. Systemic lupus erythematosus.
3. Polyarteritis nodosa.
4. Wegener's granulomatosis.
Contact lens cornea in rheumatoid arthritis
the infiltrate is an unusual feature
Acute stromal keratitis in
rheumatoid arthritis
Peripheral corneal melting in rheumatoid arthritis.
Top:
without
inflammation;
bottom:
with
inflammation
Peripheral corneal melting in rheumatoid
arthritis. Top: without inflammation; bottom:
with inflammation
Disorders of the Cornea
1. Age-related degenerations.
ARCUS SENILIS
VOGT'S WHITE LIMBAL GIRDLE
CORNEA FARINATA
CROCODILE SHAGREEN
CORNEA GUTTATA
2. Lipid keratopathy.
3. Band keratopathy.
4. Spheroidal degeneration.
5. Salzmann's nodular degeneration.
ARCUS SENILIS
It may be associated with familial and non-
familial dyslipoproteinaemias but may also
occur without any predisposing factors. It is
frequently bilateral arcus. The presence of
arcus is also age related and is found in
virtually all individuals over the age of 80.
Unilateral arcus is a rare entity that may be
associated with carotid disease or ocular
hypotony.
Examination shows bilateral lipid deposition
which starts in the superior and inferior
perilimbal
cornea
and
then
progresses
circumferentially to form a band about 1 mm
wide.
Disorders of the Cornea
VOGT'S WHITE LIMBAL GIRDLE
Bilateral, narrow, crescentic lines composed of chalk-like flecks running in the
interpalpebral fissure along the nasal and temporal limbus.
CORNEA FARINATA
Characterized by the presence of minute, bilateral, flour-like deposits in the deep
corneal stroma most prominent centrally.
CROCODILE SHAGREEN
CORNEA GUTTATA
Cornea guttata
Disorders of the Cornea
It is occurs in two settings:
1. Primary lipid keratopathy (spontaneously in an avascular cornea).
2. Secondary lipid keratopathy common and associated with previous
ocular injury or disease which results in corneal vascularization.
O/E
shows white or yellowish corneal
stromal deposits consisting of cholesterol,
fats and phospholipids. In the secondary
type
there
is
associated
corneal
vascularization. In the absence of treatment,
vascularized
lipid
keratopathy
is
a
progressive
condition
which
causes
deterioration of vision.
Control of the primary inflammatory disease and then of the lipid
deposits. Slow resorption of the lipid infiltrate can be induced by: -
1. Argon laser photocoagulation to the feeder vessels.
2. Corneal grafting where laser therapy is inappropriate or ineffective.
Treatment
Disorders of the Cornea
Deposition of calcium salts in the subepithelial space and
Bowman's membrane. The four main causes are:
1. Chronic iridocyclitis particularly in children,
2. Idiopathic in the elderly,
3. Phthisis bulbi and
4. Increased serum calcium or phosphorus levels.
Chelation is a simple and effective form of treatment for relatively mild
cases.
Excimer laser keratectomy may be used for cases with more extensive
and deeper involvement.
O/E
distribution of the lesions is in the interpalpebral fissure with a clear
space separating the sharp margin of the band from the limbus.
Slitlamp examination reveals holes in the calcium plaques which are
thought to represent nerve canals in Bowman's layer.
Treatment
Application of versenate
Epithelium is scraped off
Disorders of the Cornea
Spheroidal degeneration (corneal elastosis). It is a degenerative condition
which typically occurs in men whose working lives are spent outdoors.
The degree of severity of the degeneration correlates closely with the
length of time spent outside.
1. Corneal epithelial débridement.
2. Superficial keratectomy (temporary measure) to improve vision.
3. Lamellar or penetrating keratoplasty is required for long-term
improvement of visually incapacitating cases.
O/E
small amber-colored spheroidal granules or droplets composed of
protein in the superficial corneal stroma in the interpalpebral strip. It begins
in the periphery and spreads centrally.
The condition varies in severity from mid to severe and serious visual
impairment in later life caused by corneal opacification.
Treatment
More
advanced
nodular
forms
Early
stage
showing
corneal
haze
Disorders of the Cornea
O/E
shows discrete, elevated grey or blue grey superficial stromal
opacities, which form nodules that elevate the corneal epithelium.
These nodules are located either in scarred cornea or at the edges of
transparent cornea. The base of a nodule may be surrounded by
epithelial iron deposits.
It is invariably occurs secondary to chronic keratitis,
especially trachoma and phlyctenulosis.
Treatment
Similar
spheroidal
degeneration.
Disorders of the Cornea
The corneal dystrophies are a group of spontaneous appearing, usually
inherited, bilateral, stationary or slowly progressive corneal alterations
that develop in the absence of inflammation. Age of onset, symptoms,
mode of progression and inheritance differ in the various dystrophies.
Most present by the second decade, but some that have little effect on
vision may present in adult life.
I. Anterior dystrophies
Microcystic
Reis-Bücklers'
Meesmann's
II. Stromal dystrophies
Lattice
Macular
Granular
III. Posterior dystrophies
Fuchs' endothelial
Posterior polymorphous
IV. Ectatic dystrophies
Keratoconus
Posterior keratoconus
Keratoglobus
Pellucid marginal degeneration
Disorders of the Cornea
Common, progressive disorder in which the cornea assumes an irregular
conical shape.
Central
or
Paracentra
l
stromal
thinning
,
Apical
protrusion
and
Irregular astigmatism
.
The condition starts at around puberty and progresses slowly thereafter,
although it may become stationary at any time. Bilateral asymmetrical.
Keratoconus occurs with increased frequency in the following disorders.
Systemic disorders include
: Down's syndrome, Turner's syndrome,
Ehlers-Danlos syndrome, Marfan's syndrome, atopy, osteogenesis imperfecta and
mitral valve prolapse.
Ocular associations include:
vernal disease, Leber's congenital
amaurosis, retinitis pigmentosa, blue sclera, aniridia and ectopia lentis. The
wearing of hard contact lenses and constant eye rubbing has also been proposed
as possible predisposing factors.
The aetiology of keratoconus is obscure.
Disorders of the Cornea
Easy to miss, can be detected by the following methods of examination:
1. Retinoscopy shows an irregular 'scissor' reflex.
2. Keratometry initially shows irregular astigmatism.
3. Photokeratoscopy or Placido's disc
shows irregularity of the reflected
ring contours.
1. Slitlamp biomicroscopy shows very fine, deep, stromal, oblique striae
(Vogt's lines) which disappear with external pressure on the globe.
Prominent corneal nerves may also be present.
Disorders of the Cornea
Onset is between the ages of 10 and 20 years, with impaired
vision in one eye caused by progressive astigmatism and myopia.
The patient may report the need for frequent changes in spectacle
correction or a decreased tolerance to contact lens wear.
Subsequently, the astigmatism becomes irregular
Early signs
Disorders of the Cornea
Consist of the following:
• Progressive central or paracentral corneal thinning. This is
associated with poor visual acuity.
• Bulging of the lower lid when the patient looks down (Munson's sign).
• Epithelial iron deposits (Fleischer's ring) may surround the base of
the cone.
• Central and paracentral corneal scarring in severe cases.
• Acute hydrops results from ruptures in Descemet's membrane and
acute leakage of fluid into the corneal stroma and epithelium. This
causes a sudden drop in visual acuity associated with discomfort and
watering. Acute episodes are initially treated with hypertonic saline
and patching or a soft bandage contact lens.
Late signs
Disorders of the Cornea
1. Spectacle correction
in very early cases can correct regular
astigmatism and very low amounts of irregular astigmatism.
2. Contact lenses
provide a regular refracting surface over the
cone. Advances in both lens designs and materials have greatly
increased the proportion of keratoconus patients who can be
fitted with contact lenses and only between 5% and 10% require
surgery.
3. Corneal cross linking
4. Corneal rings
is an effective procedure especially if there is no
central corneal scarring.
5. Penetrating keratoplasty
is
indicated
in
patients
with
advanced progressive disease, especially with significant corneal
scarring. The visual results are excellent with a low risk of
allograft rejection.
MANAGEMENT
Disorders of the Cornea
1. Exposure keratopathy
2. Neurotrophic keratopathy
3.Recurrent corneal erosion syndrome
4. Metabolic keratopathy
a. MUCOPOLYSACCHARIDOSES
b. WILSON'S DISEASE
Disorders of the Cornea
1. Exposure keratopathy
It is caused by improper wetting of the corneal surface by the precorneal
tear film because of the inability of the lids to resurface the cornea with
each blink. Important causes include facial nerve palsy, severe proptosis
and scarring of the eyelids.
2. Neurotrophic keratopathy
It is occurs in an anaesthetic
cornea. It appears that the corneal
sensory nerves are very important in
maintaining the health of the corneal
epithelium.
Causes section of the fifth nerve,
herpes simplex and herpes zoster
keratitis, diabetes and leprosy.
Disorders of the Cornea
3. Recurrent Corneal Erosion Syndrome
It is a disturbance of the corneal epithelial basement membrane
complex which results in defective adhesion and recurrent breakdown
of the epithelium. The condition is most commonly caused by
superficial corneal trauma, especially from a scratch. It may also occur
in certain corneal dystrophies as already described.
Presentation
is typically on waking with a sudden onset of unilateral
pain, lacrimation, photophobia and blurred vision. It is troublesome in
diabetic patients.
O/E: -
during the acute stage shows a corneal abrasion. It is also
important to examine the fellow eye for evidence of microcystic
dystrophy.
Disorders of the Cornea
TREATMENT OF ACUTE EROSIONS
1. Pressure patching for 24 hours, combined with a
2. Mild cycloplegic and a
3. Prophylactic antibiotic ointment, will usually suffice in most mild
cases.
4. Débridement in severe cases. It provides a smooth basement
membrane substrate which can be resurfaced with healthy
epithelium.
1. Lubrication
with artificial tears four times daily.
2. Bandage contact lenses
with low water content can be tried if
lubrication is ineffective.
3. Superficial epithelial keratectomy
may be necessary for severely
recalcitrant cases.
4. Anterior
stromal
puncture
is
an
alternative
treatment
for
recalcitrant erosions. The Nd: YAG laser can also be used to perform
stromal punctures.
PROPHYLACTIC TREATMENT
Disorders of the Cornea
4. Metabolic keratopathy
A.
MUCOPOLYSACCHARIDOSES
B. WILSON'S DISEASE
Wilson's disease (hepatolenticular degeneration) is a rare
condition caused by a deficiency of the
α2-globulin ceruloplasmin
.
It is characterized by a widespread deposition of copper in the
tissues and becomes manifest in one of three ways: (1) liver
disease, (2) neurological involvement of the basal ganglia or (3)
psychiatric features.
Corneal copper deposition is present in nearly all patients. The
classic
Kayser-Fleischer ring
is located at the peripheral part of
Descemet's membrane.
It will be disappear with penicillamine therapy.
Some patients also have a green 'sunflower' cataract.
Is an operation in which abnormal host tissue is replaced by
healthy donor corneal tissue. The graft may be partial thickness
(lamellar) or full thickness (penetrating).
1. Optical indications
are primarily improvement of visual acuity by
replacing opaque corneal tissue with clear donor tissue. Currently, the most
common indication is pseudophakic bullous keratopathy, keratoconus,
corneal dystrophies and degenerations, and scarring caused by various
types of keratitis and trauma.
2. Tectonic indications
are restoration or preservation of corneal anatomy in
eyes with severe structural changes such as stromal thinning and
descemetoceles.
3. Therapeutic indication
is removal of inflamed corneal tissue in eyes
unresponsive to conventional antimicrobial or antiviral therapy.
4. Cosmetic indication
is improvement of the appearance of the eye.
Penetrating keratoplasty
Disorders of the Cornea
Donor tissue should ideally be removed less than 6 hours after death.
Disorders of the Cornea
Donor tissue should ideally be removed less than 6 hours after death.
SURGICA
L
PROCEDUR
E
Suturing of
donor button
Excision of
host tissue by
trephination
Completion
with
scissors
Postoperative
appearance of
continuous running
suture, securing the graft
Early
Early failure is characterized by cloudiness of the graft from the
first postoperative day. It is caused by endothelial dysfunction
resulting from defective donor endothelium or surgical trauma at the
time of operation.
Late
Late failure is most frequently the result of immune graft rejection.
GRAFT FAILURE
Disorders of the Cornea
Treatment
Prompt administration of hourly topical steroids and periocular
steroid
injections.
In
severe
resistant
cases,
systemic
immunosuppressive agents may be necessary.
Keratic precipitates and oedema of graft associated
with late failure of penetrating keratoplasty
1. Opacification of the superficial one-third of the corneal
stroma not caused by potentially recurrent disease.
2. Marginal corneal thinning or infiltration as in recurrent
pterygium, Terrien's marginal degeneration, and limbal
dermoids or other tumours.
3. Localized thinning or descemetocele formation.
Disorders of the Cornea
Lamellar keratoplasty
Figure 5.79 Subretinal exudation in posterior scleritis
Scleromalacia perforans
More advanced scleral necrosis
Necrotizing scleritis with inflammation
Early scleral necrosis
Necrotizing scleritis with inflammation
Early avascular patch
More advanced
avascularity
Nodular episcleritis -- note
deep scleral part of the slit
beam is not displaced
non-necrotizing diffuse scleritis
non-necrotizing nodular scleritis
non-necrotizing nodular scleritis
Simple sectoral episcleritis
Applied anatomy of anterior vascular coats in
relation to episcleritis and scleritis
Trephine keratotomy
0.3 mm deep
Annular keratectomy
Spreading technique
1 mm undermined
Lens edges designed
to fit keratectomy
.
Principles of photorefractive keratectomy with excimer laser
Appearance of cornea following radial keratotomy
Figure 5.65 Potential complications of contact lens wear
Figure 4.3 Papillary reaction
involving the upper palpebral
conjunctiva
Figure 5.64 Giant papillary conjunctivitis
Therapeutic indications for contact lens wear
Kayser-Fleischer ring in Wilson's disease
Treatment by
anterior stromal
punctures
Corneal epithelial
abnormalities
following
resolution of an
acute attack
Recurrent corneal erosion syndrome
Hydrops
Keratoconus bilateral Munson's sign
Keratoconus, Vogt's lines
Corneal mapping showing irregularity
Hydrops
K
e
ra
toc
on
us
,
V
og
t's
l
ine
s
Corneal mapping showing irregularity
Keratoconus bilateral Munson's sign
Salzmann's nodular degeneration
More
advanced
nodular
forms
Early
stage
showing
corneal
haze
Application of versenate
Epithelium is scraped off
Band keratopathy
Figure 5.44 Treatment of hand keratopathy by chelation.
Top: epithelium is scraped off; bottom: application of
versenate
Lipid keratopathy
Appearance of
normal endothelium
Cornea guttata
Anterior
crocodile
shagreen
&
arcus
senilis
Vogt's
white
limbal
girdle
&
cornea
farinata
Peripheral sclerokeratitis in
polyarteritis nodosa early involvement
Peripheral sclerokeratitis in polyarteritis
nodosa. late involvement with extensive
thinning and scarring
Figure 5.36 Contact lens cornea
in rheumatoid arthritis the infiltrate
is an unusual feature
Figure 5.37 Acute stromal
keratitis in rheumatoid arthritis
Figure
5.38
Peripheral
corneal
melting
in
rheumatoid
arthritis.
Top: without inflammation; bottom:
with inflammation
Figure
5.38
Peripheral
corneal
melting
in
rheumatoid
arthritis.
Top: without inflammation; bottom:
with inflammation
Early Mooren's ulcer
Advanced
Mooren's ulcer
with
circumferential involvement
Mooren's ulcer with central spread
Healing Mooren's ulcer with
corneal vascularization
and opacification
Yellow-white lipid
deposition
Pseudopterygium
Circumferential thinning
Various stages of
phlyctenulosis
Healed corneal phlycten
Limbal phlycten
Conjunctival phlycten
Phlyctenulosis
Severe thinning
Rosacea keratitis
pannus formation
and scarring
Rosacea keratitis
peripheral
vascularization
Skin lesions in acne rosacea
Rhinophyma
Skin lesions in acne rosacea
Hypertrophy of sebaceous glands
Skin lesions in acne rosacea
telangiectasis of chin
Skin lesions in acne rosacea
a severe cheek involvement
Catarrhal ulcer
Dellen
Mucous plaque keratitis in herpes zoster
Lipid keratopathy
Mucus secreting conjunctivitis &
lipid filled granulomata in herpes zoster
Scalloping keratitis in herpes zoster
Herpetic disciform keratitis
Herpetic stromal
necrotic keratitis
Catarrhal ulcer
Small dendritic ulcer
Large herpetic dendritic ulcer
stained with fluorescein
Herpetic geographical ulcer
Old interstitial keratitis
Non-perfused (ghost vessels) in interstitial keratitis
Acanthamoeba keratitis
Pneumococcal keratitis
with hypopyon
Pseudomonas keratitis
Puntate epithelial keratitis
Corneal filaments
Superior limbic keratoconjunctivitis