KERATOCONUS: A REVIEW OF CORNEAL ANATOMY AND ECTASIA
1. KERATOCONUS
Refreactive and Contact Lens Sub Division
Ophthalmology Departement
Medical Faculty of Andalas University
M. Djamil Hospital Padang
2021
FITRAH
Literature Review
3. Introduction
first time in 1729
Benedict Duddell
in 1854 John Nottingham
documented this disease in
more depth in his book
"Practical Observations of
the Corneal Cone and Short
Vision and Other Related
Defects of the Eye"
Keratoconus
6. higher in the
Middle East.
6
Introduction
prevalence of keratoconus is 50 per 100,000 with
an annual incidence of 2 per 100,000.
7. Cornea Anatomy
Cornea transparent avascular connective
tissue the primary infectious and
structural barrier of the eye
8. The horizontal diameter 11-12
mm and 1.0 mm larger than the
vertical diameter
0.5 mm thick at the center and
gradually increases to the
periphery
The shape prolated flatter in
the periphery and steeper
centrally
Corneal Anatomy
11. Epithelium
50 μm thick and 5%-10% of total corneal thickness
basal cells corneal epithelial cells capable of
mitosis
basal cells attached to the underlying basement
membrane by a hemidesmosomal system
12. Epithelium
as a barrier
serve as
an optical interface
maintaining a
constant level of
stromal hydration
major roles of the
corneal epithelium
13. Bowman Layer
posterior to the epithelial
basal lamina
8-12 μm thick, composed of
type I and type IV collagen
fibers
acellular, does not regenerate
when damaged
14. Stroma
90% of the corneal thickness
Stromal cells keratocytes
responsible for collagen synthesis
15. Stromal Injury
Severe chemical injuries deplete
stromal keratocytes
initiate collagenolytic processes
undermine the structural integrity
Adjacent keratocytes migrate into
areas of damaged stroma
play a critical role in the
maintenance and regeneration
16. Type I is the major
collagen component of
the corneal stroma
constitutes
approximately 70% of the
total stromal dry weight
Proteoglycans the
second most abundant
biological constituents
of the cornea
constitute approximately
10% of the dry weight of
the cornea.
Stroma
17. Descemet Membrane
O 10-12 μm thick
O present between the endothelium and
the posterior stroma.
O Type I is the most abundant collagen in
the Descemet membrane.
18. Endothelium
single layer,
composed of
polygonal cells
approximately 2000-
3000 cells/mm2
hemidesmosomes
promote adhesion to
Descemet membrane
barrier between the
aqueous humor and
the corneal stroma
20. Definition
Keratoconus occurs bilaterally
and is characterized by a non-
inflammatory condition
causes posterior corneal
ectasia and thinning of the
stromal layer leading to
protrusion
cause high myopia and irregular
astigmatism that affects visual
quality
21. Definition
O epithelial cell is disrupted the entire cell
is usually lost leaving a defect
O A variety of factors may retard the rate of
reepithelialization following chemical injury
the inflammatory response and structural
damage to the epithelial basement
membrane.
23. O Recovery dependent on the centripetal
migration of cells from the most proximal
region of viable epithelium.
O 24-30 hours mitosis begins to restore the
epithelial cell population.
Epithelial Injury
25. Chemical Trauma
O Acids and alkalis interact with tissues in
fundamentally differently ways.
O Alkalis dissociate into cations and hydroxyl
ions upon contacting the eye.
26. Chemical Trauma
cation
penetration of alkali
and react with the
carboxyl groups of
stromal collagen
and extensive
hydrolysis of the
corneal matrix
hydroxyl ion
saponification of
cellular membranes
resulting in cell
disruption and death
27. O acids penetrate the corneal stroma than
alkalis
O the hydrogen ion mediates damage due
to pH alteration
O the anion precipitation and denaturation
of proteins in the corneal epithelium and
anterior stroma.
Chemical Trauma in Cornea
28. O Precipitation of the epithelial proteins
affords a degree of protection by providing
a physical barrier against further ingress.
O The end result of a very severe acid injury
often indistinguishable from that of an
alkaline injury.
Chemical Trauma in Cornea
29. Chemical Trauma in Cornea
Grade
of Injury
Clinical Findings Prognosis
Grade I No corneal opacity
No limbal ischemia
Good
Grade II Corneal haziness,but visible iris
details
Ischemia < 1/3 of limbus
Good
Grade III Significant corneal haziness to
obscure iris details
Ischemia 1/3 to ½ of limbus
guarded
Grade IV Cornea is opaque, no view of iris or
pupil
Ischemia > ½ of limbus
Poor
30. Corneal Melting in
Chemical Trauma
O Corneal melting common prelude to the
development of corneal perforation.
O This process occurs from conditions
infections, sterile inflammation, surgical,
or chemical injury to the cornea.
31.
32. Corneal Melting in
Chemical Trauma
Strong chemicals exert their destructive effect directly
damaging cellular and extracellular matrices
indirectly by initiating an inflammatory process
Corneal melting influenced by the excessive
tissue degradative proteases
these proteases are the MMPs
33. O Resident corneal cells keratocytes and
infiltrating macrophages releasing active
MMPs release of proinflammatory cytokines
the melting process
O process of repair injury, fibroblasts
simultaneously synthesize both collagen and
collagenase participate both in ulceration
and repair.
Corneal Melting in
Chemical Trauma
34. Conclusion
O Chemical trauma caused by acid or alkaline
O The severity of the chemical injury depends on
concentration and pH of the solution, the extent
of ocular surface exposure, chemical
penetration, and the duration of ocular
exposure.
O Acid precipitate protein in the corneal
epithelium and anterior stroma which functions
as a tissue barrier.
35. O Alkali saponification with membran cells,
hydrolyzes the extracellular matrix, causing
apoptosis and necrosis of corneal tissue.
O Indirect, corneal melting also results from
inflammatory factors.
Conclusion
First in overview this paper start from introduction, anatomy physiology of the pupil, pupillary examination and CONCLUSION
Ocular chemical injuries are true ophthalmic emergencies due to the potential for permanent corneal and intraocular damage.
2. Where strong alkalis and acids are involved, significant exposure results in severe injury to both the ocular surface and intraocular structures.
the severity of the chemical injury depends on a number of factors including a) concentration and pH of the solution, b) the extent of ocular surface exposure, chemical penetration and c) the duration of ocular exposure.
Chemical injury can be acidic or alkaline
2. acids causing injury include sulfuric, hydrochloric, nitric, and hydrofluoric.
3. Alkalis causing eye injury include ammonium hydroxide, sodium hydroxide, potassium hydroxide, magnesium hydroxide, and calcium hydroxide
The cornea is a transparent avascular connective tissue that acts as the primary infectious and structural barrier of the eye.
2. Its clarity is the result of many factors including the structural anatomy and physiology of its cellular components.
In the average adult, the horizontal diameter of the cornea is 11 to 12 mm and about 1.0 mm larger than the vertical diameter.
2. It is approximately 0.5 mm thick at the center and gradually increases in thickness to the periphery
3. The shape of the cornea is prolated flatter in the periphery and steeper centrally
The cornea consists of the following histologic layers: • epithelium with basement membrane • Bowman layer • stroma • Descemet membrane • endothelium
The epithelium is composed of 4-6 layers, which include 1-2 layers of superficial squamous cells, 2-3 layers of wing cells, and the innermost layer of the columnar basal cells.
The epithelium is typically approximately 50 μm thick and constitutes 5%-10% of total corneal thickness.
2. basal cells are the only corneal epithelial cells capable of mitosis.
3. The basal cells are attached to the underlying basement membrane by a hemidesmosomal system.
The major roles of the corneal epithelium are to act as a barrier, assist in maintaining a constant level of stromal hydration and to serve as an optical interface.
The Bowman layer, or Bowman membrane, is immediately posterior to the epithelial basal lamina.
2. This layer is 8- 12 μm thick and is composed of randomly packed type I and type IV collagen fibers that are 30 nm in diameter.
3. It is acellular, and it does not regenerate when damaged.
The stroma makes up 90% of the corneal thickness.
2. Stromal cells are known as keratocytes.
3. Keratocytes responsible for collagen synthesis.
Severe chemical injuries deplete stromal keratocytes and 2. initiate collagenolytic processes which undermine the structural integrity of the corneal stroma. 3. Adjacent keratocytes migrate into areas of damaged stroma 4. where they play a critical role in the maintenance and regeneration of stromal tissue.
The Descemet membrane is a specialized basement membrane, 10-12 μm thick, present between the endothelium and the posterior stroma.
And consist Type I collagen.
The corneal endothelium is a single layer posterior to the Descemet membrane and is composed of polygonal cells.
2. the normal endothelial cell count is approximately 3000/mm2.
3. The basal surface of the endothelium contains hemidesmosomes that promote adhesion to Descemet membrane.
4. The endothelium functions as a permeability barrier between the aqueous humor and the corneal stroma.
When any portion of an epithelial cell is disrupted, the entire cell is usually lost, leaving a defect in the epithelial layer.
2. A variety of factors may retard the rate of reepithelialization following chemical injury including the inflammatory response and structural damage to the epithelial basement membrane.
Neutrophils appear in the wound within 2 to 6 hours 2. engage in the proteolytic debridement of necrotic cellular and extracellular debris.
3. Within 1 until 2 weeks of the initial insult, myofibroblasts increased expression of matrix metaloproteinase (MMPs), 4. which is a proteolytic enzyme responsible for matrix extraseluler (ECM) remodeling
When any portion of an epithelial cell is disrupted, the entire cell is usually lost, leaving a defect in the epithelial layer.
2. A variety of factors may retard the rate of reepithelialization following chemical injury including the inflammatory response and structural damage to the epithelial basement membrane.
Recovery from epithelial injury is dependent on the centripetal migration of cells from the most proximal region of viable epithelium.
By 24 to 30 hours after injury, mitosis begins to restore the epithelial cell population.
Endothelial cells do not have the ability to mitosis,and If the endothelium is injured, healing occurs mainly via cell migration, rearrangement, and enlargement of the residual cells.
The cation is responsible for the penetration of alkali and react with the carboxyl groups of stromal collagen and extensive hydrolysis of the corneal matrix.
2. the hydroxyl ion causing saponification of cellular membranes resulting in cell disruption and death.
In general, acids penetrate the corneal stroma much less readily than alkalis.
2. The hydrogen ion mediates damage due to pH alteration, while the anion causes precipitation and denaturation of proteins in the corneal epithelium and anterior stroma.
Classification of chemical injury are differentiated based upon the extent of epithelial damage, stromal edema denoting degree of penetration, and limbal ischemic.
2. This is the table of Hugges classification modified by Roper Hall for chemical trauma
Corneal melting is a common prelude to the development of corneal perforation.
2. This process occurs from conditions such as infections, sterile inflammation, surgical, or chemical injury to the cornea.
this shows a corneal melting scheme in chemical trauma and other causes. in chemical trauma tissue denaturation occurs and release collagenase enzime. This enzime causes collagen and proteoglycan destruction.
Strong chemicals exert their destructive effect directly by damaging cellular and extracellular matrices and 2. indirectly by initiating an inflammatory process that is not necessarily time-limited.
3. Corneal melting to be influenced by the excessive tissue degradative proteases.
4. these proteases are the matrix metalloproteinases (MMPs)
Resident corneal cells such as keratocytes and infiltrating macrophages are also capable of releasing active MMPs, as well as drive the melting process by the release of proinflammatory cytokines.
2. process of repair after chemical trauma, fibroblasts can simultaneously synthesize both collagen and collagenase, the same cells to participate both in ulceration and repair.
