REVIEW/UPDATE

Anatomy and physiology of the cornea

Derek W. DelMonte, MD, Terry Kim, MD

The importance of the cornea to the ocular structure and visual system is often overlooked
because of the cornea’s unassuming transparent nature. The cornea lacks the neurobiological
sophistication of the retina and the dynamic movement of the lens; yet, without its clarity, the
eye would not be able to perform its necessary functions. The complexity of structure and function
necessary to maintain such elegant simplicity is the wonder that draws us to one of the most
important components of our visual system.
Financial Disclosure: Neither author has a financial or proprietary interest in any material or
method mentioned.
J Cataract Refract Surg 2011; 37:588–598 Q 2011 ASCRS and ESCRS

Editor’s Note: In this issue, we begin a series of review arti-
cles that will provide a framework for understanding what
we do and do not know about corneal biomechanics and
methods to evaluate this important topic. The article in
this issue provides a basic understanding of corneal anat-
omy and physiology. Subsequent articles, which will be
published during 2011, will review the status of the corneal
endothelium after refractive surgery and provide an intro-
duction to our understanding of corneal biomechanics and
the means by which we measure corneal biomechanical
properties, including topography, tomography, and wave-
front analysis.
The cornea is a transparent avascular connective tis-
sue that acts as the primary infectious and structural
barrier of the eye. Together with the overlying tear
film, it also provides a proper anterior refractive sur-
face for the eye. Its clarity is the result of many factors
including the structural anatomy and physiology of its
cellular components. In this article, we describe the
intricate and delicate balance of cellular components
and factors that create the most important refractive
component of our ocular system.
ANATOMY OF THE CORNEA
In the average adult, the horizontal diameter of the
cornea is 11.5 to 12.0 mm1 and about 1.0 mm larger
than the vertical diameter. It is approximately
0.5 mm thick at the center and gradually increases in
thickness toward the periphery. The shape of the cor-
nea is prolatedflatter in the periphery and steeper
centrallydwhich creates an aspheric optical system.
Corneal shape and curvature are governed by the
intrinsic biomechanical structure and extrinsic envi-
ronment. Anterior corneal stromal rigidity appears to
be particularly important in maintaining the corneal
curvature.2 Organizational differences in the collagen
bundles of the anterior stroma may contribute to
a tighter cohesive strength in this area and may also
explain why the anterior curvature resists change to
stromal hydration much more than the posterior
stroma, which tends to more easily develop folds.
Stromal hydration also appears to affect the cornea’s
response to strain and shear forces.3
The human cornea consists of 5 recognized layers, 3
cellular (epithelium, stroma, endothelium) and 2 inter-
face (Bowman membrane, Descemet membrane)
(Figure 1).

Submitted: June 29, 2010. Epithelium

Final revision submitted: October 27, 2010.
Accepted: October 29, 2010.
From the Department of Ophthalmology, Duke University Eye Center,
Duke University Medical Center, Durham, North Carolina, USA.
Corresponding author: Terry Kim, MD, Duke University School of
Medicine, Cornea and External Disease Service, Refractive Surgery
Service, Duke University Eye Center, 2351 Erwin Road, Duke
University Eye Center, DUMC 3802, Durham, North Carolina
27710-3802, USA. E-mail: terry.kim@duke.edu.
The epithelial surface of the cornea creates the first
barrier to the outside environment and is an integral
part of the tear film–cornea interface that is critical to
the refractive power of the eye. It is a stratified, non-
keratinizing squamous layer characterized by extreme
uniformity from limbus to limbus.
Embryologically, the corneal epithelium is derived
from surface ectoderm between 5 and 6 weeks of ges-
tation. It is composed of nonkeratinized, stratified

588 Q 2011 ASCRS and ESCRS 0886-3350/$ - see front matter

Published by Elsevier Inc. doi:10.1016/j.jcrs.2010.12.037
 REVIEW/UPDATE: ANATOMY AND PHYSIOLOGY OF THE CORNEA
Figure 1. Light micrograph of normal endothelium (original magni-
fication 100). Note the single-cell endothelial layer with a Descemet
membrane of uniform thickness (epithelial surface at top of figure).
Reprinted with permission of Ophthalmology.4 Copyright 2008
Elsevier.
squamous epithelium that is 4 to 6 cell layers thick
(40 mm to 50 mm).4 As mentioned earlier, the epithe-
lium is covered with a tear film, which is optically
important in smoothing out microirregularities of the
anterior epithelial surface. The air–tear film interface,
together with the underlying cornea, provides two
thirds of the total refractive power of the eye.
The corneal epithelium and overlying tear film have
a symbiotic relationship both anatomically and physi-
ologically. The mucinous layer of the tear film, which
is in direct contact with the corneal epithelium, is pro-
duced by the conjunctival goblet cells and interacts
closely with the corneal epithelial cell glycocalyx to al-
low hydrophilic spreading of the tear film with each
eyelid blink. It has been suggested that the epithelium
itself may contribute to this mucinous layer, but this is
unproven.5 Loss of the glycocalyx from injury or dis-
ease results in loss of tear-film stability and subsequent
breakdown of the ocular optical system. The tear film
is the primary protector of the corneal surface from
microbial invasion, as well as from chemical, toxic,
and foreign-body damage. The tear film also supplies
immunological and growth factors that are critical for
epithelial health, proliferation, and repair.6
Corneal epithelial cells have an average lifespan of 7
to 10 days7 and routinely undergo orderly involution,
apoptosis (programmed cell death), and desquama-
tion. This process results in complete turnover of the
corneal epithelial layer every week as deeper cells re-
place the desquamating superficial cells in an orderly,
apically directed fashion. The most superficial corneal
epithelial cells form a mean of 2 to 3 layers of flat po-
lygonal cells. These cells have extensive apical micro-
villi and microplicae, which in turn are covered by
a fine, closely apposed, charged glycocalyceal layer.4
This layer’s apical membrane projections increase the
J CATARACT REFRACT SURG - VOL 37, MARCH 2011
589
Figure 2. Cross-sectional view of the corneal epithelial cell layer.
Reprinted with permission of Ophthalmology.4 Copyright 2008
Elsevier.
surface area of contact and adherence between the
tear film’s mucinous layer and the cell membrane
(Figure 2). As discussed earlier, this is critical for
a smooth and clear optical system.
These surface cells maintain tight junctional com-
plexes between their neighbors, which prohibit tears
from entering the intercellular spaces. This can be
demonstrated clinically by observing a healthy epithe-
lial surface’s ability to repel dyes such as fluorescein
and rose bengal. This barrier also prevents toxins
and microbes from entering deeper corneal layers.
Beneath the superficial cell layer and just anterior to
the deepest basal layer of the epithelium are the supra-
basal or wing cells. This layer is 2 to 3 cells deep and
consists of cells that are less flat than the overlying su-
perficial cells but possess similar tight lateral intercel-
lular junctions.
The deepest cellular layer of the corneal epithelium
is the basal layer, which comprises a single cell layer of
columnar epithelium approximately 20 mm tall. Be-
sides the stem cells and transient amplifying cells,
basal cells are the only corneal epithelial cells capable
of mitosis.8 They are the source of wing and superficial
cells and possess lateral intercellular junctions charac-
terized by gap junctions and zonulae adherens. The
basal cells are attached to the underlying basement
membrane by a hemidesmosomal system. This strong
attachment is what prevents the epithelium from sep-
arating from the underlying corneal layers. Abnormal-
ities in this bonding system may result clinically in
recurrent corneal erosion syndromes or nonhealing
epithelial defects. Epithelial stem cells, which serve
as an important source of new corneal epithelium,
have been localized to the limbal basal epithelium.
As the cells migrate to the central cornea, they differen-
tiate into transient amplifying cells (cells capable of
590 REVIEW/UPDATE: ANATOMY AND PHYSIOLOGY OF THE CORNEA
Figure 3. Hypothetical scheme of limbal stem cell niche. Reprinted
with permission of Cell Research.9 Copyright 2007 Macmillan Pub-
lishers Ltd.
multiple but limited cellular division) and basal cells
(Figure 3).9
The epithelial basement membrane, approximately
0.05 mm thick, comprises type IV collagen and laminin
secreted by the basal cells. If damaged, fibronectin
levels increase and the process of healing can take up
to 6 weeks. During this time, the epithelial bond to
the underlying, newly laid basement membrane tends
to be unstable and weak.
Bowman Layer
Bowman layer (or Bowman membrane) lies just an-
terior to the stroma and is not a true membrane but
rather the acellular condensate of the most anterior
portion of the stroma. This smooth layer is approxi-
mately 15 mm thick and helps the cornea maintain its
shape. When disrupted, it will not regenerate and
can form a scar (Figure 4).
Stroma
The corneal stroma provides the bulk of the struc-
tural framework of the cornea and comprises roughly
80% to 85% of its thickness. Embryologically, it is the
result of a second wave of neural crest migration that
occurs in the seventh week of gestation, after establish-
ment of the primitive endothelium. The stroma differs
from other collagenous structures in its transparency,
which is the result of precise organization of the stro-
mal fibers and extracellular matrix (ECM).10,11 The col-
lagen fibers are arranged in parallel bundles called
fibrils, and these fibrils are packed in parallel arranged
layers or lamellae. The stroma of the human eye con-
tains 200 to 250 distinct lamella, each layer arranged
at right angles relative to fibers in adjacent lamellae.11
The peripheral stroma is thicker than the central
J CATARACT REFRACT SURG - VOL 37, MARCH 2011
Figure 4. Bowman scarring seen after herpes simplex keratitis. Note
the abrupt termination of Bowman membrane. Reprinted with per-
mission of Cornea.6 Copyright 2005 Elsevier.
stroma, and the collagen fibrils may change direction
to run circumferentially as they approach the limbus.12
This highly organized network reduces forward light
scatter and contributes to the transparency and
mechanical strength of the cornea.
An additional feature of the stroma is that the ultra-
structure within the organization of the lamella ap-
pears to vary based on the depth within the stroma.
Deeper layers are more strictly organized than super-
ficial layers, and this difference accounts for the
greater ease of surgical dissection in a particular plane
as one approaches the posterior depths of the corneal
stroma. This variation in stromal organization also
accounts for the differences in response to corneal
edema, as mentioned previously. Descemet folds are
the result of asymmetric swelling of the posterior
stroma imposed by the structurally more rigid anterior
cornea and structural restriction imposed by the lim-
bus.13 Stromal swelling is therefore directed posteri-
orly and results in relative flattening of the posterior
surface, which can push Descemet membrane into
multiple folds that become visible as striae.
Stromal collagen fibrils are composed of type I colla-
gen in a heterodimeric complex with type V collagen
to obtain their unique and narrow diameter.14 These
complexes are surrounded by specialized proteogly-
cans, consisting of keratan sulfate or chondroitin
sulfate/dermatan sulfate side chains, which help reg-
ulate hydration and structural properties.
Keratocytes are the major cell type of the stroma and
are involved in maintaining the ECM environment
(Figure 5). They are able to synthesize collagen
molecules and glycosaminoglycans while also creating
matrix metalloproteases (MMPs)dall crucial in main-
taining stromal homeostasis. Most of these keratocytes
reside in the anterior stroma and contain corneal
 REVIEW/UPDATE: ANATOMY AND PHYSIOLOGY OF THE CORNEA
“crystallins,” representing 25% to 30% of soluble pro-
tein in the cells. These crystallins appear to be respon-
sible for reducing backscatter of light from the
keratocytes and maintaining corneal transparency.15
Descemet Membrane
Beginning in utero at the 8-week stage, endothelial
cells continuously secrete Descemet membrane. The
anterior 3 mm secreted prior to birth has a distinctive
banded appearance when viewed by electron
Figure 6. Micrograph illustrating Descemet membrane (DM) located
between the posterior aspect of the corneal stroma (S) and the under-
lying endothelium (EN). The anterior “banded” region (A) is se-
creted by the endothelial cells during fetal development and is
more highly organized than the posterior “amorphous region” (P),
which is secreted after birth. Reprinted with permission of Principles
and Practice of Ophthalmology.13 Copyright 2008 Elsevier.
J CATARACT REFRACT SURG - VOL 37, MARCH 2011
591
Figure 5. Transmission electron micros-
copy of the human corneal stroma. A:
Keratocyte localized between stromal la-
mellae. B: Higher magnification view
showing a keratocyte in relation to colla-
gen fibers coursing in various directions.
Reprinted with permission of Cornea.6
Copyright 2005 Elsevier.
microscopy, but Descemet membrane produced after
birth is unbanded and has an amorphous ultrastruc-
tural texture. Descemet can accumulate up to 10 mm
in thickness with age (Figure 6).
Endothelium
The endothelial layer of the cornea maintains cor-
neal clarity by ensuring it remains in a relatively
deturgesced state. The intact human endothelium is
a monolayer, which appears as a honeycomb-like
mosaic when viewed from the posterior side (Figure 7).
In early embryogenesis, the posterior cornea is lined
with a neural crest-derived monolayer of orderly ar-
ranged cuboidal cells.16 Over time, these cells flatten
and become tightly adherent to one another. Immedi-
ately anterior to the flattened layer is a discontinuous
homogeneous acellular layer, which in time becomes
Descemet membrane.17 At birth, the endothelial
monolayer is approximately 10 mm thick and consists
of a uniform thickness layer of cells that spans the en-
tire posterior corneal surface and fuses with the cells of
the trabecular meshwork.17 Similarly, Descemet mem-
brane becomes continuous and uniform, fusing
peripherally with the trabecular beams.17 The fusion
site, known as Schwalbe line, is a gonioscopic land-
mark that defines the end of Descemet membrane
and the start of the trabecular meshwork.
The individual cells continue to flatten over time
and stabilize at approximately 4 mm in thickness in
adulthood. Adjacent cells share extensive lateral inter-
digitations and possess gap and tight junctions along
their lateral borders. The lateral membranes contain
a high density of NaC, KC-ATPase pump sites.18
The basal surface of the endothelium contains numer-
ous hemidesmosomes that promote adhesion to
Descemet membrane.
Endothelial cell density and topography continue
to change throughout life. From the second to eighth
592 REVIEW/UPDATE: ANATOMY AND PHYSIOLOGY OF THE CORNEA

Figure 7. Specular photomicrograph of normal endothelium. Note Figure 8. Major corneal loading forces in the steady state. Reprinted
the dark well-defined cell borders, the regular hexagonal array, with permission of Ophthalmology.4 Copyright 2008 Elsevier.
and the uniform cell size. Reprinted with permission of Cornea.6
Copyright 2005 Elsevier.

decades of life, the cell density declines from 3000 (ie, Fuchs endothelial dystrophy), but the remaining
to 4000 cells/mm2 to around 2600 cells/mm2, and cells have the capacity to “stretch” and take over
the percentage of hexagonal cells declines from ap- the space of the degenerated endothelial cells. As this
proximately 75% to approximately 60%.19 The central process occurs, the remaining cells grow in size (poly-
endothelial cell density decreases at an average rate of megathism) and lose their hexagonal shape (pleomor-
0.6% per year in normal corneas.20 phism) (Figure 9).
As mentioned, the stroma is maintained in a rela-
tively deturgesced state (78% water content) by the ac- Blood Supply of the Cornea
tivity of the endothelial cells.21 This dehydration is
mediated by a pump–leak process as fluid egresses Although the normal human cornea is avascular, it
from the corneal stroma down the osmotic gradient relies on components of the blood to remain healthy.
from a relatively hypo-osmotic stroma toward a rela- These components are supplied by tiny vessels at the
tively hypertonic aqueous humor. This passive bulk outermost edge of the cornea as well as components
fluid movement requires no energy but is fueled by supplied by end branches of the facial and ophthalmic
the energy-requiring processes of transporting ions arteries via the aqueous humor and tear film.
to generate the osmotic gradient. The 2 most important
ion transport systems are the membrane-bound NaC Nerve Supply of the Cornea
and KC-ATPase sites and the intracellular carbonic The cornea is one of the most heavily innervated and
anhydrase pathway. Activity in both these pathways most sensitive tissues in the body. Corneal nerves and
produces a net flux of ions from the stroma to the aque-
ous humor. The barrier portion of the endothelium is
unique in that it is permeable to some degree, permit-
ting the ion flux necessary to establish the osmotic
gradient (Figure 8).17
Endothelial cells have no mitotic activity in vivo;
however, humans are born with a significant reserve.
Cell density is approximately 3500 cells/mm2 at birth,
but this number decreases gradually throughout life at
approximately 0.6% per year. It has been observed that
eyes with endothelial cell counts below 500 cells/mm2
may be at risk for the development of corneal edema.
Endothelial cell morphology (size and shape) also ap-
pears to correlate with pump function. An increase in
cell size (polymegathism) and an increase in variation
of cell shape (pleomorphism) correlate to reduced abil-
Figure 9. Specular photomicrograph of Fuchs dystrophy. Note dark
ity of the endothelial cells to deturgesce the cornea.22 areas that represent guttae adjacent to areas of enlarged endothelial
The number of endothelial cells decreases with age, cells. (Spacing of grid 0.1 mm) Reprinted with permission of Oph-
trauma, inflammation, and other disease processes thalmology.4 Copyright 2008 Elsevier.

J CATARACT REFRACT SURG - VOL 37, MARCH 2011

 REVIEW/UPDATE: ANATOMY AND PHYSIOLOGY OF THE CORNEA
sensation are derived from the nasociliary branch of
the first (ophthalmic) division of the trigeminal nerve.
In the superficial cornea, the nerves enter the stroma
radially in thick trunks forming plexiform arrange-
ments, which eventually perforate Bowman mem-
brane to provide a rich plexus beneath the basal
epithelial layer.23 The cornea also contains autonomic
sympathetic nerve fibers.
CORNEAL RESPONSES TO INJURY
Epithelial Injury
When any portion of an epithelial cell is disrupted,
the entire cell is usually lost, leaving a defect in the ep-
ithelial layer. The most common form of injury to the
epithelium is mechanical, but thermal and chemical in-
juries are also possible. When a mechanical force cre-
ates a break in the epithelial barrier, cells at the edge
of the abrasion begin to cover the defect within min-
utes by a combination of cell migration and cell
spreading. This process is preceded by almost immedi-
ate preparatory cellular changes of an anatomical,
physiological, and biochemical nature, including the
creation of cell membrane extensions, disappearance
of hemidesmosome adhesions from the basal cells,
and increase in mitochondrial energy production.
This early nonmitotic wound coverage phase can
proceed at the remarkable rate of 60 to 80 mm per
hour.24 Studies have shown that the migrating sheet
of epithelial cells is attached most firmly to the under-
lying substrate at the leading margin, possibly sug-
gesting that the leading cells are “pulling” the
epithelial sheet as it migrates.25 The ECM protein fi-
bronectin is thought to be a key element in the media-
tion of cell-to-substrate adhesion and cell migration.
By 24 to 30 hours after injury, mitosis begins to re-
store the epithelial cell population. Only the basal cells,
transient amplifying cells, and limbal stem cells par-
take in this reconstitutive mitosis.8
Stromal Injury
The separation of the stroma from the other cellular
layers of the cornea by the Bowman layer and Desce-
met membrane is necessary for the normal homeosta-
sis of the cornea, and the disruption of this strict
organization is associated with activation of the stro-
mal wound-healing process. Stromal wound healing
consists of 3 stages: repair, regeneration, and remodel-
ing.14 Similar to the wound-healing process in skin
wounds, stromal wound healing has been shown to in-
volve a complex interplay of cytokines, growth factors,
and chemokines; however, an important distinction is
the absence of a vascular component to the healing.26
The activation and migration of stromal keratocytes
are the first responses to a stromal injury and can occur
J CATARACT REFRACT SURG - VOL 37, MARCH 2011
593
within hours. These cells take on a more fibroblast-like
appearance and behavior as they become activated.27
The keratocytes within the area of injury undergo
apoptosis, peaking 4 hours after the initial insult.28
Apoptosis appears to modulate the wound-healing
response by influencing the activation of adjacent
keratocytes.
Within 1 to 2 weeks of the initial insult, myofibro-
blasts with contractile properties enter the injured
area and become involved in the stromal remodeling.
These cells use increased expression of MMPs, which
are a family of proteolytic enzymes responsible for
ECM remodeling, cell–matrix interaction, inflamma-
tory cell recruitment, and cytokine activation.29 In
the cornea, MMPs are thought to be very important
in the complex reorganization of collagen in the stro-
mal wound.14 This theory is supported by research
looking at complex laser in situ keratomileusis
wounds that has found increased levels of MMPs, par-
ticularly in areas of significant wound trauma with
interface fibrosis.30 It has been proposed that
overexpression of these MMPs, along with activated
inflammatory cytokines, may be responsible for loss
of specific type IV collagen isoforms in the epithelial
basement membrane, leading to scarring or haze.
The interaction between these cytokines, MMPs, and
other mediators, rather than the mere presence or ab-
sence of these proteins, often plays a decisive role in
regulating the complex remodeling process during
corneal wound healing.31 This process can take
months or even years to complete; the end result some-
times reduces corneal clarity long after primary
wound healing has occurred.
Endothelial Injury
Aside from full-thickness penetrating injuries, endo-
thelial injury primarily results from rapid focal distor-
tion of the cellular layer. This disruption is similar to
the injuries seen from excessive corneal bending in
large-incision surgeries such as extracapsular cataract
extraction and/or from endothelial trauma caused
by high fluid turbulence during cataract surgery. Clin-
ically, these injuries are seen as “snail-track” lesions or
serpentine gray lines on the endothelium.
As discussed earlier, endothelial cells do not appear
to undergo mitosis in vivo, which means the damaged
cells are rapidly replaced by enlargement of the sur-
rounding cells and their centripetal migration into
the injured region. The process of resurfacing the in-
jured area is completed in 3 stages that can take several
weeks. The first stage is characterized by the establish-
ment of initial coverage of the wound by migration of
adjacent endothelial cells, which forms a temporary
incomplete barrier with reduced pump sites and
594 REVIEW/UPDATE: ANATOMY AND PHYSIOLOGY OF THE CORNEA
incompletely formed tight junctions. In the second
stage, the barrier (ie, tight junctions) and subsequently
the number and quality of pump sites return to normal
levels, the endothelial cells form irregular polygons,
the corneal thickness typically returns to normal, and
transparency is restored. The third stage involves re-
modeling of the endothelial cells to form more regular
hexagons, which can continue for several months.17
With more severe trauma, as a result of keratoconus,
and as a possible complication of incisional anterior
segment surgery, the underlying Descemet membrane
may be torn or ruptured. If this occurs, migrating en-
dothelial cells are required to produce new Descemet
membrane. As seen with acute corneal hydrops, focal
corneal edema may be seen early, which resolves
when the break is repaired.
One must consider other stressors in endothelial in-
jury as surface trauma is less problematic here than
with the more superficial corneal layers. The endothe-
lium has a restricted response to stress. Mild stress
may result in changes in cell size and shape, whereas
greater stress may result in cell loss as well as irrevers-
ible alterations in the endothelial cytoskeleton.32 Sour-
ces of stress may be metabolic (from hypoxia or
hyperglycemia) or toxic (from drugs or their preserva-
tives) or caused by alterations in pH or osmolarity. For
example, contact lenses cause a hypoxic stress of vary-
ing degrees to the endothelium.33 Over time, this may
result in alteration of the morphology, microanatomy,
and possibly the function of the endothelium.22 Hy-
perglycemia is another common metabolic stress that
may produce changes in the endothelium. Compared
with the corneal endothelium in age-matched controls,
the corneal endothelium in patients with type 1 and
type 2 diabetes has a lower mean cell density and
greater pleomorphism and polymegathism.34
SURGERY AND THE CORNEA
Since the first phacoemulsification surgery performed
by Kelman in the 1960s,35 intraocular surgery has ad-
vanced rapidly. With this has come the need to ensure
corneal health and clarity during the intraoperative
and postoperative course. Nothing is worse than per-
forming surgery to improve visual potential only to
be foiled by decreased corneal clarity due to prevent-
able corneal injury. For this reason, ophthalmic sur-
geons should be aware of the potential causes of
corneal injury and know how to treat the injury should
it occur.
Epithelium
Epithelial injury during intraocular surgery is not
rare but is generally mechanical and can be treated
in the same manner as any other mechanical injury
J CATARACT REFRACT SURG - VOL 37, MARCH 2011
to the corneal epithelium with minimal long-term
complications.
Bowman Layer and Stroma
Corneal refractive surgery, similar to intraocular
surgery, requires close attention to corneal anatomy
and physiology. Corneal haze and progressive ectasia
are stromal complications of corneal refractive surgery
that must be considered and addressed by surgeons
who perform refractive procedures. For example,
many people have found that corneal haze, which
was a significant complication after photorefractive
keratectomy, was seen less frequently after the intro-
duction of flap-based surgeries that spared Bowman
layer. Corneal haze appears to be related to increased
initiation of cytokine messaging cascades and in-
creased activity of stromal keratocytes when this bar-
rier is breached, resulting in altered stromal healing
patterns, as discussed above.36 Reports have docu-
mented irregularities in basement membrane configu-
ration, the presence of vacuoles in and around
keratocytes, and disorganization in the lamellar struc-
ture of the corneal stroma, all related to the activated
keratocytes.13,36 The incidence of visually significant
haze has decreased with continued advances in laser
technology, such as smaller spot sizes and larger abla-
tion zones, as well as advances in postoperative man-
agement, such as new steroid regimens and the use of
mitomycin-C.37
The increasing demand for a 20/20 uncorrected vi-
sual outcome after cataract surgery is driving more
cataract surgeons to use incisional astigmatic keratoto-
my to correct existing astigmatism at the time of pha-
coemulsification. Although these treatments are not
new to the world of refractive surgery, they are having
a resurgence outside the traditional use by subspe-
cialty trained refractive surgeons. These procedures
rely on the biomechanical structure of the cornea, mak-
ing it imperative that surgeons know the effects of in-
cision length, depth, and axis. Early work by Bates38
and later Lans39 identified 4 major rules governing in-
cisional corneal outcomes: (1) deeper incisions into the
stroma provide a greater effect; (2) wound healing
and scarring of the incisions induce further effect; (3)
arcuate incisions result in flattening in the axis of the in-
cision; and (4) radial incisions result in central flatten-
ing and peripheral corneal steepening.13 Since that
time, corneal incisional refractive surgery has been
very successful but comes with its own set of complica-
tions, including decreased corneal stability, risk for in-
fectious keratitis, and over- or undercorrection.
Descemet Membrane and Endothelium
Descemet membrane injury and detachment is an
uncommon but serious complication of anterior
 REVIEW/UPDATE: ANATOMY AND PHYSIOLOGY OF THE CORNEA
segment surgery that has the potential to lead to signif-
icant endothelial cell loss in some cases.40 It is esti-
mated that Descemet detachment occurs in 0.5% of
cataract surgeries; although most injuries remain small
and localized to the wound, some can extend to the
visual axis, resulting in significant morbidity.41 It
must be remembered that healing of Descemet breaks
requires endothelial cell migration and deposition of
a new basement membrane, a process that is much eas-
ier if the edges remain in close proximity. For this rea-
son, many surgeons place air or gas bubbles in the
anterior chamber of the eye to hold the loose mem-
brane tags against the posterior cornea as the healing
process takes place or, in larger detachments, use
a 10-0 nylon suture to reappose the detachment
mechanically.42,43
One of the most serious complications after intraoc-
ular surgery is corneal edema, which was noted
frequently during the early years of phacoemulsifica-
tion surgery and is largely due to endothelial damage
at the time of surgery. In several studies, 44–46 the cen-
tral endothelial cell loss after phacoemulsification
ranges from 4% to 25%. Many factors likely affect the
corneal endothelium during a phacoemulsification
procedure and these can be divided into 4 groups:
(1) direct mechanical trauma to the endothelium
from the incision and inadvertent touch of the endo-
thelium by lens fragments, instruments, or intraocular
lenses during the procedure; (2) ultrasound energy
affecting the endothelium directly or (3) via the gener-
ation of hydroxyl radicals; and (4) the biochemical and
mechanical effects of the irrigating solution (nature,
volume, turbulence).47,48
Direct trauma to the endothelium is a risk when in-
struments or other objects are placed in the confined
space of the anterior chamber. Care must be taken to
avoid touching the delicate endothelial cells inadver-
tently, as even minor trauma can result in significant
cell death. This is supported by studies reporting
that dense nuclear fragments floating in the anterior
chamber with high turbulence are a risk for endothe-
lial trauma.49,50 For this reason, Osher51 and others
suggest a “slow motion” phacoemulsification tech-
nique that may minimize this trauma.
One major advance in intraocular surgery is oph-
thalmic viscosurgical devices (OVDs) (composed of
hydroxypropyl methylcellulose, chondroitin sulfate,
or sodium hyaluronate). These devices significantly
protect the endothelium against intraoperative
trauma.52 Different OVDs have different physical
properties (eg, rheology, shear rate, and osmotic
strength) and may provide different levels of endothe-
lial protection from mechanical and ultrasonic insults.
The ultrasonic energy delivered to the eye during
phacoemulsification is important for removing
J CATARACT REFRACT SURG - VOL 37, MARCH 2011
595
cataracts through a small incision, but it can damage
other ocular structures, particularly the delicate cor-
neal endothelium. During early phacoemulsification
surgery, the level of corneal endothelial cell loss was
high and many patients developed corneal failure. Nu-
merous studies found that the level of ultrasound
power used during surgery was directly proportional
to the endothelial cell loss, often attributed to direct
mechanical trauma from the sonic wave as well as
thermal injury.53,54 With the development of better
ways to protect the cornea through OVDs and
methods to modulate and decrease the phaco energy,
the rate of pseudophakic bullous keratopathy has de-
creased dramatically. By delivering smaller pulses or
bursts of energy in variable patterns, the phaco effi-
ciency can be maximized while the total amount of
phaco energy, phaco time, and phaco-generated heat
within the eye is decreased, thus minimizing endothe-
lial trauma.55
Elevated levels of oxygen-free radical species have
been identified in the eyes of patients who recently
had phacoemulsification surgery.56 These free radicals
are thought to be the result of ultrasound oscillations
that induce acoustic cavitations, leading to dissocia-
tion of water vapor.57 Several recent studies propose
that these free radicals are a significant source of endo-
thelial damage after cataract extraction by inducing
the apoptosis cascade.58
Fluidics also play an important role in corneal health
during intraocular surgery.59 It is critical to minimize
the mechanical trauma from the turbulent flow of irri-
gating solutions in a confined space as well as to
maintain the delicate biochemical composition of the
anterior chamber during the procedure.
With all the ophthalmic solutions, medications, and
other agents currently used during routine phaco-
emulsification cataract surgery, it is important to
know the pH and osmotic tolerance range of the hu-
man corneal endothelium. Studies show that the cor-
neal endothelium has a pH tolerance between 6.8
and 8.2, which is similar to that of the natural aqueous
humor bicarbonate buffer system.60 During cataract
surgery, the osmolality of the anterior chamber can
easily vary because of the variety of drugs and solu-
tions used in irrigation or injection of the eye. This var-
iation can cause the endothelial cells to become
swollen, degenerated, apoptotic, or even necrotic. If
all the essential ions are present, corneal endothelial
cells tolerate a wide range of osmolalities from 250 to
350 mOsmoles.61 Therefore, both the pH and osmolal-
ity of the intraocular solution are critical in maintain-
ing the health of the corneal endothelium.
It is important to monitor the composition of not
only the phacoemulsification irrigating solution, but
also the many other fluids used intraocularly during
596 REVIEW/UPDATE: ANATOMY AND PHYSIOLOGY OF THE CORNEA
surgery. Medications such as epinephrine, anesthetic
agents, and miotic agents are used routinely but
must be properly buffered, used in specific concentra-
tions, and at specific temperatures to ensure endothe-
lial health.41,62 Many preservatives in ocular
medications, such as methylparaben and benzalko-
nium, are toxic to the corneal endothelium.63 For this
reason, all intraocular medications should be free of
preservatives or other unnecessary additives.
Toxic anterior segment syndrome (TASS), an ex-
treme example of endothelial toxicity, is an acute ster-
ile anterior segment inflammation that develops after
anterior segment surgery. Findings associated with
TASS typically present within 12 to 48 hours of sur-
gery and include diffuse limbus-to-limbus corneal
edema secondary to widespread damage to the cor-
neal endothelium. Several large studies have not
been able to identify a single factor responsible for
this syndrome; however, problems with the cleaning
and sterilization process of surgical instruments may
be responsible.64
CONCLUSION
About the size of a postage stamp and less than half
the thickness of a United States dime, the human cor-
nea is one of the marvels of the human body. Transpar-
ent and refractive, it offers us a clear view of the world
around us while protecting the delicate contents of the
human visual system. It is crucial that ophthalmic
surgeons appreciate the importance of this tough yet
vulnerable tissue when planning and performing in-
traocular and refractive corneal surgery.
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