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OPTOMETRY
REVIEW
Ciro Costagliola* MD Corneal oedema is a common sign of acute or protracted corneal disease of various
Vito Romano* MD aetiologies. In this paper, we review the causes and pathophysiological bases of corneal
Eliana Forbice† MD oedema, as well as discussing the goals and modalities of its medical treatment. Corneal
Martina Angi† MD oedema, if adequately understood and appropriately treated, generally shows a good
Arduino Pascotto* prognosis.
Tiziana Boccia*
Francesco Semeraro† MD
* Eye Clinic, Department of Health Sciences,
University of Molise, Campobasso, Italy
†
Eye Clinic, Department of Ophthalmology,
University of Brescia, Brescia, Italy
E-mail: elianaforbice@email.it
Key words: corneal dystrophy, corneal oedema, endothelial pump, stromal swelling pressure
The cornea protects the eye from the envi- tests, will usually lead to the correct diagno- epithelium and the endothelium, endothe-
ronment and pathogens, as well as having an sis and treatment. Usually oedema is revers- lial pump, tear evaporation and intraocular
important role in the transmission and ible, disappearing when the underlying pressure.2
refraction of light, guaranteed by numerous disease is cured. However, chronic oedema
mechanisms that regulate corneal hydration requires symptomatic treatment and is Stromal swelling pressure
and maintain its transparency. Many proc- usually the result of irreversible damage to The state of corneal hydration can increase
esses work together to accomplish this task, the endothelium. Medical treatment aims at up to 98 per cent, when the cornea is placed
including properly functioning epithelium improving visual acuity and reducing dis- in an aqueous medium, with proportional
and endothelium and a healthy interaction comfort. The present review discusses the increase in its thickness. Stromal proteogly-
between stromal structural components, pathophysiology and treatment of corneal cans associated with collagen bind water and
such as collagen and proteoglycans. oedema. create a strong inward pressure gradient
When one of these delicate processes is called swelling pressure. Stromal swelling
altered, extracellular fluid accumulates in- is due to interfibrillary imbibition of
side the cornea leading to corneal oedema, PATHOPHYSIOLOGY water, not to swelling of collagen fibrils. If
with loss of transparency. Corneal oedema glycosaminoglycans are removed from the
is a common sign of acute or protracted Corneal transparency is primarily depend- stroma, a marked reduction in swelling
corneal disease of various aetiologies. ent on the ability of the cornea to remain occurs, indicating that glycosaminoglycans
Cogan1 emphasised that two distinct in a dehydrated state. Ideally, the human are the major cause of this hydration
phenomena encompass the term corneal cornea maintains a 78 per cent hydration phenomenon.3
oedema: stromal oedema and epithelial level. Any major deviation can lead to Histologically, ultrastructurally and bio-
oedema. Both may occur independently, corneal opacity, as it has an inherent ten- chemically, there are differences between
produce different symptoms and have differ- dency to imbibe water and swell. As corneal the anterior third and posterior two-thirds of
ent causes (Table 1). swelling causes an increase in corneal thick- the cornea. The anterior stroma contains
Making a differential diagnosis of corneal ness, corneal thickness and hydration are less water than the posterior. The cause
oedema can be very challenging but under- linearly related. of such differences is a greater amount of
standing its normal physiology, together There are five primary factors that play a glucose in the posterior stroma, as well as
with an accurate medical history, a full clini- role in corneal hydration, namely, stromal an uneven distribution of proteoglycans
cal examination and some specific ancillary swelling pressure, barrier function of the throughout the cornea. Dermatan sulphate
© 2013 The Authors Clinical and Experimental Optometry 96.6 November 2013
Clinical and Experimental Optometry © 2013 Optometrists Association Australia 529
Corneal oedema Costagliola, Romano, Forbice, Angi, Pascotto, Boccia and Semeraro
Clinical and Experimental Optometry 96.6 November 2013 © 2013 The Authors
530 Clinical and Experimental Optometry © 2013 Optometrists Association Australia
Corneal oedema Costagliola, Romano, Forbice, Angi, Pascotto, Boccia and Semeraro
© 2013 The Authors Clinical and Experimental Optometry 96.6 November 2013
Clinical and Experimental Optometry © 2013 Optometrists Association Australia 531
Corneal oedema Costagliola, Romano, Forbice, Angi, Pascotto, Boccia and Semeraro
intraocular use in humans as much as possi- Dystrophic causes improved success with corneal transplanta-
ble, no matter what the concentration. tion, avascular subepithelial fibrous scarring
Fuchs’ endothelial corneal dystrophy was occurs between the epithelium and Bow-
INTRAOCULAR ANTIBIOTICS first described by Fuchs34 in 1910, as bilateral man’s layer, best seen with tangential
Gentamycin sulphate, vancomycin or corneal stromal and epithelial oedema in illumination. Peripheral superficial corneal
both have historically been used as intra- elderly patients. Fuchs’ dystrophy is a slowly neovascularisation can also occur. Subepi-
ocular antibiotics;27,28 however, concerns progressive disease with initial onset in the thelial scarring may eliminate the recurrent
about vancomycin-resistant organisms fifth through seventh decades of life. Fifty erosions but the irregularity of the surface
and aminoglycoside-related macular toxicity per cent of the time, there is family cluster- and the loss of transparency further reduce
have favoured the introduction of cefo- ing with an autosomal dominant inheritance vision.
taxime, a third-generation cephalosporin pattern.35–39 Females are predisposed to
that has broad Gram-negative coverage Fuchs’ dystrophy and develop corneal guttae
and sufficient activity against Gram-positive 2.5 times more frequently than males, pro- Inflammatory causes
organisms. No evidence of toxicity was gressing to corneal oedema 5.7 times more Inflammation of either the cornea or the
found when 0.25% cefotaxime solution was often than males. The initial manifestation anterior chamber from the iris and/or the
instilled into the anterior chamber and in Fuchs’ dystrophy is central corneal guttae. trabecular meshwork, can lead to deposition
there was no significant endothelial damage The guttae appear as dark spots on the of leukocytes on the endothelium, giving
in terms of cell density or morphology after posterior corneal surface by direct illumi- origin to keratic precipitates. These can
three months.29 nation and are highlighted in retroillu- form a variety of patterns, according to the
INTRAOCULAR INDOCYANINE GREEN mination, where they resemble dewdrops. underlying disease,42 including diffuse
Intraocular indocyanine green has been Pigment dusting is often present on the non-specific spattering (ankylosing spond-
used to stain both the internal limiting mem- endothelium and may be difficult to differ- ylitis),43 focal aggregation (herpes simplex
brane in vitreoretinal surgery and the ante- entiate from guttae. Patients at this early keratitis) and central, inferior, elliptical
rior capsule in cataract surgery. Holley and stage of the disease are not symptomatic. or triangular pattern44 (sarcoid uveitis). The
colleagues30 studied the effects of intraocu- Over time, the guttae spread peripherally endothelium can also becomes directly
lar indocyanine green on the human and and may also coalesce centrally, producing a target by inflammatory processes, such as
rabbit corneal endothelium. They showed beaten-metal appearance associated with in allograft reactions, where antigens on
that human cornea exposed to intraocular increased pigmentation. Desçemet’s mem- the endothelial cell surface stimulate the
indocyanine green had no corneal endothe- brane becomes visibly thickened, grey and immune reaction.45
lial ultrastructural damage observed by scan- irregular. In the even more advanced stage, Whatever the origin, once polymorpho-
ning and transmission electron microscopy. fibrous thickening of Desçemet’s membrane nuclear and mononuclear leukocytes
masks the presence of guttae, that are adhere to the endothelial cell surface, they
STERILISATION DETERGENTS then described as ‘buried guttae’.40 Corneal penetrate between the cells and migrate
A relatively new issue that will need to oedema begins in the posterior stroma adja- between Desçemet’s membrane and the
be addressed by ophthalmic surgeons and cent to Desçemet’s membrane and just endothelium. If the inflammatory process
operating room personnel is enzymatic behind Bowman’s layer, causing a fine grey is mild to moderate or is appropriately
detergent-related toxicity to the corneal haze best seen with sclerotic scatter. In addi- treated, the leukocytes migrate back into
endothelium. Because ethylene oxide is now tion, swelling of the corneal stroma can the anterior chamber and the endothelial
considered an occupational carcinogen and produce fine vertical wrinkles or striae in monolayer recovers functional viability
reproductive toxin by the National Institute Desçemet’s membrane. Microcystic epithe- with resolution of the corneal oedema. If
for Occupational Safety and Health, Centers lial oedema may follow and is seen as a stip- the inflammatory process is more severe
for Disease Control and Prevention,31,32 pled pattern that stands out in sclerotic and prolonged or is inadequately treated,
there has been a greater demand for better scatter. Using fluorescein stain, the micro- endothelial cells show increasing vascuolisa-
and safer alternatives. Enzymatic detergents cystic pattern is highlighted as a disruption tion, separation from Desçemet’s mem-
are supposed to be the answer. They contain in the tear film. At this point, the patient’s brane, desquamation into the anterior
subtilisin, an exotoxin, and alpha amylase vision will be reduced, most prominently in chamber and death, resulting in persisting
enzymes that are deactivated when exposed the morning. Progressive stromal oedema corneal oedema.
to temperatures exceeding 140°C. Nowadays results in a ground-glass appearance, with Desçemet’s membrane is remarkably
most autoclaves reach maximal tempera- marked thickening of the central cornea. resistant to the proteolytic enzymes elabo-
tures of 120°C to 130°C33 and hence, if The epithelial microcystic changes may rated by microorganisms, leukocytes and
surgical instruments are not rinsed thor- coalesce to form bullae, which can lead to epithelial cells. It resists destruction in the
oughly, residual active detergents are intro- epithelial erosions and fingerprint lines. presence of severe keratitis, iridocyclitis
duced into the eye and can be toxic for the Irregularity of the corneal surface and and endophthalmitis, and acts as a barrier
corneal endothelium. In vitro experiments stromal haze further reduce vision. Confocal that prevents the passage of leukocytes and
on both human and rabbit corneas have microscopy has aided in the diagnosis most microorganisms between the anterior
shown a dose-related increase in corneal of advanced Fuchs’ endothelial dystrophy, chamber and the corneal stroma.46 Fungi
thickness and corneal endothelial ultra- where corneal oedema may obscure visuali- are an exception; many elaborate enzymes
structural damage when exposed to enzy- sation of the endothelium.41 In end-stage enable them to penetrate Desçemet’s mem-
matic detergents. disease, infrequently seen today because of brane. Inflammation directed specifically at
Clinical and Experimental Optometry 96.6 November 2013 © 2013 The Authors
532 Clinical and Experimental Optometry © 2013 Optometrists Association Australia
Corneal oedema Costagliola, Romano, Forbice, Angi, Pascotto, Boccia and Semeraro
Desçemet’s membrane may also occur but it control. In a multicentre clinical trial com- instil the ointment at bedtime to prevent
is rare. paring prednisolone sodium phosphate, visual problems when instilled during the
1.0%, to placebo as adjunctive therapy for day.
the treatment of bacterial corneal ulcers, Another solution is an emulsion of
TREATMENT they found no overall difference in visual polyoxyethylene, which is a surface active
acuity after three months and no safety con- agent that has one hydrophilic and one
The treatment of corneal oedema depends
cerns with adjunctive corticosteroid therapy hydrophobic part on the molecule and
on the specific cause and the symptoms of
for bacterial corneal ulcers.54 Similarly, Pseu- probably extracts water from the epithelium
the individual patient. This can vary from no
domonas aeruginosa corneal ulcers do not by osmosis. Silicone oil (350 centistokes)
treatment in an asymptomatic patient with
appear to respond better to treatment than smooths the irregular corneal surface and
early Fuchs’ dystrophy to keratoplasty in a
other bacterial ulcers.55 has a mollifying effect that is clinically useful
patient with painful bullous keratopathy and
in epithelial oedema when instilled several
significant visual loss. A stepwise approach to
times a day.
the treatment of corneal oedema is the best
INTRAOCULAR PRESSURE Anhydrous glycerine is another hyper-
approach to follow. In the case of secondary
Both acute and chronic increase in IOP can tonic preparation that can have a dramatic
oedema (inflammation, infection, trauma,
lead to corneal oedema. In such cases, but transient effect on corneal oedema. As it
glaucoma et cetera) treatment must be
decreasing the IOP can improve or resolve is the most effective dehydrating agent used,
directed at eliminating the underlying
the corneal oedema and prevent further it causes considerable stinging on applica-
aetiology.
damage to endothelial cells. tion and gives rise to chronic conjunctival
Among the pressure-lowering agents, injection and photophobia. It is so irritating
Control of associated carbonic anhydrase inhibitors deserve that it should be instilled after application
abnormalities special attention for their relationship with of a topical anaesthetic. This agent is very
corneal oedema. Inhibition of corneal car- useful for diagnostic purposes, as it allows
INFLAMMATION / INFECTION bonic anhydrase pumps may decrease the better visualisation of the corneal layers and
Topical corticosteroids are effective and outflow of fluid from stroma to aqueous, the anterior chamber. In the case of corneal
useful in reducing anterior segment inflam- leading to corneal oedema. This class of damage by ultraviolet light, treatment
mation and consequently corneal oedema. pressure-lowering agents should be used should be accompanied by ascorbic acid, as
Dexamethasone suppresses the new lym- with caution in eyes with compromised it is a potent antioxidant that neutralises free
phatic vessel growth. These findings identify corneal endothelium. radicals.58
a novel mechanism of glucocorticoid action,
the suppression of corneal lymphangio- BANDAGE CONTACT LENS
genesis, through the suppression of Management of primary Placement of an extended-wear bandage
macrophage infiltration, pro-inflammatory corneal oedema contact lens on the cornea can provide relief
cytokine expression and direct inhibition of from the discomfort of bullous keratopathy
proliferation of lymphatic endothelial cells. HYPERTONIC AGENTS and is used in the setting of poor visual
The steroids block corneal lymphangiogen- Mild oedema can be treated with hypertonic potential or when surgical intervention
esis, which is the main risk factor for immune eye drops and ointment, aimed at increasing is not recommended or is delayed. The
rejections after corneal transplantation and the tonicity of the tear film and drawing fluid contact lens chosen should have high
herpetic stromal keratitis.47,48 The topical out of the cornea and into the tears by osmo- oxygen transmissibility. The use of a silicone
corticosteroid regimen used in herpetic sis;56,57 however, for an osmotic gradient to hydrogel or rigid gas-permeable lens is safe
stromal keratitis reduces persistence or occur, the epithelium has to be intact and to and effective for the treatment of bullous
progression of stromal inflammation.49 The function as a semi-permeable membrane keratopathy,59 although theoretically, the
different anti-lymphangiogenic potency of that allows water but not electrolytes to pass. rigid gas-permeable lenses provide more
these drugs should be taken into account Moreover, this treatment is most effective for total oxygen to the entire cornea.60 The
when using steroids in clinical practice. epithelial oedema, as stromal oedema is comfort provided by this modality must be
While older corticosteroids, such as dexam- usually caused by endothelial dysfunction. weighed against the risk of contact lens-
ethasone and prednisolone acetate, offer In selected patients, vision and comfort can induced infectious corneal ulcer. Regular
good anti-inflammatory efficacy, clinically often be improved for months and occasion- follow-up visits reduce the risk of complica-
significant increases in IOP (10 mmHg or ally years with this therapy. tions. In suspected cases, we use broad-
more) are often associated with their use. Hypertonic solution, such as five per cent spectrum fortified antibiotic drops after
Loteprednol etabonate offers potent anti- sodium chloride drops or ointment, can be appropriate laboratory workup. As a pre-
inflammatory efficacy but with decreased also used for the symptomatic medical treat- ventive measure, you can use an antibiotic
impact on IOP.50 Several researchers have ment of more advanced chronic corneal against Gram-negative organisms once per
investigated the effect of corticosteroids on oedema with epithelial bullae. These solutes day but we do not recommend it because it
endothelial cell function, suggesting that penetrate the epithelium poorly and there- can create resistance. In one study, antibiotic
they may induce activation of the pump fore, can attract the more easily diffusible use reduced the microbiota on the lids but
function.51–53 They can also be beneficial in water from the epithelial bullae. Sooner did not affect the microbiota of the throat or
corneal oedema, due to non-viral infections or later the oedema progresses and may change resistance to the antibiotic.61 In addi-
once the infectious component is well under require surgical treatment. We prefer to tion, the use of the lens on a cornea with an
© 2013 The Authors Clinical and Experimental Optometry 96.6 November 2013
Clinical and Experimental Optometry © 2013 Optometrists Association Australia 533
Corneal oedema Costagliola, Romano, Forbice, Angi, Pascotto, Boccia and Semeraro
already compromised endothelium should In conclusion, corneal oedema is a 18. Irvine AR Jr. The role of the endothelium in
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