Vol.14
No. 1, Januray, 2004
EDITORIAL
Pseudophakic
or Aphakic Bullous Keratopathy: Management Strategies and
Prevention
Corneal edema
resulting from cataract extraction is called pseudophakic or
aphakic bullous keratopathy. Pathologically, bullous
keratopathy is caused by changes in the corneal endothelium,
allowing the cornea to be in an abnormal state of hydration.
As endothelial cells are damaged,, the remaining cells
rearrange themselves to cover the posterior corneal surface.
These cells are shaped iregularly and enlarged. The
Descemet membrane is produced in increased amounts by any
pathologic process that affects the endothelial cells,
resulting in cornea guttata. As the endothelium becomes
increasingly unable to act as a pump to deturgesce the cornea,
the stroma begins to swell, especialy in the central cornea.
As the stroma swells, the cornea thickens and folds are seen
in the Descemet membrane. The edema may fluctuate in
response to changing intraocular pressure. Epithelial
edema manifests as fluid accumulation between the basal
epithelial cells. As more fluid accumulates, blisters,
and then bullae, develop.
Patients with
bullous keratopathy demonstrate decreased visual acuity and
pain or discomfort. Pain or discomfort associated with
corneal edema results from exposure of corneal nerves to an
often noxious environment. As the edema progresses and
bullae are formed, rupture of bullae results in pain,
photophobia, and epiphora.
Surgical
trauma, most commonly during cataract extraction, can damage
the endothelium, causing a period of postoperative edema that
resolves in most cases. Most corneas recover, but some
do not. Knowledge of the preoperative status of corneal
endothelium may help to reduce this complication. Preoperative
clinical specular microscopy is used to examine the quality
and quantity of endothelial cells. Significant
correlation has been found between variation in cell size and
the development of postoperative corneal edema. Endothelium
with a greater degree of pleomorphism reacts more adversely to
intraocular surgery and requires a longer time for corneal
deturgescence. The type of cataract surgery also has an
impact on how much trauma occurs to the endothelium.
Routine uncomplicated phacoemulsification surgery results in
9% endothelial cell loss 1 year postoperatively, while an
average of 16% endothelial cell loss is associated with phakic
anterior chamber intraocular lens surgery.
Regardless of
surgery type and whether an intraocular lens is implanted,
continuing endothelial loss greater than the usual 1% per year
occurs in patients who have had cataract extraction.
Corneal edema usually develops within 1 year after the
endothelial cell density falls below 500 cells/mm, but no
absolute lower limit to the number of cells has been found to
be associated with stromal edema. The type of lens
implanted also is significant in determining the amount of
endothelial cell loss over time. persistent low-grade
inflammation and intermittent contact of the implant with the
corneal endothelium may cause PBK.
While
mechanical trauma to the endothelium during surgery is
considered to be the most significant factor influencing
postoperative corneal edema, other factors can adversely
affect the endothelium. Toxic substances used to
disinfect instruments may inadvertently be introduced into the
eye, if inadequate rinsing of instruments allows some of the
substances to remain in the small lumens of the instruments.
Water, and not saline, should be used to rinse the
instruments. Viscoelastics can reduce touch between the
cornea and the intraocular lens during lens insertion, and
they can deepen the anterior chamber to minimize endothelial
damage in the event of a shallow anterior chamber.
Reusable cannulas with viscoelastic can result in toxic
residues being introduced into the eye; therefore, disposable
cannulas should be used whenever possible. Viscoelastics
are used routinely to maintain anterior chamber depth, to
protect the endothelium, and to facilitate placement of
intraocular lenses.
Therapy of
pseudophakic and aphakic bullous keratopathy is performed to
reduce discomfort or to increase visual acuity. The
corneal edema associated with bullous keratopathy is chronic
and usually non-inflammatory. A number of treatment
options are available. The reduction of intraocular
pressure is an important treatment for corneal edema, because
increased intraocular pressure can compromise endothelial
function and lead to epithelial edema and further endothelial
damage. Epithelial edema often can be managed with
topical hypertonic agents such as sodium chloride (5%)
ointment or drops. Hydrophilic contact lenses, on an
extended-wear basis, can be used to decrease pain associated
with epithelial bullae. It is thought that the lens acts
as an effective precorneal protective layer and shields the
abnormal epithelium from the environment and prevents bullae
from bursting. In the presence of low grade
inflammation, topical steroids can be useful, since low-grade
anterior uveitis, not infrequently, is associated with chronic
corneal edema.
Surgical
treatments for bullous keratopathy include conjunctival flap,
cauterization of the Bowman layer, anterior stromal
micropuncture, excimer laser phototherpeutic keratectomy (PTK),
annular keratotomy, and penetrating keratoplasty. A
conjunctival flap is an excellent manner to decrease painful
symptoms in eyes with painful bullous keratopathy.
Recently, amniotic membrane has been used successfully to
cover swollen corneas and to decrease pain. Neither of
these procedures tends to improve the vision.
Cauterization of the Bowman layer is performed for pain
relief. This procedure is thought to produce a dense
fibrous barrier between the corneal stroma and the epithelium
that fluid cannot permeate into the epithelial cells and
produce bullous changes. Anterior stromal micropuncture
and excimer laser PTK also have been used with some success to
cause scarring of the superficial cornea and to decrease
painful symptoms. Annular keratotomy has been used to treat
the pain associated with bullous keratopathy in eyes with poor
visual potential. A partial-thickness corneal incision
is made with a trephine and relieves pain by severing branches
of corneal ciliary nerves to decrease corneal sensation.
Penetrating keratoplasty is the only surgical treatment that
relieves pain, while attempting to restore visual acuity. In
patients with pseudophakic bullous keratopathy, the
intraocular lens may be removed or exchanged at the time of
transplant. Displaced lenses causing recurrent uveitis,
closed loop, or anterior chamber iris supported lenses
generally should be removed.
Surgical
techniques of cataract extraction have resulted in a reduction
in the number of bullous keratopathy cases; however, bullous
keratopathy still constitutes a major indication of
penetrating keratoplasty. Penetrating keratoplasty techniques
also have improved, but cystoid macular edema associated with
previous intraocular surgery may limit its effectiveness in
improving visual acuity. The decision to proceed with
penetrating keratoplasty must be made while fully aware of the
risks of infection, secondary glaucoma, and graft rejection,
but it still remains the treatment most likely to markedly
improve visual acuity.
Sudesh Kumar
Arya
Deptt. of Opthalmology
Govt. Medical College & Hospital, Chandigarh
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