| Lasikinformer 2005-07-09, 5:54 pm |
| Here are some excerpts from an article about LASIK dry eye. He forgets to
mention the nerve-cutting aspect
of the LASIK procedure ("suck, saw, and sizzle"), which should figure
prominently in any discussion of LASIK dry eye.
http://www.ophthalmologymanagement....p?article=86170
Minimizing Post-LASIK Dry Eye
BY ERIC DONNENFELD, M.D., F.A.C.S.
Dry eye following LASIK is arguably the most common problem facing
refractive surgeons today. All refractive procedures, and especially LASIK,
impact ocular surface and tear film dynamics. They affect corneal sensation,
aqueous tear production, wound healing, and the incidence of epithelial
defects.
With LASIK, interaction between the ocular surface and the eyelid is
affected because the excimer laser alters the anterior curvature of the
cornea by removing stromal tissue.
LASIK-associated dry eye can be caused by:
? high pressure induced by the suction ring during flap creation, which may
damage the conjunctival goblet cells and compromise the mucin layer of the
tear film.
? significant alterations to the corneal curvature that occur after LASIK,
which alter tear wetting as the lids move over the modified ocular surface
? medicamentosum caused by epithelial-toxic antibiotics, nonsteroidal
anti-inflammatory (NSAID) drops, and preservatives such as benzalkonium
chloride (BAK), which may induce transient dry eye symptoms.
Because intact corneal sensation drives tear production, corneal denervation
associated with LASIK is the most significant cause of post-LASIK dry eye.
During LASIK, the corneal nerve trunks are severed by the microkeratome, and
the anterior stromal nerves are disrupted by photoablation. Both processes
damage corneal innervation. The reduction in corneal neuronal feedback to
the brain stem reduces brain stem innervation of the lacrimal glands,
diminishing tear production.
Sensory Denervation: A Self-Perpetuating Cycle
The recognition that the ocular surface and the lacrimal glands function as
an integrated unit represents a major advance in our understanding of dry
eye syndrome. Communication between the ocular surface and the lacrimal
glands occurs through a sensory/autonomic neural reflex loop. The sensory
nerves innervating the ocular surface connect with efferent autonomic nerves
in the brain stem that stimulate secretion of tear fluid and proteins by the
lacrimal glands. Ocular surface sensitivity lessens as aqueous tear
production and clearance decrease, which exacerbates dry eye because the
decreased sensory-stimulated reflex tearing diminishes the ability of the
lacrimal glands to respond to ocular surface insults, creating a
self-perpetuating cycle between the lacrimal glands and the ocular surface.
The anesthetic cornea created by the LASIK flap and photoablation worsens
dry eye by reducing the afferent pathways from the cornea to the brain stem,
which reduces the efferent signal from the brain stem to the lacrimal glands
to produce tears. It has been reported that even with unaltered tear
production post-LASIK there is corneal staining, leading to the notion that
neurotrophic keratitis rather than dry eye may be responsible for some of
the corneal changes following LASIK.
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