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Contact complications as requested by Joycweb
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| The other link I provided today is not the one I meant to post.
Here's the one I intended to post. I couldn't find it on a google
search earlier. This link is the a-to-z of contact lens
complications.
http://www.emedicine.com/OPH/topic651.htm
The scariest part of the article is that it claims:
"Approximately 1 out of every 20 contact lens wearers develops a
contact lens–related complication each year. These problems range from
self-limiting to sight threatening, which require rapid diagnosis and
treatment to prevent vision loss"
========================================
Contact Lens Complications
Last Updated: September 1, 2004 Rate this Article
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AUTHOR INFORMATION Section 1 of 9
Author Information Introduction Lids Tear Film Conjunctiva Corneal
Epithelium Corneal Stroma Corneal Endothelium And Summary Bibliography
Author: John Stamler, MD, PhD, Clinical Assistant Professor,
Department of Ophthalmology, university of Iowa
John Stamler, MD, PhD, is a member of the following medical societies:
American Academy of Ophthalmology, and Sigma Xi
Editor(s): Andrew Lawton, MD, Medical Director of Neuro-Ophthalmology
Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health
Medical Center; Donald S Fong, MD, MPH, Assistant Clinical Professor
of Ophthalmology, UCLA School of Medicine; Consulting Physician,
Department of Ophthalmology, Southern California Permanente Medical
Group; Christopher J Rapuano, MD, Co-Chairman of Refractive Surgery
Department, Associate Professor, Cornea Service, Wills Eye Hospital,
Jefferson Medical College; Lance L Brown, OD, MD, Ophthalmologist,
Regional Eye Center, Affiliated With Freeman Hospital and St John's
Hospital, Joplin, Missouri; and Hampton Roy, Sr, MD, Clinical
Associate Professor, Department of Ophthalmology, university of
Arkansas for Medical Sciences
INTRODUCTION Section 2 of 9
Author Information Introduction Lids Tear Film Conjunctiva Corneal
Epithelium Corneal Stroma Corneal Endothelium And Summary Bibliography
Approximately 1 out of every 20 contact lens wearers develops a
contact lens–related complication each year. These problems range from
self-limiting to sight threatening, which require rapid diagnosis and
treatment to prevent vision loss. With millions of individuals wearing
contact lenses, even a small percentage of complications create a
major public health problem. Contact lens complications are as varied
as they are common, involving the lids, conjunctiva, and all layers of
the cornea (ie, epithelium, stroma, endothelium). It is convenient to
group them according to which anatomical structure is primarily
affected. LIDS Section 3 of 9
Author Information Introduction Lids Tear Film Conjunctiva Corneal
Epithelium Corneal Stroma Corneal Endothelium And Summary Bibliography
A rigid contact lens can dislocate from the cornea and settle into the
upper fornix. Eventually, the lens may erode through the conjunctiva
and enter the soft tissues of the lid where it can remain relatively
asymptomatic. Alternatively, the tissues around the contact lens can
become irritated and inflamed producing a sterile abscess. The lens
foreign body can incite the formulation of granulation tissue around
the lens, encapsulating it in a cystlike structure.
A mechanical ptosis occasionally is the result of the mass of lens,
scar, and fibrous tissue in the lid. An embedded contact lens also can
produce enough scarring and contraction of the lid tissues to produce
a lid retraction. The contact lens need not migrate into the lid
tissues to produce ptosis. A ptotic lid can result simply from severe
giant papillary conjunctivitis (GPC).
Often, ptosis can be seen in contact lens wearers without any
inflammation, lens migration, or other definite cause. Hard contact
lens wearers may develop ptosis from levator aponeurosis disinsertion
from years of repeated stretching of the lid during lens removal. A
second proposed mechanism is that the repeated trauma of the lens edge
rubbing against the palpebral conjunctiva produces chronic
inflammation and edema in the soft tissues of the lid. Because all or
part of the ptosis may resolve with discontinuation of contact lens
wear, it is recommended that patients stop wearing their lenses for a
period of time prior to surgical correction of the ptosis. TEAR FILM
Section 4 of 9
Author Information Introduction Lids Tear Film Conjunctiva Corneal
Epithelium Corneal Stroma Corneal Endothelium And Summary Bibliography
The tear film provides a smooth and transparent refractive surface,
essential moisture, and oxygen to the epithelial cells. Tears also
contain immunoglobulins, complement, and other proteins, which help
protect against infection. The health of the ocular surface is
entirely dependent upon an adequate quantity and quality of tear film,
both of which can be altered by the presence of contact lenses.
Bacteria and debris are collected in the tear film, wiped by the lid
blink, and rinsed away from the surface of the eye. The presence of a
contact lens on the eye substantially reduces the interchange of tears
across the ocular surface. Rigid lenses reduce the tear exchange
compared to no contact lens wear. Soft lenses reduce the tear exchange
to an even greater extent and the larger the diameter, the greater the
reduction.
The effect of contact lenses on the tear film can vary from one part
of the cornea to another part of the cornea. Tear film instability
exists in the interpalpebral fissure in the periphery of the cornea,
the so-called 3- and 9-o'clock areas, in wearers of rigid contact
lenses. It is typical for rigid lenses to produce corneal staining at
these sites. Epithelial damage in these areas is associated with
instability and abnormalities in the mucin layer of the tear film.
In addition to the mixing of tears, the content of the tears can be
altered by the presence of contact lenses. Overnight wear increases
the levels of tear proteins compared to daily wear or no wear of
contact lenses.
Quick Find
Author Information
Introduction
Lids
Tear Film
Conjunctiva
Corneal Epithelium
Corneal Stroma
Corneal Endothelium And Summary
Bibliography
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Continuing Education
CME available for this topic. Click here to take this CME.
Patient Education
Eye and Vision Center
Contact Lenses Overview
Causes for Contact Lenses
Contact Lenses Symptoms
Contact Lenses Treatment
CONJUNCTIVA Section 5 of 9
Author Information Introduction Lids Tear Film Conjunctiva Corneal
Epithelium Corneal Stroma Corneal Endothelium And Summary Bibliography
Conjunctival Abnormalities
Contact Allergy
A contact dermatitis hypersensitivity reaction can be produced by one
of a host of chemicals, which are found in contact lens solutions. A
typical reaction consists of marked itching with varying amounts of
injection, burning, redness, tearing, mucoid discharge, and
occasionally chemosis. In addition, the lid may become edematous and
erythematous. Cold compresses and the elimination of the offending
chemical usually relieves symptoms. A short course of topical steroids
can be used in particularly severe instances.
Giant Papillary Conjunctivitis
Approximately 1-3% of contact lens wearers eventually develop a
symptom complex of GPC consisting of conjunctival injection, mucoid
discharge, itching, tear film debris, coated lenses, blurred vision,
excess lens movement, and blurred vision. These symptoms may remain
minimal or progress to complete lens intolerance. The tarsal
conjunctiva becomes inflamed and hypertrophied. This inflammatory
hypertrophy is morphologically similar to the papillary hypertrophy of
vernal conjunctivitis.
The etiology of GPC is multifactorial and begins with the formation of
deposits on the surface of the lens. The constant trauma of the
blinking lid rubbing on the surface of the lens exposes the deposits
to the conjunctival lymphatic system. The antigens associated with the
deposits incite an immune response in the conjunctiva. This condition
can occur whenever a foreign substance chronically rubs the tarsal
conjunctiva, such as ocular prostheses, exposed scleral buckles, nylon
sutures, and gas-permeable contact lenses but most commonly is
associated with soft contact lenses.
Typically, papillae 0.3 mm or larger are seen surrounded by thickened
and hypervascular conjunctiva. The hyperplastic epithelium extends
down into the underlying stoma. The epithelium is infiltrated with
mast cells and the stroma is infiltrated with basophils and
eosinophils. The symptoms of GPC are exacerbated by anything that
increases the contact of the lens deposits with the tarsal conjunctiva
(increased numbers of deposits, increased size of the contact lens,
and increased wearing time, especially overnight wear).
Treatment of GPC consists of reducing the amount of contact between
the deposits and the conjunctiva. Frequent enzymatic cleaning of the
contact lenses, frequent replacement of contact lenses (disposable
lenses), reduction in wearing time, and the use of lenses that resist
deposit formation are effective treatments.
Medications that suppress the immune response also can be used.
Topical steroids also reduce symptoms; however, the risk of
complications limits their use. Topical mast cell stabilizers, such as
4% cromolyn, have some effectiveness in reducing symptoms of GPC.
Medical treatments generally are used for a short duration in acute
exacerbations. The most effective treatment usually is reduced wearing
time and switching to disposable contact lenses.
Contact Lens–induced Superior Limbic Keratoconjunctivitis
Contact lens–induced superior limbic keratoconjunctivitis (CL-SLK) is
an immunologic reaction in the peripheral conjunctiva produced by
contact lens wear that is similar to that seen in Theodore superior
limbic keratoconjunctivitis (SLK). It is characterized by conjunctival
thickening, erythema, and a variable amount of fluorescein staining of
the superior bulbar conjunctiva.
The keratinized epithelium loses many of its goblet cells and is
invaded by neutrophils. Foreign body sensation, photophobia, tearing,
burning, occasional itching, and reduced visual acuity due to punctate
epitheliopathy are typical symptoms of CL-SLK.
Although similar in name, CL-SLK is a separate and distinct entity
from Theodore SLK. CL-SLK can be differentiated by a lack of
filaments, minimal tarsal papillary reaction, impaired vision, and
lack of association with thyroid disease. It also is not limited to
the superior conjunctiva but can be circumferential.
CL-SLK may be caused by excessive lens movement or sensitivity to
thimerosal. Treatment consists of discontinuing contact lens wear
until the epithelium returns to normal and the symptoms resolve.
Refitting with better fitting lenses, using preservative-free
solutions with a hydrogen peroxide disinfecting system or switching to
rigid gas-permeable (RGP) contact lenses may permit a resumption of
contact lens wear. CORNEAL EPITHELIUM Section 6 of 9
Author Information Introduction Lids Tear Film Conjunctiva Corneal
Epithelium Corneal Stroma Corneal Endothelium And Summary Bibliography
Mechanical Epithelial Defects
The contact lens is a foreign body, which rubs across and is pressed
against the corneal epithelium with each blink, thousands of times
each day. Surprisingly, this only occasionally results in an abrasion.
Corneal abrasions from contact lens wear need to be recognized and
treated because they indicate chronic epithelial stress due to the
contact lens. Epithelial defects can allow bacteria to penetrate the
cornea, resulting in a stromal infection. Chronic corneal epithelial
trauma can stimulate subepithelial fibrosis in the absence of an
infection. The specific abrasion pattern often provides the necessary
clues to indicate what problem can be corrected to improve the comfort
and safety of the patient.
Manipulation of a contact lens during insertion and removal can
traumatize the epithelium creating painful abrasions of a variety of
shapes and sizes. These abrasions usually heal quite rapidly with
simple lubrication or patching. Debris trapped under a contact lens or
a chip or tear in the edge of a contact lens can produce dramatic
curvilinear abrasions. Removal of the debris or replacement of the
damaged contact lens is all that is needed to treat this problem.
Punctate epithelial erosions occur commonly with contact lens wear and
have several causes. Three staining patterns are characteristic for
rigid lenses, as follows: central, peripheral, and 3- and 9-o'clock
positions. If a lens is too flat for the particular cornea, it may
produce central punctate staining. A steep cornea, such as in
keratoconus where the lens rubs on the tip of the cone, is a typical
example. A lens that is too steep for the cornea can produce
peripheral punctate staining patterns, often in a superior arcuate
shape. A poorly moving lens or one with a large optical zone may
produce superior arcuate staining.
The most common staining pattern occurs between the lens and the
limbus in the interpalpebral fissure (at the 3- and 9-o'clock
positions). This epitheliopathy is caused by the contact lens lifting
the lid away from the cornea and poor tear stability with subsequent
drying of the cornea. This often is exacerbated by an incomplete
blink. A small amount of 3- and 9-o'clock staining is benign, but
persistent epithelial erosions can lead to dellen formation,
neovascularization, Salzmann-type elevated lesions and pseudopterygium
formation. This type of punctate staining is alleviated by decreasing
the distance from the lens to the limbus with a larger lens, reducing
edge lift with a thinner-edged lens or steeper fit, or refitting with
a lens that rests under the upper lid (alignment fit).
Punctate staining by soft lenses is not as common as with rigid lenses
but can occur. Soft lenses that cause excessive desiccation can cause
an inferior central or inferior arcuate pattern. Usually, these
patients have minor symptoms of mild irritation or slightly decreased
vision. Refitting with a higher water content lens or RGP lens usually
eliminates the problem.
Epithelial splitting is a common finding in asymptomatic soft contact
lens wearers. This finding often is overlooked on a routine
examination because it usually does not cause severe symptoms and may
be covered by the upper lid. Epithelial splits are horizontal, linear,
white, faintly staining epithelial defects in the superior cornea,
which often are asymptomatic during lens wear and produce mild foreign
body sensation after the lens has been removed. The splits usually
heal after the lenses have been out for 24 hours and refitting with
RGP lenses prevents recurrence.
Chemical Epithelial Defects
Various contact lens chemical solutions can produce a range of
epithelial defects from marked erosions to less extensive punctate
defects. Surfactant cleaning solutions that are left on the lens after
cleaning usually cause immediate pain, redness, photophobia, and
tearing upon lens insertion. These symptoms typically disappear after
1 or 2 days.
If hydrogen peroxide is placed on the eye, it can cause
intraepithelial and subepithelial gas bubbles. These bubbles have a
dramatic appearance and can cause significant but usually temporary
vision loss. The bubbles typically resolve without permanent sequelae
within minutes to hours. However, hydrogen peroxide can cause a
permanent refractive change by altering the shape of the cornea.
Enzyme cleaner and chemical disinfection solutions can cause more
subtle and intermittent punctate epithelial defects. This condition
may require careful investigation and systematic elimination of
various lens care products to identify and remove the offending agent.
Use of preservative-free solutions and proper use of hydrogen peroxide
disinfection usually solves this problem.
Hypoxia
Because the oxygen requirements of the cornea are met by direct
diffusion of oxygen from the corneal surface, the barrier of the
contact lens reduces the amount of available oxygen. Contact lens wear
(especially with a closed lid during sleep) can cause acute hypoxia.
If mild, hypoxia produces epithelial edema and temporary blurred
vision; if severe, it can cause epithelial cell death and
desquamation. Patients usually experience discomfort and remove the
contact lenses before the acute hypoxia becomes severe. Typically, the
conjunctiva is hyperemic and the epithelium has fine punctate defects,
producing temporary decreased vision and photophobia.
Chronic hypoxia produces a variety of more subtle effects such as
epithelial microcysts. Contact lens users who sleep in their lenses
are prone to developing epithelial microcysts. These transparent
epithelial inclusions of degenerated epithelium are about 10-15 mm,
begin in the deep epithelium, and slowly migrate anteriorly. Upon
reaching the surface, they rupture, creating depressions that pool
with fluorescein. Epithelial microcysts seldom produce any significant
symptoms other than mild decrease in vision. Surprisingly, it takes
several weeks for the microcysts to disappear after discontinuation of
the contact lenses. Either the mitotic rate is reduced below normal or
the microcysts continue to be produced long after the contact lenses
are removed.
One of the hallmarks of chronic corneal hypoxia is superficial
neovascularization, especially along the superior limbus.
Neovascularization of less than 2 mm from the limbus is not visually
significant and generally is well tolerated but is a sign of hypoxia
and may be a harbinger of more significant problems. Rarely, deep
stromal neovascularization can occur. Changing to lenses that are
thinner or contain materials with greater oxygen permeability, have
greater lens movement, and decreasing wear time (especially
eliminating overnight wear) can greatly reduce the risk of
progression.
Chronic hypoxia has been implicated as a cause of the decreased
corneal sensitivity that occurs with prolonged contact lens wear and
may be partly the reason why some patients have increased comfort with
long-term wear and why they often have decreased comfort with a change
from polymethyl methacrylate (PMMA) to gas-permeable contact lenses.
The corneal epithelium is thinner in contact lens wearers. This change
may be due to chronic hypoxia and decreased mitotic activity. In
addition to thinning of the epithelium, extended wear is associated
with decreased epithelial shedding, increased cell size, and increased
binding of Pseudomonas aeruginosa to the cell surface. All of these
effects could reduce the resistance of the cornea to bacterial
infection. The thinner epithelium poses less of a barrier to bacterial
penetration. The reduced shedding of epithelial cells allows the
attached bacteria to remain on the eye for longer periods of time. The
increased binding of bacteria, such as P aeruginosa, enables greater
numbers of bacteria to attach to the epithelial surface.
The physiology of the corneal epithelium also is altered by contact
lens wear. The barrier function of the epithelium is reduced and the
permeability to fluorescein is doubled after as little as 2 weeks of
soft contact lens wear. Similarly, rigid contact lenses can alter the
epithelial permeability.
Superficial Immunologic Reactions
A variety of chemicals in contact lens solutions can elicit
superficial toxic or immune reactions. The typical response is a fine
punctate keratopathy, conjunctival injection, tearing, itching, and
occasionally chemosis.
The preservative, thimerosal, which is now rarely used, produced a
keratoconjunctivitis in as many as 10% of contact lens wearers who
used thimerosal-preserved products. Essentially, it has disappeared
from use but other chemicals used as preservatives or disinfectives
can produce similar pathology, so recognition of this condition is
helpful.
The earliest symptoms are mild and nonspecific (eg, foreign body
sensation, conjunctival hyperemia, variable mixed follicular-papillary
hypertrophy), which present gradually after weeks or years of
uneventful contact lens wear. The superior limbus becomes
progressively more hyperemic and a triangle of punctate keratopathy
extends downward from involved limbus toward the central cornea. If
allowed to proceed, the epitheliopathy may progress to an opaque
pannus with microcysts.
A problem associated with the use of chemical disinfection systems and
seen with increasing frequency is the development of small, gray,
epithelial, granular opacities that resemble the epithelial opacities
of Thygeson superficial punctate keratopathy. The round, gray-white
granules appear to be on the surface of the epithelium and are
scattered randomly across the cornea. They are similar to Thygeson
superficial punctate keratopathy, but they tend to be small and stain
less intensely with fluorescein. These opacities are associated with
symptoms of foreign body sensation, tearing, photophobia, lens
intolerance, and conjunctival injection. The symptoms resolve over a
few days after the chemical disinfecting solution is discontinued.
Thimerosal and other chemicals used in disinfection systems also can
produce subepithelial infiltrates similar to those seen in adenoviral
conjunctivitis. Changing to a preservative-free hydrogen peroxide
based disinfection system or to gas-permeable lenses allows these
deposits and infiltrates to resolve. However, it may take weeks for
the pathology to disappear. CORNEAL STROMA Section 7 of 9
Author Information Introduction Lids Tear Film Conjunctiva Corneal
Epithelium Corneal Stroma Corneal Endothelium And Summary Bibliography
Sterile Infiltrates
Contact lens wear can induce a distinctive sterile keratitis, which
presents as a sudden onset of an anterior stromal or subepithelial
polymorphonuclear leukocyte and mononuclear cell infiltrate typically
in the periphery of the cornea. The infiltrates usually are small
(0.1-2 mm) and may be single or in groups. The infiltrates may be
round, oval, or arcuate and may underlie either an intact epithelium
or an epithelial defect.
Histologic examination of biopsy specimens of these infiltrates
reveals focal areas of full-thickness loss of epithelium with
surrounding thin areas of epithelium. The polymorphonuclear leukocyte
infiltrates were localized directly under the Bowman layer, and patchy
areas of necrosis were present. The specimens did not reveal any
microorganisms.
The etiology of these sterile infiltrates may involve an
immune-mediated reaction to bacterial toxins from colonized contact
lenses. Staphylococcal organisms have been isolated from contact lens
wearers that have sterile infiltrates. The infiltrates tend to resolve
with no loss of vision leaving behind only a faint scar in the
anterior stroma after a short course of topical steroids or simple
elimination of contact lens wear.
Usually, sterile infiltrates can be differentiated from infectious
infiltrates on clinical signs and symptoms alone. Sterile infiltrates
tend to be multiple, peripheral, associated with less pain, minimal
anterior chamber inflammation, and with less of an epithelial defect
than infectious ulcers. However, if doubt exists, they should be
treated as presumed infectious ulcers.
Bacterial Infectious Keratitis
Microbial keratitis is an uncommon but potentially devastating
complication of contact lens wear. The eye is under constant threat of
infection by bacteria present on the lids and in the tears.
Fortunately, the eye has many defense mechanisms with which to fend of
the bacterial invaders.
The lids constantly wipe the ocular surface, mechanically dislodging
bacteria and epithelial cells from the surface. The constant flow of
tears across the eye continually washes away bacteria and debris from
the eye and into the nasolacrimal ducts. The tears not only have a
dilutional effect but also contain immunoglobulins, lysozyme, and
compliment, which can inactivate potential pathogens.
The multiple layers of epithelial cells provide a formidable barrier
to bacterial infection. The mucin-coated surface is resistant to
bacterial adhesion. The constant shedding of desquamating epithelial
cells rid the eye of attached bacteria. The multiple layers of
epithelial cells give the ocular surface extra security. If one layer
of cells is penetrated, it can be sloughed, while the remaining layers
remain to provide continued protection.
The cornea is richly innervated with sensory nerves, which respond to
bacterial toxins, inflammation, and epithelial defects. The resulting
pain increases tearing and blinking resulting in increased protection.
All of these protective mechanisms are affected adversely by contact
lens wear. The contact lens is a barrier between the epithelial
surface and the lid preventing the wiping action of the lid. Tear
exchange is reduced markedly under the contact lens, creating a
stagnant pool of tears next to the cornea.
Contact lens wear reduces the thickness of the epithelium, the rate of
cell turnover and desquamation, and increases the ability of bacteria
to adhere to epithelial cells. With the reduced corneal sensitivity
associated with contact lens wear, the early stages of infection may
not be felt as much; thus, the reflex tearing and blinking responses
may be blunted.
Contact lenses also cause breaks in the epithelium (punctate erosions,
abrasions, and splits), which allow direct access of pathogens to the
stroma. The epithelium of the contact lens wearer is thinner, less
sensitive, and relatively hypoxic; all of these factors reduce the
ability of the epithelium to repair itself and repel invading
organisms.
One in 2,500 daily contact lens wearers and 1 in 500 overnight wearers
in the US develop bacterial keratitis each year. A variety of both
gram-positive and gram-negative organisms have been isolated from
corneal infections. However, the most commonly cultured pathogens have
been P aeruginosa, Staphylococcus aureus, and Staphylococcus
epidermidis. This trend may be changing in the direction of increased
frequency of gram-positive organisms. The high association of P
aeruginosa may be because of its ability to invade corneal epithelial
cells.
Case reports of contact lens–associated corneal infections first
appeared in the ophthalmic literature 2 decades ago. Contact lenses
were implicated as a causative factor, but it was not until the
hallmark studies of Schein and colleagues that the incidence and
relative risk of contact lens–associated corneal infections was
elucidated. They found the incidence of ulcerative keratitis in New
England to be 4.1 in 10,000 daily contact lens wearers per year.
Incidence in extended contact lens wearers was even greater at 20.9
per 10,000. When the actual wearing patterns of users were studied,
they found that patients who slept in their lenses had a 10- to
15-fold higher risk of developing an infection. Incidence in the
United Kingdom and the Netherlands is similar.
The introduction of disposable lenses did not reduce the risk of
infection; in fact, the risk of infectious keratitis in disposable
lens wearers was increased relative to daily wear soft or
gas-permeable lenses. More recent studies also have found the risk of
microbial keratitis to be increased with disposable contact lenses
even when other risk factors were controlled. However, the primary
risk factor for developing contact lens–related bacterial keratitis is
sleeping with the lenses in. Similar to cosmetic contact lenses,
aphakic extended wear increases the risk of infection.
Surprisingly, and contrary to common supposition, poor lens hygiene
does not appear to increase this risk of contact lens–associated
bacterial keratitis. Perhaps this is because contact lenses become
contaminated with bacteria shortly after they are placed on the eye
and approximately one half of contact lens disinfecting solutions have
been found to be contaminated with bacteria.
Breaks in the corneal epithelium probably are important predisposing
factors to bacterial keratitis. However, they are not a necessary
precondition. P aeruginosa can penetrate intact epithelium, and
bacterial keratitis can occur on the surface of the intact epithelium.
The symptoms of bacterial keratitis usually present acutely (within 24
h) and include pain, photophobia, tearing, purulent discharge, and
reduced vision. Early in the course of the disease a whitish-to-yellow
stromal infiltrate develops under an epithelial defect in the presence
of anterior chamber reaction and conjunctival injection. This
progresses to stromal and epithelial edema, anterior chamber reaction,
hypopyon, and eventually, stromal necrosis. Often gram-negative
bacteria induce an immune precipitate (Wessely ring) to form around
the nidus of infection.
The firm diagnosis of bacterial infection is made with a positive
culture; however, even with the best culture techniques, cultures
often are negative and treatment must be empirical. The mainstay of
treatment has consisted of broad-spectrum topical antibiotics (eg,
combination of cefazolin 50 mg/mL and tobramycin 14 mg/mL)
administered at frequent intervals, starting at every 15-30 minutes,
and less frequent as the clinical response allows. These doses of
antibiotics are quite toxic and need to be tapered to prevent
epithelial damage.
Ciprofloxacin 0.3% and ofloxacin 0.3% may be as effective in treating
bacterial keratitis as the traditional combination of fortified
antibiotics and are commercially available. However, with the
ever-changing spectrum of microbial resistance, it is recommended to
culture every serious keratitis and treat according to the antibiotic
sensitivities. Fortunately, with prompt antibiotic therapy most
bacterial corneal infections can be cured with little sequelae.
Acanthamoeba Keratitis
The protozoan, Acanthamoeba, causes a particularly difficult infection
to treat. Acanthamoeba is found widely in nature and has been isolated
from random samples of soil, water, and air. It can gain access to
contact lens solutions and contact lenses from any of these sources,
but tap water is a common culprit. Tap water should never be used to
rinse contact lenses, store contact lenses, or make saline solution
because of the risk of Acanthamoeba infection.
The symptoms of infection occur more gradually than in bacterial
keratitis. It often takes several days or weeks before the symptoms
progress to the point that the patient seeks attention. The early
signs and symptoms are foreign body sensation, mild blurred vision,
and redness. This progresses to pain, conjunctival injection, rough
epithelium, and thickened corneal nerves on slit lamp examination. As
the infection progresses, the pain becomes severe, out of proportion
to the apparent amount of inflammation, and a characteristic central
ring infiltrate forms.
Acanthamoeba feed on bacteria and are cultured on a lawn of
Escherichia coli. Corneal scrapings or biopsy specimens are placed on
the E coli-layered agar and inspected for the characteristic tracks
that the trophozoites make as they eat their way across the dish.
Diagnosis and therapy are both aided by scraping a large amount of
epithelium for culture. Acanthamoeba cysts also can be identified from
corneal scrapings using Giemsa and calcofluor white stains.
The Acanthamoeba organism exists in 2 states, motile trophozoite and
dormant cyst. The cyst form has great resistance to amebicidal drugs
and can lie dormant in the cornea for months. Therefore, topical
antimicrobials are started at a high frequency of every hour and
reduced according to the severity of the toxicity and symptoms. The
traditional therapy of propamidine (Brolene) and neomycin (Neosporin)
supplemented with miconazole, clotrimazole, and oral ketoconazole is
being replaced by polyhexamethylene biguanide (PHMB). In a
concentration of 0.02%, PHMB if effective in killing both cysts and
trophozoites of many different strains and displays relatively little
corneal toxicity. Therapy is continued every 1-2 hours until clinical
improvement is evident, which often is 1-2 weeks. The frequency of
dosing is reduced gradually to 4 times a day. Treatment usually is
continued for a number of months until all inflammation has resolved.
Therapy with PHMB is complicated by the lack of commercially available
solution. PHMB is not licensed for ocular use in any country. However,
the compound is readily available and several pharmacies are willing
to formulate the proper dosage and ship the preparation.
Prognosis depends greatly on how early in the course of the disease
the infection is diagnosed and therapy instituted. If caught early,
medical cures are usual. However, if it progresses to the ring
infiltrate stage, which typically takes about 6 weeks, a medical cure
is quite difficult and surgery may be required. Amoeba other than
Acanthamoeba also can cause an infectious keratitis. The amoebae
Vahlkampfia jugosa and Naegleria species have been cultured from the
contact lenses of patients with keratitis. The former patient
responded well to treatment of PHMB and the later was lost to
follow-up.
Tight Lens (Acute Red Eye) Syndrome
A contact lens occasionally can become tightly adherent to the eye and
produce marked, diffuse stromal inflammation and an anterior chamber
reaction. The resultant pain, photophobia, injection, and tearing are
typically acute and severe. The epithelium has punctate staining,
diffuse or peripheral infiltrates in the anterior stroma. The symptoms
resolve with removal of the contact lens; the infiltrates may take a
few days to disappear. A short course of topical steroids will speed
the resolution of the symptoms.
Corneal Warpage
Prolonged contact lens wear may produce gradual and unpredictable
changes in the contour of the cornea-corneal warpage. The astigmatism
or the general steepness may be either increased or decreased.
Typically, corneal warpage produces an irregular astigmatism, which
reduces the best spectacle correction. Corneal warpage commonly is
seen with hard lenses but also can occur with soft contact lens wear.
Corneas usually regain a stable and regular shape after
discontinuation of the contact lenses, but it may take weeks or even
months.
Contact Lens–induced Keratoconus
The possibility of a causal relationship between keratoconus and
contact lenses is controversial. A high percentage (20-30%) of
patients with keratoconus have worn contact lenses at the time of
diagnosis; however, no causal connection may exist because patients
with keratoconus tend to have myopia and irregular astigmatism, they
would be expected to prefer rigid contact lenses to spectacles.
The strongest evidence to support the hypothesis that wearing contact
lenses can cause keratoconus in certain susceptible individuals has
been presented by Macsai and colleagues. In their series of patients
with keratoconus, a difference existed in those who wore contact
lenses at the time of diagnosis (older age, flatter corneas, and more
superior cones) than those who wore glasses when diagnosed. They also
reported 2 patients who wore contact lenses in only 1 eye and
developed keratoconus in only that eye. This evidence is very
suggestive that long-term wear of contact lenses can produce
keratoconus in susceptible individuals.
The concept that structural changes in the corneal stroma can be
produced by contact lenses is supported by studies, which have found a
correlation between a reduced thickness, an increased steepness, and a
greater irregularity in the corneas of long-term contact lens wearers
compared to normals. Furthermore, keratocyte density appears to be
reduced in contact lens wearers.
The myopic progression found in adolescents does not appear to be
influenced by contact lens wear. In this study, 175 adolescents aged
11-14 years were assigned randomly to spectacle or contact lens wear.
After 3 years, no difference was noted in spherical equivalent change.
Contact lenses wear did not increase or decrease the amount of myopia.
CORNEAL ENDOTHELIUM AND SUMMARY Section 8 of 9
Author Information Introduction Lids Tear Film Conjunctiva Corneal
Epithelium Corneal Stroma Corneal Endothelium And Summary Bibliography
Corneal Endothelium
Contact lens wear also may compromise the corneal endothelium. Wearers
have a greater variation in endothelial cell size (polymegethism) and
an increased frequency of nonhexagonal cells (polymorphism) than do
nonwearers. Along with the dramatic alteration in endothelial cell
morphology, a small decrease in endothelial cell density also has been
found in long-term contact lens wearers in both soft and PMMA lenses
and in RGP.
Deswelling rates are reduced in contact lens wearers and may indicate
a compromised pump reserve or increased endothelial cell permeability
in these corneas. However, using fluorophotometric methodology, Bourne
et al were unable to demonstrate any significant differences in
permeability or pump function in contact lens wearers. Therefore, it
appears clear that morphological changes occur in the endothelium with
contact lens wear. However, it is not clear that this difference in
morphology is translated to a difference in function.
Summary
All eyes are altered by contact lens wear. Abnormalities of the lids,
conjunctiva, epithelium, stroma, and endothelium are produced. The
changes run the gamut from incidental findings without any apparent
functional significance to severely painful and sight-threatening
pathology. Fortunately, the large majority of contact lens wearers
enjoy the benefits of comfort and excellent vision without
experiencing any significant ill effects. The more we learn about the
complications of contact lens wear, the more we can help our patients
treat and avoid them.
Patient Education
For excellent patient education resources, visit eMedicine's Eye and
Vision Center. Also, see eMedicine's patient education article Contact
Lenses. BIBLIOGRAPHY Section 9 of 9
Author Information Introduction Lids Tear Film Conjunctiva Corneal
Epithelium Corneal Stroma Corneal Endothelium And Summary Bibliography
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"RM" <rm@yahoo.com> schreef in bericht
news:ld9bm0pf7kirv4s1abbqv7o4623efi6139@4ax.com...
> The other link I provided today is not the one I meant to post.
> Here's the one I intended to post. I couldn't find it on a google
> search earlier. This link is the a-to-z of contact lens
> complications.
>
> http://www.emedicine.com/OPH/topic651.htm
>
> The scariest part of the article is that it claims:
> "Approximately 1 out of every 20 contact lens wearers develops a
> contact lens-related complication each year. These problems range from
> self-limiting to sight threatening, which require rapid diagnosis and
> treatment to prevent vision loss"
>
Ragnar or should I say Sandy.(IMHO two of a kind)
Ragnar, this is exactly the type of posting which makes you angry when done
by Sandy.
What is your agenda?
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"RM" <rm@yahoo.com> schreef in bericht
news:ld9bm0pf7kirv4s1abbqv7o4623efi6139@4ax.com...
> The other link I provided today is not the one I meant to post.
> Here's the one I intended to post. I couldn't find it on a google
> search earlier. This link is the a-to-z of contact lens
> complications.
>
> http://www.emedicine.com/OPH/topic651.htm
>
> The scariest part of the article is that it claims:
> "Approximately 1 out of every 20 contact lens wearers develops a
> contact lens-related complication each year. These problems range from
> self-limiting to sight threatening, which require rapid diagnosis and
> treatment to prevent vision loss"
Who is this, Sandy or Ragnar?
Seeing the type of posting I should say it must be Sandy, this type of
postings did make Ragnar furious so I take it for granted he never wrote
this one..
Right Sandy, there are complications with contactlenses which gladly most of
the time are to be treated well.
However Sandy, there are complications when having LASIK done which only are
to be solved with the help of these contactlenses.
--
Jan (normally Dutch spoken)
Neither pro, nor anti, LASIK,LASEK,PRK etc......
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| joyceb 2004-10-08, 2:08 am |
| Thank you! That's a lot of very useful information, especially that
related to the effects of contacts (both hard and soft) on tear film.
In some of my other reading, I have learned some about how important
tears are to our ocular health. Never occurred to me that contacts
might interfere with them.
I wonder why my eye doc has never found it appropriate to either
mention the potential for both short- and long-term effects or point
me towards such information? Not that it would have necessarily
changed my mind about getting contacts -- honestly, it probably
wouldn't have. But it's still a very peculiar feeling -- the
realization that I got my contacts without once even thinking that
there might be physiological ramifications. Millions of people wear
them, right? And if there were any real potential for problems, my
doc would have mentioned it, right? But until now I'd never heard
anything from any source that would make me think that contacts had
any more potential for problems than eyeglasses. Naive? Undoubtedly.
Stupid? Probably.
I find myself, after reading so much about LASIK (and now contacts)
experiencing a bit of a sea change in my attitude toward what I can
generically term "messin' around with my body." I think about how
much our scientists and doctors have learned about human physiology in
the last 100 years, then extrapolate what we might learn in the next
100 years, and what comes to mind is, "We have no idea what we're
messing around with." In fact, it seems almost self-evident that by
the time we reach the 22nd century, we will run across an article on
the web describing some medical opinion from 2004 and think to
ourselves, "What a bunch of arrogant, clueless barbarians." My
goodness, it was only thirty or forty years ago that babies were
routinely delivered with forceps, and under full anesthesia (including
me and my three brothers!), and breastfeeding was pooh-poohed as
inferior to formula. Now such practices are almost unthinkable. I
wonder what will be said in 2104 about LASIK? About my contacts?
Fear not -- I have no intention of sinking into a Luddite stupor. But
my radar is on now.
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| Glenn - USAEyes.org 2004-10-08, 11:08 am |
| Things have gone seriously wrong when one cannot distinguish if the
nature of a post is from Ragnar or from Keller. 8^)
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"Glenn - USAEyes.org" <glenn.hageleSTOPSPAM@USAEyes.org> schreef in bericht
news:4sadm0t797fj4ud8k3r8jh07nbptmk13v9@4ax.com...
> Things have gone seriously wrong when one cannot distinguish if the
> nature of a post is from Ragnar or from Keller. 8^)
The methods they use are the same, the agenda's differs.
--
Jan (normally Dutch spoken)
Neither pro, nor anti, LASIK,LASEK,PRK etc......
|
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