Download Complications of Contact Lenses

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Complications of
Contact Lenses
Maruee Kishore Pahuja
MBBS, DOMS
Maruee Kishore Pahuja MBBS, DOMS
Natasha Eye Care and Research Center, Eyelight Laser and Eye Care Pvt. Ltd.
Pimple Saudagar, Pune
C
ontact lenses are medical devices being used to
correct vision but their role in cosmetic or therapeutic
applications is no less. In 1888, the German ophthalmologist
Adolf Gaston Eugen Fick constructed and fitted the first
successful contact lens1 and optical correction via contact
lens have come a long way since then. With rising demand,
the expectations from these devices has increased. Hence,
the importance of adequately explaining the potential
complications to prospective users, and dealing effectively
with those complications, is even more prudent. Most
contact lens related complications can be avoided by a
proper pre-fitting assessment, evaluation of the lens fit and
detail instructions on its use including regular aftercare
visits . The key to identifying a contact lens related problem
is thorough history taking and a detailed anterior eye
assessment with and without the contact lens in the eye.
Grading scales have been developed to assist practitioners
in recording the level of severity of ocular complications of
contact lens wear2.
Abnormal blinking can cause contact lens surface
drying4, deposition on the lens surface, corneal epithelial
desiccation5, post lens tear stagnation6, hypoxia,
hypercapnia and 3 & 9 o clock staining7.
Blink training[8]
and altering lens design and fit can improve blinking and
avoid the related complications.
Blepharoptosis
Eyelid ptosis can occur in younger adult
patients who wear contact lenses. Due to continuous micro
trauma from insertion and removal of the lenses, blink
induced lens rubbing, contact lens migration9 and papillary
conjunctivitis.
It happens mainly in rigid corneal lens
wearers10, but can also happen in soft lens wearers. The
patient will most likely complaint of poor cosmesis
when
the ptosis is excessive.
Ptosis in contact lens wearers occurs
due to lid oedema caused by papillary conjunctivitis or due
to levator aponeurosis.
The list of potential contact lens related complications is
long and varied, ranging from relatively benign dry eye
to potentially sight-threatening microbial keratitis. In this
article, we shall discuss several common complications
that the lens-wearing patients may experience.
Blinking Abnormalities
According to Abelson and Holly3
blinking can be classified into four types:
•
Complete blink – the upper eyelid covers more than
67%of the cornea
•
Incomplete blink- the upper eyelid covers less than
67%of the cornea •
Twitch blink- a small movement of the upper eyelid •
Forced blink – lower lid raises to complete eye closure.
Figure 1: Meibomian Gland Dysfunction
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Contact Lens: Complications of Contact Lenses
If it is due to papillary conjunctivitis, cure the papillary
conjunctivitis. If it is due to rigid gas permeable corneal
lenses then refit the patient with soft lenses. In severe cases,
surgical intervention is required.
Meibomian Gland Dysfunction
It has been found that contact lens wear is associated with
a decrease in the number of functional meibomian glands,
which may be a cause of dry eye in contact lens patients11.
Daniel Nelson, defined meibomian gland dysfunction as
a “chronic, diffuse abnormality of the meibomian glands,
commonly characterized by terminal duct obstruction
and/or qualitative/quantitative changes in the glandular
secretion. This may result in alteration of the tear film,
symptoms of eye irritation, clinically apparent inflammation
and ocular surface disease”12.
Symptoms of MGD include foreign body sensation,
burning, itching, watering and fluctuating or decreased
vision. The diagnosis of MGD is difficult because many of
the symptoms mirror the everyday complaints by contact
lens wearers13.
One method to assess the stability of the tear film is by
performing a tear break-up test (TBUT). A TBUT can be
performed noninvasively using a Keeler Tearscope, a
non-automated keratomoter or a topographer, or it can be
performed invasively using NaFL and a cobalt blue filter
at the slit lamp. In normal control eyes the values of the
fluorescein TBUT can range from 3 to 132 seconds, with
an average of 27 seconds14. In dry eye patients, TBUT is
reduced to mean values lower than 5 seconds, but the
inter-individual variability is still high15. Despite the wide
variation in TBUT among individual subjects, there is
general agreement that a TBUT shorter than 10 seconds
reflects tear film instability, whereas a TBUT shorter than 5
seconds is a marker of definite dry eye16.
If these signs are present in contact lens patients complaining
of reduced wear time or contact lens intolerance, the patient
may be suffering from meibomian gland dysfunction.
Depending on the type and etiology of MGD, it can be
treated with warm compresses, lid scrubs, mechanical
expression, antibiotics, calcineurin inhibitors and
cyclosporine essential fatty acids, artificial tears, topical lid
supplements or surfactant cleaning.
Dry Eye
Dry eye is a multifactorial disease of the tears and ocular
surface that results in symptoms of discomfort, visual
disturbance, tear film instability with potential damage
to the ocular surface. It is accompanied by increased
osmolarity of the tear film and inflammation of the ocular
surface17. Contact lens–related dry eye may be explained
mechanistically by increased tear film thinning times
(evaporation or dewetting) resulting in increased tear film
32 l DOS Times - Vol. 20, No. 9 March, 2015
osmolality. Other contributing factors include the use of
high-water-content lenses, which have traditionally been
reported to be associated with less patient comfort than
lower-water-content lenses, potentially due to spoilation
and deposition18. Symptoms of dryness are often cited as
the primary reason patients drop out of contact lens wear19.
Evaluate the tear volume, tear film structure and quality,
tear film stability. The tear volume in prospective and
current contact lens wearers can be assessed by observing
the height of the lower lacrimal tear prism. Using optical
coherence tomography, Chen et al. demonstrated that tear
meniscus volumes in dry eye symptomatic wearers are
lower than in asymptomatic wearers at baseline and during
lens wear20.
Tear film structure can be assessed clinically by observing
the corneal surface in specular relection21 or by using a
tearscope. It has been observed by Young and Efron that
the lipid layer was either absent or very thin on all hydrogel
lenses rigid lenses, although there was a tendency of higher
water content lenses to support a thin lipid layer. The
aqueous layer was generally found to be thicker on lenses
of high water content22,23.
Tear film stability can be assessed by TBUT as discussed
earlier. Young and Efron demonstrated that tear break
up occurs within 3 to 10 seconds on the front surface of
hydrogel lenses, and that longer pre lens tear film non
invasive tear break up times (PLTF NIBUTs) were generally
associated with higher water content lenses.
Tissue damage to the surface of the cornea and conjunctiva
can occur during contact lens wear as a consequence of
disruption of tear layer. Guilon and Maisa reported that
lissamine green conjunctival staining could discriminate
symptomatic from asymptomatic contact lens wearers24.
An excess of a particular tear component coupled with
compromised structural integrity of the tears leading to rapid
tear break up and excessive surface drying, are intrinsic
factors thought to be conductive to deposit formation
on lens surface. Indeed there is some clinical evidence
to support the notion that lens deposition is a particular
problem in dry eye patients wearing contact lenses.
Symptoms of dryness are often cited as the primary reason
patients drop out of contact lens wear. The lens induced
changes cause increased osmolarity of tears, change in - pH
of tears, composition of tears, tear film break up and the
temperature profile of the tear film.
This can be treated by either changing the lens material,
lens solution, rewetting drops, nutritional supplements and
by control of evaporation and omega- 6 fatty acids26.
Mucin Balls
Mucin balls are spherical and translucent or opalescent
bodies sandwiched between a CL and the cornea that can
be observed within minutes after lens insertion. They are
Contact Lens
composed primarily of mucin, and their sizes have been
reported to range between 20 and 200 μm in diameter27-28.
These depressions are best observed with fluorescein
instilled in the eye as the dye pools in the imprinted areas
and are usually resolved within 24 hrs. Mucin balls and
mucin ball–induced depressions are not associated with
decreased lens-wearing comfort or compromised vision,
and patients are usually asymptomatic29,30. Mucin balls
are seen most often with higher modulus materials. Most
common in extended wear of silicon hydrogel lenses, but
not exclusive to these lenses.
A subset of the population is predisposed to develop mucin
balls irrespective of the soft contact lens type worn, but lens
type influences the degree of mucin ball formation. The
mechanical interaction of a lens with the surface layer of the
epithelium and the tear film in association with the blinking
forces of the lid is involved in mucin ball formation31.
The obvious strategy for preventing mucin ball formation,
should this be the aim of the clinician to re-fit the patient
with a lens type that is not made from silicon hydrogel. This
may create a dilemma because silicone hydrogel lenses are
the only lens type indicated for extended wear. Therefore,
optimizing lens fit, advising the patient to use lubricating
drops before sleeping and after waking could minimize
mucin ball formation.
Contact Lens-Induced Papillary Conjunctivitis
Contact lens–induced papillary conjunctivitis (CLPC) is an
inflammation of the upper palpebral conjunctiva and is one
of the main reasons for CL discontinuation. It is characterized
by enlarged papillae (>0.3 mm), hyperemia, and mucus
strands. Patients who have CLPC can be asymptomatic
or experience acute ocular discomfort with complaints
of itching, mucus or ropy discharge, lens awareness, and
blurred vision, which are the results of increased frontsurface lens deposits and excessive lens movement33-34. The
CLPC is managed by frequent cleaning and replacement
of lenses, reducing wearing time, changing in lens-wearing
modality to DD wear, and refitting into a different lens
type or material35-37. On discontinuation of the lens, there
is usually a rapid relief in symptoms, with ocular signs
dissipating over the course of several days, sometimes
longer.
The cause of CLPC is still not well understood, but several
factors have been suggested as possible causes. Since
the advent of SiHy CLs and the report of two clinical
presentations of CLPC, the paradigm has shifted to suggest
that perhaps local CLPC is caused by mechanical trauma
and general CLPC is a hypersensitivity reaction, caused by
lens surface deposits, lens coatings, or solution38-41.
CLPC has been associated with delayed tear clearance,
which might increase the protein and inflammatory
mediator concentrations in the tear film and contribute to
Figure 2: Induced Papillary Conjunctivitis
the pathogenesis or aggravate the severity of CLPC42. Of
interest, MGD is common for patients with CLPC43, but
no association was found between MGD and delayed tear
clearance. It has been proposed that a tear clearance test
be incorporated in the eye examination for CL wearers
with CLPC, as the treatment modality can be adjusted
accordingly. In cases of decreased tear clearance, nonpreserved steroids may be indicated. If tear clearance
is normal, then changing the lens material may be
recommended first, because mechanical trauma may be a
more significant contributor compared with inflammation.
Contact Lens-Induced Epithelial Erosions
Corneal epithelial erosions related to CL wear are epithelial
defects with a wide range of clinical presentations44. In
general, they can be characterized as localized, wellcircumscribed lesions that can be as small as 0.1 mm in
diameter or encompass a much larger area of the cornea.
45
. They can present anywhere on the cornea, but 87.5%
have been found inferiorly and, more commonly, near the
vertical midline just below the pupil. The lesions can be
superficial, affecting only the first one to three layers of the
epithelium or deep into the basement membrane, and stain
with sodium fluorescein with no underlying infiltrates.
Alternatively, the epithelium may become detached
centrally but remain adherent at the border, representing
an early stage of development. There is no mucopurulent
discharge, and there may be localized limbal and bulbar
conjunctival injection. Patients may be asymptomatic or
experience foreign body sensation, especially on awakening
if lenses are worn overnight, or sharp pain exists on lens
removal. Although the aim of management is to reduce
pain, prevent infection, and promote re-epithelialization,
there is no consensus on how best to do so. In general,
lens wear discontinuation, ocular lubricants in the form of
drops, gels, or ointments, and prophylactic antibiotics are
all believed to help with the healing process. Bandage CLs
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Contact Lens: Complications of Contact Lenses
are avoided in cases of CL-induced erosion to reduce the
risk of infection.
Epithelial Microcysts
Small (15-50µm), irregular shaped inclusions usually found
in the para-central to mid-peripheral zones of the cornea.
Observation is best with retro-illumination. Microcysts
show reversed illumination due to a suspected higher
refractive index than the surrounding tissue.
The presence of epithelial microcysts in the corneal
epithelium is a good clinical indicator of chronic hypoxia.
Unlike disposable contact lenses, silicone hydrogel lenses
do not induce an increase in epithelial microcysts when
worn on extended wear basis46.
Microcysts can be a valuable “red flag,” indicating the
patient needs a lens with higher oxygen transmissibility.
Don’t be alarmed if you observe an initial increase in
microcysts after refitting a patient with a more oxygenpermeable contact lens. The additional oxygen will “flush
out” microcysts from deeper epithelial layers over the first
month or two after switching lens materials47.
Corneal Oedema
Corneal edema, or swelling, occurs when there is an
inadequate supply of oxygen reaching the cornea due to
contact lens wear. Following sleep with lenses, the cornea
showed evidence of gross stromal edema (striae and folds
in the posterior cornea) that reduced or disappeared during
the day depending on the level of edema finally reached48,49.
Symptoms of corneal edema include blurred or foggy
vision, seeing rainbows around lights, redness, and possibly
irritation or pain.
Since oxygen starvation is the primary cause of contact
lens- induced oedema, strategies are directed towards
mechanisms for increasing corneal oxygen availability
during lens wear. Changing to a higher Dk, reducing the
lens thickness, increasing the edge lift, a smaller lens
diameter will prove helpful in alleviating contact lens
induced oedema.
Complications of corneal edema include corneal abrasion,
a tight lens syndrome and corneal ulcers or infection.
Corneal Infiltrates and Ulcers
The development of a corneal ulcer unfortunately is a
common complication of contact lens use. Soft contact
lenses have a higher risk of corneal ulcer than rigid lenses,
but all lenses have some risk. A corneal ulcer starts when
a bacteria (or rarely a fungus or parasite) infects an area of
breakdown in the corneal surface. The surface may break
down, forming a small corneal abrasion, due to routine
lens use.
34 l DOS Times - Vol. 20, No. 9 March, 2015
Overwear of lenses, improper cleaning of lenses, extended
wear use of lenses, and overly tight lenses may increase
the risk of developing this surface breakdown. Normally, a
corneal abrasion, even if tiny, is uncomfortable. However,
a contact lens can act as a bandage on the eye masking
symptoms, and some contact users develop a lack of
sensitivity of the cornea.
Once an infection begins, most people experience severe
symptoms. The eye typically becomes red and painful.
There may be tearing or discharge and sensitivity to light.
The vision may be variably blurred. The most important
thing to do initially is to remove the contact lens. A corneal
ulcer needs to be treated intensively with antibiotic eye
drops, and often a culture of the infected cornea, or of
the lens or lens case is performed. Frequent follow-up
appointments will help you determine if the infection is
being adequately treated with the antibiotics. Usually a
week or two of antibiotic eye drops is needed, and contact
lenses cannot be worn during this time.
A successfully treated corneal ulcer may still leave a scar,
which could affect the vision.
It is important to avoid situations which can lead to corneal
ulcer, such as over wear of lenses, poor disinfection
techniques, swimming with contact lenses in, and ignoring
symptoms of pain or redness50.
When contact lens patients present with infiltrates, consider
non-infectious causes, including extended wear, hypoxia,
poor hygiene, case contamination, solution sensitivity and
normal flora or bacterial toxins51.
Solution toxicity and hypersensitivity have been identified
as a potential cause of corneal infiltrates.
Hydrogen peroxide systems are a potential alternative
in cases of hypersensitivity to multipurpose solutions. In
fact, the lowest incidence of corneal infiltrative events
was reported in silicone hydrogel wearers using hydrogen
peroxide systems52.
A prospective study looked at the risk of non- ulcerative
contact lens complications and showed that there is a
lower rate of complications in patients wearing daily
disposable vs. planned replacement lenses; Silicone
hydrogel lenses wear was associated with a two-fold risk
for “sterile keratitis.” Other factors that increased risk for
non-infectious infiltrates included occasional and habitual
overnight wear, less than 10 years of wear, poor hand
hygiene and smoking53.
Endothelial Changes
Contact lenses may induce short- and long-term corneal
endothelial changes.
The endothelial bleb response is a short-term, reversible
change noted with contact lens wearers. One physiological
Contact Lens
factor causing endothelial blebs and polymegathism is a
local acidic pH change at the endothelium, which happens
due to hypercapnia and hypoxia induced due to certain
contact lens wear.
Long-term endothelial changes such as polymegethism
(increased variation in cell size) and pleomorphism (a
decrease in the frequency of hexagonal cells) have also
been detected in polymethylmethacrylate, rigid gas
permeable, and daily and extended wear soft contact lens
patients. Differences in endothelial morphometry between
the central and mid-peripheral regions of the cornea have
also been noted in hard lens wearers54.
Morphologically, the endothelial cells of contact lens
wearers showed greater variability in size and shape
compared to controls. The mean endothelial cell size in
contact lens wearers was smaller than that of controls. It has
been found that the gas permeable lens wearers had more
hexagonal and less pentagonal cells55.
From a clinical perspective, it is essential to take note of
the presence of significant endothelial polymegathism
and to take action to minimize the metabolic stress to
the cornea. Strategies for alleviating contact lens induced
hypercapnia and hypoxia include; fitting soft or rigid lenses
made from materials of higher gas permeability, reducing
lens thickness, sleeping in extended wear less frequently,
changing from extended wear lens wear to daily wear and
reducing lens wearing time.
References
1.
”Adolf Eugen Fick (1852-1937)”. Retrieved 26 March 2015.
2. Grading scales for contact lens complications. Efron N Ophthalmic
Physiol Opt. 1998 Mar;18(2):182-6.
3. Abelson MB Holly FJ. A tentative mechanism for inferior punctate
keratopathy. Am J Ophthalmol 1977;83:866-70
4.
Alonso-CaneiroD, Iskander DR, Collins MJ. Tear film surface quality
with soft lenses using dynamic- area-high-speed videokeratoscopy.
Eye Contact Lens 2009;35:227-31
5.
Guillon JP, Gillion M ,Malgouyres S. Corneal dessication stainingwith
hydrogel lenses:Tear filam and contact lens factors. Ophthal Physiol
Opt 1990;10:343-8
6. Paugh JR , Stapleton F , Keay L, Ho A . A tear exchange under
hydrogel contact lenses : methodological considerations. Invest
Opthalmol Vis Sci 2001;42:2813-20
7. Van der Worp E, De Brabender J, Swarbrick H ,Hendrikse F.
Eyeblinkfrequency and type in relation to 3- and 9-o’clock
stainingand gas permeable contact lens variables. OptomVis
Sci2008;85:857-66
8.
Collins M, Heron H, Larsen R, Lindner R. Blinking patterns in soft
contact lens wearers can be altered with training.Am J Optom
Physiol Opt 1987;64:100-3
9. John G. Yassin, Robert H. White, Gerard M. Shannon. Blepharoptosis
As a Complication of Contact Lens Migration American Journal of
Ophthalmology 1971;72:536–37
10. Kersten RC, de ConcilisC, Kulwin DR. Acquired ptosis in the young
and middle agedadult population. Ophthalmology 1995;102:924-8
11. Arita R, Itoh K, Inoue K, et al. Contact lens wear is associated with
decrease of meibomian glands. Opthalmology. 2009; Mar 116:379–
84.
12. International Workshop Previews MGD Report. Rev Ophthalmology.
2010;17(6/1).
13. Henriquez AS, Korb DR. Meibomian glands and contact lens wear.
Br J Ophthalmol. 1981 Feb;65:108-11.
14. Norn MS Desiccation of the precorneal film. I. Corneal wetting-time.
Acta Ophthalmol (Copenh). 1969; 47:865-80.
15. Pflugfelder SC, Tseng SC, Sanabria O, et al. Evaluation of subjective
assessments and objective diagnostic tests for diagnosing tear-film
disorders known to cause ocular irritation. Cornea. 1998;17:38–56.
16. Shimazaki J. Definition and criteria of dry eye. Ganka. 1995;37:765–
70.
17. The Definition and Classification of Dry Eye Disease: Report of the
Definition and Classification Subcommittee of the International Dry
Eye Work Shop (2007).
18. Jason J. Nichols and Loraine T. Sinnott Tear Film, Contact Lens, and
Patient-Related Factors Associated with Contact Lens–Related Dry
Eye Invest. Ophthalmol. Vis. Sci. April 2006 vol. 47 no. 4 1319-1328
19. Jeffrey Krohn, O.D. Dry eye symptoms in contact lens wearing
patients can present in several ways. Fortunately, there are also
several ways to uniquely treat each presentation. Review of Cornea
and Contact Lenses. March 2012
20. Chen Q ,Wang J, Shen M,et al . Lower volumes of tear menisci in
contact lens wearers with dry eye symptoms. Invest Opthalmol Vis
Sci 2009;50:3159-63
21. Koby ES. Microscopie de l’Oeil vivant, Paris:Masonet Cie;1924
22. Young G, Efron N . Characteristics of the pre-lens tear film during
hydrogel contact lens wear . Opthalmic Physiol Opt 1991;11:53-8
23. Guillon M, Guillon JP , Mapstone V. Rigid gas permeable lenses
in vivi wettability . Trans Br Contact Lens Assoc 1989;Conference
Proceedings:24
24. Guillon M , Maissa C . Bulbar conjunctival staining in contact lens
wearers and non lens wearers and its association with symptomology.
Contact Lens Ant Eye 2005;28:67-73
25. Doughman DJ. The nature of ’spots ‘ on soft lenses . Ann Opthalmol
1975;7:345-8
26. Kokke KH, Morris JA , Lawrenson jg. Oral omega-6 essential fatty
acid treatment in contact lens associated dry eye. Contact Lens Ant
Eye2008;31:141-6
27. Meng C. Lin, O.D., Ph.D, Thao N. Yeh, O.D.Mechanical
Complications Induced by Silicone Hydrogel Contact Lenses. EYE
AND CONTACT LENSES
28. Millar TJ, Papas EB, Ozkan J, et al. Clinical appearance and
microscopic analysis of mucin balls associated with contact lens
wear. Cornea 2003;22: 740–745.
29. Dumbleton K, Jones L, Chalmers R, et al. Clinical characterization
of spherical post-lens debris associated with lotrafilcon high-Dk
silicone lenses. CLAO J 2000;26:186–192.
30. Pritchard N, Jones L, Dumbleton K, et al. Epithelial inclusions
in association with mucin ball development in high-oxygen
permeability hydrogel lenses. Optom Vis Sci 2000;77:68–72.
31. Tan J1, Keay L, Jalbert I, Naduvilath TJ, Sweeney DF, Holden BA.
Mucin balls with wear of conventional and silicone hydrogel contact
lenses. Optom Vis Sci. 2003 Apr;80(4):291-7.
www. dosonline.org l 35
Contact Lens: Complications of Contact Lenses
32. Sankaridurg P, Sweeney DF, Naduvilath T, et al. Papillary response
in contact lens papillary conjunctivitis is either general or localised.
ARVO Meeting Abstracts 2001;42:S596.
33. Alemany A, Redal A. Giant papillary conjunctivitis in soft and rigid
lens wear. Contactologia 1991;13:14–17.
34. Roth H. Studies on the etiology and treatment of giant papillary
conjunctivitis in contact lens wearers. Contactologia 1991;13E:55–
60.
35. Donshik PC, Ballow M, Luistro A, et al. Treatment of contact lensinduced giant papillary conjunctivitis. CLAO J 1984;10:346–350.
36.Katelaris CH. Giant papillary conjunctivitis—A review. Acta
Ophthalmol Scand Suppl 1999;228:17–20.
37. Sankaridurg P, Skotnitsky C, Pearce D, et al. Contact lens papillary
conjunctivitis: A review. Optom Pract 2001;2:19–28.
38. Skotnitsky CC, Naduvilath TJ, Sweeney DF, et al. Two presentations
of contact lens-induced papillary conjunctivitis (CLPC) in hydrogel
lens wear: Local and general. Optom Vis Sci 2006;83:27–36.
39. Donshik PC. Giant papillary conjunctivitis. Trans Am Ophthalmol
Soc 1994;92:687–744.
40. Molinari JF, Stanek S. Meibomian gland status and prevalence of
giant papillary conjunctivitis in contact lens wearers. Optometry
2000;71:459–461.
41. Zhao Z, Fu H, Skotnitsky CC, et al. IgE antibody on worn highly
oxygenpermeable silicone hydrogel contact lenses from patients
with contact lensinduced papillary conjunctivitis (CLPC). Eye
Contact Lens 2008;34:117– 121.
42. Chang SW, Chang CJ. Delayed tear clearance in contact lens
associated papillary conjunctivitis. Curr Eye Res 2001;22:253–257.
43. Mathers WD, Billborough M. Meibomian gland function and giant
papillary conjunctivitis. Am J Ophthalmol 1992;114:188–192.
36 l DOS Times - Vol. 20, No. 9 March, 2015
46.. Patrick M. Ladage The effects of Silicone hydrogel lenses on the
corneal epithelium
47. THOMAS G. QUINN Slit Lamp Examination: Back to Basics. Contact
Lens Spectrum.
48. Keith H. Carlson, William M. Bourne, and Richard F. Drubaker
Effect of Long-Term Contact Lens Wear on Corneal Endothelial Cell
Morphology and Function Investigative Ophthalmology & Visual
Science, Vol. 29, No. 2, February 1988.
49. Drien A. Holden, George W. Merrz, and John J. McNolly Corneal
Swelling Response to Contact Lenses Worn Under Extended Wear
Conditions.
50. Contact Lenses and Related Problems, Richmond Eye Associates,
P.C
51. Baum J, Dabezies OH Jr. Pathogenesis and treatment of “sterile”
midperipheral corneal infiltrates associated with soft contact lens
use. Cornea. 2000;19:777-81.
52. Carnt NA, Evans VE, Naduvilath TJ, et al. Contact lens-related
adverse events and the silicone hydrogel lenses and daily wear care
system used. Arch Ophthalmol. 2009;127:1616-23.
53. Radford CF, Minassian D, Dart JK, et al. Risk factors for nonulcerative
contact lens complications in an ophthalmic accident and
emergency department: a case-control study. Ophthalmology. 2009
Mar;116:385-92. 54. MacRae SM1, Matsuda M, Shellans S. Corneal endothelial changes
associated with contact lens wear. CLAO J. 1989;15:82-7.
55. Keith H. Carlson, William M. Bourne, and Richard F. Drubaker
Effect of Long-Term Contact Lens Wear on Corneal Endothelial Cell
Morphology and Function : Investigative Ophthalmology & Visual
Science, Vol. 29, No. 2, February 1988.