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198 Cards in this Set

  • Front
  • Back
List examples of non-ideal patients.
-surgeons, engineers, architects
-uncorrected hyperopes
-astigs > 0.75
-unreasonable expectations
-very steep/flat Ks
Daily wear
put on same pair of lenses next day
wear one a day and throw away at end of day
Name 4 aspheric/simultaneous vision lenses
-blanchard essentials
-conforma VFL 3
-Lifestyle Hi-ridder
What are 5 things that make aspheric/sim vision lenses unique?
-posterior (F2) surface
-steep fit
-needs some translation
-thin design
-amount of add det by eccentricity
Name 4 Translating/Alternating lenses
=TruForm Solitaire II
-TruForm Llevations
-Metro Optics MetroSeg
-Fused Kontacts Tangent Streak
Name 5 things that make translating/Alternating lenses unique.
-Posterior (F2) spherical
-Fit Flate to average K
-Excellent optics
-needs to translate, need good lid structure
-thicker design (0.2-0.4mm truncation 1.25 - 3 D prism
Who are ideal pts for aspheric/simultaneous vision lenses?
-early presbyopes (comp users, intermediate dist, athletes)
-critical vision not essential
Who are ideal pts for Translating/Alternating vision lenses?
-Mode to advance presbyopes
-requires critical vision
What type of anatomy and fit do you need for Aspheric/Simultaneous vision lenses?
-lower lid tonicity - not a critical factor
-lrg pupil in normal rm illumination
-follow manufacturer's guidlines
-lens needs to center
-steeper fit
What type of anatomy and fit do you need for translating/Alternating vision lenses?
-good lower lid tonicity (lower lid is 1 mm above or below limbus)
-less pupil sz dependent
-lens needs to translate
-ave k - 0.75
What are the powers for the series I, II, III in the Blanchard Essential lenses?
-Series I +0.50 to +1.50
-Series II +1.75 to +2.25
-Series III +2.50 and up
Which series has more add?
Series III
If you need more distance what will use in the Blanchard Essentials?
-Essentials Xtra
If you need even more add what will you use in the Blanchard Essentials?
- CSA add, ADDS +1.50, +2.25, and +2.75
Describe the fitting strategy for Blanchard Essentials.
1. Hx: vocation, avocation, goals
2. Ks
3. Ref
WTR up to 2.50, ATR up to 0.75
4. Pupil < 5.5 mm
5. Choose lens (start w/ series II)
6. Distance OR
7. Place OR in trial frame and demonstrate new VA
When do you use the phoropter and when do you use loose lenses?
-use phoropter if in situ VA worse than 20/70
-if in situ VA better than 20/70 refine w/ +/-0.25D until 20/25 resolvable
-est multifocal wearers - do loose lens over ref - no phoropter
What do you do if an aspheric multifocal lens rides to high - poor dist VA?
-steepen BC
-increase center thickness
-thin edge of lens (so lid won't catch on it as much)
What do you do if an aspheric multifocal lens rides to low - poor near VA?
-flatten BC if lens too tight
-increase OAD if lens too loose
5 characteristics of GP segmented multifocals
-translating = alternating = segmented designs
-thicker, prism ballasted
-good dist and near vision (higher add) - those who need precise vision
-usually fit on flat K
-lower lid must be <2.0 mm from lower limbus
How would you fit a metroseg? tangent streak bifocal?
Metroseg: avg K or flatter fit, spherical BC

Tangent Streak BF: -0.75 flatther than average K, Spherical BC
What is the design of a metroseg? tangent streak BF?
Metroseg: curved/crescent seg, less sensitive to rotation, thin design

Tangent Streak BF: also avaiable in trifocal
What are some extras about metroseg? tangent streak BF?
Metroseg: stable enar vision w/ up to 30 deg rot, available in toric parameters, no truncation, prism ballasted

Tangent Streak BF: Optics are great, toric options available, needs MORE prism than most lenses
How would you adjust a translating design that doesn't translate? (poor near vision, good distance vision)
-decrease prism
-truncate and compensate by increasing seg height
-flatten BC and change power to compensate
How would you adjust a translating design if upper lid pushes down on lens down? (poor near vision, good distance vision)
-increase OAD/OZ
-Thin upper edge
How would you adjust a translating lens if the
Len translates, but pupil not intercepting seg? (poor near vision, good distance vision)
-increase seg height
-can chk by hainv pt tilt head up
What adjustments would you make if the translating lens gives poor or inconsistent vision?
-lens decenters sup - poor dist vision (need to steepen BC and compensate power)
-lens decenters inferior - poor near vision (flatten BC and compensate power)
What adjustments would you make if the translating lens gives poor distance vision?
-Distance too small and seg height too higher (increase OAD, lower seg height)
What is the difference in fit b/w Llevations and Solitaire II?
-Ave K or flatter fit
-spherial BC
-Aspheric front surface

Solitaire II
-Ave K or flatter fit
-Spherical BC
-Aspheric front surface
What is the difference in design b/w Llevations and Solitaire II?
-Also comes in thin design
-aspheric intermediate area

Solitaire II:
-large dist and near section
-sm aspheric mid-range
What is the difference in extras for Llevation and Solitaire II?
-reference lines for practicioners - pt do not perceive
-intermediate = 55% of Add,
-WD 30'' = pwr can be changed
-low prism 1.25D

Solitaire II:
-ref line for doctors, not pts
-solitaire thin - ant slab off feature - less prism
-w/ or w/o truncation
-low and high add
Name 6 MF SCL?
1. Acuvue BF
2. Soflens MF
3. PureVision MF
4. Ciba Focus Progressive
5. Frequency 55 MF
6. Proclear MF
What are some characteristics of Acuvue BF?
-concentrict design - either works or it doesn't
-pupil independent
-variety of lighting conditions
-can alter dist and near Rx independent of each other
-intermediate vision? (switch to aspheric MF or bias 1 eye for D/N and other eye I/N)
What are 3 characterisitics of Aspheric Designs?
-tend to better w/ hyperopes
-pupil size dependent
-near center, distance periphery
What are some differences b/w softlens 66 MF and purevision MF? (they are both made by B and L)
Soflens 66 MF:
-2 wk replacement
-not silicon hydrogel

-monthly replacement
-silicon hydrogel

for both can choose distance and near independent of ea other (low add +1.50, high add +2.50)
Characteristics of CIBA?
-can't choose D and N power independent of ea other
-monthly, daily replacement
How do you calc the CLP for CIBA lenses?
Distance Srx (EDS it, vertex it) + 1/2ADD = CLP
Characteristics of Freq 55 and proclear MF?
-D lens = dominant eye
-N lens = non-dom eye
-young prebyopes
-doesn't work if intolerant to monovision
-better add effect
-can change dist and near power indepedent of each other
3 prescriptions to avoid for multifocals
-astigmatism (proclear toric MF)
-mild hyperopic astigmat (+1.00 - 0.75 x 090)
-Essential emmetropes
Intolerant to monovision?
-avoid centrad designs
-choose aspheric designs or concentric designs
Glare at night? Pupils too large?
-switch designs (usu centrade to aspheric or concentric)
-single vision distance and multifocal)
Presbyopic and sleeping in lenses?
-purevision MF
-wearing SL 66 MF (consider switching into purevision MF, fairly seamless change, may need more plus in distance rx)
What is the number one reason for CL dropouts?
Discomfort (28%)
Describe the onset of presbyopia?
Age <40 5%
Age 40-42 45% (steep cliff)
Age 42-44 50%
Age >44 1%
Describe the interest of presbyopes in CLs?
-over 50% of the vision care pop is presbyopes
-27% of presbyopes are interested in CL
What two issues cause most of the problems in CL pts?
What are short term effects that can happen to the epithelium when you have CL-induced relative hypoxia?
What are long term effects that can happen to the epithelium when you have CL-induced relative hypoxia?
-reduced O2 consumption
-increased fragility
-reduced sensitivity
-reduced cell mitosis
What are short term effects that can happen to the stroma when you have CL-induced relative hypoxia?
What are long term effects that can happen to the stroma when you have CL-induced relative hypoxia?
What are short term effects that can happen to the endothelium when you have CL-induced relative hypoxia?
What are long term effects that can happen to the endothelium when you have CL-induced relative hypoxia?
How has the cornea adapted for hypoxia?
-cornea withstands grtr shifts in O2 than most body tissues
-cornea derives most O2 exogenously, rather than a vascular bed
-est that only 15% of corneal glucose comes from aerobic means
-corneal epithelium has an enzyme to prevent vascularization in hypoxia
-cornea DN show same struc. insult to hypoxia that stroma and endo shw
-corneal epi cells have a low number of mitochondria (site of aerobic respiration)
-the lens has no mitochondria (transparent tissues have little to none)
Where does the O2 to the cornea come from?
-limbal vasculature
Where is the oxygen utilized?
-epithelium to provide energy for tissue replication, growth and maintenance
-accomplishes this by metabolism of glucose
-glucose is supplied by the aqueous and glycogen is stored in the epithelium
Where else is the oxygen used?
-endo (high metabolic rate, sig O2 available from aqueous)
What are the relative consuptions of O2 in the epithelium, stroma, endothelium?
epi 40%
stroma 39% (huge chunk)
endo 21% (1 cell thick)
what can be said about the endothelium
end tissue is 5X more active than the same vol of epi tissue
-stroma is sort of inactive
4 events taht will happen if a t/r is a decrease of O2 beyond critical lvls
1. cornea cannot perform aerobic glycolosis
2. glycogen stores become depleted
3. lactic acid accumulates in the corneal tissue
4. osmotic load leads to edema of the stroma and epi
Whether the cornea can supply adequate amounts of O2 depends on what 3 things?
1. O2 available at the atmospheric surface (in tears)
2. O2 at the aq surface
3. permeability of the tissue to O2 transfer
how much O2 is
-at sea lvl
-Denver (5,000 ft)
-Mexico City
-Mt. Everest
-at sea lvl (155 mmHg)
-Denver (5,000 ft) (134 mmHg)
-Mexico City (118 mmHg)
-Mt. Everest (52 mmHg)
If the tears were fully saturated w/ atmospheric O2, the O2 tension at the surface of the cornea would be?
155 mmHg (21% O2)
what 3 things in the presence of a CL, does O2 availablity depend on?
-oxygen transmissibility of the CL material (Dk/t)
-Wehter the lens is a non-moving hydrogel or from a rigid lens that moves on the eye
-daily or extended wear lens modalities
How much O2 does the cornea need
-min Dk is 125
Def. of critical O2 requirement.
the min O2 tension (or O2%) at which the cornea can survivie indefinitely w/o compromise in its normal function
Critical O2 reuirements are expressed as?
O2 tension (mmHg)
How do you convert the tension to the O2%?
divide tension by 7.4

155mmHg/7.4 = 21%
55mmHg/7.4 = 8%
How do we define dysfunction? (7)
1. corneal swelling or edema levels
2. cell mitosis rates
3. Microcyst production
4. epithelial junctional integrity
5. loss of corneal sensitivity
6. limbal vasculature
7. endothelial anatomy and function
How much is corneal O2 reduced by in a closed eye state

from 21% 155 mmHg to approximately 8% (55 mmHg) in the closed eye state
under closed eye conditions, O2 is supplied to the cornea by the (blank)
capillary plexus of the superior conjunctiva
What is the fraction of the ppl that have nocturnal lagophthalmos?
1/3 of the population
recent, well designed studies suggest that the cornea needs how much O2 to prevent dysfunction?
escess of 10% O2 (75 mmHg)
5 things that happen when eyes are closed?
1. O2 lvl red
2. lid action on the lens is eliminated
3. decrease in tear and stromal pH
4. increase in corneal temp
5. increase in tear osmolarity
how much O2 can the eye get from the superior palpebral conj?
55 mmHg (8% O2)
What did Holden and Mertz (1984) attempt to do?
they attempted to define the critical O2 tension lvl required in a closed eye state during EW
What did they find?
the level they found was 18%, which is a difficult lvl to achieve w/ previous CL materials
As a compromise, the suggested standard was set at ....?
In the group of subjects in teh study what did 12% mean?
this was the lvl at which no residula corneal swelling remained during the daily wear phase (open eye phase) of the extended wear cycle
DK =
Dk/t =
equivalent oxygen percentage
What does the EOP run from?
0-21% (21% is the full amnt of O2 available in atmostpheric oxygen)
What does an EOP of 7% mean?
if a CL delivered 7% EOP, it would allow 1/3 of the O2 availble in the atmosphere to reach the cornea
What is the needed EOP to prevent residula corneal swelling during the daily wear phase of EW?
LEC #4
LEC #5
LEC #5
the formation and extension of vascular capillaries w/in and into an avascular cornea
the formation and extension of vascular capillaries w/in and into a PREVIOUSLY vascularized cornea
Limbal Hyperemia
(limbal injection, limbal engorgement) - increased blood flow, resulting in distention of the limbal blood vessels
-hyperemia may be active, when due to dilation of b.v. or passive, when the drainage is hindered
Vessel Penetration
-Apparent ingrowth of vessels
-towards the corneal apex
-measured from the coneoscleral juctnion
increase in the number of vessels
Vascular pannus
-vascularization adn connective tissue deposition beneath epi
-usu in sup limbal region
What did the study by McMonnies use for their reference point?
limit of visible iris
What did McMonnies say the limbal vessel filling measured inferiorly was for ...
-non-Cl weareres
-HCL weareres
-SCL wearers
-non-Cl weareres (0.13 mm)
-HCL weareres (0.22 mm)
-SCL wearers (0.47 mm)
what did McMonnies show and conclude from their study?
they showed that vasostimulating agenst could prodcue an identical response to that of SCL
they concluded that the SCL response is actually filling of nomrally empty capillaies rather than true vessel penetration
What are 3 types of vascular patterns that can occur
1. Superificial vascularization
2. Deep stromal vascularization
3. VAscular pannus
Superificial vascularization

how do you know they are superficial vessels?
-episcleral branches of the anterior ciliry artery form a plexus around the libus known as the superficial marginal arcade
-they are continuous w/ the superivicial marginal arcades
What is the best way to observe superficial vascularization?
-direct focus of direct retro-illlum, high mag - indiv blood corpuscles can often be seen at this mag
Deep stromal vascularization
large feeder vessel emergin sharply from the limbus
-rapidly dev into finer, wildly tortuous branches
Active (inflammtory) pannus
-avascular and composed of supepithelial inflammatory cells
Fibrovascular (Degenerative) Pannus
-ingrowth of collagen and vessels and often containts fatty plaques
Grading scale for CL induced corneal vascularization
Grading scale for CL induced corneal vascularization
Vessels enchroaching onto the cornea but not exceeding:
0.4 mm w/ DW HCL
0.6 mm w/ DW SCL
1.4 mm w/ EW SCL
Caution, take action
Vessels encroachmen exceeding Grade 1 and extending as far as (but not entering the pupil area)
Danger; cease lens wear
Vessel encroachment into the pupil area
What should you document for a vascular response of the cornea to CL wear?
-location - by deg, as part of an arc portion of a circle, pos on the clock, quadrant
-depth - superficial, deep
-penetration - mm from limbus
What is the FDA's def of sig vascularization?
penetration of vessels in excess of 1.5 mm
What are 5 ocular/systemic cond that may lead to neo?
1. acne rosacea
2. trachoma
3. keratitis
4. DM
5. renal dz
What are 3 theories for why vascularization occurs?
angiogenic suppression
Metabolic Theories:
-hypoxia in other body tissues stim vascularization so it stands to reason that the cornea may be similar
Metabolic Theories:
Lactic Acid
accumulation of lactic acid due to changeover into anaerobic drainage may lead to corneal vascularization
Metabolic Theories:
stromal edmea alone may be a stim to vascularization - shown in rabbit models
Metabolic theories:
Stroma Softening
-chronic edema may cause a breakkwn of stromal ground substance and collagen
-loss of compactness reduces the physical barrier to vessel penetration
Angiogenic Suppression theory
Cornea has a factor that acts to restrain cell diviion and migration of cells into the cornea
-CL may suppress this factor
Vasostimulation Theories:
free cellular elements
PMNs and macrophages have been implcated in vasogenesis, so may be part of the inflammatory response
Vasostimulation Theories:
Humoral componenets
plasma constituents have the potential to be vasogenic - like Prostaglandins and fibrin
Vasostimulation Theories:
Epithelial cell facotrs
released w/ trauma as a vasogenic factor
Vasostimulation Theories:
Extrinsic substances
Subst in CL soln may be vasogenia
-at least 20 chem have been identified
Neural control theory: what did research show when the corenas were surgically denervated
showed increase rates of corneal vascularization
-since we know that CLs decrease corneal sensitivity, neural contral may be at hand
CL indeced Vascularization Model
CL creates tissue hypoxia leading to corneal edema adn stromal softening
-CL can cause mech injurty to the cornea, resulting in a release of enzymes, inflammatory cells migrate to the area and release vaso-stim agents causing vascularization
What are some causative factors for vasoproliferation?
-peripheral corneal edema
-trauma from decentered rigid lens across the limbus
-tight fitting lens that interferes w/ blood/lymph drainage
-decentered rigid lens that cuases chronic limbal epithelial microabrasions
-entrapment of cellular debris and metabolic byproducts
Management of vasoproliferation?
-improve lens design
-improve lens fit
-decrease wearing time
-increase avail O2
-use of preservative free care sys
LEC #6
What are some METABOLIC CL complications in the epithelium?
-lens overewra
-tight lens syndrom (CLARE)
-Central corneal clouding
What are some METABOLIC CL complications in the strom?
What are some METABOLIC CL complications in the endo?
what are some tear surfacing disorders?
-peripheral corneal dessication
-inf corneal staining
-dimple veiling
Corneal distortion
corneal warpage
corneal abrasion
what are some toxic and allergic disorders?
-toxic keratopathy
-thimerosal keratopathy
-CL induced papillary hypertrophy
-allergies and CL wear
Sterile keratitis
sterile corneal infiltrates
Microbial keratitis
microbial keratitis
What is the etiology of Contact lens induced papillary hypertrophy?
deposits on SCL, mech irritation
What are the signs and sx of Contact lens induced papillary hypertrophy?
-increased mucous secretion
-dev of papillae on the upper tarsal conj
What zone does RGPs affect the most?
zone 3 (lash margin)
What zones SCLs affect the most?
Zone 1 and 2
Describe Grade 1 CLIPH.
-mild itching
-increase in mucus AM
-no signs
-slight hyperemia
Describe Grade 2 CLIPH.
-increase mucus AM
-lens awareness
-blurred VA late in day
-enlrg papillae
-mucus over papillae
-slight to mod hyperemia of upper lid
-mild coating of CL
-Rare SPK superiorly
Describe Grade 3 CLIPH.
-mod to servere itching esp on CL removal
-mod-sev mucus
-increase lens awareness
-mod blur of VA
-decentered CL
-enlargement of papillae (>1mm), tips may stain heavy mucus over papillae
-hyperemia of upper lid and edmatous
-mod coatings of CL
-may have SPK superiorly
Describe Grade 4 CLIPH.
-sev itching
-sev mucu-lids stuck shut in AM
-reduction or dicont of CL wear
-mod blur of VA
-decentered CL
-giant papillae (>1mm); tips may stain; flattened on top
-heavy musu over papillae
-hyperemia of upper lid and edmatous
-severe coating of CL
-may have SPK and/or infiltration
tx for CLIPH
-lens deprivation
-decrease wear time
-increase enzyme regimen
-refit: 2 wk vs extended wear materials, daily vs 2 wk
-topical anti-histamines, mast cell stabilizers, steroids, combo drugs
Systemic eye allergy drugs
-must ravel thru bld stream to reach the target tissue
-longer onset time
-undesirable side effects (dry eye and drowsiness)
-Rx and OTC
-lotadine (Claritin), Cetirizine (Zyrtec), Fexofenadine (Allegra)
Antihistamine/vasocontrictor combos
agents with only a vasoconstrictor, such as tetrahydrazoline (Visine) have no anti-allergy effect
-OTC cobos contain antihis (antazoline, pheniramine) to reduce itching and a vasocontstrictor (tetrahydrazonline, naphazoline) to red redness and swelling
-last 2 hours, w/ QID dosing no all day relief, sig tachyphylaxis possible
-loteprednol (Alrex) - temp relief of seasonal allergic conjunctivitis - last ditch (Pred-Forte, Vexol)
-have grtr effectiveness thatn other meds but grtr risk of short term and long term side effects - cats and increase IOP
-may be used for conj problems - vernal, atopic, GPC, and drug induced conjuntivitis
-for redness, swelling, ithcing
-longer durations of action than OTC antihis
-Levocasbatin (livostin) and emedastine (emadine)
Mast cell stabilizers
-only for itching and works to a minimal extene
-need loading period
-cromolyn (crolom, opticrom) and lodoxamid (alomide) dosed qid
-nedrocromil (alocril) is dosed BID; pemirolast (Alamast) dosed QID
Dual action drugs
-fast acting antihis
-long duration due to mast cell stabilizer
-effective when dosed twice daily
-olopatadine (Patanol), Azelastine (optivar), and ketotifen (Zaditor)
Peripheral Corneal Desiccation Syndrome (3-9 staining)
-RGP wearer
-incomplete blinks: fluid balance
-inadeq spread of mucin
-improper edge design
-excessive edge lift
tx of Peripheral Corneal Desiccation Syndrome (3-9 staining)
-increase OAD
-plus edge for interpalpebral fit
-minus edge for lid attachment
-steepen the secondary curve
-refit to SCLs
Vascular Limbal Keratitis (VLK) etiology
-large dia
-low edge lift
Signs and Sx of VLK?
-complain of slight irritation in area of VLK (inflam, invasive vascularization)
management of VLK
-rev and non-scarring
Tx of VLK
-smaller dia
-flatter and wider peripheral curves
-therapeutic intervention: coualr lub, decongestants, NSAIDS,steroids
-pt asym
-prolong hypoxia
-trapped cellular debris and disorganized cell growth
-sm irregular in shape
-onset 2-6 mo
-increase in number after deprivation
-disappear 1-3 mo
How do you grade Microcysts
0 no microcysts

1 <50, central and paracentral cornea

2 > 50 central and paracentral cornea

3 >50 microcysts, tend to be coalesced, staining

4 numverous dense, coalesced microcysts + staining
management for microcysts less than 50?
monitor periodically
management for microcysts more than 50?
-decreased thickness
-increase dk
-decrease wear time
what if you're not able to red number of microcysts?
-refit to daily wear
What are mucin balls?
-appear pearly and opalescent
-small spheres underneath CL
-associated w/ overnight silicone hydrogel wear
who are more prone to mucin balls?
-30 day EW
-steeper corneas (>44)
-lack of lubricating drops
what do mucin balls lv?
dimple veiling-like staining pattern after removal of lens
what is the tx of mucin balls?
-fit steeper BC
-red number of overnights
-include rewetting drop
How would you describe CL associated red eye (CLARE)
-EW hydrogel or sihy
-uniocpain/FB sensation
-red eye
-VA normal
-SEIs in mid-periphery or limbal
-limbal inj
-no AC reac or lid edema
-well fitted or tight lens
CLARE is associated w/?
non-ulcerative sterile keratitis
-associated w/ colonization of Gram - (primarly pseudomonas)
-can include serratia marcesens and H. influenzae
-can be recurrent (in continuous wear Sihy 29%)
Tx of CLARE?
-remove lense
-discont lens wear
-ocular lubrication
-conservation tx warrants AB use for 48 hours w/ follow-up and re-eval
etiology of striae?
What are some DDX of striae?
-endothelial folds and edematous corneal formations (ECF)
How do you differentiate b/w corneal nerves and striae?
striae are central, vertical, deep stroma

corneal nerves - anywhere, anterior stroma, bifurcated, can follow to limbus
how do you manage Striae?
-increase Dk/L
-decrease wear time
what 3 things can striae be present w/?
would would you do if severe edema exists, ECF, striae, microcystic edema?
-topical hypertonics
Sx of corneal infiltrates?
-or complain of slight irritation
etiology of corneal infiltrates?
-toxicity reaction
management of corneal infiltrates?
-change solns
-r/o corneal ulcer
CL Induced Peripheral Ulcer presnts in what way?
whitish gray focal anterior stromal infiltrate
periphery or mid periphery
0.1 -2.0 mm
What can cause CLPU?
-colonization of bac on lens surface
-gram +, staph aureus and epidermis
-DW but now EW
sx of CLPU?
-or mod FB
What is a DDX of CLPU?
What can you see in the epithelium w/ a CLPU?
-epi resurfaces over lesion, leaves a well-demarcated grayish scar
tx of CLPU
-milder sx - quick resolution w/ discontinuation
-discont lens wear
-broad spec AB
-close monitoring for first 24 hours
Microbial Keratitis (MK) sx?
-may or may not have discharge
MK etiology?
epithelial trauma, hypoxia, contaminated soln, extended wear CL
Management of MK?
-discont lens wear
-2gtt q15 min for 6 hours
-then 2 gtt q30min for 18 hours,
-next day 2gtt q1hr for 24 hours,
-2gtt GID for 12 days of broad spectrum AB (fluoroquinalones)
Epithelial splitting (SEALS) etiology?
-large dia, thin, high water CL
-tight fitting low water CL, silicone, high Dk Soft lenses
-hypoxia, edge design, papillary hypertrophy, SLK
Management of epithelial splitting
different lens design, different water content, different material
Corneal Wrinkling etiology
mech forces imposed on the cornea by the weight of the lid and lens
-thick RGP
-mid-water content, thin HEMA soft lens
management of corneal wrinkling?
-discont lens wear
etiology of polymegathism?
-prolonged hypoxia
management of polymegathism
no reversible
superficial punctate keratitis (SPK) etiology?
variable depending on the staining pattern
smile face
tight lens
bleph, SLK, conj
inf. libus
bleph, lagophthalmos
nasal/temp, pinguecula
dimple veiling, poor fitting relationship
management of SPK?
varies w/ etio
-art tears
-removal of irritant or refit of the lens
-AB for prophylaxis if indicated based on area and density of staining observed
read LEC #7