Contact lens physio Flashcards
physio criteria for well-tolerated cl
absence of clinically significant lens-related physio problems
no sig. corneal staining
no vertical striae
no sig. papillary conj. changes
absence of limbal vessel engorgement and vessel penetration
no sig. conj. injection
less than 6% central corneal thickness inc. after 6 hours wear
epithelial microvilli
intermeshed w/ secreted glycocalyx to attach to mucin layer of the pre-corneal tear film
corneal metabolism
metabolic pump - endothelial pumps control flow of lfuids
oxygen glucose metabolism
acidosis (lactate buildup) leading to edema
corneal sensitivity
corneal edema types
central circular clouding (CCC) - epithelial
-typically produced hard pmma cl wear
vertical striae (stromal): folds -typical of soft cl wear
striate keratopathy (fold in descemet's) -more severe with bolus keratopathy
microcystic edema
-typical in extended wear cl
superficial punctate keratitis (SPK)
epithelial microcysts
chronic edema leading to neovascularization: perilimbal enlargement can lead to neovascularization
Central circular clouding (CCC)
PMMA edema
most likely won’t encounter because more oxygen is transmitted to newer cls
central epithelial haze
edematous myopic shift great deal of light scatter
less tight jxn
spectacle blur - blurred vision caused by edema experienced by patients
caused by epithelial edema and associated light scatter
grades 1-4 (4 max)
temporary myopic shift causing refractive blur
steepening of central Ks correspond to location of optical zone of rigid lens
epithelial microcysts
commonly seen in those that sleep in hydrogel (hema) lenses
occurs after 2-3 months of extended wear
can number up to 50-100 per eye
asymptomatic
sign that cornea is experiencing long-term oxygen deprivation causing damage to deep layers of epithelial cells (cystic formations) with entrapped BM elements – distorted packets of basement membrane with cystic formation from sleeping in soft cl
microcyst display reversed illumination
microcyst vs vacuole in high mag slit lamp
microcyst display reversed illumination
vacuoles display unreversed illumination
vertical striae (stromal edema)
6-8% stromal thickening
striae tells cornea has thickened at least 6%
more edema = more striae
no steepening of central Ks, only corneal thickening
no myopic shift with epithelial edema
can develop striate keratopathy
Fuc’s dystrophy non-cl related stromal edema
pre-fuch’s : guttata of endothelium
-tiny droplets/outpouchings
fuchs: damage to endo overcomes the endothelial pump; aqueous enters stroma
- usually seen with striate keratopathy
- may require corneal transplant
severe keratoconus: corneal hydrops
total overpowering of endo pump (acute event) due to extreme ectasia (thinning) in the cone (break in descemet’s)
- occurs in advanced keratoconus
- cornea becomes white and edematous
- cornea eventually clears out
3-4 month healing time
limbus
vascular transition zone containing blood vessels
main points:
- vascular arcades
- limbal hyperemia
- vessel penetration
- neovascularization
- micropannus
limbus vascularization/ hyperemia
limbal engorgement (precursor to neovascularization)
- hypoxia cause
- mechanical irritation
- chemical response
lack of oxygen directly looking at limbal region
perilimbal injection
sign of cl-induced corneal edema especially in cases of EW
general conj. injection or redness is not a sign of corneal edema
- infection
- inflammation
- not due to oxygen
disappears when refitted from hema to silicone hydrogels
neovascularization
typically response to lack of oxygen (hypoxia)
extended wear vascularization
chronic corneal staining - loss of epithelial cells scattered across surface
toxic (thimerosal)
disease (staph toxin)
may or may not be perminant -> ghost vessels remain
neo vessels are more fragile and can produce intra-corneal hemes
the conjunctiva - cl related
goblet cells and mucus secretion
accessory glands of kraus and wolfring (aqueous tears)
papillae
follicles
mast cells and allergic rxn
-GPC
normal microbial flora
inflammation and infection
non-cl vs cl-related palpebral conj. changes
folliculosis: mostly occur in lower lid for virals, std usually in upper lid
- typically viral or chlamydial response (look for water and swolen preauricular nodes)
- giant follicles of upper lid must be differentiated from GPC papillae
papillae: caused by mast cell production, can occur upper lids -> swuared off elevation and central stalk, more opaque than follicles
- characteristics
- mast cell infusion and degranulation
- GPC
papillae classification
junctional papillae:found on tarsal plate
micropapillae: found in city dwellers from environmental exposure
macropapillae: inflammation due to allergies, CL can be treated with medication - clinically significant finding and should intervene
giant papillae: upper lid
chemosis (allergic swelling)
type 1 (immediate) hypersensitivity response
not directly caused by CL wear
the lids
anatomy
blinking
bell’s phenomenon
palpebral fissure (aperture)
glands of zeis and moll
meibomian glands (and MG dysfxn)
palpebral conjunctival zones
5 zones
lids inspection
can have phthiriasis palpebrarum -> crab lice
-tx: removal, destruction, delousing
evert lid
inspect meibomian glands and suderiferous glands
-sweat gland can produce foreing body sensation
capped glands
aka blocked meibomian glands
mybomian gland dysfxn aka posterior blepharitis
MGD: keratinized plugs -whitish zones
dry eyes
caused by plugged glands
infrared meibomography can show lids assessment
meibomiam gland fxn important in cl because prevents quick evaporation
MGD treatment
warm heat
bruder mask
manual expression
expression with aid of instruments
lipiflow system
mibo termoflo
cornea and conj stains
sodium fluorescein: cobalt filter to observe fluorescein dye
- used to observe patterns on RGP lenses
- can be enhanced with wratten yellow filter
- corneal abrasion observed w/ fluorescein
- intercellular
rose bengal and lissamine green
-intracellular staining
contacts in contact with tear
tears
- keep cornea moist
- provide oxygen
- maintain smooth surface for even refraction
- wash away debris
- destroy microorganisms
- remove metabolites
tear film layers
old layer:
- lipid
- aqueous
- mucus
holly model:
- superficial lipid layer
- dilute mucin solution
- mucin coacervate
- absorbed mucin layer
- corneal epithelium
current model:
- mucin likely form gradient
- superficial mucin interact w/ lipid layer to dec. surface tension
- bottom mucin help aqueous fluid stay on cell membrane
- different mucins: secreted by goblet and nongoblet epithelial cells
- membrane spanning mucin and mucin like glycoproteins near cell membrane form glycocalyx
newest tear film model
DEWS II
two phase model of tear film with lipid layer overlying a mucoaqueous phase
lipid layer contains polar and non-polar lipids.
mucoaqueous layer contains 4 major mucins and over 1500 diff. proteins and peptids and overlies the carbohydrate-rich glycocalyx of apical epithelium
glycocalyx
produced by corneal epithelial surface cells
help bind mucins onto corneal surface
dry eye and osmolarity
when osmolarity > 312 mOsm/L, dry eye occurs
tonicity effects and CL
hypertonicity: low salt enviroment -> water sucked in
hypotonicity: water pushed out -> reducing corneal edema
precorneal tear film - aqueous layer
derived from main and accessory lacrimal glands
comprises 90% tear volume in normals
contains H2O, electrolytes, O2, lysozyme, lactoferrins, IgA, peroxidases and albumins
precorneal tear film - mucin layer
derived from conj. goblet cells
act as wetting agent
allows spread of stable tear film
role in expulsion of foreign bodies
TBUT - tear breakup time
interval between complete blink and first randomly distributed dry spot
tear film break up viewed with fluorescein stain on patient with dry eye.
normal >10 sec
schirmer test
normal = 10 - 15 mms / 5 min
external ocular biota
sparse coonization of ocular surface
- lids 60% of cases
- conj 40% of cases
mainly gram pos. species
- coagulase-neg. staphylococci
- corynebacterium spp.
other: propionibacterium spp. S.aureus, microccus spp., bacillus spp.
gran-neg. organisms isolated infrequently (<5%)
CL related peripheral ulcer
sterile infiltrates
CLPU associated with ocular carriage of gram-pos. bacteria especially S.aureus
toxin released cause inflammatory rxn in eye
sterile infiltrates associated with bacterial contamination of storage case
hypersensitive ulcer not infectious
basically heal themselves but scarring occurs
seen in CL sleepers
Biofilm
fxn consortia of microorganisms, organized at interfaces, within exopolymer matrix
resist antimicrobials by physical exclusion and phenotypic alteration
role: explains unexpected persistence of organisms in storages cases
- may play part in pathogenesis of infection
CL acute red eye
CLARE
-caused by endotoxins released by gram - microbes adherent to extended wear lenses
pseudomonas aeruginosa
severe red eye and pain
sleeping in soft lens and large gram neg buildup
pseudomonas corneal ulcer microbial keratitis (MK)
sight theatening
vision lost 24-48 hours if penetrates cornea
