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
