5.2.1 manage soft aftercare Flashcards
Go through a routine of soft cl aftercare
- H&S- (rfv, sx check like in an ee, details of current cl wear and compliance (how long wearing the type of lens, how old current pair, how often do you replace, have you tried any different lens types in the past and why stopped, have you ever stopped wearing, how many days per week, how many hours comfortable lens wear, how long would you like to wear them, how often sleep/shower/swim in lenses, do you have back up specs FINISH OFF), MH+OH, needs from cl’s)
- VA
- Over refraction (and oculomotor balance)
- Slit-lamp assessment of lens fit and condition (centration–>coverage- blink, lag, pushup-determine of lens too tight, too loose or acceptable/good–>lens condition)
- Observe px remove lenses
- Slit lamp assessment of the anterior eye and tear film asessment (first non-invasive
(optional-assessment of corneal shape (topography/keratometry to monitor, other clinical checks like ophthalmoscopy if needed, refraction if indicated) - Summary of outcome with advice and attention to rfv and re-education of lens wear and care, emergency advise
- Review date and advise if need any other examination if not up to date
What type of deposits do different cl materials attract?
Silicone Hydrogel material attracts lipid
Hydrogel material attract protein
How does modulus affect handling and corneal interaction?
Lower modulus lenses are harder to handle but are softer and less likely to cause issues on cornea
Higher modulus lenses are easier to handle but can cause Superior Epithelial Arcuate Leasions (SEALS)
How does Lid Wiper Epitheliopathy (LWE) relate to lens type and eyelids?
A lens with a higher coefficient of friction is more likely to cause LWE.
Px with tighter lids influence the lens too
What is the incidence of Microbial Keratitis (MK) in daily soft cl wear compared to daily disposable, RGP and extended wear?
0.02-0.04%, it is slightly lower in dd wear and RGP wear
Increases to 0.2% in extended wear
What is the gross anatomy of the cornea?
epithelium–>Bowman’s–>Stroma–>Descemet and Dua’s—> endothelium
What is the epithelium and how does a foreign body affect this?
It makes up approx 10% of total corneal thickness
smooth surface
absorbs oxygen and nutrients
cells attach and organise at basement membrane
if any foreign body goes onto it, it is superficial if it only involves the epithelium and heals uneventfully
What is Bowman’s layer and how does a fb affect this?
Transparent compacted collagen
Acellular anterior layer which protects the stroma
once injured it cannot regenerate= necessary replacement by epithelial tissue or stromal scar tissue
What is the stroma and how does a fb affect this?
90% of corneal thickness
water and collagen
unique shape, arrangement and spacing of collagen allows transparency and strength
A fb disrupts the regular arrangement and spacing of collagen fibrils, leading to scarring
What is Descemet’s Membrane/Dua’s?
Thin strong layer with a protective barrier against infection and injuries
What is the endothelium?
Thin, single hexagonal cell layer
Keeps cornea transparent by regulating the water content of the stroma- done by ion transport via HCO3 (bicarbonate) and Na+-K+ ion pumps
cannot regenerate and cells reduce throughout life
minimum 700 cells/mm2 required for integrity function and metabolism, if less than 500 cells/mm2 then function fails
What are corneal nerves and how do fb affect it?
located in the stroma
most rich innervation of nerves in cornea compared to all body tissue (400times more than skin) and is innervated by ophthalmic division of 5th cranial nerve (trigeminal)
maintains anatomical integrity and function of the cornea, in particular the epithelium- loss of sensory innervation causes reduced function of epithelial cells and leads to epithelium breakdown
corneal abrasion stimulates nerves causing pain and photophobia
How doe eyelids protect against disease?
dislodge bacteria, epithelial cells and fb
How do tears protect against disease?
Mechanical: flushing out fbs
Biochemical: immune molecules with bactericidal properties use tears as a medium: secretory lgA helps prevent bacteria adhering to epithelium, lactoferrin limits bacterial growth and biofilm formation by destabilizing bacterial membranes
How does the epithelium protect against disease?
- smooth surface prevents microbial adherence
- continuous epithelial turnover
- multiple layers
- tight cell junctions (basal lamina pores smaller than bacteria) and cell polarity
- corneal epithelial cells express immune receptors on their surface which are targeted against pathogenic products
How do contact lenses compromise corneal defence?
- overall reduced corneal thickness
- reduced rate of epithalial cell turnover
- reduction in corneal sensitivity
- may cause breaks in epithelium
What are non-infective/inflammatory corneal infiltrates and what are the signs?
- raised tisse with immune cells confined to anterior stroma
- looks like focal areas of granular appearing grey-white opacities in anterior stroma- often associated with limbal/conjunctoval hyperaemia
- will stain with fluorescein, can be flat/raised and when viewed with optic section it is in the epithelium- it is superficial so no epithelial defect
- excess lacrimation, but no sticky discharge, localised/sectoral mild to mod bulbar conjunctival redness
- no eyelid involvement/ac reaction
- smaller than ulcers (<1mm) found in periphery (<2mm from limbus) and often multiple in number
What causes corneal infiltrates?
inflammatory non infective
- bacteria does not invade or replicate in the cornea and usually no progressiom to infection
- cl associated infiltrative keratitis is considered to be a response to microbial (usually Staphylococcal) antigens, derived from bacteria on the cl or lid margin (microorganisms cannot usually be recovered from the lesions (in dd SIHy 0.4% per year incidence- higher in re-usable and much higher in EW)
- may be seen alone or with an ulcer
Who is more at risk of corneal ifiltrates (non-infective/inflammatory) that are alone (without an ulcer)?
- cl px- immune response to lens material interaction with cornea/overwear/EW
- Immune response to viral keratitis
- Response to pathogens on the eyelid margin
- Smoking
- Poor hand hygiene
What are sx of corneal infiltrates?
Asx to mod discomfort and fb sensation
no/mild photophobia and no visual loss
How to investigate corneal infiltrates to differentially diagnose against ulcers?
- Use optic section on slit lamp to check depth and whether lesion is raised or flat (infiltrate) or excavated (ulcer)
- Check AC for cells/flare and hypopyon (signs of ulcer not infiltrate)
- Use fluorescein to rule out makor epithelial loss (ulcer)
How to manage corneal infiltrates?
- Non infected infiltrates:
- artificial tears to provide sx relief
- temporarily discontinue lens wear
- manage any blepharitis
What are corneal infected ulcers (microbial keratitis) and what are the signs?
-melting of tisse due to enzymes released by microbes or as part of an immune response
Edges: excavated lesion in anterior stroma with rolled and indistint edges
Staining: stains well with fluorescein with pooling and seepage into surrounding cornea
Oedema: may have stromal oedema throughout cornea
Redness: Severe redness in usually entire bulbar conjunctiva
Discharge: often sticky (mucopurulent) discharge which may coat the corneal ulcer
Eyelid: mod to severe lid involvement with swelling and in severe cases ptosis
Anterior Chamber: may be AC reaction-uveitis type with cells/flare and with hypopyon in severe cases
Location/size: large depressed lesion (>2mm) in midperiphery or corneal centre (>3mm in from limbus), although initially present peripherally
