contact lenses 4 - complications and aftercare Flashcards
in what 3 moments is contact lens dropout most likely to occur?
-when first fitted with contact lenses
-once becoming an established contact lens wearer
-when reaching presbyopia
most common reasons for these are discomfort and poor vision
what are the main problems new spherical lens wearers have to overcome?
handling and discomfort
what are the main problems new toric and multifocal lens wearers have to overcome?
visual problems
how can you make sure patients are happy with vision aspect of CLs when they are first fitted with them?
- Personalised prescribing for initial lens selection
- Ensure patient is happy with vision at fitting, especially torics and multifocals
- Match lens features to patient requirements (visual task analysis)
how can you make sure patients are happy with the handling aspect of CLs when they are first fitted with them?
- Teach experience
- Follow-up call to check progress and reassure
- Offer additional support, change lens brand, increase modulus
what is contact lens discomfort (CLD)? How is it different to CL related dry eye or CL induced dry eye?
-episodic or persistent adverse ocular sensations related to lens wear, may or may not affect vision and lead to decreased wearing time and CL dropout
-as CLD describes px with pre-existing dry
eye, which may be exaggerated by CL wear whereas the others did not have dry eye before but after having worn the lenses for a while, they now do
how can you manage a patient with CLD?
- determine the most likely cause
- identify corresponding treatment strategy
- stepwise application of treatments to achieve the maximum effect e.g.
-adjust replacement frequency
-change the lens material and/ or design
-tear supplementation
-dietary supplementation
-improve the environment
what are the signs contact lens wear has affected the tear film?
-reduced tear film stability due to thinner/absent lipid layer so increased evaporation
-increased osmolarity
-increased inflammatory mediators where sub clinical inflammation was found in even asymptomatic patients
-ocular surface temperature
-deposition of tear film protein and lipid onto the lens surface only take minutes
what aspects of CLs affects meibomian gland morphology and function?
- Duration of wear
- Type of lens
- Modulus
how do you manage establish lens wearers to prevent them from dropping out?
- Offer convenient options to meet patients changing needs
- Choose products for optimum comfort
- Proactively manage MGD and dry eye
- Offer new lens options
why can presbyopia cause CL dropout?
as increasing prevalence of dry eye with age is likely to impact CL comfort
how do you clinically manage patients with presbyopia who are CL wearers to prevent dropout?
- Inform patients 40 years+ that near vision changes over time and presbyopic contact lens options are available
- Personalised prescribing - tailor vision correction to individual patient requirements (visual task analysis)
- Choose products for optimum comfort
- Use the fitting guide when fitting multifocals
- Set realistic expectations & explain adaptation issues
- Provide both contact lenses and spectacles to meet the spectrum of
patient needs
what are the 3 dyes that can be used to check corneal staining?
-sodium fluorescein
-rose bengal
-lissamine green
what are the types of sodium fluorescein dyes?
- 1 or 2% solution (minim)
- Fluoret (fluorescein impregnated paper strips)
- High molecular weight Fluoresoft (fluorexon)
when may you use high molecular weight fluoresoft fluorescein?
may be used in specialist cl fitting where you need fluorescein to aid the fit of the lens without dying the CL like other forms of fluorescein would
otherwise not commonly used as it doesn’t fluoresce well
why is rose bengal stain not used much anymore?
t is very painful and this can be made worse with UV lights as well
what is lissamine green stain good for?
great for dry eye assessment but not used often as it’s difficult to get a hold of
how do you observe corneal staining? how do you set up the slit lamp? What mag should you use?
-in a z shape so scan from bottom to top
-Direct illumination, ~2mm wide beam,
beam 45º angle, max illumination
-Start at 16x, increase for greater detail
how can you assess corneal staining?
-using grading scales - CCLRU and effron (grade 1-5 based on which the staining looks most similar to)
-the best way being to draw what you see on record & indicate depth one reason being a small amount of deep staining is more serious than large amounts of superficial staining (this is especially true for effron)
how does CCLRU grading for corneal staining work?
you can grade the staining in each of the 3 categories being:
-corneal staining type
-corneal staining depth
-corneal staining extent
why can patients sometimes not be able to tell they have a foreign body in their soft CL?
because the soft CL can sometimes act as a bandage where it depresses the scratch created on the cornea as soft CLs generally do not move.
what are the three types of corneal staining?
-punctates = most common usually seen as small superficial dots
-diffuse - a vast array of closely separated punctates
-coalescent/ patch which is confluent patch of diffuse staining
what are the categories of things that can cause corneal staining?
- Mechanical
- Exposure
- Metabolic
- Toxic
- Allergic
- Infectious
how do you manage foreign body staining?
- Remove lens
- Check FB has gone, evert lid
- Replace lens if damaged
*Use lubricants/ artificial tears to promote healing and reduce discomfort while blinking - Monitor until resolved
how do you differentiate between toxicity staining caused by rgp cleaner / peroxide vs cl solution?
-rgp cleaner/ peroxide is unilateral ( usually unilateral as people usually don’t do it to both eyes) and cl solution is usually bilateral and symmetrical
what are signs of toxicity staining caused by cl solution?
-bilateral and symmetrical
-diffuse SPEE (superficial punctate epithelial erosion) across the whole cornea
-stinging on lens insertion
-cl intolerance
-takes weeks/ months to develop
how do you manage acute toxicity staining?
acute = peroxide/ RGP cleaner
* Remove lens
* Irrigate
* Monitor
* Educate patient
how do you manage chronic toxicity staining?
- Replace lenses
- Trial alternative solution
- Monitor
for SICS, what solution lens combos is it associated with?
Polyhexanide (PHMB) preserved lens care solutions & Group II lenses
what is SICS staining?
solution induced corneal staining - asymptomatic, transient and reversible staining and sometimes considered benign as initially thought to be a response to preservative interaction with lens deposits
how can you manage SICS staining?
-rub and rinse RGPs before overnight soaking
-always teach and remind patients to rub and rinse their lenses on removal
-change to a PHMB free solution
-change to a peroxide preservative free solution
-change to daily disposables
what is 3 and 9 o’clock staining?
in RGP wearers where sometimes the lens lift causes areas of the cornea to not get wet and this sometimes. This can sometimes be triggered by incomplete/ infrequent blinking
how can you manage 3 and 9 o’clock staining?
-refit of the lenses with a bigger diameter- changing the lens to one with an amended diameter due to it being too flat or too steep
-recommend lubricant drops to help the corneal heal.
what is seal staining?
-superior epithelial arcuate lesion and is usually missed as it’s found on the top of the cornea
-typically more common when RGPs were very stiff as this combined with the force of the eyelid caused mechanical chaffing of the cornea but now has a mechanical aetiology in soft lens wearers
how do you manage SEAL staining?
- Lenses out initially
- Recommence lens wear &
monitor - Refit with tighter lens
- Refit with lower modulus lens
what is a smile stain? What is it caused by?
-inferior and arcuate so looks like a smile
-Caused because of dehydration (dessication) of the inferior cornea as the lens causes teg tear film to evaporate Fairly common and can be caused by incomplete blink or dry eye (poor humidity)
how do you manage smile staining?
- Incomplete blinking- give
exercises - Lens drying- refit
- Dry environment- increase
humidity
what is an epithelial plug? How do you manage it?
staining caused by full thickness epithelial loss due to severe and prolonged hypoxia e.g. sleeping in CLs so you need to refer urgently as has ability to impair vision and cause scarring due to it being in the central cornea
what is clpu?
contact lens peripheral ulcer and causes stromal degeneration and overlying epithelial defect - usually caused by non compliance
how do you manage CLPU?
remove the lens (this greatly improves the comfort) and monitor carefully
what is indentation/ musin ball staining?
not true staining but occurs when something has pushed back into the epithelium (e.g. air bubbles) causing an indent which the fluorescein pools into but is not actual staining
how do you manage indentation staining?
- irrigate and if it goes away, then you know it’s not actual staining
-otherwise refit the lens
why is hypoxia bad?
causes a build up of lactate which the body finds difficult to remove and so builds up as a by product of anaerobic respiration
how does oxygen reach the open eye?
through the atmosphere and tear film
where does the closed eye get oxygen from?
-limbus
-palpebral conj
-CLs
how does an eye get oxygen through contact lenses?
via tear exchange in rigid lenses and through the lens material in soft ones
how can you measure oxygen performance of contact lenses?
-Dk
-Dk/t
-EOP
-oxygen flux
what is oxygen permeability?
Dk where
D = diffusivity (ease of which O2 moves through material
k = solubility (ease of O2 dissolving in material)
in Barrer (fatt) units
also un hectopascals (ISO)
what is a Fatt Dk of 1 in ISO Dk (hectopascals)?
0.75 hectopascals
what are the problems of comparing lenses with just Dk?
Higher Dk lenses are thicker and lower Dk lenses are thinner - the level of o2 that reaches the different lenses may be the same due to the thickness difference
in dk/t what is t based on?
typically the centre thickness of a -3.00D lens
what units are dk/t
barrer/cm
what are the problems with dk/t?
*Thickness varies across a single CL and between powers and designs
* Only really relevant to centre of a -3.00D lens
when is there most difference between dk between silicone and non silicone hydrogels?
at lower water content
in a thin CL is dk/t high or low?
dk/t is higher as t is smaller (so less to divide dk by
why can you sleep with certain CL lenses but not others?
Cornea needs a lens with a much higher Dk/t when the eyes are closed compared to when the eyes are open for sufficient levels of corneal oxygen to be maintained.
what are the methods of measuring oxygen on the cornea
EOP - the only in vivo method
Oxygen flux
what is EOP?
equivalent oxygen potential = the conc of oxygen that induces equivalent oxygen thirst of the cornea and ranges from 0-21%
what is oxygen flux?
Amount of O2 that reached the cornea per unit time based on ficks law
is it common for people to sleep with their contact lenses?
no
what can hypoxia cause to the corneal epithelium
-microcysts
-vacuoles
-epithelial plugs
what can hypoxia cause to the corneal stroma?
-oedema: striae, folds and haze
-neovascularisation
-microbial and sterile keratitis
what can hypoxia cause to the corneal endothelium?
-blebs
-guttata
-polymegathism
when may microcysts become something to investigate?
if there are more than 10 as this could indicate hypoxia in the corneal epithelium
for microcysts, what are the symptoms?
normally asymptomatic in terms of comfort and vision
where does microcyst formation start?
Form in the deepest layers due to disorganised cell growth and then move anteriorly and break through the surface of the cornea and that’s when they will cause corneal staining, otherwise you will only see them in white light
what kind of illumination do microcysts show compared to vacuoles?
show reversed illumination so if light is coming from the right, the left side lights up whereas vacuoles show unreversed illumination so light coming from the right hand side means the right hand side lights up because vacuoles have a lower refractive index.
how common are microcysts?
around 100% in pretty much all low Dk lenses with extended wear
how can you observe microcysts?
- 16-25x to locate- more where lens thickest
- 25x appear as grey dots direct illumination
- 40x marginal retro illumination for differential diagnosis- show reversed
illumination as cyst contents have higher refractive index
how can you grade microcysts?
-CCLRU = record the number visible
-Efron (grade 1-4)
what should you expect when treating microcysts
microcyst rebound - you will see an increase in no of microcysts - this is due to removal of the hypoxic response causing the body to increase the metabolism to promote cell growth as a healing response
what are vacuoles filled with
they are gas filled
how can you grade vacuoles?
CCLRU - count the number
are vacuoles or microcysts more common?
microcysts
what causes vacuoles?
corneal oedema secondary to hypoxia
what are the three signs of stromal oedma?
- Striae – fluid separation of collagen fibrils in posterior stroma
- Folds – physical buckling of posterior stroma
- Haze – gross separation of fibrils disrupts regular geometry
what symptoms can haze in stromal oedema cause?
blur/haloes
is some stromal oedema normal?
yes usually theres 3-4% oedmea during sleep and then the stroma deswells when you open your eyes and returns to normal thickness after about 4 hours
what causes stromal oedema?
- anaerobic respiration
- causes an osmotic imbalance
- fluid shifts into stroma from the anterior chamber
- there’s oedema as it cannot be balanced by the endothelial pump
for striae in stromal oedema, what are the signs and symptoms and at what percent of oedema do they arise
- fine, white, vertical lines in posterior stroma, 1-3mm in length
-do not affect VA
-when oedema is >5%
for folds in stromal oedema, what are the signs and symptoms and at what percent of oedema do they arise
-depressed grooves or raised ridges in endothelium
-have no affect on VA
-when oedema is >8%
for haze in stromal oedema, what are the signs and symptoms and at what percent of oedema do they arise
- stroma has hazy, granular appearance
-affects VA when oedema is >20%
-arise when oedema is >15%
how can you see each aspect of stromal oedema?
- Striae - direct, parallel-piped, 25-40x
- Folds - direct/specular, 25-40x
- Haze - sclerotic scatter, 10-25x
what is prognosis for stromal oedema
*CL induced oedema resolves within 4 hours – 7 days of lens removal
* Endothelial dystrophy & diabetes causes impaired de-swell response
* BUT if not resolved long-term, can result in stromal thinning
how can you grade stromal oedema?
-CCLRU by counting number of striae/ folds and see how much oedema that corresponds to
-efron grades 0-4
what might be a differential diagnosis to straie in stromal oedema?
corneal nerves
striae run vertically whereas corneal nerves are radially orientated
what CL will cause worse neovasc?
thick/high powered lenses
when does neovasc become severe?
when the blood vessels are seen to grow close to the pupil
what is neovascularisation?
an acute inflammatory response where new blood vessels grow into the avascular cornea
what are the signs of neovasc
- Limbal hyperaemia
- Corneal infiltrates (white blood cells)
- Vessel spikes from normal limbal vessels (acute stage)
- Lipid deposits from deep stromal vessels
*when blood vessels are not looping back at the limbus
what are the symptoms of neovascularisation?
asymptomatic but there can be visual disturbance if it enters the visual axis
what are the two potential mechanisms of neovasc?
- Hypoxic route: hypoxia triggers release of VEGF
- Hypoxia mediated inflammatory route: hypoxia-induced corneal inflammation signals release of vasostimulating factors in the stroma
what beam type, magnification and mag do you need to see neovasc?
- Use limit of visible iris as reference point to assess extent of limbal vessel
filling - Direct & indirect retro-illumination
- 16 - 40x mag
- Red-free illumination (green filter)
what is the grading for neovasc?
CCLRU - record in mm
efron - grades 1-4
how can you manage grade 1 neovasc?
- Increase O2
- Replace soft with RGP or SiH lenses
- Decrease mechanical stimulation
- WT down
- Stop EW
how can you mange grade 2 neovasc?
- May cause serious threat to vision - cease lens wear
- Require careful monitoring if returning to lens wear
Can you use NSAID’s on neovasc?
can control/ reduce it but then they have other side effects
what managemnet may be needed if neoovasc causes vision loss?
keratoplasty
what is the prognosis of neovasc?
- Vascular in-growth may
regress when CL wear ceased - Larger vessels empty to leave
‘ghost vessels’ - Smaller vessels regress
- However, ghost vessels refill if
CL wear resumed
Give a differential diagnoses to neovascularisation?
limbal hyperaemia where vessels loop back
what can cause changes in corneal endothelium in CL wearers?
-the lactate by product of anaerobic respiration in hypoxia
-hypercapnia where high CO2 combines with H20 to form carbonic acid HCO3
what are the signs and symptoms of endothelial blebs?
- Black, non-reflecting areas within endothelial mosaic
- Greater response soft vs. RGP, thicker lenses, lower Dk
- Increase in number in late evening with EW
- Px asymptomatic
what is the prevalence of endothelial blebs?
- Observed within 10 minutes of CL insertion
- 100% CL wearers
what can cause endothelial blebs?
- local oedema
- so endothelial cells bulge posteriorly
- local acidic change in pH at endothelium due to hypercapnia and hypoxia causing increased lactic acid?
local acidic change is stromal acidosis and hypercapnia is the slowing of co2 efflux
how do you observe endothelial blebs?
40x specular reflection
how can you grade endothelial blebs?
efron grading 0-4
what are endothelial guttata?
the focal accumulation of collagen on Descemet’s membrane formed by abnormal endothelial cells causing disruption to the regular end. mosaic - reduced cell density = reduced pump function
asymmetric, bilateral and progressive
how are endothelial guttata different to endothelial blebs?
-guttata are not really CL related while blebs are
-guttata are larger and permanent while blebs are smaller and not permanent
what are the signs of guttata?
small dark spots in the central cornea
what disease are endothelial guttata associated with?
can be a precursor to fuchs endothelial dystrophy
what is the prevalence of endothelial polymegathism?
- Normal age-related change
- CL wear accelerates this change
what are the signs and symptoms of endothelial polymegathism?
- Cell density & regularity decreases: In 25-year-old diameters 1:5, In advanced case in CL wear 1:20
*Connected with corneal exhaustion syndrome? Causes loss of endothelial pump function - Asymptomatic
what causes endothelilal polymegathism?
the chronic response to CL wear induced hypoxia and hypercapnia
how can you observe end. polymegathism?
40x specular reflection
what is the grading system for end. polymegathism?
-efron: 0-4
-CCLRU: 1-4
what is the management and prognosis to endothelial polymegathism?
-unclear of needs management
-irreversible so prognosis is poor
what contact lenses is lens damage more common in?
soft, thin and disposable lenses
what can cause lens damage?
- Manufacture defects
- Poor lens handling
- Lenses trapped in cases
what are signs and symptoms of the patient having inserted a damaged contact lens?
- Discomfort
- Associated bulbar conj/limbal redness
what are the management options for patients that have used damaged CLs?
*Replace lens
* Re-teach patient
* Change manufacturer / lens type: 2 weekly lens or RGP/ one with higher modulus so its thicker and less easily damaged
* Change type of lens case - maybe go for a flat case if the lenses are getting trapped
if a patient tells you they think they lost their CL in their eye, what should you do?
-assume the lens is still in the eye
-load their eye with fluorescein so its easier to see as the lens will absorb some of the dye
-lubricate eye and evert upper lid to sweep the CL with a cotton bud if it’s there
why are contact lens deposits bad?
- Reduce lens surface wettability = discomfort
- Cause inflammatory complications
- Contaminate the lens case
- Be a food source for microorganisms
what are the two types of lens deposits?
-intrinsic
-extrinsic
what are the types of intrinsic lens deposits?
-protein, lipid, mucin and calcium deposits
-jelly bumps
-mucin balls
what are the types of extrinsic lens deposits?
-environmental
-lifestyle
-non compliance
what is the most common intrinsic contact lens contamination?
protein - specifically lysozyme, found in tears as part of the innate immune system by killing gram positive bacteria but becomes problematic if it denatures
what lenses are protein deposits most likely to form in?
group III and group IV
what lenses are lipid deposits most common in?
group II high WC non ionic lenses and mainly in SiH lenses
what can make lipid deposits on lenses worse?
cosmetics or MGD
what are jelly bump deposits made of?
made of protein, lipid and calcium in layered combinations
how common are mucin ball lens deposits?
affect around 50% of siH wearers
what kind of lens are mucin ball deposits associated with?
looser and stiffer lens as shear forces roll up mucin into balls - especially common if the patient sleeps with their lenses
what are the variables that affect lens deposition?
MDG - affects tear composition
The length of wear tine if the lens
Lens replacement frequency
Having higher water content lenses as when they dry out, deposits stick on
Environmental pollution and work environment
Type of contact lens solution
Compliance
Wearing makeup
how can you manage lens deposits?
- Replace lens
- Review compliance
- Address contributing factors- make-up, MGD
- Increase replacement frequency
- Change lens material / type
- Change care regime – MPS to hydrogen peroxide solution as the latter does not need rubbing and rinsing so may increase compliance
- Additional lens cleaning products
what are the steps to good contact lens insertion?
- Wash & dry hands
- Apply lenses
- Empty case
- Rinse with solution
- Wipe with tissue
- Place case & caps face down on
clean tissue
what are the steps for good contact lens removal?
- Wash & dry hands
- Remove lens
- Rub & rinse lens (NEVER WITH WATER)
- Fill case with fresh solution (REPLACE LENS CASE REGURLARLY - at least every three months)
- Insert lens, re-cap case & leave
for at least MRDT
in terms of deposits how are SiH different to standard hydrogels?
-they have more lipid deposits
-they have less protein deposits but these are more likely to be denatured
what might you recommend to patients whose lens deposits dont seem to be going away with the standard management options
recommend premium contact lens solutions like B+L Replenish, alcon ever moist and alcon bio true because they:
*include Surfactant & wetting agents
* Remove lens surface deposits to promote wettability
* Condition the lens surface to enhance and promote wettability
what additional cleaning products can you recommend to patients getting lens deposits on their CLs?
- Surfactant Cleaner
- Enzymes used to remove denatured or bound tear proteins
- Progent (Menicon) which is a weekly protein remover, disinfectant and intensive cleaner
compatible with all rigid contact lenses
what patients are surfactant cleaners recommended for and give an example
- Mainly used for patients with very greasy lenses or stubborn
deposits - Ote Clean / i-clean - alcohol based – lipid solvent and wetting agent
give and example of an enzyme you can use as a cleaning product for patients with deposits on their CLs
Amiclair (Abatron) – tablet formulation, triple enzyme formulation
(removes protein, lipid & mucin)
where on the eyes can you see contact lens induced papillary conjunctivitis?
on the upper tarsal conjunctiva - not really seen on the inferior eyelid as it does not move much on bink and does not really interact with the contact lens
what is clpc?
contact lens induced papillary conjunctivitis - an inflammatory condition of the upper tarsal conjunctiva so hypersensitivity reaction which is linked with lens deposits and mechanical trauma caused by lens movement and the lens edge rubbing on the tarsal conjunctiva
what are the signs of CLPC?
-redness and small papillae: early
-thickened tarsal conjunctiva giving it a cobblestone appearance
why should you always evert the upper and lower lid in CL appts
because you need to check for any signs of CLPC as if thats the case the px should not wear cls until it resolves
why not always check for CLPC with fluorescein?
because fluorescein lets you see the papillae but you need to check for redness first as that will be the initial sign and for that you need a white light ideally no staining to best pick it up
how can you grade cclru?
using effron - you can grade roughness and redness
what do papillae in CLPC consist of?
connective tissue infiltrated with cells
associated with inflammatory reactions
what are the symptoms of CLPC?
- Itching
- Lens intolerance
- Burning, photophobia,
lacrimation, foreign body
sensation, redness - Sticky mucous discharge
- Reduced quality of vision with
lenses
how can you observe for CLPC?
- Evert top & bottom lids- 10-15x
mag. - Observe central tarsal plate
- Observe redness/roughness
- “cobblestone appearance”
- compare to lower lid (baseline)
- Mucus formation?
- Vessels may show at papillae
apex (40x mag)
what are the two distinct forms of CLPC?
localised and generalised
what is the difference between localised and generalised CLPC?
-localised papillae tend to be confined to the tarsal conjunctiva near the lid margin whereas generalised - the enlarged papillae are present across the entire palpebral conjunctiva
-localised may be more mechanical related whereas generalised may be more immune related?
when may you do pharmacological intervention of CLPC?
if the grading is more than 2
what are the pharmacological treatments for CLPC?
what are the non pharmacological treatments for CLPC?
what is the prognosis of CLPC?
-symptoms resolve once CL wear is stopped
-papillae can take 2 weeks - 6 months to resolve
-large papillae apex may scar giving whiteish appearance
what may GPC be associated with
typically not CL wear
* Ocular prostheses
* Nylon sutures
* Scleral buckles
* Elevated corneal abnormalities
* Blebs
what are some causes of ocular surface hyperaemia?
- Inflammation / Infection
- Metabolic – hypoxia
- Hypoxia (inverse relationship of limbal hyperaemia
& Dk) - Mechanical- localised hyperaemia when lens
defect, poor lens fit, lens - Toxic / allergic
- Exposure
what are the symptoms of ocular surface hyperaemia?
-discomfort
-pain (could be due to infection)
what does limbal redness tell you in soft CLs?
the more the limbal redness, the lower the DK/t and so indicates corneal hypoxia
how do you manage ocular surface hyperaemia?
- Identify cause & if acute / chronic
*refit the lens so change the type, design, material or modality
*change the care system
*improve ocular hygiene and compliance
*address any dry eye
what are differential diagnoses to limbal hyperaemia?
- Superior limbal keratoconjunctvitis (SLK)
- Neovascularisation
what is sterile keratitis?
an inflammation of the cornea caused by toxins, proteins and enzymes being released by bacteria and causing an indirect pathogenic effect - it is not a direct microbial infection
what are the types of sterile keratitis?
-infiltrates (accumulation of inflammatory cells)
-infiltrative keratitis
-CLPU
-CLARE
what can cause corneal infiltrates?
-trauma
-hypoxia
-allergy
-CLARE
what are the signs of corneal infiltrates?
◼Dull, grey, grainy hazy appearance, <1.2mm diameter
◼Sub-epithelial or intra-epithelial
◼Typically observed near limbus
what are the symptoms of corneal infiltrates?
generally none
how can you observe corneal infilatrates?
- Direct/indirect illum
- 16-30x mag
- Typically associated with localised bulbar and limbal hyperaemia
graded using efron
what is infiltrative keratitis associated with?
commonly associated with daily and monthly wear lenses
what are the signs of infiltrative keratitis?
◼Usually unilateral, small multiple focal infiltrates (up to
0.4mm) in or mid-periph or periph cornea
◼Overlying epithelial involvement- punctate or erosion
◼No AC involvement
what are the symptoms of infiltrative keratitis?
can be asymptomatic or can have mild to moderate irritation and lacrimation
how can you manage sterile keratitis?
-Generally self limiting - once the patient takes the lenses out it should get better but you should call the patient back in a few days to check
-Any doubt it’s not improving, refer to HES as it could be MK
-Sometimes they can give a prophylactic antibiotic to make sure there ulcers do not infect and lead to MK
-Make sure patients do not throw away their lenses so you can examine the culture
-Prognosis is usually very good
-You need to make sure to educate the patient after as often this has been due to non compliance
-Make sure the Px does not put the lenses back in their eyes until you give them the go ahead or else they may get a rebound effect
what causes CLPU?
where gram positive bacteria release toxins from enzymes and trigger an inflammatory response
how can you be more sure that CLPU is not microbial keratitis
as clpu occurs on the periphery whereas MK is more central and CLPU symptoms improve when the lenses come out whereas in MK the symptoms do not improve after taking out the lenses
how can you observe CLPU?
◼Direct illumination
◼16-30x mag
what are the signs of CLPU?
◼Single circular lesion (0.5-1.5mm), periph or mid-periph,
associated limbal & bulbar hyp.
◼NaFl diffuses into stroma- glow/halo
◼Slight ant chamber activity?
◼Scar remains
what are the symptoms of CLPU?
moderate to severe pain with lacrimation and FB sensation
this improves on lens removal
what causes CLARE?
where proteases released by bacteria get trapped under the CL and trigger an acute unilateral inflammatory response
what are the signs of CLARE?
Conj & limbal hyperaemia, corneal infiltrates near limbus, AC flare, endothelial bedewing
what are the symptoms of CLARE?
-starts in the morning
-painful red eye
-tearing
-photophobia
what are the predisposing factors to microbial keratitis?
-px is immunocompromised
-poor compliance
-poor hygiene
-prolonged exposure to debris/ toxins/ antigens trapped in post lens tear film
-microbes adhered to the contact lens as they get retained on the corneal surface
basically hypoxia and epithelial break
what are the signs of MK?
Redness, lid swelling, lacrimation, photophobia, loss of VA
* Infiltrates, stromal haze, epithelial break & ulcer
* Focal ulcer progression, creamy, purulent ulcer, AC flare, iritis, hypopyon
* Stromal melt & perforation
what are the symptoms of MK?
- Initially – FB sensation / pain that does not improve or worsens on lens
removal - Later – very severe, extreme pain
which bacteria is the most common cause of MK?
pseudomonas
what are the signs and symptoms of pseudomonas keratitis?
- Corneal oedema & ring abscess (defined as circular infiltrate with less
dense centre) - Mucopurulent discharge common
- Reduced VA, injection, lid oedema, anterior uveitis (hypopyon
possibly) - Corneal melt & perforation (in as little as 24-36 hours)
- Loss of aqueous = Retinal detachment
-symptom of severe pain
where can you be at risk of getting acanthamoeba keratitis?
swimming pools, hot tubs, air soil, water, your nose
what are the signs of acanthamoeba keratitis?
- Dendritic, patchy stromal infiltrates
- or radial keratoneuritis- circular formation of opacities
- Perineural infiltrates (infiltrates running along nerves –
occur in approx 60% cases) - Scleritis
what are the symptoms of acanthamoeba keratitis?
patient is complaining of severe pain even though the signs dont seem to warrant such severe pain
what kind of lenses is MK most likely in?
soft lenses compared to hard
what is a differential diagnosis to acanthamoeba keratitis?
herpes dendritic ulcer due to herpes simplex
what is fusarium keratitis and where is it most likely? What are the signs?
keratitis caused by fungus found in soil,
vegetation and water, in tropical and subtropical climates
signs are large white infiltrate with fluffy or branching margins
what are the modifiable risk factors of MK?
Occasional ON wear
Poor lens cleaning
Improper cleaning of lens case and replacement
Poor hygiene
poor/ no hand washing
swimming/ showering
Poor GH
Smoking
Purchase on internet so not being educated in teach
Hypoxia
Mechanical trauma
Lens deposits
what are the non-modifiable risk factors of MK?
Younger age
Male gender
Socioeconomic status
Warmer climate
Poor GH
how can you help differentiate between sterile and infective keratitis?
use PEDAL
Pain
Epithelial defect
Discharge
Anterior chamber reaction
Location
look at the table that differentiates between sterile and infective keratitis
page 10 in google doc op2502 term 2
how do you manage any infective keratitis?
-urgent referral to eye casualty and take the lenses and case + corneal scraping for culture identification
-treatment is specific to the causative microbe so bacterial keratitis treated with topical antibiotic and ak is treated with biguanides (PHMB) and diamidines
