CL - Contact Lens Complications - Week -1 Flashcards
What are the 4 broad causes of contact lens complications?
Inflammation (e.g. allergy, immune response)
Mechanical (e.g. rubbing, poor fit)
Microbiological (i.e. infection)
Hypoxia
What are 6 common risk multipliers for contact lens complications?
dry eye male smoker extended wear lifestyle compliance
What should be covered in the history of a contact lens wearing patient? (10)
PC: VA? Photophobic? Pain? Red? Discharge? Onset + duration? EW? Lens characteristics (type, age, replacement) Care system (rub/rinse?) Compliance GH, Ocular medications (Rx + OTC) Tap water/swimming/showering
What 3 dyes can we use to assess ocular surface damage?
Fluorescein (NaFl)
Rose Bengal
Lissamine Green
What do Rose bengal and lissamine green stain?
damaged cells and devitalized areas of the surface
Which is more toxic: rose bengal or lissamine green? How can we minimise discomfort for the more toxic dye?
Rose bengal is more toxic to the ocular surface and thus causes stinging. (can use topical anaesthetic to minimise discomfort)
How should we score ocular conditions on grading scales?
To the first decimal
How should we manage corneal staining if the cause of staining is infection, toxic, allergic or inflammatory?
treat the overall condition
How should we manage corneal staining if the cause is hypoxia?
increase Dk/t or decrease WT (wearing time)
What happens to a CL patient with epithelial loss?
nerve ends get exposed, resulting in pain
How long does superficial staining of the cornea take to heal? What about deep staining?
Superficial: 24 hours
Deep: 1-2 days
For how long should a patient cease contact lens wear if they have deep corneal staining?
2-4 days while treating the cause
How can we manage corneal staining if the stroma is affected?
consider prophylactic antibiotics (CHL 0.5%) (or aminoglycoside for better gram -ve cover)
How does the eye protect itself from infection? (3)
Cell shedding + wiping action of blnking
Irrigation by lacrimal secretions
Antimicrobial defenses (tear lysosoyme, immunoglobulins, anti-microbial peptides on ocular surface)
What does PEDAL stand for? (differentiating ulcer vs infiltrate)
Pain Epithelial defect Discharge AC reaction Location (central/paracentral) (bonus: lid swelling/oedema)
How does the staining of an ulcer compare to infiltrate?
Ulcer: 1:1 staining defect/lesion ratio
Infiltrate: small staining
How does the level of conjunctival infection of an ulcer compare to infiltrate?
Ulcer: generalised conj injection
Infiltrate: sector skewed injection
How does the number of lesions in an ulcer compare to infiltrate?
Ulcer: usually single lesion
Infiltrate: can be multiple lesions
What microbe is most commonly responsible for MK?
Pseudomonas
How does pseudomonas aeruginosa cause damage? (2)
Exotoxins inhibit protein synthesis Biofilm generation (glycocalyx; polysaccharide)
Where can you find acanthamoeba? (4)
Soil, air, fresh water, tap water
What percentage of keratitis is due to acanthamoeba? What percentage of acanthamoeba keratitis is due to contact lens wear?
<1%
85%
When is acanthamoeba keratitis often diagnosed?
When bacterial management not working (e.g. improving, but never getting better)
When must you refer any corneal lesion?
when the lesion is on the visual axis
How can you manage MK?
Fluoroquinolones - g15min loading, then g1hr
In accordance with SCUT: How does high dose steroid treatment affect visual outcomes in patients with culture-positive bacterial keratitis? What was the odds ratio
Better visual outcomes. Odds ratio of better outcomes with high dose steroids was 5.49
In accordance with SCUT (steroids for corneal ulcers trial): what factors were significantly associated with visual outcomes? (5)
high-dose steroid treatment visual acuity on presentation age group cause of keratisis infiltrate size/location
Are infiltrates unilateral or bilateral
Can be either uni or bi-lateral
Are infiltrates symptomatic?
Can be either
How much epithelial excavation occurs with infiltrate?
only slight excavation
Name 3 possible causes of infiltrates in a contact lens wearer
Poor compliance
MG dysfunction/bleph
Hypersensitivity (e.g. to lens, solution, bacteria)
How can we treat infiltrates? (4) When should we review? (1)
Cease lens wear Steroid/antibiotic Change lens type/modality/WT/replacement If suspect infection - tx as infection Review 24 hours
What is CLARE? What patients is it common in?
Contact Lens Acute Red Eye: immune response to acute or chronic hypoxia.
Common in EW patients
Can CLARE present with bacterial presence?
yes. May or may not have presence of high bacterial load on the contact lenses that is being trapped in close proximity to the ocular surface
How may tight lenses contribute to bacterial accumulation in CLARE?
no tear exchange to flush toxins
List 5 signs of CLARE
Painful red eye +/- photophobia Diffuse + focal infiltration Corneal epithelial + stromal oedema Conj + limbal oedema, injection Peripheral, multiple? culture negative infiltrates
How do we manage CLARE? (2)
Cease lens wear
Consider steroid with or without antibiotics?
How does GPC occur?
mechanical irritation/inflammation/allergic response
What is GPC associated with? (5)
Soft (5-10%)/RGP(3-5%) CLs Prosthetic devices Exposed sutures Glaucoma filtering blebs Corneal scars
What are papillae? Where are they mainly located? Where do they first appear?
Hyperplastic conjunctival epithelium
Mostly in upper palpebral conjunctiva
First appear at margin of tarsal plate
What are the major causes of papillae? (2)
CLPC (contact lens induced papillary conjunctivitis)
Vernal conjunctivitis
What are follicles? Where are they mainly located?
Hyperplastic lymphoid tissue
Mostly found in inferior forniceal conjunctiva
What are the major causes of follicles? (2)
Viral infection
Hypersensitivity to solutions
How can you tell follicles and papillae apart?
Follicles: encircled by vessels, rice grain appearance
Papillae: central tufts of vessels, appear like cobblestones
How can we treat CLPC (CL induced papillary conjunctivitis)? (3)
Cease lens wear
Preservatives free cleaners/frequent lubrication
Reduce protein exposure (change to daily disposable if SCL, or in-office lens surface polish for RGPs and increased frequency of protein removal for any CL)
How long may grade 3-4 CLPC take to treat? What happens if left untreated for many years?
1-6 months. If untreated, you’ll get conjunctival scarring
Name 6 mechanical complications from contact lens wear?
FB staining (RGP >>> SCL) RGP and SCL binding Epithelial wrinkling (thin, high water SCL) Bubble indentations (RGP fit issue) Mucin balls SEALS
What are SEALS? Who is affected by them?
Superior Epithelial Arcuate Lesion. Affects SCL wearers (more commonly Si-H)
List 2 signs of SEALs
Epithelial split
Staining with Nafl
What causes SEALS? (3)
lens thickness
modulus
lid force (tight lids?)
How can you treat SEALS? (3)
Discontinue wear until resolves (~1-2wks)
Change SCL design (softer modulus)
Change to RGPs
How do mucin balls form? Are they punctate staining?
Form via interaction of lens surface and corneal epithelium in higher modulus lenses.
- They are NOT punctate staining. They are indentations
What complications arise from hypoxia in contact lens wearers? (6)
Epithelial cell loss, microcysts + vacuoles
Stromal transparency, striae + folds
Endothelial blebs, polymegathism, pleomorphism + bedewing
Neovascularization
Corneal exhaustion syndrome
Superior limbic keratoconjunctivitis (SLKC)
What causes neovascularisation? (4)
Chronic oedema
Stromal softening
Mechanical irritation
Inflammatory response
Where is neovascularisation located in contact lens wearers?
located near the source of irritation (often superior lid)
What are microcysts? What contact lens problem are they associated with and when are they seen?
Pockets of cellular debris in the epithelium. Associated with days-wks of hypoxia. Now only seen in EW patients.
List 3 signs of microcysts
small inclusions in epithelium at 40x mag
Presence of a few microcysts is normal
Small NaFl stain only when they reach the epithelial surface
How can you manage microcysts? (3)
Improve Dk/L?
Decrease WT (wearing time)
Reduce or cease EW
How can you differentiate microcysts from vacuoles?
In retroillumination: MR UV
Microcysts reversed: shadow away from darkness
Unreversed Vacuoles: shadow towards darkness
How does the stroma present with 5-6% swelling? What about 10-12%?
5-6%: Striae
10%: Folds
Does polymegathism and pleomorphism of the endothelium in response to contact lens hypoxia occur after a short time or long time?
occurs as a chronic response to hypoxia (years)
How can we manage hypoxia? (3)
Increase Dk/L (increase dk or decrease lens thiccness)
Improve tear exchange (RGPs)
Reduce wearing time
What are the critical cornea O2 requirements for contact lens wear for daily wear and extended wear?
Daily wear: Dk/t of 24 (avoids oedema)
EW: Dk/t of 87 (limits to 4% oedema)
