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OD3 - Clin. Optometry Sem 1 and Preacademic Period > CL - Contact Lens Complications - Week -1 > Flashcards

CL - Contact Lens Complications - Week -1 Flashcards

1
Q

What are the 4 broad causes of contact lens complications?

A

Inflammation (e.g. allergy, immune response)
Mechanical (e.g. rubbing, poor fit)
Microbiological (i.e. infection)
Hypoxia

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2
Q

What are 6 common risk multipliers for contact lens complications?

A 
dry eye
male
smoker
extended wear
lifestyle
compliance
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3
Q

What should be covered in the history of a contact lens wearing patient? (10)

A 
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
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4
Q

What 3 dyes can we use to assess ocular surface damage?

A

Fluorescein (NaFl)
Rose Bengal
Lissamine Green

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5
Q

What do Rose bengal and lissamine green stain?

A

damaged cells and devitalized areas of the surface

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6
Q

Which is more toxic: rose bengal or lissamine green? How can we minimise discomfort for the more toxic dye?

A

Rose bengal is more toxic to the ocular surface and thus causes stinging. (can use topical anaesthetic to minimise discomfort)

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7
Q

How should we score ocular conditions on grading scales?

A

To the first decimal

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8
Q

How should we manage corneal staining if the cause of staining is infection, toxic, allergic or inflammatory?

A

treat the overall condition

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9
Q

How should we manage corneal staining if the cause is hypoxia?

A

increase Dk/t or decrease WT (wearing time)

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10
Q

What happens to a CL patient with epithelial loss?

A

nerve ends get exposed, resulting in pain

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11
Q

How long does superficial staining of the cornea take to heal? What about deep staining?

A

Superficial: 24 hours
Deep: 1-2 days

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12
Q

For how long should a patient cease contact lens wear if they have deep corneal staining?

A

2-4 days while treating the cause

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13
Q

How can we manage corneal staining if the stroma is affected?

A

consider prophylactic antibiotics (CHL 0.5%) (or aminoglycoside for better gram -ve cover)

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14
Q

How does the eye protect itself from infection? (3)

A

Cell shedding + wiping action of blnking
Irrigation by lacrimal secretions
Antimicrobial defenses (tear lysosoyme, immunoglobulins, anti-microbial peptides on ocular surface)

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15
Q

What does PEDAL stand for? (differentiating ulcer vs infiltrate)

A 
Pain
Epithelial defect
Discharge
AC reaction
Location (central/paracentral)
(bonus: lid swelling/oedema)
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16
Q

How does the staining of an ulcer compare to infiltrate?

A

Ulcer: 1:1 staining defect/lesion ratio
Infiltrate: small staining

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17
Q

How does the level of conjunctival infection of an ulcer compare to infiltrate?

A

Ulcer: generalised conj injection
Infiltrate: sector skewed injection

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18
Q

How does the number of lesions in an ulcer compare to infiltrate?

A

Ulcer: usually single lesion
Infiltrate: can be multiple lesions

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19
Q

What microbe is most commonly responsible for MK?

A

Pseudomonas

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20
Q

How does pseudomonas aeruginosa cause damage? (2)

A 
Exotoxins inhibit protein synthesis
Biofilm generation (glycocalyx; polysaccharide)
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21
Q

Where can you find acanthamoeba? (4)

A

Soil, air, fresh water, tap water

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22
Q

What percentage of keratitis is due to acanthamoeba? What percentage of acanthamoeba keratitis is due to contact lens wear?

A

<1%

85%

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23
Q

When is acanthamoeba keratitis often diagnosed?

A

When bacterial management not working (e.g. improving, but never getting better)

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24
Q

When must you refer any corneal lesion?

A

when the lesion is on the visual axis

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25
Q

How can you manage MK?

A

Fluoroquinolones - g15min loading, then g1hr

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26
Q

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

A

Better visual outcomes. Odds ratio of better outcomes with high dose steroids was 5.49

27
Q

In accordance with SCUT (steroids for corneal ulcers trial): what factors were significantly associated with visual outcomes? (5)

A 
high-dose steroid treatment
visual acuity on presentation
age group
cause of keratisis
infiltrate size/location
28
Q

Are infiltrates unilateral or bilateral

A

Can be either uni or bi-lateral

29
Q

Are infiltrates symptomatic?

A

Can be either

30
Q

How much epithelial excavation occurs with infiltrate?

A

only slight excavation

31
Q

Name 3 possible causes of infiltrates in a contact lens wearer

A

Poor compliance
MG dysfunction/bleph
Hypersensitivity (e.g. to lens, solution, bacteria)

32
Q

How can we treat infiltrates? (4) When should we review? (1)

A 
Cease lens wear
Steroid/antibiotic
Change lens type/modality/WT/replacement
If suspect infection - tx as infection
Review 24 hours
33
Q

What is CLARE? What patients is it common in?

A

Contact Lens Acute Red Eye: immune response to acute or chronic hypoxia.
Common in EW patients

34
Q

Can CLARE present with bacterial presence?

A

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

35
Q

How may tight lenses contribute to bacterial accumulation in CLARE?

A

no tear exchange to flush toxins

36
Q

List 5 signs of CLARE

A 
Painful red eye +/- photophobia
Diffuse + focal infiltration
Corneal epithelial + stromal oedema
Conj + limbal oedema, injection
Peripheral, multiple? culture negative infiltrates
37
Q

How do we manage CLARE? (2)

A

Cease lens wear

Consider steroid with or without antibiotics?

38
Q

How does GPC occur?

A

mechanical irritation/inflammation/allergic response

39
Q

What is GPC associated with? (5)

A 
Soft (5-10%)/RGP(3-5%) CLs
Prosthetic devices
Exposed sutures
Glaucoma filtering blebs
Corneal scars
40
Q

What are papillae? Where are they mainly located? Where do they first appear?

A

Hyperplastic conjunctival epithelium
Mostly in upper palpebral conjunctiva
First appear at margin of tarsal plate

41
Q

What are the major causes of papillae? (2)

A

CLPC (contact lens induced papillary conjunctivitis)

Vernal conjunctivitis

42
Q

What are follicles? Where are they mainly located?

A

Hyperplastic lymphoid tissue

Mostly found in inferior forniceal conjunctiva

43
Q

What are the major causes of follicles? (2)

A

Viral infection

Hypersensitivity to solutions

44
Q

How can you tell follicles and papillae apart?

A

Follicles: encircled by vessels, rice grain appearance
Papillae: central tufts of vessels, appear like cobblestones

45
Q

How can we treat CLPC (CL induced papillary conjunctivitis)? (3)

A

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)

46
Q

How long may grade 3-4 CLPC take to treat? What happens if left untreated for many years?

A

1-6 months. If untreated, you’ll get conjunctival scarring

47
Q

Name 6 mechanical complications from contact lens wear?

A 
FB staining (RGP >>> SCL)
RGP and SCL binding
Epithelial wrinkling (thin, high water SCL)
Bubble indentations (RGP fit issue)
Mucin balls
SEALS
48
Q

What are SEALS? Who is affected by them?

A

Superior Epithelial Arcuate Lesion. Affects SCL wearers (more commonly Si-H)

49
Q

List 2 signs of SEALs

A

Epithelial split

Staining with Nafl

50
Q

What causes SEALS? (3)

A

lens thickness
modulus
lid force (tight lids?)

51
Q

How can you treat SEALS? (3)

A

Discontinue wear until resolves (~1-2wks)
Change SCL design (softer modulus)
Change to RGPs

52
Q

How do mucin balls form? Are they punctate staining?

A

Form via interaction of lens surface and corneal epithelium in higher modulus lenses.

  • They are NOT punctate staining. They are indentations
53
Q

What complications arise from hypoxia in contact lens wearers? (6)

A

Epithelial cell loss, microcysts + vacuoles
Stromal transparency, striae + folds
Endothelial blebs, polymegathism, pleomorphism + bedewing
Neovascularization
Corneal exhaustion syndrome
Superior limbic keratoconjunctivitis (SLKC)

54
Q

What causes neovascularisation? (4)

A

Chronic oedema
Stromal softening
Mechanical irritation
Inflammatory response

55
Q

Where is neovascularisation located in contact lens wearers?

A

located near the source of irritation (often superior lid)

56
Q

What are microcysts? What contact lens problem are they associated with and when are they seen?

A

Pockets of cellular debris in the epithelium. Associated with days-wks of hypoxia. Now only seen in EW patients.

57
Q

List 3 signs of microcysts

A

small inclusions in epithelium at 40x mag
Presence of a few microcysts is normal
Small NaFl stain only when they reach the epithelial surface

58
Q

How can you manage microcysts? (3)

A

Improve Dk/L?
Decrease WT (wearing time)
Reduce or cease EW

59
Q

How can you differentiate microcysts from vacuoles?

A

In retroillumination: MR UV
Microcysts reversed: shadow away from darkness
Unreversed Vacuoles: shadow towards darkness

60
Q

How does the stroma present with 5-6% swelling? What about 10-12%?

A

5-6%: Striae

10%: Folds

61
Q

Does polymegathism and pleomorphism of the endothelium in response to contact lens hypoxia occur after a short time or long time?

A

occurs as a chronic response to hypoxia (years)

62
Q

How can we manage hypoxia? (3)

A

Increase Dk/L (increase dk or decrease lens thiccness)
Improve tear exchange (RGPs)
Reduce wearing time

63
Q

What are the critical cornea O2 requirements for contact lens wear for daily wear and extended wear?

A

Daily wear: Dk/t of 24 (avoids oedema)

EW: Dk/t of 87 (limits to 4% oedema)

OD3 - Clin. Optometry Sem 1 and Preacademic Period (25 decks)

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