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Contact lenses > Lecture 11-12 Soft lens complications > Flashcards

Lecture 11-12 Soft lens complications Flashcards

1
Q

How can you classify soft contact lens complications?

A

Metabolic influences- hypoxia, osmolarity
Chemical influences- pH
Toxic Reaction-preservatives
Allergic Reaction-hypersensitivity to deposits
Mechanical influences- breakages, modulus
Tear deficiency- dehydration of lens
Infection-bacterial

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2
Q

What corneal complications can you get?

A

corneal staining
epithelial wrinkling
microcysts
oedema
endothelial blebs
endothelial bedewing
neovascularization

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3
Q

What is the prevalence of staining in CL and non-CL wearers?

What can corneal staining cause?

A

CL wearers: 60%
non-CL wearers: 35%

-CL tolerance
-Central staining will effect vision
-Increased risk of infection

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4
Q

How can you describe corneal staining?

A

TYPE: punctate, coalesced, confluent
LOCATION: central, peripheral, use a clock face
EXTENT: diffuse or localised
DEPTH: epithelial, stromal

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5
Q

Describe SMILE staining
What causes it?
What is the management?

A

-punctate staining located inferiorly

-dry environments, e.g., air con
-incomplete blink

*Dry eye drops
*Treat underling MGD if present
*Blinking exercise
*Modify environment
*Lens changes

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6
Q

Describe diffuse punctate staining
What causes it?
What is the management?

A

*Covers whole cornea, limbus, and conjunctiva

*Can be due to toxicity or dryness

*Short term: stay out of lenses until resolved
*Lubrication for symptomatic relief
*Review within 2-3/7
*Long term: Address change like change solution or fit with dailies

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7
Q

Describe mechanical staining
What causes it?
What is the management?

A

*Foreign Body Tracks

*FB can get caught under lens
*Px blinks and this causes rubbing causing abrasion
*More likely with RGP

*Remove lenses, review in 3-7/7
*lubrication for symptomatic relief
*Resume lens wear when resolved
*Consider refitting if lenses are tight fitting

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8
Q

Describe SEAL
What is this associated with?
What is the management?

A

*Superior Epithelial Arcuate Lesion
-superior punctate staining

*Commonly associated with first generation SiHy (high modulus)
*These are rare now with improved contact lens materials
*Occasional symptoms of irritation

*Management
*Remove lenses, review within 7/7
*Refit with lower modulus lens
*Possible RGP fitting

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9
Q

What are the principles of Management?

A

*Remove the lenses
*Epithelium heals in 48 hours
*Review – Period will depend on severity and depth but usually within 2-7 days
*Advise patient on risk of infection, symptoms, and actions to take if occurs. E.g., contact practice, A&E if out of hours
*Consider use of lubricants
*Prophylactic antibiotics – How would you supply
*Possible referral if very severe
*Once resolved address underlying cause

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10
Q

What are the signs of hypoxia?

A

microcysts
vacuoles
oedema
neovascularisation

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11
Q

1.Why do microcysts appear?
2.What are they?
3.How can differentiate between microcysts and vacuoles?
4.Why do you get vacuoles? Where?
5.What is the management for vacuoles and microcysts?

A

1-hypoxia

2-superficial epithelial vesicles

3-Microcysts show on reversed illumination (when light comes from the right, you will get a shadow on the right side and illuminated left side)
-Vacuoles are fluid-filled so NO reverse illumination

4-chronic hypoxia
-mid-peripheral cornea

  1. address hypoxia
    change lens and wear time
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12
Q

What signs can you get for oedema?

What is the management?

A

-Striae (5%)
-Folds (8%)
-Haze (15%)

remove lenses
manage wear time
change lenses

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13
Q

What is vascularisation?

What is neovascularisation?

What is vasopoliferation?

A

*Vascularisation: ‘normal’ vascular capillaries within cornea/limbus region. Encroachment is ~ 0.2mm especially in superior cornea

*Neovascularisation: Formation of new blood vessels in areas which were previously avascular

*Vasoproliferation: Increase in number of vessels
*Episcleral branches of the anterior ciliary artery form a plexus around the limbus (superficial marginal arcade). Small branches form at right angles to the plexus and encroach the cornea

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14
Q

Why does neovascularisation happen?

A

METABOLIC THEORY
CL causes hypoxia: upregulation of vascular endothelial growth factor which promote neovasc.

-lactic acid: may be produced as a consequence of hypoxia OR tight fitting lens may impede venous drainage leading to build up of lactic acid in peripheral cornea

-stromal softening: chronic oedema may lead to stromal softening. this reduces the physical barrier for vessel to grow.
-oedema is associated with neovasc

VASOGENIC FACTORS
*Local Vaso stimulatory factors produced causing corneal vascularisation
*The factors create a concentration gradient which the vessels then grow along
*This is usually proceeded by inflammation
leucocytes produce the Vaso stimulatory factors

Neural theory
*Corneal nerves may play a role in vessel growth
*Contact lens wear is associated with changing corneal nerves and sensitivity

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15
Q

How can the appearance of neovascualrisation differ?

A

superficial: vessels can leak extra vascular lipid-like fluid
-can cross line of sight in severe cases

deep stromal:
-can occur at all levels of stroma
-numerous tortuous vessels may develop
-loss of vision
-pattern of vessels may reflect breakdown of stromal tissue

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16
Q

What is the management of neovascularisation?

A

*Cease lens wear
*Monitor recovery
*May leave ghost vessels (suggests previous neovasc but not current, don’t treat)
*Ghost vessels are vulnerable to refilling
*Refit with caution- SiH lenses
*Monitor frequently
*Greater movement on fitting

17
Q

What are the symptoms of epithelial wrinkling?
What is the management?

A

-painful, vision affected

-cease lens wear
-resolves within 6 hours, can take up to a week.

18
Q

What are the symptoms of endothelial bedewing?

what is it related to?

what is the differential diagnosis and why?

What is the management?

A

*Px may be symptomatic-redness, stinging, lens intolerance

related to inflammatory cells on the endothelium

*They display reversed illumination – like epithelial microcysts (DIFFERENTIAL DIAGNOSIS)

*Due to inflammatory origin need to rule out other causes of signs/symptoms – PDS, uveitis etc

19
Q

What is the prevalence of endothelial blebs in CL patients?

What is the aetiology?

What are the signs?

How can they be viewed on a slit lamp?

A

100%

acidic shift’ CO2/lactic acid

*Appear as black non-reflecting ‘holes’
*Transient change in corneal endothelium
*Can be seen within 10 minutes of insertion, peaking around 30 minutes

-only seen on 40x mag
-viewed with specular reflection

20
Q

What eyelid related contact lens complications can you get?

A

-lid wiper epitheliopathy
-inferior corneal staining (incomplete blink)
-MGD
-Ptosis

21
Q

Who is contact lens induces ptosis more common in?

What is the cause?

A

*More common in RGP wearers
*Soft CL wear approx. 5x more common in young px who developed unexplained acquired ptosis
*Soft CL wear has been reported as the most common risk factor for ptosis in patients under 35 years old

*Cause likely to be abnormal force on eyelids during I+R or intrinsically weak levator aponeurosis

22
Q

What conjunctiva related CL complications can you get?

A

-hyperaemia
-lid wiper epitheliopathy
-conjunctival epithelial flap
-papillary conjunctivitis
-staining
-Lid Parallel conjunctival folds (LIPCOF)

23
Q

What Palpebral changes can you get?

A

hyperaemia-first sign of inflammation

papillae

follicles

concretions

24
Q

What are papillae?

A

-raised areas of palpebral conjunctiva
-have a central blood vessel
-GPC: papillae on tarsal conjunctiva bigger than 1.0mm in diameter

25
Q

What are follicles?

A

focal accumulations of white blood cells within palpebral conjunctiva without a central blood vessel
-associated with viral infections of the conjunctiva
NOT CL RELATED

26
Q

What are concretions?

A

pale yellow accumulations of inorganic type material beneath palpebral conjunctival epithelium

may cause FB sensation

NOT CL RELATED

27
Q

What are the signs of CLAPC (contact lens-associated papillary conjunctivitis)?

A

-papillae
-hyperaemia
-mucus discharge
-lens depostion
-excessive movement

28
Q

What are the symptoms of contact lens-associated papillary conjunctivitis?

A

blurred vision (lens deposits, mucus)
itching
FB sensation
not able to wear the lenses for long

29
Q

What are the causes of CLAPC?

A

*Allergic (e.g., protein deposits on lens). proteins denature which triggers hypersensitivity. indicates poor cleaning of lens.

  • mechanical (lens design, modulus of lens material)
    *Hypersensitivity reaction mediated by Immunoglobulin E (IgE)
    *Associated with soft CL wear and stiffer materials
    *Associated with sensitivity to solutions or preservatives
    *Associated with MGD and atopy
30
Q

What is the management of CLAPC?

A

Short Term:
-Remove source
-allow to resolve
-Review
-Tell them they can get a rebound with aggressive symptoms if they resume lens wear to quickly
-lubricants

Long Term:
-Improve lens care regime
-Daily disposables
-Alter lens design or material
-Manage any lid margin disease
-Review this px more regularly

31
Q

What limbus related CL complications can yuo get?

A

redness

superior limbic keratoconjunctivitis

32
Q

What is the aetiology of limbal redness?

A

*Hypoxia
*Infection / Inflammation
*Trauma
*Solution toxicity/ hypersensitivity
*Lens deposits
*Mechanical

33
Q

What is limbal redness?
Is limbal redness common?
Which material induces less limbal redness?

A

*Limbal vascular arcades- series of blood vessels within the limbus

*Mild limbal hyperaemia is common in CL wearers
*Greater impact of CL wear on limbal redness

*SiHy induce less limbal redness to hydrogel lenses towards the end of the day.

34
Q

What is the management of limbal redness?

A

*Record-use grading scale
*Cease lens wear
*Refit with high Dk lens/SiH
*Reduce wear time
*Alter lens fit
*Review care regime

35
Q

What does superior limbic keratoconjunctivitis involve?

What is superior limbic keratoconjunctivitis associated with?

What are the signs?

A

corneal epithelium, stroma, limbus, bulbar and tarsal conjunctiva

-associated with toxicity with CL solutions containing thimerosal.
-Hypoxia thought to be an aggravating factor

-superior limbic redness
-corneal staining

36
Q

What is the management of conjunctival hypereamia?

A

-Identify and address cause
-Refit- change lens design
-Refit-change lens material e.g. different modulus or Dk
-Refit- more frequent replacement
-Review care regime
-Ocular lubricants
-Consider environmental factors

37
Q

What is sectoral conjunctival hypereamia caused by?

What is interpalpebral conjunctival hypereamia caused by?

What is bulbar conjunctival hypereamia caused by?

A

specific cause e.g., infiltrate

dryness, RGP wear, allergic/mechnical

soft CL wear

38
Q

What conjunctival staining can you get in CL wear?

A

furrow staining- lens indentation

conjunctival epithelial flap
-areas of loose conjunctival tissue are in the lens-indented areas
-superior or inferior
-associated with SiHy

Management: cease CL wear, lower modulus lens

Contact lenses (19 decks)

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