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Contact lenses year 3 > Soft contact lens complications Pt 2 > Flashcards

Soft contact lens complications Pt 2 Flashcards

1
Q

how much of the eyes refractive power does the cornea account for

A

Approximately 2/3rd

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2
Q

where does the cornea gets its nutrients supply via and why

A
  • via tears and aqueous humour

- because the cornea is avascular

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3
Q

list all the 7 forms of complications affecting the cornea caused by soft contact lenses

A
  • staining
  • microcysts
  • epithelial wrinkling
  • neovascularisation
  • endothelial blebs
  • oedema
  • endothelial bedewing
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4
Q

how common is corneal staining in contact lens and non contact lens wearers

A
  • up to 60% of CL wearers

- up to 35% in non CL wearers (e.g. from poor blinking or something in the eye)

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5
Q

describe the symptoms of corneal staining

A
  • Can be asymptomatic, but depends on severity
  • May affect CL tolerance, cause lacrimation
  • Depending on location, may affect the vision (e.g. central, large and deep)
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6
Q

give 2 reasons why we should care about corneal staining

A
  • When the epithelium is breached there is an increased chance of infection
  • Can lead to scarring (esp if stroma is affected), which could affect the vision
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7
Q

list 4 ways a corneal staining can be described by

A
  • Type
  • Location
  • Extent
  • Depth
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8
Q

how many areas is the cornea decided up into and what can you represent from each area

A
  • 5 areas

- type, extent, depth can be graded for each area

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9
Q

list 6 different types and 3 different aetiologies of corneal staining

A

Types:

  • punctate
  • coalesced
  • confluent
  • SMILE/desiccation
  • 3 and 9 o’clock
  • foreign body track/mechanical

Aetiologies:

  • superior epithelial arcuate lesion SEAL
  • mucin balls
  • corneal abrasion
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10
Q

what is the outcome of a superficial (epithelial) scratch and a deeper injury to the cornea

A
  • Can heal superficial (epithelial) scratches fast
    - Deeper injuries can scar cornea, this leads to loss of
    transparency and affect vision, or can just take longer to heal than superficial
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11
Q

where is a SMILE/desiccation stain located and what 3 things is it caused by

A 
- inferiorly located 
caused by:
- desiccation
- drying
- incomplete blink
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12
Q

where is solution induced corneal staining usually located and what is it caused by

A
  • usually all over cornea
    caused by:
  • toxicity
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13
Q

what is a 3 and 9 o’clock/desiccation corneal stain caused by

A
  • desiccation
  • Poor blinking/tear film
  • Mechanical-lens characteristics
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14
Q

what type of staining is a foreign body track and what should you do when you see this

A
  • Mechanical type (FB rubbing cornea under the CL)

- take the FB out and find out where it came from incase it has a microbe

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15
Q

what type of corneal staining is a superior epithelial arcuate lesion SEAL, how deep in the cornea can it reach, what may also be a factor of this staining and what is it associated with

A
  • Mechanical-CL induced epithelial defect. Can involve
    full epithelial thickness
  • Poor tear flow may also be a
    factor
  • Associated with higher modulus (SiH) lenses and
    tight eyelids
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16
Q

what is the prevalence of a superior epithelial arcuate lesion and what is the prevalence of it being unilateral and bilateral

A
  • 2-10%
  • unilateral (~80%) more common
  • bilateral (~20%) less common
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17
Q

describe how a superior epithelial arcuate lesion is associated with higher modulus (SiH) lenses

A

The top eyelid is tight and so it pushes down the lens
- A tight eyelid also doesn’t let tears flow underneath and so debris gets trapped under the superior lens and also obstructs the tears entering

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18
Q

what are the 4 main symptoms of a Superior Epithelial Arcuate Lesion (SEAL) and explain why pain can be less common with this type of staining

A 
- can be asymptomatic 
may report:
- discomfort
- irritation
- burning
- redness

pain is less common because superior peripheral cornea is less sensitive than the centre

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19
Q

what is the management for a Superior Epithelial Arcuate Lesion (SEAL)

A
  • Cease lens wear – this reduces the chance of infection and also helps remove the cause and allow the cornea to heal
  • Wait ~1 wk
  • SEALs can reoccur
  • Refit with lower modulus lens, alter lens fit, or consider RGPs (if recurrent)
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20
Q

what is the cause of mucin balls, what size do they tend to be and what does it do to the cornea

A
  • Mucin from pre-ocular tear film/post lens tear film rolls up into balls as the px moves the eyes from blinking, the CL moves
  • ~10-50μm
  • does not move with the lens
  • The mucin balls indent cornea and stains with flourescein
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21
Q

what is mucin balls associated with, what are the risks and what are the symptoms

A
  • Associated with SiH/Higher
    modulus materials
  • not a risk of infection as cornea is just indented
  • usually asymptomatic
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22
Q

what is the management of mucin ball corneal staining

A
  • Remove lens
  • Refit with a lower modulus lens
  • Reduce no. of nights lens worn
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23
Q

which type of lens is mucin balls most common with

A

extended wear lenses

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24
Q

which type of corneal staining is serious and why

A
  • corneal abrasion
  • because the cornea is compromised
  • if it scars, it can affect vision permanently if it crosses the line of sight
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25
Q

what may a corneal abrasion be caused by with SCLs and when may it be asymptomatic

A
  • by fingernails during lens insertion/removal or by lens imperfections
  • if very superficial, px may be
    asymptomatic
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26
Q

what is the management is corneal staining caused by a corneal abrasion is seen

A
  • Assess depth and extent
  • Cease lens wear
  • Give advice about infection and symptoms
  • May need to use lubricants
  • May require prophylactic antibiotic
  • Book px in for review
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27
Q

when seeing corneal staining in a patients’ eye, in general, what 2 things will you do and list 4 things of what you will have the patient do in the mean time

A
  • Assess depth and extent
  • Book px in for review

In the meantime:

  • Cease lens wear
  • May need to use lubricants
  • May require prophylactic antibiotic
  • When resuming lens wear- advise fresh pair of lenses
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28
Q

what is microcysts due to, what shape are they and what are they described as

A
  • Due to hypoxia
  • Circular shape
  • Superficial epithelial vesicles - from an accumulation of rubbish
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29
Q

which type of soft contact lenses are microcysts mostly associated with and not seen with

A
  • more associated with low oxygen transmissibility soft lenses
  • not seen with daily wear lenses
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30
Q

where abouts in the eye are microcysts seen and what does this mean

A
  • seen within the epithelium

- hence no staining with flourescein

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31
Q

how do microcysts appear to look if they break through the epithelium, how is this shown in slit lamp and why

A
  • appear as black dots
  • show reversed illumination
  • because they have a higher refractive index than their surround
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32
Q

what are vacuoles filled with, what are they due to, where in the eye are they found and how are they shown in slit lamp

A
  • fluid filled = focal mini oedemas
  • due to chronic hypoxia
  • usually found in mid peripheral cornea
  • do not show reversed illumination - are fluid filled and have lower refractive index than surround
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33
Q

how do you tell microcysts and vacuoles apart

A

the surround of each are different refractive index to the centre, so light comes in and bends differently at the edges than it does at the centre = reversed illumination (microcysts)

34
Q

which type of SCL are both microcysts and vacuoles mainly only associated with

A

extended wear lenses with low oxygen transmissibility

which is rarely used nowadays

35
Q

what is the symptoms of microcysts and vacuoles and when do they happen the most.
How will you manage this patient

A
  • Usually asymptomatic
  • Vision OK, unless ~ 200 microcysts
  • There may be an initial increase in microcysts after cessation of EW, then resolves after a few months
  • Manage by refitting with high Dk lenses (to allow more oxygen to come through)
36
Q

what can the accumulation of vacuoles in the eye become dangerous/serious

A

because the increase in fluid (mini oedemas) can mean acanthamoeba can try and get into those intracellular spaces

37
Q

how much % of oedema is experienced by everyone during sleep

A

3%

38
Q

what is the central corneal oedema with low Dk hydrogels and rigid lenses during lens wear

A

between 1-6%

39
Q

list the 3 different stages of oedema and how much % of oedema each stage correlates to

A

Different stages of oedema:

  • Striae (5%)
  • Folds (8%)
  • Haze (15%)
40
Q

what determined the calculation for the minimum amount of dk/t required to stop corneal oedema occurring

A

Holden and Mertz criterion

Has separate equations for daily wear and extended wear

41
Q

define oxygen transmissibility

A

(Dk/t):
the amount of oxygen passing through a contact lens of specified thickness over a set amount of time and pressure difference
- D = diffusion coefficient
- k = solubility coefficient
- t = thickness of lens or sample of average lens thickness -3.00D

42
Q

define oxygen permeability

A 
O2 Permeability (Dk):
the amount of oxygen passing through the lens material over a set amount of time and pressure difference
- D = diffusion coefficient: dissolved molecules move within the material
- k = solubility coefficient: number of oxygen molecules dissolved in the material
  • ISO units are used: Pascals
  • Varies with the temperature: Increased temp = Increased Dk
43
Q

define oxygen flux

A 
O2 flux (j):
the volume of oxygen passing through a specified area of a contact lens over a set amount of time
44
Q

define equivalent oxygen percentage (EOP)

A

A percentage value of the assumed oxygen pressure existing behind a contact lens

The oxygen level at the anterior corneal surface and is expressed as the percentage concentration of oxygen in the atmosphere behind a CL

45
Q

what is epithelial wrinkling, what are the symptoms and signs

A
  • Rare complication of CL wear
  • Painful
  • Visual acuity usually affected
  • Should be visible on slit lamp, but also keratometry mires will
    be distorted
46
Q

list 4 properties of a SCL that is associated with epithelial wrinkling

A

Associated with lenses that are:

  • Made of highly elastic material
  • Extremely thin lenses
  • Mid-water content (50-55%)
  • Steep fitting
47
Q

which type of water content lens is associated with epithelial wrinkling

A

Mid-water content (50-55%)

48
Q

what is the mechanism of epithelial wrinkling and what is the action referred to as

A

the excessive elastic forces pull corneal tissue inwards from the limbus causing superficial corneal tissue to collapse and create wrinkled appearance

The action is referred to as ‘concertina-like’

49
Q

what is the management of epithelial wrinkling and what is the prognosis

A
  • Cease lens wear
  • May need to refer is severe
  • Usually resolves within 6 hrs, can take up to a week
50
Q

what is vascularisation

A

‘normal’ vascular capillaries within cornea/limbus region. Encroachment into corneal region is no more than 0.2mm

Episcleral branches of the anterior ciliary artery form a plexus around the limbus (superficial marginal arcade). Small branches form at right angles towards this plexus, they
encroach on the cornea, loop inwards (towards corneal apex).

You do not want to see these vessels not turning back

51
Q

what is neovascularisation

A

Formation of new blood vessels in areas which were previously avascular

52
Q

what is vasoproliferation

A

Increase in no. of vessels

53
Q

what are the 3 different theories of neovascularisation

A
  • Metabolic theory
  • Vasogenenic homeostasis model
  • Neural theory
54
Q

what are the 4 stages that causes the metabolic theory of neovascularisation and explain what happens in each stage to cause this

A
  • Hypoxia
    CL wear may cause hypoxia, causes upregulation of vascular endothelial growth factor, which promotes neovascularisation
- Lactic acid
Might be produced as a
consequence of hypoxia OR
tight fitting lens may impede
venous drainage leading to
build up of lactic acid in the
peripheral cornea. causes oedema
  • Oedema
    Presence of excess fluid associated with neovascularisation, but not all researchers agree.
  • Stromal softening
    Chronic oedema may lead to stromal softening, thus reducing
    the physical barrier for vessel penetration (stroma is soft so BV’s can go through)
55
Q

explain the theory behind the vasogenic homeostasis model of neovasculairsation

A
  • Corneal neovascularisation thought to be produced by local
    vasostimulatory factors
  • Vessels believed to grow in the direction of these factors
    Along a concentration gradient
  • Neovascularisation is usually preceded by inflammation, the
    leucocytes involved are thought to produce these vasostimulatory factors

In other words:
where theres inflammation, theres leukocytes, they leave behind vasostimulatory factors and the vessels are supposed to follow the vasostimulatory factors and they grow in that direction

Vasogenic suppression - describes the inhibition of
neovascularisation in this model

56
Q

explain the neural theory behind neovascularisation

A
  • Suggests corneal nerves may play a role in vessel growth
  • CL wear is also associated with changes in corneal
    neurology and sensitivity (increased with CL wear)
  • This theory implies a link between these two factors
57
Q

what 2 appearances of neovascularisation can there be

A
  • superficial
    or
  • deep stromal
58
Q

describe the appearance of superficial neovascularisation

A

corneal penetration by vessels is continuous from limbal vessels

59
Q

describe the appearance of deep stromal neovascularisation

A

Blood vessel growth in the stroma - the vessels disappear

from view at the limbus as they go into the stroma

60
Q

what happens during superficial neovascularisation and what can a severe case of it cause

A
  • Vessels can leak an extra yellowy vascular lipid-like fluid
  • In severe case may cross line of sight
  • As a consequence of the above, vision may be affected
61
Q

where in the stroma can deep stromal neovascularisation occur and what happens during this type of neovascularisation and what can occur as a result of this

A
  • CL induced stromal
    neovascularisation can occur at all levels of the stroma
  • Numerous tortuous branches may develop
  • Pattern of vessels may reflect a
    breakdown in the stromal tissue
  • Loss of vision may occur due to
    leakage of lipid or due to haemorrhaging of blood vessel (as new BV’s are fragile, can break)
62
Q

what is pannus and what it is a form of

A
  • Tissue growth from limbus towards cornea

- A form of neovascularisation

63
Q

what size of pannus is referred to as micro pannus

A

if its less than 2mm

64
Q

what are the 2 sub types of pannus

A
  • Active or inflammatory

- Degenerative or fibrovascular

65
Q

what is the active or inflammatory subtype of pannus down to

A
  • Inflammatory cells
  • Avascular
  • May lead to scarring
66
Q

what is the degenerative or fibrovascular subtype of pannus down to

A
  • Ingrowth of collagen, vessels
  • Congested vessels
  • Associated with superior limbic keratoconjunctivitis
67
Q

what is the distinguishing feature between the 2 subtype of pannus

A

active or inflammatory is avascular and degenerative or fibrovascular is full of blood vessels

68
Q

what may neovascularisation leave, even when it is managed and what risk does this have

A
  • May leave ghost vessels

- Ghost vessels are vulnerable to refilling

69
Q

list 4 things you will do to manage someone with neovascularisation

A
  • Cease lens wear
  • Monitor recovery
  • Refit with caution- SiH lenses. Thick lenses may cause problems e.g. torics
  • Monitor frequently
  • In some cases drugs (steroids) and surgery may be used but this is not common practice
70
Q

what is the prognosis if the neovascularisation crosses the line of sight

A

not much can be done about it

71
Q

what future surgery does neovascularisation not allow a px to get

A

laser surgery

72
Q

what is the prevalence of endothelial blebs amongst CL wearers, what is the symptoms, what do they appear as and why, when do they appear and how can it be viewed with SL

A
  • Prevalence 100% amongst CL wearers
  • Generally asymptomatic
  • Appear as black non-reflecting ‘holes’
  • Due to transient change in corneal endothelium
  • Appear soon after lens insertion (within 10 mins)
  • Can be viewed using specular reflection
73
Q

what is the aetiology of endothelial blebs

A

unclear, but hypoxia thought to

contribute. pH changes due to hypoxia and carbon dioxide

74
Q

which type of lenses does endothelial blebs occur more with

A
  • more with hydrogel lenses

- but can occur with rigid lenses aswell

75
Q

what is the management of endothelial blebs

A
  • Note no. of blebs (as black patches represents low oxygen cells)
  • Use higher Dk lenses, use SiH lenses (if lots of blebs)
76
Q

where are endothelial bedewing located in the eye, is it unilateral or bilateral, which type of illumination does it display and what is it associated with

A
  • Inferiorly located, just below lower pupil margin
  • Usually bilateral
  • Display reversed illumination
  • Possible association with lens wear
77
Q

what differentiates endothelial bedewing from microcysts when you see that they both have reversed illumination

A

endothelial bedewing is associated with inflammation

78
Q

what is the suggested aetiologies of endothelial bedewing and why

A
  • Aetiology is unclear
  • An inflammatory response has been suggested, symptoms suggest mild anterior uveal inflammation
  • Hypoxia
79
Q

what is the ddx of endothelial bedewing and what differentiates them

A
  • anterior uveitis/iritis

- difference is that uveitis is unilateral and endothelial bedewing is bilateral

80
Q

what are the symptoms of endothelial bedewing

A

Px may be symptomatic:

  • redness
  • stinging
  • vision affected
81
Q

what is the 3 things you should do to manage a patient with endothelial bedewing

A
  • Inflammatory cells - need to rule out other serious conditions,
    measure IOPs, ensure there is no blockage of anterior angle.
    Gonioscopy advisable
  • Based on px symptoms - reduce wear time
  • Could try refitting with higher Dk lenses/SiH
82
Q

what is the prognosis of endothelial bedewing

A
  • Can resolve within 4 months, sometimes persists for longer (so keep reviewing your px)
  • Symptoms may persist even after signs have disappeared

Contact lenses year 3 (15 decks)

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