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(2) Tri A - Contact lenses > Week 10 - SCL Complications 1 > Flashcards

Week 10 - SCL Complications 1 Flashcards

1
Q

What are the different Aetiological causes of contact lenses?

A

• Physical
• Visual
• Physiological
• Wear-related
• Pathological

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2
Q

What are some physical complications?

A

• The CL
- Fit
- Condition
- Design

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3
Q

What are some visual complications?

A

• Correct RX
• Presbyopia (CL options?)
• Binocular vision

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4
Q

What are some Physiological complications?

A

• DK
• Water content
• Environment
• Blinking

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5
Q

What are some Wear-related complications?

A

• Non-compliance
- Misunderstanding
- Deviating from instructions

• FTA (failure to attend)

• Poor personal hygiene

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6
Q

What are some Pathological complications

A

• Micro-organisms
• Condition of CL/case
• Immunological issues
• Chemical
• Environment
• Pre-existing ocular pathology

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7
Q

How can all complications be prevented?

A

• Px selection
• Lens selection
• Px education
• After care and intervention

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8
Q

What are some General causes to corneal oedema?

A

• SCL-induced corneal oedema involves the whole of the cornea & is diffuse in nature
• Mild oedema -› a natural consequence of sleep
• Usually greater centrally than peripherally
• Occurs in an anterior-posterior direction

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9
Q

What are symptoms of Corneal Oedema?

A

• Generally asymptomatic unless corneal swelling is significant
• Decreased vision examples:
- ‘spectacle’ blur
- haziness, haloes, coloured haloes
- little or no change in Rx

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10
Q

What is Striae in corneal Oedema?

A

• Posterior stroma
• Believed to be due to hypoxia
• (usually) vertical white lines 1-3mm in length
• Indicates at least 5% swelling
• Caused by separation of stromal lamellae

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11
Q

What are folds, in corneal oedema?

A

• As swelling increases (7-12%) then striae can develop into folds in the stroma and through to the endothelium
• More serious problem
• Overall haze at about 15%

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12
Q

What is diffuse corneal oedema?

A

• Involves all layers
• Signs can be subtle (or very obvious as is below)
• Pachymetry can be used to measure subtle changes

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13
Q

Corneal Oedema - management plans?

A

• Maximize CL Dk/t (priority)
• Fit Sily CLs (most effective)
• Decrease CL thickness
• Decrease CL wear
• Consider RGP lenses (especially in cases of endothelial folding)

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14
Q

What is the Prognosis for corneal oedema?

A

• Chronic oedema takes time
• Debate in the literature about length of time to resolve. Couple of weeks with no lenses (may take longer in older patients)
• Then make changes as per previous slide

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15
Q

What are epithelial micro-cysts?

A

• Can occur in:
- corneal dystrophies
- anterior eye inflammations
- anterior eye infections
- chronic hypoxia
• Related to Dk/t of CL & wear modality
• Delayed onset (2 - 3 months)
• Common, especially in SCLEW
• Low cyst count regarded as acceptable’

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16
Q

Why do epithelial micro-cysts affect vision?

A

• They reverse the appearance of images, i.e inverting them

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17
Q

What are the 3 different micro-cyst types and their description?

A

• Mucin balls: Abolished on CL removal, translucent and NaFL pooling in depression
• Microcysts: Persist on CL removal, Reversed illumination, occasional NaFL stain
• Vacuoles: Persist on CL removal, unreserved illumination, No NaFl stain

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18
Q

What are epithelial micro-cysts signs and symptoms?

A

•Small, usually round ‘dots’, relatively well defined borders
• Exhibit reversed illumination (higher refractive index of necrotic cells)
• Vary in number from a few to > 100
• Fluorescein only discloses cysts when they are ‘breaking out’ from the epithelium’s front surface
Usuall asvmptomatic unless numerous, we must find them as they indicate chronic corneal hypoxia.

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19
Q

What are the management options for epithelial microcysts?

A

• Careful monitoring, If < 10, no action needed, Increased number warrants intervention
• Increase CL Dk/t
• Decrease CL wearing time
• Cease EW
• Change to RGP
• Rebound effect after CL discontinuation or lens change
• Lengthy time to resolve - approx. 3 months for full resolution

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20
Q

What is the aetiology for corneal vascularisation?

A

• HyPOKia SiHy CLs s affected than hydrogel OLs
- excessive wearing time/over-wear
• Corneal oedema
• Epithelial Injury
-prolonged mechanical insult
-poor/suboptimal fitting
-chronically disturbed tear film (e.g. 3&9 o’clock staining)
-excessive wearing time/over-wear
• Infection

21
Q

How does corneal vascularisation actually occur?

A

• Triggering agent causes epithelial damage, which releases enzymes, inflammatory cells and vasostimulating agents. This causes vascular growth.
Chronic hypoxia induces stomal softening,

22
Q

What ate signs and symptoms of corneal vascularisation, and how is it recorded?

A

• Asymptomatic unless very severe (vision will then be affected)
• Must be looked for at every AC, make sure to check the superior cornea

• Supporting documentation/diagram(s)/photograph(s)
• Extent of radial penetration
• Location (o’clock)
• Depth (relative to corneal anatomical layers)
• Severity (grading scale)
• Assessment by corneal quadrant

23
Q

How is corneal vascularisation managed?

A

• ^ corneal O2 supply
- ^ CL Dk/t
- refit with SiHy CLs (SiHy CLs -›Decreased CV)
- refit with GP CLs
• Optimise CL fitting
• Decrease CL wearing time
- change from EW to DW
- Decrease hours of DW

24
Q

What is corneal vascularisation prognosis?

A

• Removal of stimulus leads to retreat of blood column from new blood vessels (can take months)
• Early intervention is vital to prevent permanency of new vessels
• ‘Ghost’ vessels remain unless intervention was made early (1-2 weeks), i.e. soon after onset of vascular changes
• Close monitoring if lens wear is resumed

25
Q

What are infiltrates?

A

• A relatively common CL-induced condition
• Also seen in 1% of non-CL wearers
• May be epithelial, sub-epithelial, or stromal
• Usually, the overlying epithelium is intact
• Believed to be discrete collections of inflammatory cells
• May be ‘sterile’ or infected

26
Q

What are the differences between infiltrates and ulcers?

A

Infiltrates vs ulcers as follows:
• Smaller <1mm vs larger >1mm lesions
• Peripheral vs central
• Minimal vs significant epithelial defect
• No mucus vs mucopurulent discharge
• Less vs more pain/photophobia
• Little vs significant anterior chamber reaction
• No lid involvement vs lid edema

27
Q

What are Infiltrates aetiology?

A

• Bacterial presence
• Eye closer with CL
• Hypersensitivity
• CL deposits
• Inadequate disinfection/hygiene
• Tight CL
• Mechanical trauma
• Hypoxia

28
Q

What are infiltrates appearance?

A

• May be focal, arcuate, or diffuse
• Hazy, greyish-white (0.5 mm to 2 mm)
• Tiny & circular to a wooly appearance
• Location:
- epithelial
- sub-epithelial
- stromal

29
Q

What are symptoms of Infiltrative keratitis? (IK)

A

• Range from asymptomatic to painful
• CLs can ‘mask’ the problem (bandage effect)
• Typically:
- foreign body sensation (FB)
- photophobia
- lacrimation

30
Q

What are the signs to infiltrative keratitis?

A

• Located peripherally to mid-peripherally
• Mild to moderate diffuse infiltration &/or small, focal infiltrate, possibly multiple
• In anterior stroma (sub-epithelial)
• Usually, no observable corneal edema
• Slight to moderate staining
• No anterior chamber reaction
• Moderate limbal redness
• Can be bilateral

31
Q

What is the management plan for infiltrative keratitis?

A

• CL wear must be stopped (MOST IMPORTANT)
• Monitoring
• Specific advice to patients
• Antibiotics? Artificial tears?
• Resolution (clear cornea) necessary before CL wear resumed, can take days - weeks - months

32
Q

How is risk of recurrence managed for infiltrative keratitis?

A

• Risk of recurrence, need to decrease risk
• Isolate the cause
• May need to change Cls, solutions, CL care routine, or CL wear schedule
• Re-educate patient
• Refit with daily disposables, SiHy, or GO Cls
• Use preservative free products

33
Q

What is Asymptomatic infiltrative keratitis? (AIK)

A

• Infiltration of the cornea with no symptoms
• Small infiltrates (<0.5mm)
• Usually peripheral
• Need to really look at the cornea of all CL patients, even those with no symptoms
• Similar management to symptomatic IK
Advice to patients with IK and AIK regarding signs if infection

34
Q

What is general punctate corneal staining?

A

• Common in CL wearers (approx 60%)
• Due to drying of the cornea
• Can occur in non-CL wearers
• Symptoms:
- FB sensation
- irritation/grittiness
- excessive lacrimation
- reduced CL wear time

35
Q

How is general punctate corneal staining managed?

A

• CL re-wetting drops
• Reduced wear time
• Re-fit (if soft consider silicone hydrogel or daily disposable)
• Treat underlying conditions i.e. MD, anterior blepharitis

36
Q

What is Epi Abrasion/erosion in corneal staining?

A

• Mechanical aetiology is most common
• Fingernails/fingers
• Trapped foreign body (FBs)
• CL defect
• Significant abrasion leads to disorganization of epitheliums regular cellular arrangement

37
Q

What symptoms occur with a Epi Abrasion/erosion in corneal staining?

A

• Mild to severe pain
• Photophobia
• CL bandage effect can mask symptoms until CL removal

38
Q

What Signs appear with Abrasion/erosion in corneal staining?

A

• Dense, localized staining with fluorescein
• Bulbar redness
• Lacrimation
• Stromal infiltrates possible

39
Q

What is the treatment/management of Abrasion/erosion in corneal staining?

A

• Stop usage of contact lenses
• Check for foreign bodies - where?
• Prophylactic antibiotics
- vs gram -ve bacteria, eg levifloxacin
• Monitor patient closely
• If infiltrates detected - treat as MK until proved otherwise
• Avoid corticosteroids (why?)
• Bandage SCL?

40
Q

What is CLPC?

A

• Contact lens induced papillary conjunctivitis aka giant papillary conjunctivitis
• Mainly a result of SCL wear (less common in RGPs)
• Usually bilateral
Caused by:
• CL front surface deposits
• Mechanical irritation
• Immune response
• Drying of CL surface

41
Q

what are the symptoms of CLPC?

A

• Most likely asymptomatic in early stages
• In moderate/advanced stages:
- Increased CL awareness, CL movement
- Increased mucus affecting: drying of CL surface, CL deposits/reduced or fluctuating vision
- itching
- CL intolerance
N.B. Itching/irritation symptoms can sometimes be worse without the CL as the lens can act as a bandage.

42
Q

What are the signs of CLPC?

A

• Enlarged papillae
• Roughened appearance
• Palpebral hyperaemia
• Tissue oedema
• Ptosis if chronic, widespread papillae

43
Q

What differences are there between papillae and follicles?

A

Papillae vs follicles:-
• Rice grain shape vs raised cobblestone
• Vital/chlamydial vs allergic diseases
• Usually not vs Is CL related
• Pale, translucent vs blood vessel core
• Mostly avascular vs vessels at base/central vascular tuft
• Inferior palpebral (0.2-0.4mm) vs superior palpebral (0.3-0.9mm), may have mucus

44
Q

How is CLPC managed?

A

• Modify CL wear - change to DW or daily disposable
• More frequent CL replacement
• Optimize CL care & maintenance
• Pharmacological therapy
• Patient education
• GP CLs

45
Q

How are CL deposits managed?

A

• Optimise care and maintenance
- solutions/systems used (protein removing tablets)
-care regimen applied (ensure compliance)
-CL replacement rate
• Consider daily disposables (DD CLs)

46
Q

What is the Aetiology of CL wrinkling?

A

• High minus or plus BVP
• Low water material
• Lid forces on blinking

47
Q

What are the symptoms of CL wrinkling?

A

• Severe vision I if wrinkling is over the pupil zone, milder if not over the pupil
• Onset may be rapid (minutes) to months
• Recovery: ‘prompt’ to ‘hours after’

48
Q

What are the signs of CL wrinkling?

A

• Corrugated central or mid-peripheral CL zone
• Does not change with a blink
• CL wrinkling can cause corneal wrinkling
• Now a rare occurrence

49
Q

What is the management plan for CL wrinkling?

A

• Change CL design
• Higher water content
• Thicker design
• Consider a more rigid CL material
• SiHy CLs
• Consider GP CLs

(2) Tri A - Contact lenses (16 decks)

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