Lecture 11-12 Soft lens complications Flashcards
(38 cards)
How can you classify soft contact lens complications?
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
What corneal complications can you get?
corneal staining
epithelial wrinkling
microcysts
oedema
endothelial blebs
endothelial bedewing
neovascularization
What is the prevalence of staining in CL and non-CL wearers?
What can corneal staining cause?
CL wearers: 60%
non-CL wearers: 35%
-CL tolerance
-Central staining will effect vision
-Increased risk of infection
How can you describe corneal staining?
TYPE: punctate, coalesced, confluent
LOCATION: central, peripheral, use a clock face
EXTENT: diffuse or localised
DEPTH: epithelial, stromal
Describe SMILE staining
What causes it?
What is the management?
-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
Describe diffuse punctate staining
What causes it?
What is the management?
*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
Describe mechanical staining
What causes it?
What is the management?
*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
Describe SEAL
What is this associated with?
What is the management?
*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
What are the principles of Management?
*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
What are the signs of hypoxia?
microcysts
vacuoles
oedema
neovascularisation
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?
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
- address hypoxia
change lens and wear time
What signs can you get for oedema?
What is the management?
-Striae (5%)
-Folds (8%)
-Haze (15%)
remove lenses
manage wear time
change lenses
What is vascularisation?
What is neovascularisation?
What is vasopoliferation?
*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
Why does neovascularisation happen?
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
How can the appearance of neovascualrisation differ?
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
What is the management of neovascularisation?
*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
What are the symptoms of epithelial wrinkling?
What is the management?
-painful, vision affected
-cease lens wear
-resolves within 6 hours, can take up to a week.
What are the symptoms of endothelial bedewing?
what is it related to?
what is the differential diagnosis and why?
What is the management?
*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
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?
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
What eyelid related contact lens complications can you get?
-lid wiper epitheliopathy
-inferior corneal staining (incomplete blink)
-MGD
-Ptosis
Who is contact lens induces ptosis more common in?
What is the cause?
*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
What conjunctiva related CL complications can you get?
-hyperaemia
-lid wiper epitheliopathy
-conjunctival epithelial flap
-papillary conjunctivitis
-staining
-Lid Parallel conjunctival folds (LIPCOF)
What Palpebral changes can you get?
hyperaemia-first sign of inflammation
papillae
follicles
concretions
What are papillae?
-raised areas of palpebral conjunctiva
-have a central blood vessel
-GPC: papillae on tarsal conjunctiva bigger than 1.0mm in diameter
