1. Soft contact lens complications:
Inflammation and Infection
By:
Md. Riyaj Ali
Consultant Optometrist
2. Factors of complication:
1. Physical factors
2. Visual factors
3. Physiological factors
4. Pathological factors
5. Wearer related
4. Ocular discomfort
• The most common contact lens-induced condition
• May be accompanied by redness and corneal staining
5. Ocular discomfort: Aetiology
• Wide range of physical, physiological, and psychological
factors need to be considered
• Acute discomfort aetiology
Mechanical: FB(debris trapped under lens)
Toxicity: solution mediated
Lens defect: surface, edge
Edge: shape and thickness
Lens fit(too tight, too loose)
6. Chronic ocular discomfort: Aetiology
• Drying of the lens front surface
• Drying of the exposed conjunctiva
• Depletion of post-lens tear film
• Lens fit(too tight)
• Front and back surface deposit
• Hypoxia and hypersensitivity of preserved solution
• MGD and hyposecretion of lipids
8. Ocular discomfort: Symptoms
• Discomfort can range from mild to painful
• Dryness
• Itchiness
• Grittiness(scratchiness)
• FB sensation
• Burning and pain
• Watering of eyes
9. Ocular discomfort: Signs
• Hyperaemia of the bulbar and/or palpebral
conjunctiva
• Presence of staining(sodium fluorescence,
rose bengal)
• Surface drying and deposits(tear debris)
• Surface defect or damage
11. Ocular discomfort: Management
• Optimize: lens fitting, lens care and
replacement schedule
• Change: material and lens design
• Dehydration resistant lens can be used
• Lubricants can be used
12. Ocular redness
• Common in SCL
• 16% of SCL wearers
• Three primary factors must be evaluated:
– Location of redness
– Extent of redness
– Depth of the vessels involved
14. Ocular redness: symptoms
• Asymptomatic to a hot/burning sensation
• Irritation
• Dryness
• Lens intolerance
16. Ocular redness: signs
• Location of redness (localized, diffuse, bulbar
&/or limbal due to edge defect)
• Deep &/or superficial vessels involved
• FB-induced redness is accompanied by acute
symptoms of discomfort
20. Ocular redness: management
• Isolate the cause of redness and solve it
• Infective(antibiotics may be required)
• Minimise dehydration of ocular surface & lens
surface
• If hypoxia is suspected, high Dk lens is
required
21. CLPC: aetiology
• Lens front surface deposits
• Mechanical irritation
• Drying of the lens surface
22. CLPC: symptoms
• Asymptomatic in early stages
• In moderate/ advanced stage
Increased lens awareness
Increased lens movement
Lens deposits
Drying of lens surface
• Itching
• Lens intolerance
32. Meibomian gland dysfunction(MGD)
• A cloudy or absent of meibomian gland secretion
• Bilateral, non-inflammatory clinical condition
• Meibomian gland fluid changes from clear and free-
flowing to cloudy & viscous
• Should not be confused with blepharitis because both
of them involve abnormal meibomian gland secretions
33. Meibomian gland dysfunction: aetiology
• Due to obstruction of the meibomian gland
orifices
• Keratinization of meibomian gland epithelium
• Generalized sebaceous gland dysfunction
• Secondary bacterial infection
• Advancing age
– Loss of the plumpness of the gland
– Loss of acini
– Widening of the central duct
– Gland width also decreases with age
34. Meibomian gland dysfunction:
symptoms
• Ocular irritation or dry eye sensation
• Itchiness & contact lens intolerance
• Worse in the morning
• Mild irritation to burning/stinging
• Apparent ocular redness
35. Meibomian gland dysfunction: signs
• Often bilateral
• Cheese like material block lipid-producing meibomian gland
• Protrusion of the orifices
• Short TBUT
• Tear film instability
• Lens deposits
• Corneal staining will be observed
38. Meibomian gland dysfunction:
management
• Hot and cold compress
• Digital massage for loosening the plugged
material at the orifice
• Lid scrubs with cotton buds and baby
shampoo
• In severe case, oral tetracycline, antibiotics
and steroids can be used
39. CORNEAL INFILTRATES
• Discrete collections of inflammatory
cells(leucocytes)
• Due to inflammatory response
• May be sterile or infected
• PEDAL
• Sterile- common, benign ,self limiting
• Infected-rare but sight threatening
• IK, AIK, AI
40. SIGNS
Focal, arcuate or diffuse
Location: epithelial, sub epithelial, stromal
Small if<1mm and big if>2mm
Location within cornea: peripheral-within
2mm of limbus, central, par central
Hazy greyish white
49. MANAGEMENT
Discontinue lens wear
Prophylactic antibiotics
No recommence until cornea is clear
If CLARE patient before then high
magnification examination of cornea in each
visit
Refit with daily disposable siloxane hydrogels
Use preservative solution
54. Aetiology
• Mostly mechanical
• Finger and fingernails
• Trapped foreign body
• Lens deposit
• Damaged lens surface
• Lens edge defect
• Lens tear(tearing of lens at the edge)
55. MANAGEMENT
• Prophylactic antibiotics
• Bandage contact lens
• Avoid corticosteroids
• Avoid pressure patching
• If infiltrates is detected then treat as MK
56. MICROBIAL KERATITIS(MK)
• Inflammation of corneal tissue due to effect of
infection by microbial agent
• Most serious complication
• Most likely cause is contact lens
• Extended wear has more risk
57. ALTERNATIVE NAME OF MK
Microbial Infiltrative Keratitis(MIK)
Infectious Keratitis
Corneal infection
Corneal ulcer
Bacterial Keratitis
Bacterial ulcer
58. SIGNS
Disruption of corneal epithelium
Bulbar redness
Watery or muco-purulent discharge
Ulcerative keratitis
Acute inflammation with new white spots
Localized epithelium and stromal oedema
59. • Hypopyon
• Aqueous flare
• Staining of lesion along with halos of stain
• Dendritiform epithelial defect (Acanthamoeba)
• Ring of lesions
• Infiltrates with feathery margin or satellite lesion
• Upper lid oedema
• Conjunctival chemosis
60. SYMPTOMS
• Mild irritation to severe pain in advanced case
( painful in early stage in Acanthamoeba Keratitis)
• Foreign body sensation
• Excessive tearing
• Redness
• Vision disturbance
• Swollen lids
• Discharge –clear or turbid
62. • Non compliance
• Resistance of organism to lens care product
• Hygiene/personal hygiene issue
• Lens that attract proteins
63. MANAGEMENT
• Cease lens wear
• Treat as potential infection
• Antibiotics
• No steroid until infection control
• No patching
• Monitor until resolve
• Change lens type and modality
65. CONTACT LENS INDUCED ACUTE RED
EYE(CLARE)
Acute inflammatory response with SCL EW
Redness in whole bulbar conjunctiva
Usually unilateral, can be bilateral
Most in first 3 month of wear
Spectacular appearance
Called as 3AM syndrome
Mostly in female
68. SIGNS
Mild to moderate 360 conjunctival redness
Diffuse infiltrates
Watery discharge
Minimal or no staining
Central corneal oedema
Increased mucus
Decreased lens tolerance
69. SYMPTOMS
Patient wake from painful eye or after waking
immediately notice pain
Watering
Photophopia
Irritation
70. ETIOLOGY
Extended wear(hypoxia)
Toxic response to depris under lens
Negative bacteria
Sensitive to lens care system
Tear protein accumulation on and in lens
General health
Seasonal variation
71. MANAGEMENT
Temporary discontinuation of lens
Regular lens replacement
Low toxicity lens care product
Monitor infiltrates
Restart with DW initially
Palliative measure
Caution with EW
72. CLPU
Ulceration of the corneal epithelium with
underlying inflammation of corneal stroma
Ulcer located periphery
Variants of marginal keratitis
Called as sterile-fail to culture
Other terms- peripheral sterile infiltrated
ulcer, contact lens associated sterile ulcer
Usually self limiting
73. SIGNS
Small, single, circular, dense focal infiltrates in
mid periphery of cornea
Red eye
Watery discharge
Located in anterior stroma
Overlying epithelium is compromised
Full thickness excavation of epithelium
No anterior chamber involvement
Limbal or bulbar redness
76. MANAGEMENT
• Discontinue lens wear
• Treat as MK until proved otherwise
• Monitor carefully for first 24 hours
• Prophylactic antibiotic
• If it is secondary to lid infection then lid
hygiene is useful
• Lubricants
• If Episodic occurrence then fit RGP
79. Corneal oedema & hypoxia
• Mild oedema is natural consequence after sleep
• Lack of oxygen supply during sleep (2/3rd)
approximately
• Overnight swelling range from 2.9% or 3% - 5.5%
• Pachometry is used for corneal swelling
measurement
• Oedema involves the whole of the cornea & is
diffuse in nature
81. Corneal oedema: Aetiology
• Reduce amount of oxygen
• Normal eyelid closure
• Anterior eye hypoxia
• Reduce tear film evaporation
• Stromal pH change
• Reduce endothelium pump efficacy
• Increased temperature under lenses
• Trauma
82. Signs:
Affect both the structural and functional capacity
of cornea & all layers are involve – posterior
layers
Hazy tissue
Increases visibility of stromal nerve fibers
Stromal striae
Oedema more central then peripheral
Fold’s in Decement’s membrane
83. Striae
• Seen in or near Descemet’s membrane
• Occurs in
inflammatory condition
Traumatic condition
Degenerative corneal condition
CL wear hypoxia & other CL effects
• usually vertically oriented
1-3mm whispy white line
Usually thicker than nerve fibers
85. Striae: Aetiology
• Corneal hypoxia causes stromal oedema
• Minimum of 5% corneal swelling is required
• Separation of lamellae
• Refractile effect
86. Striae: Signs
1. Under direct illumination:
• Fine, whispy, greyish, whitish or translucent
corneal lines
• Central to mid peripheral, posterial stroma
2. Under retro illumination:
• Appear black or dark line
Note: striae represent 11% ± 2% corneal swelling
87. Grades of striae:
• Grade I = ≤ 4% normal
• Grade II = 5% ,fine whispy, white , vertical
oriented line in the posterior stroma
• Grade III = 8% buckling corneal oedema
• Grade VI = 15% hazy, milky, or granular
appearance
89. Folds & black lines:
• Terms used somewhat interchangeably
• Buckling of the posterior stromal tissue and /
or the endothelium
• Limbus constrains lateral corneal expansion
• 7%-12% corneal swelling
- black line result from higher end range
swelling
92. Folds & black lines: Symptoms
• Asymptomatic unless corneal swelling is
significant
• Discomfort
• Reduce in vision
spectacle blur
Haziness, haloes, coloured haloes
93. Folds & black lines: Signs
• Presence of corneal striae
• Swelling approaches 7%-8%
• Presence of straight, black lines – viewed with
slit-lamp
• swelling exceed up to 10%- 15%, folds may
change to black lines
95. Endothelium folds: Management
• Significant increase in lens Dk/t needed
• Very short wearing time
• Refit with siloxane hydrogel or high Dk
• Offered RGP lens
97. Epithelial microcysts:
• Occurs in a variety of corneal
Dystrophies
Inflammations
Infections
Chronic hypoxia
• especially in SCL EW
• Also common in non wearers
• Low count considered as acceptable
102. Symptoms:
• Usually asymptomatic
• Associated with other ocular changes which is
symptomatic
• Vision unaffected unless numerous
Signs:
• Small ,circular dot with clear defined borders
• 10 to 50 microns in size
• Located only in central and paracentral region
103. Observation:
• With slit lamp
Angle approximately 45˚between &
microscope 1-2mm wide slit to scan
0.5 to 1mm to observe
15 x to 25x magnification to scan
30x to 40x to observe
Retro illumination
Scan laterally
104. Epithelial microcyst: Management
• Careful monitoring
• If microcysts is <10, no action is needed
• Increase lens Dk/t
• Reduce wearing time
• Rebound effect after lens discontinuation
• Lengthy time to resolve
105. Endothelial Polymegethism:
• Literally, poly(many) megethos (size)
• Endothelial mosaic contains cells of
significantly differing size
Some cells are smaller than normal
Other are larger than normal
Age related & CL induced polymegethism may
be different
107. Aetiology:
• Long term lens wear(low oxygen
transmissibility)
• Chronic hypoxia
• Lowering of stromal pH
• Age
• Disease , surgery , trauma
108. Symptoms:
• Asymptomatic slow progressive
• May be associated with other ocular problem
Signs:
• Variation in cell size/cell volume
• Associated with
Polymorphism
Increased polygonality
110. Corneal Exhaustion Syndrome(CES):
• Result of long term wear of lenses with no , or
low oxygen transmissibility
Most likely in PMMA lens
Low water, toric SCLs
Low water, high BVP spherical SCLs
• Sudden development of lens intolerance
• All layers of the cornea affected
114. CES: Management
• High Dk/t lens to prevent occurrence
• Refit the lens with higher Dk/t
Siloxane hydrogels
RGPs
115. Corneal vascularization: Introduction
• Sometime called neovascularization( new blood
vessels)
• All lenses make limbal vasculature more obvious ,
RGP lenses and siloxane hydrogels produce the
least obvious alteration
• Need to distinguish between ‘new’ vessels and
filled ghost ghost vessels
117. Corneal vascularization: Aetiology
• Long term contact lens induced hypoxia
• Individual susceptibility
• Vaso- proliferative stimuli include
Angiogenic factors( exiting vessels)
Tight fitting lens
Lactic acid build up
Oedema
Inflammatory mediators
Trauma/disease
118. Corneal vascularization: Symptoms
• Usually asymptomatic
• Vascularization may accompany with other
symptoms
• Painful anterior segment disease
119. Corneal vascularization: Signs
• Early signs are vessels spikes
• Branching capillaries from limbal arcade
Episcleral vessels
• Anterior or deep vessels
• Limbal versus clear corneal involvement
• Lipid deposits from deep vessels
• Ghost vessels
121. Cont…
• Patient education and follow up
• Optimize the fitting characteristics
• Decrease the wearing time
• Refit with siloxane hydrogel or RGPs lenses