Complications of Contact Lens

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

7. Lens deposits

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

10. Bulbar redness

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

13. Ocular redness: aetiology
• Tear deficiency: ocular &/or lens surface dehydration
• Mechanical: lens design, edge defect
• CLPC
• Toxicity(preservative enzymes & lens care product)
• Allergy(environmental, deposit & lens care products)
• Hypoxia(limbal redness & SPK)

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

18. Bulbar , superficial
redness

19. Bulbar, deep
episcleral redness

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

23. CLPC: signs
• Enlarged papillae
• Palpebral redness
• Tissue oedema
• Precursor of GPC

31. CLPC: management
• Modify lens wear
• Change lens design
• Frequent lens replacement
• Optimize lens care and maintenance
• Pharmacological therapy
• Patient education

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

36. Waxy or cheese-like material

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

41. Cont. sign
Neutrophils, macrophages, lymphocytes
None to severe red, discharging eye
Eye is white
Epithelial staining

42. SIGN OF INFILTRATIVE KERATITIS(IK)
Periphery to mid periphery
Mild to moderate diffuse infiltrates
Small, focal infiltrate, possibly multiple
Sub-epithelial(anterior stroma)
No corneal oedema
Slight to moderate staining
No anterior chamber reaction

43. SIGN OF AIK
Peripheral
Small, focal(0.4mm) or moderate diffuse
infiltrates
Anterior stroma
No corneal oedema
Punctate staining
No anterior chamber reaction
Mild to moderate limbal redness

44. SIGN OF AI
Commonly periphery but can be anywhere
Very small, focal(0.2mm), solitary
In anterior stroma
No staining
No corneal oedema
No anterior chamber reaction
No limbal redness

45. Corneal infiltrates

47. SYMPTOMS
Asymptomatic to painful
Redness
Photophobia
Foreign body sensation
Lacrimation

48. AETIOLOGY
Bacterial presence
Tight lens
Eye closure with lens
Hypoxia
Contaminated lens
Solution

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

50. CORNEAL ABRASIONS/EROSIONS
Can be caused by
• Fingers or finger nails
• Insertion and removal of lens
• Rubbing eye when lens is worn

51. Abrasion

52. SIGNS
Dense localized staining with fluorescein
Halo around abraded area
 Bulbar redness
Lacrimation
Stromal infiltrates

53. SYMPTOMS
• Pain
• Watering
• Photophobia

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

61. Etiology
• SCL EW
• Pseudomonas aeruginosa(gram negative
bacteria)
• Virus, fungi, protozoa
• Hypoxia
• Organism in stagnant PLTF
• Lens deposit

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

66. CLARE

67. CLARE

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

74. SYMPTOMS
Asymptomatic
Severe pain
Photophopia
Foreign body sensation

75. ETIOLOGY
• Bacterial toxins(Staphylococcus sp.
,Cornebacterium)
• EW
• Interaction of lens and epithelial surface
• Seasonal factor
• Silicone hydrogels wearers

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

77. CLPU

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

80. Corneal oedema
Corneal oedema

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

84. striae

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

88. Striae: Management
• Intervention is warranted by practitioner
• Increase lens Dk/t
• Reduce lens wearing time

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

90. Folds and
black lines

91. Folds &
black lines

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

94. Endothelial folds: Aetiology
• Corneal hypoxia causes stromal swelling
• Minimal of 80% corneal swelling is required
• Swelling directed posteriorly
• Buckling of
- posterior stroma
- Descemet's membrane
- endothelium

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

96. Corneal oedema: Management
• Minimize contact lens effects
- maximize lens Dk/t
-optimize lens fit
-fit siloxane hydrogels
• Decrease lens wearing time

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

98. Corneal dystrophy
microcysts

99. Mucin balls
Vacuoles

100. Bullae
Dimple veiling

101. Epithelial microcysts: Aetiology
• Extracellular accumulation of cellular debris
• Physiological stress
Acute hypoxia from thick SCL
Very low Dk/t lens

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

106. Polymegethism
polymegethism

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

109. Endothelial Polymegethism: Management
• Preventative strategy
High Dk/t lens
• Careful assessment with slit-lamp
• Increase oxygen transmissibility
• Minimal recovery expected

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

111. Intolerance

112. CES: Aetiology
• Long term wear of low Dk/t lenses
• Chronic hypoxia
• Acidosis
• Endothelial dysfunction
Symptoms:
• Reduce lens comfort
• Decrease wearing time
• Blurred or fluctuating vision
• photophobia

113. CES: Signs
• Distorted keratometer mires
• Acute oedema
• Posterior stroma haze/opacities
• Endothelial changes
Polymegethism
Distortion/bumpiness

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

116. Corneal vascularization

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

120. Corneal vascularization: Management
• Acceptable level of vessels growth
Budding
Limbal or clear cornea
• Optimize lens fitting
• Increase lens Dk/t
• Change lens solution

121. Cont…
• Patient education and follow up
• Optimize the fitting characteristics
• Decrease the wearing time
• Refit with siloxane hydrogel or RGPs lenses

122. Thank You