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Soft contact lens complications

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Complications of Contact Lens

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Soft contact lens complications

  1. 1. Soft contact lens complications: Inflammation and Infection By: Md. Riyaj Ali Consultant Optometrist
  2. 2. Factors of complication: 1. Physical factors 2. Visual factors 3. Physiological factors 4. Pathological factors 5. Wearer related
  3. 3. Ocular discomfort • The most common contact lens-induced condition • May be accompanied by redness and corneal staining
  4. 4. 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)
  5. 5. 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
  6. 6. Lens deposits
  7. 7. Ocular discomfort: Symptoms • Discomfort can range from mild to painful • Dryness • Itchiness • Grittiness(scratchiness) • FB sensation • Burning and pain • Watering of eyes
  8. 8. 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
  9. 9. Bulbar redness
  10. 10. 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
  11. 11. 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
  12. 12. 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)
  13. 13. Ocular redness: symptoms • Asymptomatic to a hot/burning sensation • Irritation • Dryness • Lens intolerance
  14. 14. 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
  15. 15. Bulbar , superficial redness
  16. 16. Bulbar, deep episcleral redness
  17. 17. 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
  18. 18. CLPC: aetiology • Lens front surface deposits • Mechanical irritation • Drying of the lens surface
  19. 19. 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
  20. 20. CLPC: signs • Enlarged papillae • Palpebral redness • Tissue oedema • Precursor of GPC
  21. 21. CLPC: management • Modify lens wear • Change lens design • Frequent lens replacement • Optimize lens care and maintenance • Pharmacological therapy • Patient education
  22. 22. 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
  23. 23. 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
  24. 24. 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
  25. 25. 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
  26. 26. Waxy or cheese-like material
  27. 27. 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
  28. 28. 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
  29. 29. 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
  30. 30. Cont. sign Neutrophils, macrophages, lymphocytes None to severe red, discharging eye Eye is white Epithelial staining
  31. 31. 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
  32. 32. 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
  33. 33. 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
  34. 34. Corneal infiltrates
  35. 35. SYMPTOMS Asymptomatic to painful Redness Photophobia Foreign body sensation Lacrimation
  36. 36. AETIOLOGY Bacterial presence Tight lens Eye closure with lens Hypoxia Contaminated lens Solution
  37. 37. 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
  38. 38. CORNEAL ABRASIONS/EROSIONS Can be caused by • Fingers or finger nails • Insertion and removal of lens • Rubbing eye when lens is worn
  39. 39. Abrasion
  40. 40. SIGNS Dense localized staining with fluorescein Halo around abraded area  Bulbar redness Lacrimation Stromal infiltrates
  41. 41. SYMPTOMS • Pain • Watering • Photophobia
  42. 42. 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)
  43. 43. MANAGEMENT • Prophylactic antibiotics • Bandage contact lens • Avoid corticosteroids • Avoid pressure patching • If infiltrates is detected then treat as MK
  44. 44. 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
  45. 45. ALTERNATIVE NAME OF MK Microbial Infiltrative Keratitis(MIK) Infectious Keratitis Corneal infection Corneal ulcer Bacterial Keratitis Bacterial ulcer
  46. 46. 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
  47. 47. • 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
  48. 48. 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
  49. 49. Etiology • SCL EW • Pseudomonas aeruginosa(gram negative bacteria) • Virus, fungi, protozoa • Hypoxia • Organism in stagnant PLTF • Lens deposit
  50. 50. • Non compliance • Resistance of organism to lens care product • Hygiene/personal hygiene issue • Lens that attract proteins
  51. 51. MANAGEMENT • Cease lens wear • Treat as potential infection • Antibiotics • No steroid until infection control • No patching • Monitor until resolve • Change lens type and modality
  52. 52. 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
  53. 53. CLARE
  54. 54. CLARE
  55. 55. SIGNS Mild to moderate 360 conjunctival redness Diffuse infiltrates Watery discharge Minimal or no staining Central corneal oedema Increased mucus Decreased lens tolerance
  56. 56. SYMPTOMS Patient wake from painful eye or after waking immediately notice pain Watering Photophopia Irritation
  57. 57. 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
  58. 58. MANAGEMENT Temporary discontinuation of lens Regular lens replacement Low toxicity lens care product Monitor infiltrates Restart with DW initially Palliative measure Caution with EW
  59. 59. 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
  60. 60. 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
  61. 61. SYMPTOMS Asymptomatic Severe pain Photophopia Foreign body sensation
  62. 62. ETIOLOGY • Bacterial toxins(Staphylococcus sp. ,Cornebacterium) • EW • Interaction of lens and epithelial surface • Seasonal factor • Silicone hydrogels wearers
  63. 63. 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
  64. 64. CLPU
  65. 65. 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
  66. 66. Corneal oedema Corneal oedema
  67. 67. 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
  68. 68. 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
  69. 69. 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
  70. 70. striae
  71. 71. Striae: Aetiology • Corneal hypoxia causes stromal oedema • Minimum of 5% corneal swelling is required • Separation of lamellae • Refractile effect
  72. 72. 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
  73. 73. 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
  74. 74. Striae: Management • Intervention is warranted by practitioner • Increase lens Dk/t • Reduce lens wearing time
  75. 75. 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
  76. 76. Folds and black lines
  77. 77. Folds & black lines
  78. 78. Folds & black lines: Symptoms • Asymptomatic unless corneal swelling is significant • Discomfort • Reduce in vision spectacle blur Haziness, haloes, coloured haloes
  79. 79. 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
  80. 80. 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
  81. 81. Endothelium folds: Management • Significant increase in lens Dk/t needed • Very short wearing time • Refit with siloxane hydrogel or high Dk • Offered RGP lens
  82. 82. Corneal oedema: Management • Minimize contact lens effects - maximize lens Dk/t -optimize lens fit -fit siloxane hydrogels • Decrease lens wearing time
  83. 83. 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
  84. 84. Corneal dystrophy microcysts
  85. 85. Mucin balls Vacuoles
  86. 86. Bullae Dimple veiling
  87. 87. Epithelial microcysts: Aetiology • Extracellular accumulation of cellular debris • Physiological stress Acute hypoxia from thick SCL Very low Dk/t lens
  88. 88. 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
  89. 89. 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
  90. 90. 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
  91. 91. 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
  92. 92. Polymegethism polymegethism
  93. 93. Aetiology: • Long term lens wear(low oxygen transmissibility) • Chronic hypoxia • Lowering of stromal pH • Age • Disease , surgery , trauma
  94. 94. Symptoms: • Asymptomatic slow progressive • May be associated with other ocular problem Signs: • Variation in cell size/cell volume • Associated with Polymorphism Increased polygonality
  95. 95. Endothelial Polymegethism: Management • Preventative strategy High Dk/t lens • Careful assessment with slit-lamp • Increase oxygen transmissibility • Minimal recovery expected
  96. 96. 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
  97. 97. Intolerance
  98. 98. 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
  99. 99. CES: Signs • Distorted keratometer mires • Acute oedema • Posterior stroma haze/opacities • Endothelial changes Polymegethism Distortion/bumpiness
  100. 100. CES: Management • High Dk/t lens to prevent occurrence • Refit the lens with higher Dk/t Siloxane hydrogels RGPs
  101. 101. 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
  102. 102. Corneal vascularization
  103. 103. 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
  104. 104. Corneal vascularization: Symptoms • Usually asymptomatic • Vascularization may accompany with other symptoms • Painful anterior segment disease
  105. 105. 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
  106. 106. Corneal vascularization: Management • Acceptable level of vessels growth Budding Limbal or clear cornea • Optimize lens fitting • Increase lens Dk/t • Change lens solution
  107. 107. Cont… • Patient education and follow up • Optimize the fitting characteristics • Decrease the wearing time • Refit with siloxane hydrogel or RGPs lenses
  108. 108. Thank You

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