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

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Soft contact lens complications

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