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RGP Complications

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Contact Lens Complications

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RGP Complications

  1. 1. Common RGP Complications
  2. 2. Objectives Complications related to Inflammation and Staining Oedema and Hypoxia Mechanical and Pressure Vision Complications Lens and Fitting Introduction Conclusion References
  3. 3. Introduction • Contact lenses are used to correct refractive error, improve visual acuity, and enhance appearance for cosmetic reasons. • Improper use of contact lenses can cause numerous complications, which are manifested in various clinical signs and symptoms. • About 4% of patients suffering from ophthalmic problems bear contact lens complications http://www.contactlensesus.com/contact-lens-complications.html
  4. 4. Causes of CLs complications • Sleeping wearing the contact lenses when guidelines do not permit extended use. • Not adhering to replacement schedule and stretching contact lens usage longer than they are designed for. • Purchasing contact lenses from unauthorized sources. • Sharing contact lenses. • Not following proper cleansing and sterilization instructions
  5. 5. Inflammation and Staining Related
  6. 6. CLPC 3 & 9 O’Clock Staining Corneal Dellen Corneal Staining Corneal Ulceration Vascularized Limbal Keratitis (VLK)
  7. 7. Contact lens induced papillary conjunctivitis (CLPC) Immunological inflammatory disease of superior/inferior tarsal conjunctiva associated with lens deposits, sutures, prostheses, corneal glue, or any persistent mechanical irritation of the conjunctiva SCLs > RGP lenses
  8. 8. At biopsy, Mackie and Wright (1978) found hyperplasia of the epithelium with many ‘downgrowths’ into the stroma, occasional inclusion cysts containing goblet cells, and eosinophilic infiltration of the epithelium and stroma. Goblet cell and basophil numbers were also higher than normal. They concluded that CLPC was an allergic reaction Mechanical interaction between the contact lens front surface and the palpebral conjunctival tissue and allergy
  9. 9. Management • Minimize wear, or discontinue temporarily • Determine cause - deposits/care and maintenance -edge shape (apex position) Therapeutic - mast cell stabilizer - combination stabilizer & antihistamine - mild steroid
  10. 10. 3 & 9 O’clock staining •Staining occurs as an arcuate band on the peripheral cornea between 3 and 5 o’clock and 7 and 9 o’clock •Staining occurs in the area not covered by the lens so sometimes referred to as exposure staining •Usually present both nasally and temporally •Accompanied by conjunctival hyperaemia Most persistent RGP after care problems More prevalent in RGP EW than in DW
  11. 11. May develop in two forms: 1. Without infiltrates 2. With infiltrates The first type has a 2-3 mm diameter fluorescein staining adjacent to the sclera but no infiltrates • Cessation of lens wear usually results in resolution in two to three days leaving no trace of existence The second type is an infiltrated lesion that affects both the stroma and epithelium. The affected tissue is elevated above the corneal surface and may subsequently ulcerate and become vascularized. • This form takes longer time to resolve and leave a permanent scar First sign: punctate or granular fluorescein staining in the 3 and 9 o’clock zones, usually accompanied by local ciliary injection
  12. 12. Symptoms •Mild forms of 3 & 9 0’clock staining are asymptomatic •Greater levels of staining are often associated with symptoms such as ocular dryness, itching, and increased lens awareness.
  13. 13. • An inhibition of blinking leading to blinks that are incomplete and a reduced blinking is the primary cause of 3 and 9’O clock staining • This leads to disturbance of the tear layer that results in corneal and conjunctival desiccation Aetiology
  14. 14. Peripheral desiccation 3 & 9 o’clock staining Incomplete blinkingDiscomfort Blinking inhibition Increased Tear Evaporation Lens-Limbus Bridging by lid margin dryness Thinned tear film Decreased tear mucus
  15. 15. Causes Patient factors • Irregularities of the conjunctiva, e.g. pinguecula, may assist in bridging of conjunctival areas by upper lid margin. • Tear film abnormalities include lipid contamination, mucin deficiency, and an inadequate aqueous layer
  16. 16. Lens factors edge lift of 0.08 mm was unlikely to cause 3 & 9 staining while lifts of 0.10 to 0.12 mm were almost certain to cause 3 & 9 staining. Environmental influences Examples include: wind and air- conditioning.
  17. 17. Management •Early detection important to initiate an appropriate management plan •Schnider et al.(1997) showed that large diameter (TDs of 9.6 & 10.2 mm) lenses were better as long as a moderately wide tear reservoir could be maintained at the lens edge.
  18. 18. • Dictated by cause • Early phase: -patient education -use of tear supplements -improve blinking -redesign lens to improve fitting -maximize lens wettability -minimize surface deposits
  19. 19. Josephson (1986) stated that 3 & 9 o’clock staining left unchecked could lead to: • A breakdown of elastic tissue locally. • Conjunctival epithelial hypertrophy. • Dellen-like changes in the cornea, with or without vascularization.
  20. 20. Corneal Dellen Described as very localized areas of peripheral corneal thinning with a sharp demarcation. Dimples or saucer-like excavations at the corneal margin that are usually elliptical in shape and parallel to the limbus
  21. 21. •Fluorescein and Rose Bengal pool in the dellen, there is no true staining because the epithelium in the depression remains intact
  22. 22. Symptoms • Dellen usually occur in absence of discomfort or pain, or only slight discomfort with the decrease in corneal sensitivity in the depression itself (Insler etal, 1989) • Vague irritation or photophobia may be reported (Gutner, 1989) • Visual acuity is not affected because only the peripheral cornea is involved.
  23. 23. Etiology Dellen formation is secondary to a localized breakdown of the tear film’s lipid layer followed by corneal surface evaporation and dehydration The resulting desiccation produces localized thinning of the underlying tissue. Continued inability of the upperlid to resurface the mucin layer of the cornea adequately, plays a crucial role in the process leading to dellen formation
  24. 24. Management •As dellen don't occur in isolation, it is important that the underlying cause be determined. •Any 3 & 9 O’clock staining should be minimized, and the RGP lens fitting characteristics should be optimized •Temporary discontinuation of lens wear allows the cornea to recover to normal thickness by re-epithelialization
  25. 25. • Baum et al.(1968, cited in Robin et al., 1986) suggest that rapid rehydration may lead to complete resolution and that delayed rehydration may result in permanent local thinning. • The risk of serious corneal sequelae is low but can include: • Vascularization. • Cicatrization. • Stromal inflammation. • Stromal degeneration leading to corneal thinning (Insler, 1990) • Chronic marginal keratopathy. • Secondary infection.
  26. 26. Corneal Ulceration •Ulceration of the cornea is rare with RGP lens use •Corneal ulceration may involve either the central or peripheral cornea •Ulceration may be associated with dense 3 & 9 O’clock staining •The infiltrate typically appears as a dense focal zone surrounded by diffuse cellular accumulation. The epithelial defect overlies this infiltrate.
  27. 27. •When the epithelium is damaged, the risk of an opportunistic bacterial invasion increases. •Microbial contamination in RGP lens wear: Acanthamoeba
  28. 28. Corneal staining Common finding in contact lens wear Indicates cell damage, weakened attachment, or cell loss Staining has also been referred to under various names by different authors, e.g. superficial punctate staining, superficial punctate keratitis or Superficial punctate keratopathy
  29. 29. • Classified by: • type • depth • location It is likely that staining with RGP lenses is greater than SCLs because of the incidence of 3 & 9 o’clock staining with RGP lenses
  30. 30. •Foreign body induced epithelial damage is normally characterized by being coarse and track like in either a random or orbital pattern and is usually unilateral. •Profuse tearing and hyperemia may result
  31. 31. •RGP lens adherence produces both true epithelial staining and tear pooling in the depression giving the appearance of circular ‘pseudostain’ •The true staining may be in the form of central patch inside the indentation ring and peripheral arcuate staining
  32. 32. •Corneal staining resulting from excessive lens movement is usually limited to the peripheral area traversed by the lens edge over time and is arcuate (incomplete circle) or full circle (doughnut-like) in appearance The stained area is normally outside the ‘average’ centered location of the lens, i.e. the cornea normally located under the centered lens is neither exposed nor traumatized by the lens edge and hence sustains no damage
  33. 33. Vascularized limbal keratitis •Rare superficial vascularized lesion bridging conjunctiva, limbus and cornea •Sequelae to chronic 3 and 9 O’clock staining •Usually in RGP EW
  34. 34. •The elevated nodule is located some 0.25-0.5mm from the limbus usually at 3 & 9’o clock or 4 & 8’o clock The lesion’s properties includes: • Vascularized superficially or deeply • Exhibits extensive staining of the cornea and less extensive staining of the conjunctiva • Associated with limbal edema • Has ill defined diffuse borders • Has moderate to severe accompanying conjunctival injection
  35. 35. Principal cause of VLK: • Mechanical insult to the limbal region by the edge of RGP lenses • Repeated lens adherence in extended wear may also play a role in the development of VLK
  36. 36. Clinically divided into 4 stages: 1. Stage-I Mild and asymptomatic Conjunctival hyperemia is apparent 2. Stage –II A response that is presumed to be inflammatory with hyperemia, peripheral staining and infiltrates Mild ocular irritation reported along with increased lens awareness. At this relatively early stage, VLK responds rapidly to suitable treatment given
  37. 37. 3. Stage –III Moderate conjuncatival hyperaemia More infiltrates More severe staining A vascular tuft emanating from the conjunctiva and reaching across the limbus leads to and terminates in an epithelial mass Wearing time decreases 4. Stage –IV An alarming increase in symptoms including photophobia, significant discomfort and possibly pain whenever the lens encroaches onto the raised lesion Mass visible to the wearer and is likely to be reported Corneal hypoesthesia may be detectable
  38. 38. Oedema and Hypoxia related complications
  39. 39. Corneal oedema • incomplete corneal coverage inherent in an RGP lens fitting: Advantageous • Tear exchange <2% with SCLs and 10-20% with RGPs
  40. 40. •Corneal oedema is very subtle with RGP materials •Negligible with DW •EW •Greater overnight corneal swelling •Striae may be visible •Folds/black lines unlikely •Rapid recovery following eye opening
  41. 41. Etiology can occur as a result of eyelid closure, RGP contact lens wear (Dk/t), or a combination of both due to insulating effects of the lens on cornea & reduced evaporative cooling brought about by evaporation occurring at front surface of lens rather than the cornea. Other contributing factors due to stimulated tear production at least in the early phases of RGP lens wear Mechanical effects Hypotonicity ↑Temperature corneal hypoxia (most contributing factor)
  42. 42. Management • Maximize the oxygen availability to the eye •By optimizing the level of oxygen transmissibility provided by the lens •fitting characteristics such as movement • In cases of EW, reduce the wearing time so that the adverse effects are minimized
  43. 43. Corneal vascularization • Conspicious sign of poor corneal physiology • less likely to occur as a result of RGP lens wear because the corneal periphery/limbus remains uncovered by the centred, well fitted lens
  44. 44. Mechanical and pressure related complications
  45. 45. Lens adherence • Observed almost from commencement of overnight rigid lens wear • 48% of RGP lens EW wearers, however when flat fitting lenses are applied, the incidence of lens adherence rise to 84% • While RGP lenses adhere to the cornea at any position, it most commonly occur in the nasal direction
  46. 46. Signs that may accompany a bound lens: •Corneal indentation (96%) •Localized corneal distortion (88%) •Central patch staining (76%) •Peripheral arcuate staining (17%)
  47. 47. • Lens adherence is an adverse response of rigid lens wear that can have dramatic and serious consequences if not properly managed. Although the phenomenon has historically been more common with overnight wear, it does occur with daily wear. Tear film debris: Debris beneath the lens showed the classic fern-like pattern characteristically observed in rigid lens adherence
  48. 48. Etiology: the “thin-film” theory • Extensive data presented by Swarbrick and colleagues suggests that rigid lens adherence in daily wear is most commonly observed with fitting relationships that create minimal post-tear lens thickness profiles, such as those seen with an alignment fitting or flat and decentered lenses. • Swarbrick’s “thin-film theory” is based on the principle that when two surfaces of similar radii of curvature come into close contact with one another, a thin film is created between the surfaces. In the presence of aqueous tear film abnormalities, this thin layer between surfaces can become viscous and mucoid, which increases the possibility of adhesion. Swarbrick HA, Holden BA. Rigid gas permeable lens binding: significance and contributing factors. American Journal of Optometry & Physiological Optics. 1987;64:815. Swarbrick HA, Holden BA.
  49. 49. Management • Patient education •Assess lenses each morning •Use ocular lubricants •Mobilize lens with lid pressure • Lens fitting •Increase tear volume •Fit with slight apical pooling •Reduce total diameter
  50. 50. Corneal warpage "Warpage" of the cornea refers to a distortion in the shape of the cornea, usually due to the use of rigid contact lenses, and especially poorly fitting rigid lenses. The type of lens most notorious for this is the "hard" type of lens, which is a non-gas-permeable lens made of a plastic called PMMA.
  51. 51. Signs • Keratometer mire distortion is one obvious clinical sign of corneal warpage. • Irregular retinoscopic reflexes • A detailed slit lamp examination is likely to show posterior stromal hazing or opacities • Indecisive subjective refraction end point
  52. 52. Symptoms •Usually, asymptomatic - otherwise minimal if lens is comfortable • Significant ‘spectacle blur’ •Corneal shape may be influenced by lens back surface design •Vision often reduced significantly upon lens removal •Effects likely to span weeks or months
  53. 53. Etiology •While apparent cause of corneal warpage with rigid lens is mechanical, the underlying cause is poor physiology (inadequate lens Dk/t). •The resulting corneal (mainly stromal) edema would appear to be root cause. However edema cannot be the sole cause of these changes because edema resolves very quickly whereas refractive and/or topographical changes resolves more slowly (Wilson et al., 1990B, Lowther, 1994)
  54. 54. Other contributing factors •Ill fitting lenses •Eccentric location •Localized heavy bearing •Excessive movement •Lid pressure translated to the cornea
  55. 55. Management Because of individual differences corneal warpage needs to be managed on a case by case basis a. Improve physiology (change to lenses with ↑ transmissibility b. Cessation (to permit cornea to return to its original shape)
  56. 56. c. Programmed withdrawal: Arner (1977) studied abrupt cessation of lens wear and found severe corneal deformations and loss of visual acuity. As a result, he advised a gradual reduction of lens wear over several weeks as a way of reducing the effects of eventual cessation
  57. 57. Vision complications Usually the result of • shortcomings of lens design, • material selection, • tear film and/or lens wettability issues, or • disturbances of the cornea Because vision problems discourage contact lens wear, attention to visual performance with contact lens is important
  58. 58. Caused by: • Poor lens wettability • Lens surface crazing • Spectacle blur • Dimple veiling • Flare
  59. 59. 1. Poor lens wettability • Rapid drying/thinning of tear film - BUT < 5 sec at any position on the surface or repeatable locations • Aqueous fringes (thin-film interference) • Haze and hydrophobic spots Vision clear immediately after blink & deteriorates very quickly subsequently
  60. 60. Etiology Environment factors Heat, wind & low humidity Formation of front surface deposits on the lens Hydrophobic surface Tear break up times (BUTs) are shorter
  61. 61. Management •Improved lens care to minimize deposits •Polishing the surface to remove tenacious deposits •Refitting with different materials •Changing the patients environment to minimize the effects of surface dehydration
  62. 62. 2. Lens surface crazing • Fissure widths range from 1 to 8 micron • The anterior central zone of the lens is affected at first but ultimately, the whole lens surface is involved • Onset can range from 3 to 24 months multiple cracks or a mesh like lattice of fissures with ‘frosting’ of the ‘islands’ between fissures
  63. 63. Possibilities include: •Flaws inherent in manufacturing process •Stresses introduced during lens fabrication • Excessive localized heating during surfacing • Susceptibility of particular polymers to normal surface heating • Inadequate annealing of rod or button lens blanks •Hydration-dehydration cycles may play a role •Lens flexure • Temperature variation Exact cause is unknown
  64. 64. Management • Replace problem lens • Change lens material •Maintain lens physiology • check/change lens care products
  65. 65. 3. Spectacle blur • Reduced spectacle vision immediately following removal of RGP lenses •Normal vision cannot be restored by altering the spectacle Rx • May improve over time (hours) or after a period of sleep
  66. 66. Blurred vision with spectacles after wearing RGP lenses may be due to: •Change in corneal shape &/or •Corneal Edema
  67. 67. Management • Improve lens fitting characteristics •Minimize bearing •Maintain lens mobility • Increase lens Dk/t significantly • Educate wearer
  68. 68. 4. Dimple veiling Small, hemispherical pits form in the epithelium, resulting in an irregular corneal surface • With lens removed, pooling of sodium fluorescein in theses pits presents Gas bubbles trapped in post-lens tear film Bubbles act more like solid than gases • Seen in the cases with excessive corneal clearance Toric cornea with spherical RGP
  69. 69. •The dimple reduces the cornea’s optical efficacy and reduced vision results •If the dimples are located centrally (within the entrance pupil zone), and are significant in number, vision may be affected • Alter lens design •Decrease clearance • Central • edge
  70. 70. 5. Flare • Subjective phenomenon • A small back optic zone diameter (BOZD) • Significant lens decentration • Larger pupil sizes (e.g. individual anatomical variation, and/or lenses worn under low light levels) • The degree, and/or asymmetry of pupil size exceeding the lens optic zone • A deficient pre- lens tear film • Both tear film deficiency and poor lens wettability
  71. 71. Management • Optimize fitting characteristics • Improve centration • Decrease lens movement •The use of continuous aspheric back surface design that has no distinct BOZD. The lack of a distinct transition reduce the magnitude of any flare resulting
  72. 72. Lens and fitting related problem
  73. 73. Blink related problem • RGP lenses modify blinking esp. in neophyte wearers • Lens edge awareness • Dry eyes • Tired eyes • Transient disturbances of vision • Discomfort • Burning
  74. 74. Management •Optimize lens edge profile or fit • Improve comfort, lens centration •As a last resort – SCLs •Consider the effect of lens geometry, lid position, an lid lens interaction before fitting rigid lenses •For high riding lenses, thickness and diameter should be increased •For low riding lenses, a change of material (to one of lower specific gravity) and an increase in diameter are effective
  75. 75. Lens flexure • Unwanted, unaccounted for, lens shape change that occurs in situ • Usually transient, doesn't exceed lens elastic limits, • Flexing: toric cornea > spherical cornea
  76. 76. •When a rigid lens is fitted to the toric cornea the influence of lid pressure, blinking and capillary attraction combine to induce some level of conformity of the lens to the cornea •Flexure depends largely on the physical properties of the lens materials, lens thickness and the fitting relationship
  77. 77. •When strictly applied the term rigid is probably a misnomer since all lenses exhibit some flexibility regardless of thickness and material properties •Lens flexure will induce a plus cylinder whose axis is aligned with flattest corneal meridian •If corneal astigmatism > total astigmatism and both are WTR, then lens flexing will decrease the amount of residual astigmatism
  78. 78. Sign •Decreased and/or variable visual acuity •Cylinder over- refraction •Change in residual astigmatism Symptoms •Vision • Variable • Reduced quality •Decreased comfort • Reduced lens intolerance •Decreased wearing time
  79. 79. Etiology •Lens flexure is related to the lens material, lens design (especially thickness), and the lens fitting characteristics (esp if fitted steeply) •If the lens is unable to withstand the forces applied by the upper lid, it is forced to closer alignment with cornea
  80. 80. • Centre of the lens too thin •Material characteristics •Large BOZD •High minus BVP • Corneal toricity • Lid force on blinking •Possibly a low lid position • Steep central fitting
  81. 81. Management •Increase lens thickness •Seek alignment or a slightly flat fitting •Choose a newer material •E.g. higher Dk with greater rigidity •Decrease the BOZD •Fit a back surface toric or a bitoric lens
  82. 82. Lens warpage •Irregular mires •Focimeter/lensometer •keratometer •Over-refraction •No precise end point •Irregular or inexplicable result •Altered lens fit/fluorescein pattern
  83. 83. Aetiology •Most common cause: inappropriate lens handling •Typically lens warpage occurs in wearers who clean lens between their thumb and fore finger
  84. 84. •Lens case issues: •Flat base •Smooth walls (eccentric storage) •Dry storage •Allowed to dry out •Thin lens design
  85. 85. Once RGP lens warps, it is usually not possible to restore lens to its original shape. A new lens of appropriate lens design, probably in a different more rigid, more stable material, is required.
  86. 86. Conclusion •Contact lens complications can affect the contact lens corrected visual acuity (VA), the lens comfort and wearing time and lens condition. •The problems arising can cause disturbances to the eyelids and ocular surfaces that can result in long-term changes and reduction in contact lens tolerance.
  87. 87. •The clinician should try to help the patient overcome the lens-related problems, not only to promote satisfactory lens wear and to prevent the patient giving up contact lenses, but to prevent future ocular infections, inflammation and eyestrain.

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