Common complications from rigid gas permeable (RGP) contact lens wear include inflammation and staining, oedema and hypoxia, and mechanical and pressure issues. Inflammation and staining complications include papillary conjunctivitis, 3 and 9 o'clock staining, corneal dellen, and vascularized limbal keratitis. Oedema and hypoxia complications include corneal oedema. Mechanical and pressure complications involve lens adherence, corneal warpage, and incomplete blinking leading to peripheral corneal desiccation and staining. Managing complications requires determining the underlying cause, such as lens design or fitting issues, and taking steps to improve lens physiology and ocular health.

1. Common RGP
Complications

2. Objectives
Complications related to
Inflammation and Staining
Oedema and Hypoxia
Mechanical and Pressure
Vision Complications
Lens and Fitting
Introduction
Conclusion
References

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. 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. Inflammation and
Staining Related

6. CLPC
3 & 9 O’Clock
Staining
Corneal Dellen
Corneal Staining
Corneal Ulceration
Vascularized Limbal
Keratitis (VLK)

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. 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. 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. 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. 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. 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. • 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. 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. 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. 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. 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. • 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. 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. 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. •Fluorescein and Rose Bengal pool in the dellen,
there is no true staining because the
epithelium in the depression remains intact

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. 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. 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. • 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. 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. •When the epithelium is damaged, the risk of
an opportunistic bacterial invasion increases.
•Microbial contamination in RGP lens wear:
Acanthamoeba

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. • 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. •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. •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. •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. 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. •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. 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. 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. 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. Oedema and Hypoxia
related complications

39. Corneal oedema
• incomplete corneal coverage inherent in an RGP
lens fitting: Advantageous
• Tear exchange <2% with SCLs and 10-20% with
RGPs

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. 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. 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. 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. Mechanical and pressure
related complications

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. Signs that may accompany a bound lens:
•Corneal indentation (96%)
•Localized corneal distortion (88%)
•Central patch staining (76%)
•Peripheral arcuate staining (17%)

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. 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. 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. 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. 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. 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. 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. Other contributing factors
•Ill fitting lenses
•Eccentric location
•Localized heavy bearing
•Excessive movement
•Lid pressure translated to the cornea

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. 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. 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. Caused by:
• Poor lens wettability
• Lens surface crazing
• Spectacle blur
• Dimple veiling
• Flare

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. 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. 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. 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. 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. Management
• Replace problem lens
• Change lens material
•Maintain lens physiology
• check/change lens care products

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. Blurred vision with spectacles after wearing
RGP lenses may be due to:
•Change in corneal shape &/or
•Corneal Edema

67. Management
• Improve lens fitting characteristics
•Minimize bearing
•Maintain lens mobility
• Increase lens Dk/t significantly
• Educate wearer

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. •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. 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. 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. Lens and fitting related
problem

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. 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. 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. •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. •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. 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. 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. • 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. 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. Lens warpage
•Irregular mires
•Focimeter/lensometer
•keratometer
•Over-refraction
•No precise end point
•Irregular or inexplicable result
•Altered lens fit/fluorescein pattern

83. Aetiology
•Most common cause: inappropriate lens
handling
•Typically lens warpage occurs in wearers who
clean lens between their thumb and fore finger

84. •Lens case issues:
•Flat base
•Smooth walls (eccentric storage)
•Dry storage
•Allowed to dry out
•Thin lens design

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. 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. •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.