rgp complications

Common RGP Complications

Hira Nath Dahal3rd year B. Optometry

Objectives

Complications related to Inflammation and Staining

Oedema and Hypoxia Mechanical and Pressure Vision Complications Lens and Fitting

Introduction

ConclusionReferences

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

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

Inflammation and Staining Related

CLPC3 & 9 O’Clock StainingCorneal DellenCorneal Staining

Corneal UlcerationVascularized Limbal Keratitis (VLK)

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

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

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

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 problemsMore prevalent in RGP EW than in DW

May develop in two forms:1. Without infiltrates2. 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

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.

• 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

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

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

Lens factorsedge 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.

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.

• Dictated by cause• Early phase:

-patient education-use of tear supplements-improve blinking-redesign lens to improve fitting-maximize lens wettability-minimize surface deposits

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.

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

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

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.

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

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

• 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.

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.

•When the epithelium is damaged, the risk of an opportunistic bacterial invasion increases.

•Microbial contamination in RGP lens wear: Acanthamoeba

Corneal staining

Common finding in contact lens wearIndicates cell damage, weakened attachment, or cell lossStaining has also been referred to under various names by different authors, e.g. superficial punctate staining, superficial punctate keratitis or Superficial punctate keratopathy

• 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

•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

•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

•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

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

•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

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

Clinically divided into 4 stages:1. Stage-I

Mild and asymptomaticConjunctival hyperemia is apparent

2. Stage –IIA response that is presumed to be inflammatory with hyperemia, peripheral staining and infiltratesMild ocular irritation reported along with increased lens awareness.At this relatively early stage, VLK responds rapidly to suitable treatment given

3. Stage –IIIModerate conjuncatival hyperaemiaMore infiltratesMore severe stainingA vascular tuft emanating from the conjunctiva and reaching across the limbus leads to and terminates in an epithelial massWearing time decreases

4. Stage –IVAn alarming increase in symptoms including photophobia, significant discomfort and possibly pain whenever the lens encroaches onto the raised lesionMass visible to the wearer and is likely to be reported Corneal hypoesthesia may be detectable

Oedema and Hypoxia related

complications

Corneal oedema

• incomplete corneal coverage inherent in an RGP lens fitting: Advantageous

• Tear exchange <2% with SCLs and 10-20% with RGPs

•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

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)

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

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

Mechanical and pressure related

complications

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

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

• 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

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.

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

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.

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

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

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)

Other contributing factors

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

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)

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

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

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

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

Etiology

Environment factors

Heat, wind & low humidity

Formation of front surface deposits on the lens

Hydrophobic surface

Tear break up times (BUTs) are shorter

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

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

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

Management

• Replace problem lens• Change lens material•Maintain lens physiology

• check/change lens care products

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

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

Management

• Improve lens fitting characteristics•Minimize bearing•Maintain lens mobility

• Increase lens Dk/t significantly• Educate wearer

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 filmBubbles act more like solid than gases

• Seen in the cases with excessive corneal clearanceToric cornea with spherical RGP

•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

5. Flare

• Subjective phenomenon

• A small back optic zone diameter (BOZD)• S

ignificant 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• B

oth tear film deficiency and poor lens wettability

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

Lens and fitting related problem

Blink related problem

• RGP lenses modify blinking esp. in neophyte wearers

• Lens edge awareness• Dry eyes• Tired eyes• Transient disturbances of vision• Discomfort• Burning

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

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

•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

•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

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

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

• 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

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

Lens warpage

•Irregular mires•Focimeter/lensometer•keratometer

•Over-refraction•No precise end point• Irregular or inexplicable result

•Altered lens fit/fluorescein pattern

Aetiology

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

•Lens case issues:•Flat base•Smooth walls (eccentric storage)•Dry storage•Allowed to dry out

•Thin lens design

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.

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.

•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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