and Treating Complications
guide to recognizing and treating most of today's contact lens complications.
By Barry A. Weissman, OD, PhD, FAAO
I trained in contact lens care in 1970, we used only PMMA lenses. Complications
included injected conjunctivae (red eyes), poor lens comfort (ranging from mild
lens awareness to substantial foreign body sensation), corneal edema (then defined
by central circular clouding [CCC] and/or distorted keratometry mires), three o'clock
and nine o'clock staining (3/9 staining), damaged/soiled lenses (common) and epithelial
Because we saw few complications, becoming
a good diagnostician then was a challenge. We could define contact lens success
as much by comfort-related tolerance as by physiology-related tolerance (Sarver
& Harris, 1971). Soft contact lenses improved initial tolerance dramatically,
but also led to a host of complications, particularly with extended wear (EW).
Figure 1. SEAL staining in a silicone hydrogel
We can now distinguish among a great many complications.
We also understand much more about their etiology and management. Fortunately, lens
wearers rarely experience vision-threatening complications (limited to microbial
keratitis [MK] and deep stromal neovascularization). Table 1 lists complications
both by anatomical order and by etiology: Mechanical, desiccation, hypoxia, toxic,
immune-mediated and infectious.
complications are simple. Others are multifactorial in etiology and complex in nature.
Still others are collateral while the lens itself isn't the cause, it complicates
Perhaps the most prevalent complications of lens
wear are those associated with care solutions and with lens soilage. Both are usually
hypersensitivity reactions. Patients commonly present with subjective ocular irritation
and dry eye symptoms. Signs can include fine corneal staining, sub-epithelial infiltrates
(infiltrative keratitis [IK] or asymptomatic infiltrative keratitis [AIK]), conjunctival
injection and/or edema, even a mimic of superior limbic keratoconjunctivitis (Mondino
& Groden, 1980; Stenson, 1983; Jones et al 2002). Subepithelial corneal infiltrates,
both round and dendritic, can be either infectious or non-infectious.
Rare reports exist of these lens/solution
reactions (especially when Thimerosal is the preservative) resulting in a devastating
destruction of corneal limbal stem cells. Patients report irritation, but clinicians
note a thick, granular, fibrovascular pannus growing over the (usually superior)
involved cornea. Treatment is discontinuation of lens wear, but often these patients
will require limbal stem cell transplantation (Jenkins et al, 1993).
Always rule out an infectious etiology
before beginning steroid treatment of any corneal infiltrate. Once the reaction
resolves, reconsider lens wear with an alternative care regimen, often peroxide-based.
You may also fit hydrogel lens wearers with daily disposable soft lenses to eliminate
all solution issues. GP lens wearers can rinse their lenses with preservative-free
saline prior to application.
Contact lens soilage and damage (cracks,
scratches, chips) can result in similar symptoms. Soft lenses are now usually replaced
before they become soiled. You can usually recondition GP lenses through polishing
and cleaning, but eventually they become warped, scratched or soiled to an extent
that they should be replaced.
Lens Complications by Layer and Etiology*
Mechanical: ptosis (associated with GP application/removal
or 2° to GPC)
Toxic: solution reactions
Immune-mediated: GPC (type I hypersensitivity, can lead
to 2° ptosis), solution reactions (type IV hypersensitivity), MGD
Mechanical: tear disruption (directly or related to MGD)
Desiccation: CL-mediated dry eye
Immune mediated: Sjögren's-syndrome mediated dry eyes
Mechanical: erosion leading to chemosis and vascular injection
oxic: solution-related chemosis and vascular injection,
Desiccation: erosion and vascular injection
Hypoxia: vascular injection
Immune-mediated: vascular injection, CLARE
Infectious: chemosis and vascular injection
CORNEAL EPITHELIUM AND ANTERIOR LIMITING LAMINA (BOWMAN'S)
Mechanical: 3/9 staining (can lead to either dellen or
VLK), CL adhesion/binding rings and corneal distortion, SEALs, foreign body or damaged
lens (edge?) erosions and abrasions, soiled CL back surface, dimple veil stain
Desiccation: 3/9 staining, inferior arcuate stain (dehydration
through soft lens)
Toxic: pan-corneal staining, erosion (medicamentosa)
Hypoxia: cluster stain, decreased mitosis (leading to thinning)
adhesion and sensitivity, microcysts and microcystic edema, ECF, corneal distortion
Immune-mediated: staining and erosion (hypersensitivity),
stem cell failure related pannus
Infectious: primarily bacterial (most often Pseudomonas,
Staphylococcal, Streptococcal), also Acanthamoeba; consider
fungal and viral infections as well
Toxic: IK or AIK
Hypoxia: CCC, acute swelling (leading to stromal striae
at 4 percent to 6 percent swelling and striate keratopathy at 10 percent swelling)
and chronic thinning (through loss of glycosaminoglycans), warpage, subepithelial
neovascularization (pannus), deep stromal neovascularization, IK
Immune-mediated: IK, edema
Infectious: direct (MK) and indirect (CLPU) infiltrates,
CORNEAL ENDOTHELIUM AND POSTERIOR LIMITING LAMINA (DESCEMET'S)
Hypoxia: blebs (acute) and polymegathism (chronic)
* Not all are primarily caused by lens wear, but by definition
complicate lens wear and deserve attention.
Corneal hypoxia has probably been the most common
complication of lens wear. Hypoxia causes corneal microcysts and microcystic edema
(MCE); pseudodendritic edematous corneal formations (ECF); decreased epithelial
mitosis, sensitivity and adhesion; CCC; changes in stromal thickness, acidosis and
striae; and endothelial blebs and polymegethism (Sarver, 1971; Korb, 1973; Zantos
& Holden, 1977; Hirji & Larke, 1979; Millidot & O'Leary, 1980; Schoessler
& Woloschak, 1981; Bergmanson et al, 1985; Bonnano & Polse, 1987). Hypoxia
can result in corneal distor-tion/warpage, which causes spectacle blur. A putative
corneal exhaustion syndrome (CES) causes previously successful long-term wearers
to suddenly become intolerant (Sweeney, 1992).
recently learned that lens-driven hypoxia causes conjunctival vascular injection
(Papas et al, 1997). Superficial corneal pannus can be associated with hypoxia (or
chronic mechanical 3/9 epithelial desiccation with GPs) (Grohe & Lebow, 1989;
Chan & Weissman, 1996). Deep stromal neovascularization is another rare complication.
Secondary intracorneal hemorrhages can also occur with deep or superficial neovascularization
regardless of etiology.
It's now clear that maintaining
tear oxygen tension at about 100 mmHg will preclude clinically significant hypoxia.
Modern lens materials with oxygen permeabilities of 50 to 100 Fatt units or greater
should provide reasonable corneal oxygenation under daily wear conditions (Brennan
& Efron, 2005). Lenses made from very high oxygen transmissible materials also
appear to provide reasonable corneal oxygenation even when used for EW.
If you observe hypoxic complications,
then enhance the lenses' oxygen transmissibility (and/or possibly adjust the lens
wear schedule) to increase corneal oxygen supply.
Damaged corneal epithelium accepts fluorescein
stain. Causes of epithelial corneal staining include desiccation (Zadnik & Mutti,
1985; Businger et al, 1989), chemical trauma (toxic or immune-mediated solution
reactions) and mechanical trauma (cracked or chipped lenses, foreign bodies trapped
between the lens and the eye, superior epithelial arcuate lesion [SEAL, also known
as epithelial splitting, Figure 1] [Malinovski et al, 1989]). Goals of acute treatment
are to decrease both subjective patient discomfort and the risk of abrasion and/or
secondary infection. Acute care includes decreasing or discontinuing lens wear and
helping the epithelium to heal by use of artificial tears in mild cases, protective
antibiotic drops in more severe cases and appropriate professional observation.
Chronic management should address the cause of corneal staining to prevent recurrence.
For example, perhaps the most common complication
of GP lens wear is 3/9 corneal staining. Moderate to severe 3/9 staining deserves
attention to decrease its potential to advance to abrasion, infection, dellen or
pseudopterygium/vascularized limbal keratitis (VLK). The principal cause of 3/9
staining is desiccation from a gap between the lens edge and the corneal surface
with low-riding GP lenses. You should first optimize the GP lens position by increasing
its diameter and/or flattening its base curve. For cases of substantial corneal
astigmatism, bitoric GP designs may be appropriate. When you note 3/9 staining in
the presence of a well-centered and mobile GP lens, consider increasing or decreasing
the edge lift and smoothing/thinning the lens edge. Also consider whether contact
lens binding is playing a role. If all attempts to remedy the problem of 3/9 staining
are unsuccessful, then consider prescribing hydrogel lenses.
The condition of a patient's lids/meibomian
glands and tear layers can often contribute to corneal staining (especially 3/9).
Lid treatment includes lid hygiene (Korb & Henriquez, 1980) and occasionally
topical antibiotic drops or bedtime ointment use. Recalcitrant blepharitis occasionally
deserves topical steroid/antibiotic treatment (while discontinuing lens wear) or
Clinicians must distinguish corneal
staining from the less worrisome "dimple veil" stain in which epithelial depressions
develop from bubbles of air, or even rolled up balls of mucin, trapped between the
lens and the ocular surface. Flattening GP base curves may help manage dimple veil
stain, but sometimes (as with keratoconus) this is impractical. You can ignore minimal
and asymptomatic epithelial dimple stain. Thick artificial tears and/or piggyback
lens systems may also prove helpful.
In the case of corneal abrasions, you must rule
out and prevent infection as well as manage symptoms (pain primarily). Patients
should temporarily discontinue lens wear to aid the healing process. Some clinicians
believe in prophylactic antibiotic treatment, while others prefer to withhold antibiotics
unless infection is suspected or proven. To decrease the risk of precipitating or
enhancing a microbial corneal infection, refrain from patching the eye and withhold
topical steroids (Clemons et al, 1987). Often, lubrication with artificial tears
and professional supervision (follow up at 24 hours or immediately if symptoms increase)
is appropriate treatment. Bandage soft lenses and topical non-steroidal anti-inflammatory
topical drops and occasionally oral pain agents may help decrease
pain during the healing process. Close professional supervision should continue
until the epithelial defect has closed. You should then address the cause of the
abrasion. For example, a patient with repeated apical corneal abrasions may have
underlying corneal basement membrane abnormalities (Cogan's microcystic map-dot-fingerprint
dystrophy) or keratoconus (Figure 2).
Acute Red Eye
Contact lens acute red eye (CLARE) primarily occurs
during EW. It probably results from indirect infectious contamination of lenses
and associated solutions and/or cases with bacteria, resulting in ocular exposure
to secondary bacterial toxins. Initial treatment is palliative, and improved lens
care and hygiene should preclude this complication.
Figure 2. Full
thickness epithelial defect/abrasion in a keratoconus patient wearing a GP lens.
Documented lid reactions besides blepharitis and
meibomian gland dysfunction (MGD) include allergic responses, giant papillary conjunctivitis
(GPC) and/or ptosis (Allansmith et al, 1977; Epstein & Putterman, 1981; Fonn
& Holden, 1986).
GPC is believed to be a hypersensitivity response.
The antigen is unknown but may be related to either lens adherent biological debris
or perhaps to mechanical conjunctival irritation from the lens edge.
Patients who have GPC should first
discontinue lens wear until asymptomatic. The signs (mucus, inflammatory tarsal
conjunctival papillae) should subside before cautiously resuming lens wear, and
you should recommend more frequent, increased use of enzyme cleaner and/or more
frequent replacement. Switching to peroxide disinfection or single-use contact lenses
is helpful. Often it's also helpful to change the lens design from hydrogel to GP
or vice-versa. In some instances, modifying the edge design is sufficient to preclude
the recurrence of GPC.
Prescribe topical mast cell-stabilizing
agents, NSAIDs, antihistamines and occasionally, steroids (with caution to minimize
the risk of secondary ocular infection, glaucoma or cataract) adjunctively when
conservative (non-medical) treatment is not a sufficient remedy (Meisler et al,
1982; Korb et al, 1983; Donshik et al, 1984).
Microbial Corneal Infection
Microbial keratitis (MK) is identified by sudden
onset of foreign body sensation or ocular pain, photophobia, "red" eye and discharge
and by clinical signs of a corneal epithelial/stromal defect with associated inflammatory
response (infiltration) (Stein et al, 1988). MK is often accompanied by anterior
chamber reaction (including hypopyon in some cases), ocular discharge, lid swelling
and conjunctival injection and it's commonly unilateral. Poor lens care and hygiene,
travel, smoking, male gender and young adult age may be risk factors. Overnight
orthokeratology may be an additional risk factor. MK has an incidence of about
20 per 10,000 people who use contact lenses for EW wear and about 4 per 10,000 people
using lenses for daily wear per year (Schein et al, 1989; Poggio et al, 1989; Cheng
et al, 1999). Recent reports suggest that increased risk with EW persists despite
dramatic improvements in oxygen transmissibility with soft silicone hydrogel lenses
(Schein et al, 2005).
Because MK is sight threatening, always assume
that suspicious-looking lesions are infectious and treat them aggressively. If any
signs or symptoms occur, immediately discontinue lens wear in both eyes to decrease
the potential for bilateral disease.
Bacterial MK (usually attributable
to Gram-negative Pseudomonas aeruginosa, but also Gram-positive Staphylococcus
aureus and Staphylococcus epidermidis) is primarily associated with EW
or continuous wear (Mondino et al, 1986). Poor lens care compliance, especially
exposing lenses to fresh water (swimming), also appears to be a major risk factor
for Acanthamoeba MK (Figure 3) (Shehr-Green et al, 1989).
Acanthamoeba MK in a soft lens patient who
occasionally rinsed his lenses with tap water.
Managing MK begins with initial timely
recognition. Clinicians at hospitals and university medical centers usually obtain
cultures and smears of all suspicious lesions. Community doctors alternatively often
treat peripheral and small suspected corneal infections empirically (McDonnell et
Begin treatment with an initial "loading"
dose using antibiotic drops every fifteen minutes for the first hour or two of treatment,
followed by additional drops every hour while the patient is awake. Many clinicians
believe fourth-generation fluoroquinolone monotherapy (this is an off-label use
these agents are FDA-approved only for treating conjunctivitis) is as effective
as dual therapy with "fortified" aminoglycosides (gentamicin, tobramycin, amikacin)
in addition to a cephalosporin or vancomycin, particularly for small and peripheral
suspected bacterial infections. Have patients follow up frequently, often at 24-hour
intervals if not sooner.
Modify treatment by a patient's clinical
progress as well as the laboratory identification of microorganisms and their antibiotic
sensitivities. Avoid adjunctive patching. The early use of topical steroids is usually
contraindicated, but some doctors will intervene with steroids early with the intention
of limiting scar formation from stromal infiltration. This treatment runs the risk
of allowing inadequately controlled infections of such microbes as Pseudomonas
sp, herpes and Acanthamoeba to escape therapy.
Always consider the possibility of
fungal, herpetic, mycobacterial and Acanthamoeba MK in any contact lens-related
keratitis, especially in cases of chronic disease with initially negative culture
results and failure to respond to antibiotic therapy. Increase clinical suspicion
of Acanthamoeba when the patient reports extreme ocular pain or when you
observe an unusual epitheliopathy (reminiscent of herpetic epithelial disease) or
peripheral corneal radial neuropathy. Special culture techniques are available for
Acanthamoeba infections, but tissue biopsy is often necessary.
Medical treatment of Acanthamoeba
keratitis often employs combinations of antibiotic, antifungal, antiparasitic and
biocide/cationic antiseptic agents (Berger et al, 1990). Even considering the current
concerns about contact lens solutions and fungal keratitis, fungal MK has been extremely
rare among cosmetic lens wearers, but antifungal pharmaceutical agents (both commercial
and custom-made) are available. It's important to note that herpetic, atypical mycobacterium
and Acanthamoeba infections often mimic fungal corneal ulcers and vice-versa.
Misdiagnosis and medical failures are common when treating MK caused by these microorganisms.
Adenoviral and herpes viral corneal
infections can occur during lens wear. No causative association has been proposed
for such viral infections. Patients should discontinue lens wear during viral infections.
Patients should probably discard contact
lenses that they've worn during the early stages of an active infection and apply
new lenses and replace their storage case once the infection has resolved.
MK associated with lens wear, while
rare, remains a concern, and management remains complex. Aggressive and complex
medical treatment including subconjunctival injections and/or systemic antibiotic
treatment with hospitalization and perhaps cor-neal transplantation
may be necessary, especially in cases of indolent, refractory or non-bacterial corneal
infections. Hallmarks of successful treatment/healing include decreasing pain, reduced
inflammatory signs and closing of epithelial defects. It's prudent to refer patients
who have severe or refractory inflammatory or infectious ocular disease to a corneal
and external eye disease specialist.
General Treatment Recommendations
The most effective way to address lens complications
is to prevent them from occurring. One way patients can preclude many complications
is to maintain lens care and hygiene, consistent with both common sense and FDA-approved
manufacturers' guidelines. Restricting contact lens use to daily wear also should
reduce the occurrence of severe complications.
It's also important that lens wearers, especially
those who elect EW, understand their role in their own protection. They should return
at reasonable intervals for routine care and immediately should symptoms occur.
You should always have emergency services available so that symptomatic patients
may receive appropriate care in a timely manner.
To obtain references, visit
and click on document #127.
Dr. Weissman is a Professor of Ophthalmology
at Jules Stein Eye Institute and at the Department of Ophthalmology, David Geffen
School of Medicine at UCLA.
Contact Lens Spectrum, Issue: June 2006