Article Date: 6/1/2006

LENS COMPLICATIONS
Assessing and Treating Complications
A guide to recognizing and treating most of today's contact lens complications.
By Barry A. Weissman, OD, PhD, FAAO

When 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 abrasion (rare).

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 wearer.

Complications Today

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. 

Some 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 wear.

Solution Problems

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.

Hypoxia

TABLE 1

Contact Lens Complications by Layer and Etiology*

LIDS
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
Infectious: blepharitis

TEAR LAYER
Mechanical: tear disruption (directly or related to MGD)
Desiccation: CL-mediated dry eye
Immune mediated: Sjögren's-syndrome mediated dry eyes

BULBAR CONJUNCTIVA
Mechanical: erosion leading to chemosis and vascular injection
oxic:
solution-related chemosis and vascular injection, occasionally CL-SLK
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

CORNEAL STROMA
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, edema

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). 

We've 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.

Corneal Staining

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 oral antibiotics.

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.

Corneal Abrasion

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.

Lid Complications

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).

Figure 3. 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 al, 1992).

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 www.clspectrum.com/references.asp 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