Complications Consult

Tear film environment disrupted by introduction of a contact lens

A practitioner describes the signs, symptoms and treatments for contact lens-induced dry eye.
Amar Agarwal, MS, FRCS, FRCOphth
Amar Agarwal

Sometimes described as “minimal sicca syndrome,” contact lens-induced dry eye, or CLIDE, forces a borderline keratoconjunctivitis sicca patient into a full manifest of symptoms and findings that is associated directly with the introduction of a contact lens onto the ocular surface (Figure 1). The lens acts as an obstacle and competitor to the natural tear film, which can cause a reaction in the eye and lead to changes in its natural tear film physiology and metabolism. This can lead to intolerance, inflammation and a compromise of the ocular surface. My special guest in this column is Kenneth Daniels, OD, FAAO, of Hopewell, N.J., to explain how to handle this problem.

Amar Agarwal, MS, FRCS, FRCOphth

Complications Consult

The normal tear film environment is attacked by the introduction of a contact lens. Initially, there is a reflexive increase in tear production. However, over time, tear production will “fatigue” the system, decreasing the efforts of the lacrimal system and increasing the potential for contact lens deposits, microbial infection, corneal infiltration, corneal edema and, ultimately, patient dissatisfaction and intolerance to contact lenses.

The contact lens will disrupt the homeostatic balance of the tear film, requiring a new balance to be established between the pre-lens ocular tear film and the post-lens ocular tear film/pre-corneal tear film. As deposits or surface film accumulates, blinking compresses the tear film and removes the lipid-contaminated, hydrophobic mucus and debris from the lens tear surface. The integrity of the pre-corneal and lens tear film is directly proportional to the ability to maintain proper contact lens wetability and lens surface hydration.

If the lipid layer is poor, the evaporative process increases, leading to a greater loss of aqueous and the induction of a forward osmotic draw across the contact lens surface, which leads to lens dehydration and corneal desiccation. With lens dehydration, the hydrophilic lens will steepen mechanically, pulling on a weakened epithelial surface and allowing for corneal compromise visualized as central corneal epithelial desiccation and/or cell juncture splitting or separation.

As well, when the ocular surface becomes “unprotected,” there is the development of neuronal hyposensitivity and a barrier effect created by the contact lens interface. As the contact lens develops a substantial dehydration, it will tend to vault away from the ocular surface and leave an exposed gap between the post-lens surface and the corneal surface. The gap, however, is not fluid-filled and leaves the ocular surface unprotected, leading to compromise of the epithelium and aberration to neural regulation and biofeedback to the lid structure.

Symptoms

Patients with CLIDE will present with a somewhat-chronic contact lens acute red eye. They will say that their eyes feel tired and are always red, particularly later in the day. It would also be noted that they have difficulty in lens removal and describe a feeling of relief upon lens removal. Patients will proceed with vigorous eye rubbing after lens removal. In some cases of difficult lens removal, the eye feels overly sensitive with an increase in injection due to the inadvertent removal of superficial epithelial tissue and neuronal exposure due to epithelial compromise during lens wear. Supplementation drops may or may not benefit the patients, leading to self-limitation of lens wear or even discontinuance of lens wear.

Observations

The clinician will observe a contact lens acute red eye without infection that appears to be chronic in nature. There may be mild to moderate corneal staining due to lens vault. The lens may appear somewhat immobile, suggesting induced tight lens syndrome or small petechial hemorrhages on the conjunctiva juxtaposed to the lens edge or on the paralimbal conjunctiva. There is no apparent discharge or follicular nor papillary reaction. Tear film spreading abnormalities will be seen with the use of various diagnostic testing such as Schirmer strips, lissamine green, assessment of the tear breakup time, sodium fluorescein staining of the cornea and conjunctiva, and assessment of the lacrimal lake-marginal tear volume (Figures 2 and 3).


Classical appearance of a CLIDE patient exhibiting circumlimbal injection, marginal erythema, conjunctival injection and immobile lenses.


Disrupted tear film spread with subsequent paracentral punctate keratopathy associated with CLIDE.


Lissamine green staining of the conjunctiva in a CLIDE patient.

Images: Agarwal A, Daniels K

Treatment

The treatment for dry eye and CLIDE is to relieve the underlying problem by first identifying the portion of the tear film that is dysfunctional. Once identified, the treatment should be biased to complement the lens with minimal complexity to the patient. With the use of ocular lubricants as a supplement or stimulant, the eye becomes subjectively comfortable, but little is known regarding their long-term effect on the various tear film structures and corneal physiology. With respect to supplement interaction with the material and the materials interaction with the eye, the contact lens design and material are the key to long-term comfort and physiological balance in the potential success of the contact lens patient.

In order to achieve the proper tear film balance, the CLIDE patient must be treated as a normal “dry eye” patient. Following a flow chart of treatment, such as proper tear and nutritional supplementation, is the first step. The selection of supplementation and/or medicines is critical. If the patient presents symptomatically and objectively as a dry eye patient but has a “white” noninflamed conjunctiva, the use of goblet cell-mucin enhancers in the conjunctiva with lacrimal gland stimulus, ie. cyclosporine, would be considered appropriate. If the patient appears with a “red” inflamed dry eye, then intervention with steroids would be deemed more appropriate. This may also be complemented with the use of nutritional supplementation of omega-3 and omega-6 essential oils (fish and seed oil sources), which have a natural nonsteroidal anti-inflammatory effect. As well, tear and lens rehydration is well accomplished by using anti-oxidant or electrolyte balanced tear supplements. At the same time, a clinical decision must be made to refrain from contact lens use or limit it during the initial stages of therapy. Punctal occlusion should be reserved for long-term lens comfort maintenance until positive results are established with topical and oral therapies.

Material selection is critical in the treatment of the CLIDE patient. Always consider rigid gas permeable lenses first for borderline dry eye patients. A deficient or unstable tear film requires high oxygen permeability and a lens with low surface reactivity that moves adequately to minimize the risk of complications. Also consider the hydrogel-based materials of high water, non-ionic character, such as hioxifilcon and phosphocholine. Silicone hydrogel materials may be appropriate for oxygen enhancement but are not promising when treating defined CLIDE patients. Silicone hydrogels would be highly desirable once the CLIDE patient has been treated and the eye has resumed a feasible level of comfort and proper tear film balance.

For More Information:
References:
  • Agarwal A. Handbook of Ophthalmology. Thorofare, NJ: SLACK Incorporated; 2005.
  • Agarwal A, Agarwal A, Agarwal S. Four Volume Textbook of Ophthalmology. New Delhi, India: Jaypee Brothers; 2000.
  • Daniels KM. Contact lens induced dry eye. In: Agarwal A, ed. Dry Eye: A Practical Guide to Ocular Surface Disorders. Thorofare, NJ: SLACK Incorporated; 2006:317-332.
  • State of the art management of chronic dry eye: A growing public health concern. Clinician. 2006:24(16).
Amar Agarwal, MS, FRCS, FRCOphth
Amar Agarwal

Sometimes described as “minimal sicca syndrome,” contact lens-induced dry eye, or CLIDE, forces a borderline keratoconjunctivitis sicca patient into a full manifest of symptoms and findings that is associated directly with the introduction of a contact lens onto the ocular surface (Figure 1). The lens acts as an obstacle and competitor to the natural tear film, which can cause a reaction in the eye and lead to changes in its natural tear film physiology and metabolism. This can lead to intolerance, inflammation and a compromise of the ocular surface. My special guest in this column is Kenneth Daniels, OD, FAAO, of Hopewell, N.J., to explain how to handle this problem.

Amar Agarwal, MS, FRCS, FRCOphth

Complications Consult

The normal tear film environment is attacked by the introduction of a contact lens. Initially, there is a reflexive increase in tear production. However, over time, tear production will “fatigue” the system, decreasing the efforts of the lacrimal system and increasing the potential for contact lens deposits, microbial infection, corneal infiltration, corneal edema and, ultimately, patient dissatisfaction and intolerance to contact lenses.

The contact lens will disrupt the homeostatic balance of the tear film, requiring a new balance to be established between the pre-lens ocular tear film and the post-lens ocular tear film/pre-corneal tear film. As deposits or surface film accumulates, blinking compresses the tear film and removes the lipid-contaminated, hydrophobic mucus and debris from the lens tear surface. The integrity of the pre-corneal and lens tear film is directly proportional to the ability to maintain proper contact lens wetability and lens surface hydration.

If the lipid layer is poor, the evaporative process increases, leading to a greater loss of aqueous and the induction of a forward osmotic draw across the contact lens surface, which leads to lens dehydration and corneal desiccation. With lens dehydration, the hydrophilic lens will steepen mechanically, pulling on a weakened epithelial surface and allowing for corneal compromise visualized as central corneal epithelial desiccation and/or cell juncture splitting or separation.

As well, when the ocular surface becomes “unprotected,” there is the development of neuronal hyposensitivity and a barrier effect created by the contact lens interface. As the contact lens develops a substantial dehydration, it will tend to vault away from the ocular surface and leave an exposed gap between the post-lens surface and the corneal surface. The gap, however, is not fluid-filled and leaves the ocular surface unprotected, leading to compromise of the epithelium and aberration to neural regulation and biofeedback to the lid structure.

Symptoms

Patients with CLIDE will present with a somewhat-chronic contact lens acute red eye. They will say that their eyes feel tired and are always red, particularly later in the day. It would also be noted that they have difficulty in lens removal and describe a feeling of relief upon lens removal. Patients will proceed with vigorous eye rubbing after lens removal. In some cases of difficult lens removal, the eye feels overly sensitive with an increase in injection due to the inadvertent removal of superficial epithelial tissue and neuronal exposure due to epithelial compromise during lens wear. Supplementation drops may or may not benefit the patients, leading to self-limitation of lens wear or even discontinuance of lens wear.

Observations

The clinician will observe a contact lens acute red eye without infection that appears to be chronic in nature. There may be mild to moderate corneal staining due to lens vault. The lens may appear somewhat immobile, suggesting induced tight lens syndrome or small petechial hemorrhages on the conjunctiva juxtaposed to the lens edge or on the paralimbal conjunctiva. There is no apparent discharge or follicular nor papillary reaction. Tear film spreading abnormalities will be seen with the use of various diagnostic testing such as Schirmer strips, lissamine green, assessment of the tear breakup time, sodium fluorescein staining of the cornea and conjunctiva, and assessment of the lacrimal lake-marginal tear volume (Figures 2 and 3).


Classical appearance of a CLIDE patient exhibiting circumlimbal injection, marginal erythema, conjunctival injection and immobile lenses.


Disrupted tear film spread with subsequent paracentral punctate keratopathy associated with CLIDE.


Lissamine green staining of the conjunctiva in a CLIDE patient.

Images: Agarwal A, Daniels K

Treatment

The treatment for dry eye and CLIDE is to relieve the underlying problem by first identifying the portion of the tear film that is dysfunctional. Once identified, the treatment should be biased to complement the lens with minimal complexity to the patient. With the use of ocular lubricants as a supplement or stimulant, the eye becomes subjectively comfortable, but little is known regarding their long-term effect on the various tear film structures and corneal physiology. With respect to supplement interaction with the material and the materials interaction with the eye, the contact lens design and material are the key to long-term comfort and physiological balance in the potential success of the contact lens patient.

In order to achieve the proper tear film balance, the CLIDE patient must be treated as a normal “dry eye” patient. Following a flow chart of treatment, such as proper tear and nutritional supplementation, is the first step. The selection of supplementation and/or medicines is critical. If the patient presents symptomatically and objectively as a dry eye patient but has a “white” noninflamed conjunctiva, the use of goblet cell-mucin enhancers in the conjunctiva with lacrimal gland stimulus, ie. cyclosporine, would be considered appropriate. If the patient appears with a “red” inflamed dry eye, then intervention with steroids would be deemed more appropriate. This may also be complemented with the use of nutritional supplementation of omega-3 and omega-6 essential oils (fish and seed oil sources), which have a natural nonsteroidal anti-inflammatory effect. As well, tear and lens rehydration is well accomplished by using anti-oxidant or electrolyte balanced tear supplements. At the same time, a clinical decision must be made to refrain from contact lens use or limit it during the initial stages of therapy. Punctal occlusion should be reserved for long-term lens comfort maintenance until positive results are established with topical and oral therapies.

Material selection is critical in the treatment of the CLIDE patient. Always consider rigid gas permeable lenses first for borderline dry eye patients. A deficient or unstable tear film requires high oxygen permeability and a lens with low surface reactivity that moves adequately to minimize the risk of complications. Also consider the hydrogel-based materials of high water, non-ionic character, such as hioxifilcon and phosphocholine. Silicone hydrogel materials may be appropriate for oxygen enhancement but are not promising when treating defined CLIDE patients. Silicone hydrogels would be highly desirable once the CLIDE patient has been treated and the eye has resumed a feasible level of comfort and proper tear film balance.

For More Information:
References:
  • Agarwal A. Handbook of Ophthalmology. Thorofare, NJ: SLACK Incorporated; 2005.
  • Agarwal A, Agarwal A, Agarwal S. Four Volume Textbook of Ophthalmology. New Delhi, India: Jaypee Brothers; 2000.
  • Daniels KM. Contact lens induced dry eye. In: Agarwal A, ed. Dry Eye: A Practical Guide to Ocular Surface Disorders. Thorofare, NJ: SLACK Incorporated; 2006:317-332.
  • State of the art management of chronic dry eye: A growing public health concern. Clinician. 2006:24(16).