Dry Eye Disease
For contact lens use to be successful, the tear film must be of good quality and sufficient amount. Tear film consists of a layer of water, lipids, and aqua and mucin components. The function of the tear film is to act as a cleansing and protective surface of the eye. Occasionally there are insufficient tears to keep the eye comfortable, this is known as dry eye disease.
Insufficient tears can be defined as decreased production or quality (decreased amounts of water, lipids, or mucin components) of tears. This insufficiency can cause damage to the interpalpebral ocular surface. It is the resulting inflammation and structural changes of the eye that causes discomfort for the contact lens wearer.
When tear insufficiency is caused by decreased mucin the moistness of the eye is decreased. When insufficient or abnormal lipid production is the cause, the stability of the tear film is decreased. When aqueous deficiency is the cause there is decrease volume of tears. Eyelid abnormalities or abnormal blinking results in poor tear film distribution. Eye surface abnormalities result in decrease tear film stability. No matter what factor is affected, dry eye disease is the result.
Dry eye disease can be classified as evaporative dry eye and tear deficient dry eye. Tear deficient dry eye can be further sub-divided into Sjogren’s syndrome related and non-Sjogren’s syndrome related. Sjogren’s syndrome related dry eye is associated with systemic abnormalities.
Evaporative dry eye is caused by ocular surface abnormalities, contact lens wear, eyelid pathologies, blepharitis, and lipid insufficiency. Additionally, neurohormonal interactions play a role in evaporative dry eye. Evaporative dry eye is associated with meibomian gland disease.
The tear film is responsible for moistening and lubricating contact lenses. Proper tear levels aid in proper oxygen flow to the cornea. Additionally, proteins protect the eye surface, and decrease bacterial contamination. Contact lenses can increase evaporation leading to dry eye.
Evaporation of the tear film, resulting in tear film instability results in meibomian gland disease. It is interesting to note that the presence of estrogen and androgen receptors in the meibomian glands is similar to those found on the lachrymal gland surface and ocular surface. These glands are controlled by hormonal interactions. This may be a part of the androgen disturbance found in the tear deficient dry eye. It has been found that increase evaporation dry eye correlates with increase tear deficiency.
Tear deficient dry eye is often related to decrease tear production. Proteins such as lysozome and lactoferrin, normally found in tears, showed decrease incidence in patients with dry eye. Topical solutions composed of different types of liquids, polysaccharides, and polymers are commercially available to replace tear volume. Often a variety of minerals, vitamins, and electrolytes, have been added to these solutions to improve lachrymal function. These do not solve the problem, only sooth the patient.
Studies have shown that decrease production of the hormone androgen, causes inflammation of the eye. The presence of post-inflammatory cytokines in the tears and conjunctiva of dry eye patients support the fact that inflammation leads to tear deficient dry eye. This explains the increase incidence of dry eye disease in the elderly and post-menopausal women, and adds to the correlation of tear deficient and evaporative dry eye disease.
It is a natural conclusion then that the most successful use of contact lenses will be in patients with good tear production and stability.