MILESTONES OF DRY EYE DISEASE

Efioshiomoshi Kings Topah OD, MSc

Our understanding of dry eye disorders has improved dramatically in the past several years as it is one of the common presentations seen by optometrists with a prevalence reportedly varying from 5% to as high as 73.5%1,2. This increased prevalence globally has prompted clinicians drive to understanding in details which enhanced the ability to diagnose and treat patients who have these traditionally challenging conditions. This article looks at the milestones of dry eye disease as it enhances our understanding of its natural history, diagnosis, and treatment of dry eye disorders – beginning with the underlying mechanisms.

Classifying dry eye disorders

Common to virtually all dry eye disorders is a loss of water from the tear film, which increases its concentration (osmolarity) above the normal limit of 311mOsm/L3. Tear film osmolarity increases when water is lost from the tear film, while solutes, such as sodium and potassium, are not. This loss of water and increase in osmolarity may result from any condition which either decreases tear production or increases tear evaporation. Increased tear osmolarity is the link between changes in the lacrimal glands and lids, and disease of the ocular surface.

Studies of pre-clinical models of lacrimal gland disease and meibomian gland dysfunction show that the ocular surface changes of dry eye disease are dependent upon and proportional to increases in tear film osmolarity4-10. Clinical studies agree with these findings11,12. Decreased tear secretion may result from any condition which damages the lacrimal gland or its excretory ducts. Autoimmune disease with inflammation of the tear gland is the most common cause. Less common causes include cicatricial ocular surface conditions. Tear secretion also may be decreased by any condition that decreases corneal sensation13, including diabetes, herpes zoster, long-term contact lens wear and surgery which involves corneal incisions or ablates corneal nerves. Increased tear evaporation may occur in one of two ways:

1. Long-standing posterior blepharitis causing meibomian gland dysfunction. When these glands function properly, they produce an oil layer which coats the tear film and retards evaporation.

2. A large palpebral fissure width, occurring either naturally, secondary to cosmetic surgery or with thyroid eye disease14, places evaporative stress on the tear film. Evaporation is proportional to the palpebral-fissure surface area. Increased evaporation also explains why symptoms become worse with exposure to air conditioning, dry heat, low humidity or wind.

Milestones of dry eye

While studies of human disease have shown the ocular surface changes which occur with dry eye, the study of pre-clinical models of keratoconjunctivitis sicca (KCS) helps us to depict the natural pattern of these changes. We now know that dry eye disease evolves

 through a sequence of four milestones:

• Loss of water from the tear film with an increase in tear osmolarity

• Decreased conjunctival globlet-cell density and decreased corneal glycogen

• Increased corneal epithelial desquamation

• Destabilisation of the cornea-tear interface

Decreased tear production or increased tear evaporation is rapidly reflected by an increase in tear osmolarity, and soon thereafter by a decrease in goblet cell density. The loss of goblet cells is significant because they produce mucus, the major lubricant in the tear film, and serve in the defence of the ocular surface (mucus fired from goblet cells helps trap foreign matter and expel it from the eye).

The increase in the osmotic gradient between the tear film and the ocular surface, in addition to decreasing goblet cells, pulls water between conjunctival epithelial cells. This action breaks the delicate attachments between these cells and increases conjunctival cell desquamation. In agreement with the decrease in goblet cells is a decrease in corneal glycogen. This loss of glycogen is clinically important because glycogen is the energy source for the sliding step of corneal wound healing wound healing. However, the cornea does not stay unaffected forever. Much later in the natural history of the disease, after resisting changes in the tear film, the attachments between corneal cells finally loosen. The result is an increase in corneal desquamation with a resultant decrease in corneal barrier function. Even later in the natural history of the disease, changes in the corneal epithelial cell surface become severe, resulting in a loss of corneal surface glycoproteins and destabilisation of the cornea-tear interface (the attachment between the cornea and the tears).

In summary, understanding the natural history of the disease is crucial for properly interpreting and evaluating clinical work up and appreciating treatment advances (Table 1).

Table 1: Milestones of dry eye disease

Check table here

https://drive.google.com/file/d/1RdgLmHXGundLV80RoedhaYLbg-446hzd/view?usp=drivesdk

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