Keratoconjunctivitis sicca (KCS) is the medical term for a chronic condition commonly referred to as dry eye disease. This disorder is characterized by an inadequate or unstable tear film that fails to properly lubricate the eye’s surface. While KCS can be a symptom of systemic autoimmune diseases, notably Sjögren’s Syndrome, the majority of cases occur independently.
Understanding Keratoconjunctivitis Sicca
The surface of the eye requires a continuous, stable tear film for lubrication, nourishment, and protection. This film is composed of three distinct layers: a mucus layer, a thick middle aqueous (watery) layer, and a thin outer lipid (oil) layer. When this delicate balance is disrupted, the ocular surface dries out and sustains damage. This desiccation leads to a cycle of inflammation and tissue injury on the conjunctiva and cornea.
A person experiencing KCS typically reports a persistent gritty or foreign body sensation, as if sand is in the eye. Common symptoms include burning, stinging, redness, and increased light sensitivity. Paradoxically, some individuals experience excessive tearing as a reflex response to the underlying irritation. Fluctuating vision, which may temporarily clear with a blink, is also frequent due to tear film instability.
Primary Drivers of Non-Autoimmune Dry Eye
Non-autoimmune KCS is categorized into two types: evaporative, where tears disappear too quickly, and aqueous-deficient, where not enough tears are produced. Evaporative dry eye is the more prevalent type, often stemming from Meibomian Gland Dysfunction (MGD). The meibomian glands secrete the lipid layer of the tear film; when they are blocked or inflamed, the tear film lacks this protective oil barrier. Without the lipid layer, the watery component of the tears evaporates rapidly.
Lifestyle and environment significantly contribute to evaporative loss. Extended use of digital screens reduces the spontaneous blink rate, decreasing tear film spread and inhibiting meibum expression. Environmental factors like low humidity, air conditioning, fans, and wind accelerate tear evaporation from the ocular surface. Furthermore, certain systemic medications, including antihistamines, diuretics, and some antidepressants, can diminish aqueous tear production.
The aqueous-deficient form of KCS, unrelated to Sjögren’s Syndrome, often involves age-related atrophy of the lacrimal glands. As people age, the volume of aqueous tear production naturally declines, leading to insufficient hydration. This deficiency is particularly common in postmenopausal women, suggesting a hormonal link to lacrimal gland function.
Diagnostic Steps to Rule Out Sjogren’s
The diagnosis of KCS involves objective clinical tests assessing the quantity and quality of the tear film. The Schirmer’s test measures tear production using a small strip of filter paper placed under the lower eyelid. Tear Break-Up Time (TBUT) involves applying a fluorescent dye and measuring how quickly the film destabilizes between blinks. Ocular surface damage is also assessed using dyes like fluorescein or lissamine green, which stain dried areas of corneal and conjunctival tissue.
To specifically rule out Sjögren’s Syndrome, a systemic autoimmune condition, the physician orders specific blood work. These serologic tests check for the presence of certain autoantibodies. The most indicative markers are anti-SSA (Ro) and anti-SSB (La) antibodies, along with antinuclear antibodies (ANA) and rheumatoid factor. The absence of these specific autoimmune markers confirms the diagnosis of non-Sjögren’s dry eye. In rare cases, a minor salivary gland biopsy may be performed to check for characteristic lymphocytic infiltration that defines the systemic disorder.
Customized Treatment Approaches
Management strategies for KCS are tailored to whether the primary driver is evaporative or aqueous-deficient. For the common evaporative KCS linked to MGD, treatment focuses on restoring meibomian gland function and improving the lipid layer. This involves regular warm compresses and gentle lid hygiene to express stagnant oil secretions. Oral omega-3 supplements are often recommended to improve the quality of the oil produced by the glands.
Aqueous-deficient KCS requires methods to supplement existing tears or stimulate greater production. Low-viscosity, preservative-free artificial tears are the initial approach to replace lost volume. For moderate to severe cases, punctal plugs may be inserted into the tear drainage ducts to conserve natural tears. Prescription topical anti-inflammatory medications, such as cyclosporine or lifitegrast, interrupt the cycle of inflammation, allowing the eye to produce more functional tears.