Background
Keratitis sicca, or keratoconjunctivitis sicca (dry eye syndrome), is a relatively common inflammatory condition characterized by inadequate tear film protection of the cornea. There are multiple causes that produce either inadequate tear production or abnormal tear film constitution, resulting in excessively fast evaporation or premature destruction of the tear film.
There is no racial predilection for keratitis sicca; however, a female preponderance appears to exist. Sjögren syndrome (a triad of dry eye, dry mouth, and autoimmune connective-tissue disorder) is significantly more common in women (9:1), and milder forms of keratitis sicca also are more common in females than in males.
Patient education
Regular dental examinations are important because dry mouth, a component of Sjögren syndrome, significantly increases the risk of dental problems, and women should receive regular checkups from their gynecologists.
Patients with Sjögren syndrome can obtain up-to-date information from the following organization:
Sjögren’s Syndrome Foundation
6707 Democracy Boulevard
Suite 325
Bethesda, MD 20817
Phone: (301) 530-4420 or (800) 475-6473
Fax: (301) 530-4415
For patient education information, see Eye and Vision Center, as well as Dry Eye Syndrome, Pink Eye, and Sjögren's Syndrome.
See also the following:
Pathophysiology
The tear film is constituted by 3 layers, as follows: (1) a lipid layer (0.11 µm thick), produced by the Meibomian glands of the upper and lower lid margin; (2) an aqueous layer (7.0 µm thick), produced by the main and accessory lacrimal glands of Krause and Wolfring; and (3) a hydrophilic mucin layer (0.02-0.05 µm thick), produced by the conjunctival goblet cells. Any abnormality of 1 of the 3 layers produces an unstable tear film and symptoms of keratitis sicca.
A tear layer frequently affected is the aqueous layer, resulting in aqueous tear deficiency (ATD) or lacrimal hyposecretion. A classification scheme stratifies patients with dry eye into those with aqueous tear deficiency and those with increased evaporative loss.
Patients with keratitis sicca have elevated levels of tear nerve growth factor (NGF); these levels were decreased with 0.1% prednisolone.[1] Data suggest that ocular surface nerve growth factor may play an important role in ocular surface inflammation processes associated with dry eyes.
Etiology
The causes for keratitis sicca are multiple and can be multifactorial. They can be classified into 3 categories by the element of the tear layer that is mostly affected, as follows: (1) those affecting the aqueous tear layer, (2) those affecting the lipid tear layer, and (3) those affecting the mucin tear layer.
Causes of lipid tear layer abnormalities
The most common disorders associated with abnormalities of the lipid tear layer are blepharitis and rosacea. The severity of the dry eye symptoms appears to correlate to lipid layer thickness. It is now generally recognized that increased evaporation due to a compromised lipid layer is one of the most common etiologies for hyperosmolarity of the tear film.[2]
Causes of aqueous tear layer abnormalities
Idiopathic disease, congenital alacrima, and systemic vitamin A deficiency (xerophthalmia) are the most common conditions associated with aqueous tear deficiency.
Other etiologies include the following:
- Lacrimal gland ablation
- Sensory denervation
- Collagen vascular diseases (eg, rheumatoid arthritis [RA], Wegener granulomatosis, and systemic lupus erythematosus [SLE])
- Sjögren syndrome (see Sjögren Syndrome under Clinical)
- Infiltration of the lacrimal glands by sarcoidosis or tumors
- Postradiation fibrosis of the lacrimal glands
- Conjunctival scarring as a result of ocular pemphigoid, Stevens-Johnson syndrome, trachoma, chemical/thermal burns, and atopic disease
- Drug etiologies include oral contraceptives, antihistamines, beta-blockers, phenothiazine, and atropine
Causes of mucin tear layer abnormalities
The following are the most common conditions resulting in abnormalities of the mucin tear layer:
- Vitamin A deficiency
- Trachoma
- Diphtheric keratoconjunctivitis
- Mucocutaneous disorders
- Topical medications
Prognosis
The prognosis with keratitis sicca varies with the severity of the condition. Most patients have mild-to-moderate cases, and they can be treated symptomatically with lubricants, providing good relief of symptoms.
Patients with Sjögren syndrome or prolonged untreated dry eye represent a subgroup of patients with a worse prognosis and a more prolonged treatment regimen.
Complications
Significant punctate epitheliopathy can lead to corneal erosions, corneal ulceration (both sterile and infected), corneal neovascularization, corneal scarring, corneal thinning, and even corneal perforation.
Lee HK, Ryu IH, Seo KY, Hong S, Kim HC, Kim EK. Topical 0.1% prednisolone lowers nerve growth factor expression in keratoconjunctivitis sicca patients. Ophthalmology. Feb 2006;113(2):198-205. [Medline].
Foulks GN. The correlation between the tear film lipid layer and dry eye disease. Surv Ophthalmol. Jul-Aug 2007;52(4):369-74. [Medline].
Fujita M, Igarashi T, Kurai T, Sakane M, Yoshino S, Takahashi H. Correlation between dry eye and rheumatoid arthritis activity. Am J Ophthalmol. Nov 2005;140(5):808-13. [Medline].
Geerling G, Tost FH. Surgical occlusion of the lacrimal drainage system. Dev Ophthalmol. 2008;41:213-29. [Medline].
Barber LD, Pflugfelder SC, Tauber J, Foulks GN. Phase III safety evaluation of cyclosporine 0.1% ophthalmic emulsion administered twice daily to dry eye disease patients for up to 3 years. Ophthalmology. Oct 2005;112(10):1790-4. [Medline].
Stonecipher K, Perry HD, Gross RH, Kerney DL. The impact of topical cyclosporine A emulsion 0.05% on the outcomes of patients with keratoconjunctivitis sicca. Curr Med Res Opin. Jul 2005;21(7):1057-63. [Medline].

