الفهرس 
Pathogenesis and causes of dry eyeOnly 14 pages are availabe for public view
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Abstract
The LFU includes the lacrimal glands, ocular surface (cornea and conjunctiva), eyelids, meibomian glands, and associated autonomic, sensory and motor nerves. The tear film consists of 3 layers: mucous (produced by conjunctival goblet cells and by corneal and conjunctival epithelial cells), aqueous (secreted by the lacrimal glands), and lipid (secreted primarily by the meibomian glands).
It has been known for many years that DED is a common clinical problem. Surveys over the last 20 years have estimated the prevalence of DED to be between 5% to more than 30% at various ages. The prevalence increases with age. In addition to age, other factors may increase the risk of DED, such as, autoimmune diseases and post menopausal estrogen therapy which has been associated with a 70 percent increase in risk of dry eye. Other risk factors may include chronic diseases such as diabetes mellitus, a diet rich in high fatty acids and use of certain medications such as steroids.
DED is a multifactorial disorder of the tear film and ocular surface that results in eye discomfort, visual disturbance, and possible ocular surface damage. Dysfunction of any LFU component can lead to DED by altering the volume, composition, distribution, and/or clearance of the tear film. There are two major etiologic categories of DED: aqueous deficient and evaporative. However, regardless of etiology, tear hyperosmolarity and tear film instability have been identified as global, mutually reinforcing mechanisms. In addition, inflammation is a key factor in perpetuating DED.
Currently there are no uniform diagnostic criteria. DED is considered a symptomatic disease; assessment of symptoms is considered of primary importance, and may be aided by use of a validated symptom questionnaire. Combinations of various diagnostic tests (including measurements of tear film instability, ocular surface damage, and aqueous tear flow) have been used to evaluate clinical signs, but although diagnostic tests are useful for confirming the diagnosis, they often correlate poorly with symptoms. Measurement of tear osmolarity might provide a “gold standard” of diagnosis, but a practical tear osmolarity test is not yet widely available. Measurement of tear film instability by means of a TBUT test has good overall accuracy and may be more repeatable than many other diagnostic tests.
The management of dry eye disease (DED) encompasses both pharmacologic and nonpharmacologic approaches, including avoidance of exacerbating factors, eyelid hygiene, tear supplementation, tear retention, tear stimulation, anti-inflammatory agents and surgery as mucus membrane, salivary gland, amniotic membrane, limbal stem cell transplantation, lid surgery and tarsorrhaphy.
Artificial tears are the mainstay of DED therapy but, although they improve symptoms and objective findings, there is no evidence that they can resolve the underlying inflammation in DED. Topical corticosteroids are effective anti- inflammatory agents, but are not recommended for long-term use because of their adverse-effect profiles. Topical cyclosporine currently the only pharmacologic treatment approved by the US Food and Drug Administration specifically for DED is safe for long-term use and is disease-modifying rather than merely palliative. Treatment selection is guided primarily by DED severity. Recently published guidelines propose a severity classification based on clinical signs and symptoms, with treatment recommendations according to severity level.
Surgical interventions for severe cases of dry eye may be one of the following, punctal patch technique for long lasting punctal occlusion, surgical moving of the lacrimal punctum to dry dock, cisternoplasty, tarsorrhaphy, microvascular sub-mandibular transplantation, conjunctival graft of the minor salivary gland, limbal stem cells, conjunctival stem cells transplantation and amniotic membranetransplantation