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Abstract Dry eye is a serious public problem and dry eye syndrome statistics are staggening and on rise. In fact, they have almost doubled in the last seven years world wide, dry eye is an under diagnosed problem. The prevalence of dry eye has increased in recent years due to the general ageing of the population, increased medication use and increase in environmental allergens and irritants. Dry eye syndrome is a disorder that involves both the ocular surface and the tear film. Many patients with dry eye symptoms produce a normal quantity of aqueous tears but have other tear film and/ or ocular surface disorders. The definition of dry eye has been expanded to include any anomaly in a gland associated with tear production or an anomaly in lid and /or blinking function in which the quality and /or quantity of the tear film is adversely affected and there is an inability to maintain a healthy ocular surface. The multifactorial nature of dry eye conditions has produced the term. “Tear film and Ocular surface disorders” as an alternative to the term dry eye. This recognizes the intimate relationship between the ocular surface and the tear film and the cycle of tear film instability and ocular surface damage characteristic of dry eye. It also acknowledges recent suggestions that dry eye represents a dysfunction of an integrated ocular surface-lacrimal gland unit. Delayed tear clearance play a dynamic role in the pathogenesis of dry eye syndrome and ocular surface irritation. Several inflammatory cytokines are elevated in delayed tear clearance so inflammation is a exacerbating factor in dry eye syndrome investigators have recommended a revision of the classification of dry eye, given its multifactorial nature. The major dry eye categorizes proposed were tear deficient dry eye and evaporative dry eye. In the tear deficient category were sjogren’s syndrome and non-sjogren’s syndrome forms of aqueous tear deficiency. Evaporative forms of dry eye were oil deficient (meibomain gland anomalies), lid surfacing and blinking anomalies, chronic allergy/toxicity, contact lens-related anomalies and cicatricial ocular surface disease. The meibomian gland plays an essential role in maintenance of ocular surface integrity and the preservation of visual acuity. This tissue through its synthesis and secretion of lipids at the margin, is primarily responsible for promoting of the pre ocular tear film. Meibomian gland dysfunction and in particular mebomian gland obstruction makes an important contribution to ocular surface disease which is termed meibomian keratoconjuctivitis. Patients with blepharitis frequently have meibomian gland dysfunction with loss of meibomian glands (DROP out). This explains that dry eye often occurs in patients with chronic belpharitis. Recent studies proved that the meibomian gland is an androgen target organ and that androgens influence the lipid profile within this tissue and promote the formation of the tear film’s lipid layer. Meibomian gland anomalies are commonly reported in sjogren’s syndrome whish is an androgen deficient that may serve to lessen tissue function as well as to promote (but not cause) the auto immune process in lacrimal gland. While there are many tests for dry eye assessment, there remains a great disparity among the symptoms and signs in many dry eye patients. Determining the cause of dry eye patients when minimal clinical signs are present is difficult and the diagnosis is complicated further when there is a lack of correlation between symptoms and objective tests. In an attempt to overcome these problems and to standardize the diagnostic criteria for dry eye, the National dry eye institute/ industry report has produced the following global criteria for clinical diagnosis of dry eye: 1- A validated test for dry eye symptoms. 2- Reduced tear film stability. 3- Ocular surface staining. 4- Tear hypersomolarity. Clinical differential diagnosis of dry eye types can be made primarily on the basis of biomicroscopic signs. Diagnosis of dry eye syndrome can be classified clinically into: A- Clinical diagnosis of tear deficient dry eye include: a- History b- Tear secretion tests which include the shirmer test and jones test, phenol red thread test (PRT), fluorophotometry, and fluorescein clearance test. c- A number of biomicroscopic signs are specifically associated with tear deficient eye. These include a scant inferior tear meniscus, dull pre corneal tear film specular reflection, lid parallel conjuctival folds, tear film mucous depris and mucin filaments. B- Clinical diagnosis of evaporative dry eye include a- Diagnosis of meibomian gland anomalies: Various classification systems for MGD have been proposed. They have been based on biomicroscopic signs, tear film stability, ocular surface staining, morphological characteristics of meibomian glands and secretion, osmolarity, meibomography and lipid tear interference patterns. b- Diagnosis of chronic allergy and toxicity: It depends mainly on history and biomicroscopic features of allergy and toxicity. c- Diagnosis of lid surfacing / blinking anomalies: It based on gross external examination and slit lamp biomicroscopic examination. Dry eye treatment includes psychological and educational, medical, non surgical and surgical treatment. Education of the patient is a crucial step in determining success or failure of treatment in many patients. The patient must understand that treatment must be continous and prolonged. The primary goals of dry eye treatment should to improve symptoms, reduce tear osmolarity, improve tear film stability and reverse ocular surface damage. While artificial tear supplementation remains the main treatment for all forms of dry eye, other treatments include tear conservation and tear stimulation for tear deficient dry eye, anti-inflammatory agents in allergy/ toxicity related dry eye and surgical treatment for lid/ blinking anomalies and ocular surface disease. Because inflammation is a contributing factor in dry eye syndrome, anti-inflammatory (eg. steroids) or immuno modulatory (e.g. cyclosporine A) therapy for chronic dry eye conditions may facilitate ocular surface healing. The primary goal of meibomitis treatment is to reduce inflammation. This can be achieved by hot compresses and lid massage and when necessary systemic treatment with low dose doxycycline. Other recent lines of treatment of MGD include topical androgen supplementation, castor oil DROPs, tear lipid substitutes and food rich in essential fatty acids omega-3 S. |