Medical Management of Dry Eye Disease - Mechanical Behavior of the Tear Film
Fluids can be classified according to the way they behave under sheer stress. A perfect fluid has no resistance to shear stress and therefore lacks vis¬cosity. Fluids that are not perfect are classified as either newtonian if their viscosity is constant for different rates of shear, or non-newtonian if they become less viscous over time when a shear force is applied. This property of non-newtonian fluids is termed thixotropy - these are fluids that are both viscous and elastic. Tears have thixotropic properties but most artificial tears do not. The linear charged polymers (carboxymethylcellulose and hyaluronic acid) are the only agents used in artificial tears that have shear-thinning characteristics of non-newtonian fluids. It has been proposed that tears behave like a fluid during blinking but more like a gel between blinks.
Regulation of Tear Film Components
Regulation of the stability of the tear film is under hormonal and neuronal control. Androgen receptors have been identified in meibomian tissue, while oestrogen and progesterone receptors have been identified in conjunctiva and lacrimal gland . Postmenopausal women and the elderly may be relatively androgen-deficient and this may account for some of the involutional changes seen in periocular tissue.
Androgens (testosterone) may also act as a natural suppressor of inflammation . Hormone treatments have been evaluated to treat some of the involutional changes associated with dry eye disease. Nerve fibres have been demonstrated adjacent to the lacrimal gland, goblet cells, and meibomian glands. The role of these fibres in maintaining the tear film is unclear although parasympathetic (acetylcholine- and VIP-dependent) fibres stimulate aqueous and protein secretion from the lacrimal gland, and VIP end¬ings at the basement membrane may stimulate mucus secretion from the goblet cells.
Inflammation and Dry Eye Disease
A T-lymphocyte infiltrate is present in the conjunctiva and accessory glands of 80% of patients with dry eye disease. There is also an increased expression of HLA class II antigens, markers of apoptosis (Fas-Fas ligand), and inflammatory cytokines in the epithelium. Although this is thought to be a pri¬mary event in Sjogren's syndrome, secondary inflammation from surface fric¬tion during blinking is probably an aggravating factor in the majority of patients with dry eye disease. Inflammation may thus be both the cause and the result of dry eye, amplifying and perpetuating disease. The presence of inflammation is the rationale for the use of steroid and immunosuppression in the treatment of dry eye disease in patients with and without Sjogren's syndrome .
Guidelines for Clinical Management
Dry eye disease is generally not curable and management is structured around the control of symptoms and the prevention of surface damage. Clinical tests have a low sensitivity and specificity and they are not a reliable basis for management. Fortunately, in the great majority of patients the disease is not sight-threatening. The choice of treatment depends on the severity of the dis¬ease, and one or more of the following measures may be used alone or in com¬bination. Initial treatment is with artificial tears that lubricate the surface and reduce lid friction, although they usually only provide relief for a short time period after drop instillation. The goal of treatment is to improve eye comfort and vision at a frequency of treatment that can be reduced to a minimum. Guidelines have been produced to indicate the level of management that is appropriate according to the severity of disease . There is a placebo effect and some patients wish to continue using artificial tears without clinical signs of dry eye. A benefit with regard to patient symptoms is more difficult to achieve than a resolution of ocular signs .
General Measures
(1)Patient education. Discuss the nature of the condition to establish a realistic expectation of outcome, provide reassurance, and encourage compli¬ance with treatment.
(2)Review of the home and work environment. Emphasize the importance of blinking when reading or using a video display unit. Eliminate dry air condi¬tioning and wind if possible. A reduction in room temperature and central heat¬ing will minimize tear evaporation. Humidifiers are usually disappointing because they do not increase room humidity sufficiently. Working directives and open plan offices can limit the ability of employers to implement these rec¬ommendations. A local increase in humidity can be achieved with moist cham¬ber goggles or side shields to glasses if this is cosmetically acceptable.
(3)Discontinue toxic topical treatments if possible. Numerous systemic treatments have been associated with symptoms of dry eye, e.g. thiazide diuret¬ics, anticholinergics, tricyclic antidepressants, ^-blockers, isotretinoin (13-cis- retinoic acid), and antihistaminines (loratadine, cetrizine). The excipients (e.g. benzalkonium chloride, EDTA) in drops used for other reasons, e.g. glaucoma medications, may aggravate surface damage. The preservative benzalkonium chloride can be particularly toxic to the epithelium.
(4)Aids should be provided for patients with a loss of dexterity (e.g. rheumatoid arthritis). Single unit dose dispensers for preservative free drops may not be appropriate. Stiff plastic dropper bottles can be held and squeezed in a nutcracker or an eyedrop bottle squeezer (available commercially).
Fluids can be classified according to the way they behave under sheer stress. A perfect fluid has no resistance to shear stress and therefore lacks vis¬cosity. Fluids that are not perfect are classified as either newtonian if their viscosity is constant for different rates of shear, or non-newtonian if they become less viscous over time when a shear force is applied. This property of non-newtonian fluids is termed thixotropy - these are fluids that are both viscous and elastic. Tears have thixotropic properties but most artificial tears do not. The linear charged polymers (carboxymethylcellulose and hyaluronic acid) are the only agents used in artificial tears that have shear-thinning characteristics of non-newtonian fluids. It has been proposed that tears behave like a fluid during blinking but more like a gel between blinks.
Regulation of Tear Film Components
Regulation of the stability of the tear film is under hormonal and neuronal control. Androgen receptors have been identified in meibomian tissue, while oestrogen and progesterone receptors have been identified in conjunctiva and lacrimal gland . Postmenopausal women and the elderly may be relatively androgen-deficient and this may account for some of the involutional changes seen in periocular tissue.
Androgens (testosterone) may also act as a natural suppressor of inflammation . Hormone treatments have been evaluated to treat some of the involutional changes associated with dry eye disease. Nerve fibres have been demonstrated adjacent to the lacrimal gland, goblet cells, and meibomian glands. The role of these fibres in maintaining the tear film is unclear although parasympathetic (acetylcholine- and VIP-dependent) fibres stimulate aqueous and protein secretion from the lacrimal gland, and VIP end¬ings at the basement membrane may stimulate mucus secretion from the goblet cells.
Inflammation and Dry Eye Disease
A T-lymphocyte infiltrate is present in the conjunctiva and accessory glands of 80% of patients with dry eye disease. There is also an increased expression of HLA class II antigens, markers of apoptosis (Fas-Fas ligand), and inflammatory cytokines in the epithelium. Although this is thought to be a pri¬mary event in Sjogren's syndrome, secondary inflammation from surface fric¬tion during blinking is probably an aggravating factor in the majority of patients with dry eye disease. Inflammation may thus be both the cause and the result of dry eye, amplifying and perpetuating disease. The presence of inflammation is the rationale for the use of steroid and immunosuppression in the treatment of dry eye disease in patients with and without Sjogren's syndrome .
Guidelines for Clinical Management
Dry eye disease is generally not curable and management is structured around the control of symptoms and the prevention of surface damage. Clinical tests have a low sensitivity and specificity and they are not a reliable basis for management. Fortunately, in the great majority of patients the disease is not sight-threatening. The choice of treatment depends on the severity of the dis¬ease, and one or more of the following measures may be used alone or in com¬bination. Initial treatment is with artificial tears that lubricate the surface and reduce lid friction, although they usually only provide relief for a short time period after drop instillation. The goal of treatment is to improve eye comfort and vision at a frequency of treatment that can be reduced to a minimum. Guidelines have been produced to indicate the level of management that is appropriate according to the severity of disease . There is a placebo effect and some patients wish to continue using artificial tears without clinical signs of dry eye. A benefit with regard to patient symptoms is more difficult to achieve than a resolution of ocular signs .
General Measures
(1)Patient education. Discuss the nature of the condition to establish a realistic expectation of outcome, provide reassurance, and encourage compli¬ance with treatment.
(2)Review of the home and work environment. Emphasize the importance of blinking when reading or using a video display unit. Eliminate dry air condi¬tioning and wind if possible. A reduction in room temperature and central heat¬ing will minimize tear evaporation. Humidifiers are usually disappointing because they do not increase room humidity sufficiently. Working directives and open plan offices can limit the ability of employers to implement these rec¬ommendations. A local increase in humidity can be achieved with moist cham¬ber goggles or side shields to glasses if this is cosmetically acceptable.
(3)Discontinue toxic topical treatments if possible. Numerous systemic treatments have been associated with symptoms of dry eye, e.g. thiazide diuret¬ics, anticholinergics, tricyclic antidepressants, ^-blockers, isotretinoin (13-cis- retinoic acid), and antihistaminines (loratadine, cetrizine). The excipients (e.g. benzalkonium chloride, EDTA) in drops used for other reasons, e.g. glaucoma medications, may aggravate surface damage. The preservative benzalkonium chloride can be particularly toxic to the epithelium.
(4)Aids should be provided for patients with a loss of dexterity (e.g. rheumatoid arthritis). Single unit dose dispensers for preservative free drops may not be appropriate. Stiff plastic dropper bottles can be held and squeezed in a nutcracker or an eyedrop bottle squeezer (available commercially).
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