DRY EYE SYNDROME
A complex syndrome with a high impact on vision functionality.
The ocular surface is normally covered by a hydrolipidic tear film that is able to protect the corneal and conjunctival epithelium from the external environment. Evidence support a two-layered model of the tear film, involving a thin surface lipid layer overlying a thicker mucous-aqueous mixed layer. The mucin component of this latter layer helps to wet the eye’s surface, which in turn allows the water aqueous component to spread over an otherwise non-wetting surface. In case of exposure to external or environmental stresses such as wind, sun, dried air, salted water, smoke, bright light, air conditioning, heating, prolonged use of computer, or use of contact lenses, the tear film may be altered or not sufficient to exert its protective function, causing symptoms such as irritation, burning, redness and foreign body sensation, typical symptoms of dry eye. Tear film alterations can be also initiated by conditions that affect the surface of the eye, such as vitamin A deficiency, eye allergies and use of preservatives in topical drugs.
Dry Eye mechanism and definition
The core mechanism of dry eye disease is evaporation-induced tear hyperosmolarity (higher salt concentration than normal) which is the trigger for a cascade of events leading to eye surface damage and inflammation. The new definition of Dry Eye Disease, infact, is the following: “Dry multifactorial disease of the ocular surface characterized by loss of homeostasis of the tear film and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage and neurosensory abnormalities play etiological roles.” (Definition of Tear Film & Ocular Society Dry Eye Workshop II).
LASIK surgery and the Dry Eye Syndrome
The alteration of the tear film can be determined by a reduced production of the tear liquid or increased of the same liquid evaporation, in particular a decreased ocular surface sensitivity, as may occur with ocular surface inflammation, contact lenses, corneal surgery - including refractive surgery, leads to reduced aqueous production by the lacrimal glands. Especially, dry eyes are a remarkably frequent consequence of LASIK surgery (Laser-assisted in situ keratomileusis). There are multiple theories as to how LASIK contributes to the pathophysiology of dry eyes: the main proposed cause is iatrogenic corneal nerve damage. LASIK disrupts both the dense sub-basal nerve plexus and stromal corneal nerves in the creation of the anterior stromal flap and excimer laser ablation of the cornea. Another common case is dry eyes associated with menopause, infact it was demonstrated an increasing incidence of this issue in people getting older and more frequently among females.
Corneal and conjunctival epithelial damage
In general, in critical conditions as may occur with ocular surface inflammation, contact lenses, corneal surgery, the corneal and conjunctival epithelium is more exposed to pathogens accession and to erosion caused by constant rubbing of the eyelid on the eye surface. The epithelial damage is histologically shown by the reduction in the number of goblet mucipare cells and the abnormal structures of corneal and conjunctival epithelia and of the cells membranes which form them. This type of damage is clinically detected by colorimetric assays with specific dyes (Fluorescein, Rose Bengal or lissamine green), and the degree of staining is related to the intensity of damage caused by ocular dryness.
Artificial tears as treatment
Artificial tears are habitually used as the first therapeutic option for the treatment of Dry Eye in any stage of severity, instilling ophthalmic solutions able to maintain properly humidified and lubricate the ocular surface. These ophthalmic solutions are usually designed using the chemical and physical properties of hydrophilic polymers, which, retaining water in the ocular surface, perform a moistening and lubricating action. The ideal composition must be compatible with physiological characteristics of the ocular surface epithelium and, in case of damage, must be able to create a microenvironment in which the epithelium can restore its normal structure and functions.
Bibliography:
•Changes in the tear film and ocular surface from dry eye syndrome, Johnson ME and Murphy PJ, Progr in Retinal and Eye Res, 2004:23, 449-474.
• Post-LASIK dry eye. Roni M Shtein. Expert Rev Ophthalmol. 2011 October ; 6(5): 575–582
• Tear film and ocular surface tests in animal models of dry eye: uses and limitations, Barabino S, Chen W and Dana MR., Exp Eye Res, 2004: 79, 613-621.
• Artificial tear solutions, Lemp MA, Int Ophthalmol Clin 1973:13, 221-9
• Menoapuse and dry eye. A possible relationship, Versura P, Campos EC, Gynecol ENdocrinol. 2005 May; 20(5): 289-98, Review.
• TFOS DEWS II Report Executive Summary. Jennifer P. Craig, J. Daniel Nelson, Dimitri T. Azar, Carlos Belmonte, Anthony J. Bron, Sunil K. Chauhan, Cintia S. de Paiva, Jos e A.P. Gomes, Katherine M. Hammitt, Lyndon Jones, Jason J. Nichols, Kelly K. Nichols, Gary D. Novack, Fiona J. Stapleton, Mark D.P. Willcox, James S. Wolffsohn, David A. Sullivan. The Ocular Surface (2017)