MGD Diagnosis and Treatment

Abstract

The identification of the starting cause or main pathogenic factors of dry eye can be of great help for planning an appropriate therapy. DED can be divided into conditions in which the production of the aqueous component of tears is inadequate [aqueous deficient dry eye (ADDE)] and conditions in which this is not the case. Unfortunately, standard DED symptom questionnaires are not designed to differentiate between ADDE and EDE; however, if the symptoms described are more frequent in the morning or are associated with the lids rather than the eye in general, this could be indicative of some form of blepharitis or meibomian gland dysfunction (MGD). The recollection of personal habits, such as lid rubbing, is also of interest, and a history of chalazion or hordeolum or of skin diseases is also suggestive. In clear-cut cases, a normal tear secretion with thick meniscus but low break-up time (BUT) and/or bad dynamic behavior of the lipid layer should suggest increased evaporation as the main source of dysfunction, while a thin, scanty meniscus or a Schirmer’s test score <5 mm per 5 min associated with a low BUT or poordynamic lipid behavior makes us think of aqueous deficiency. Unfortunately, the clinical picture frequently is not so sharp. Nevertheless, the combination of the results of the different clinically available tests and the addition of one or more other tests, such as interferometry, meibometry, meniscometry and meiboscopy as well as direct evaporimetry, if available, will allow us to address the therapy toward the particular dysfunction active on the ocular surface or ameliorate the vicious cycles that are the basis of the problem, correcting, if possible, the failures that cause the disease.