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  • Title: Tear film dynamics in floppy eyelid syndrome.
    Author: Liu DT, Di Pascuale MA, Sawai J, Gao YY, Tseng SC.
    Journal: Invest Ophthalmol Vis Sci; 2005 Apr; 46(4):1188-94. PubMed ID: 15790878.
    Abstract:
    PURPOSE: Floppy eyelid syndrome (FES) presents nonspecific ocular surface irritation. The hypothesis for the current study was that one contributing factor is the abnormality in tear film dynamics. METHODS: Sixteen patients with FES were consecutively examined. Tear film dynamics were evaluated by kinetic tear interference images, infrared thermometry, water evaporation rate, tear break-up time, and fluorescein clearance test. Data showing evaporation rate and thermometry were compared with those of 10 normal subjects. RESULTS: There was a high correlation between the eye with the worse symptoms and the eyes with the more severe floppy lids (P < 0.01) and with ocular surface evaporation rate (P = 0.02). Except for one patient, all others showed abnormal tear film, with an average tear break-up time of 2.9 +/- 3.7 seconds. Kinetic analysis of tear interference images revealed that lipid spread in a vertical or mixed pattern in 18 eyes (75%) with a delayed spread time (P = 0.0007), indicating that most of the patients had lipid tear deficiency. The ocular skin temperature and water evaporation rate were higher in the FES group (P = 0.0003 and 0.026, respectively). Nearly all patients with FES showed eyelid hyperpigmentation. The ocular surface evaporation rate in the FES group was also higher than that of the normal subjects (P < 0.0001). Multiple regression analysis showed that a vertical pattern of lipid spread had a significant influence on ocular surface evaporation rate (P = 0.003). CONCLUSIONS: Tear film abnormality is prevalent in patients with FES and is characterized by lipid tear deficiency, leading to rapid tear evaporation. The FES lid skin is also characterized by high temperature, high water evaporation rate, and hyperpigmentation. Studies directed to investigating the linkage of lid changes and meibomian gland dysfunction may shed new lights on the pathogenesis of FES.
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