Eiki Goto1, Scheffer C G Tseng. 1. Ocular Surface Center and Ocular Surface Research and Education Foundation, Miami, Florida, USA.
Abstract
PURPOSE: Kinetic analysis of sequential tear interference images was used to investigate how the precorneal lipid film spread and distributed in aqueous tear deficiency (ATD) dry eye. METHODS: One eye of 17 patients with ATD was randomly selected for this noncomparative case series. Twelve patients also had noninflamed meibomian gland dysfunction (MGD). Sequential images were digitized and analyzed on computer. Data were further compared in 9 of the 17 cases before and after punctal occlusion (PO). Outcome measures included speed and pattern of lipid spread and resultant lipid layer thickness in the superior, central, and inferior cornea. Intensity and red/green/blue (RGB) color spectra of the tear interference image were compared before and after PO. RESULTS: After lid blinking, it took a longer time (2.2 +/- 1.1 second) to reach a stable lipid film in all eyes with ATD compared with normal subjects (P < 0.0001). Because of this retarded spread, the thickest lipid film was located at the inferior cornea adjacent to the lid margin, with a gradient spreading toward the superior cornea (P = 0.01). As a result, the lipid film was thinner than normal on the superior cornea in 10 of 17 (59%) ATD eyes. Fifteen of 17 eyes (88%) showed vertical streaking, rather than a normal horizontal propagation pattern on the superior cornea. Such a lipid-deficient state and uneven distribution did not correlate with the presence or absence of MGD. The lipid spread time was shortened (P = 0.008), the distribution of the lipid film was more even, and the thickness approached normal in all nine eyes after PO. CONCLUSIONS: In this study, kinetic analysis of tear interference images provided evidence that retardation of lipid spread is, but MGD is not, the main reason for the increased thickness of precorneal lipid film in the inferior cornea of eyes with ATD. As a result, lipid film is deficient in the superior cornea and unevenly distributed, further destabilizing the tear film. The fact that PO significantly improves lipid spread, evenness, and thickness suggests that the performance of lipid film is also dictated by the amount of aqueous tear fluid. These findings provide new insight into the interaction between the lipid film and the aqueous tear fluid.
PURPOSE: Kinetic analysis of sequential tear interference images was used to investigate how the precorneal lipid film spread and distributed in aqueous tear deficiency (ATD) dry eye. METHODS: One eye of 17 patients with ATD was randomly selected for this noncomparative case series. Twelve patients also had noninflamed meibomian gland dysfunction (MGD). Sequential images were digitized and analyzed on computer. Data were further compared in 9 of the 17 cases before and after punctal occlusion (PO). Outcome measures included speed and pattern of lipid spread and resultant lipid layer thickness in the superior, central, and inferior cornea. Intensity and red/green/blue (RGB) color spectra of the tear interference image were compared before and after PO. RESULTS: After lid blinking, it took a longer time (2.2 +/- 1.1 second) to reach a stable lipid film in all eyes with ATD compared with normal subjects (P < 0.0001). Because of this retarded spread, the thickest lipid film was located at the inferior cornea adjacent to the lid margin, with a gradient spreading toward the superior cornea (P = 0.01). As a result, the lipid film was thinner than normal on the superior cornea in 10 of 17 (59%) ATD eyes. Fifteen of 17 eyes (88%) showed vertical streaking, rather than a normal horizontal propagation pattern on the superior cornea. Such a lipid-deficient state and uneven distribution did not correlate with the presence or absence of MGD. The lipid spread time was shortened (P = 0.008), the distribution of the lipid film was more even, and the thickness approached normal in all nine eyes after PO. CONCLUSIONS: In this study, kinetic analysis of tear interference images provided evidence that retardation of lipid spread is, but MGD is not, the main reason for the increased thickness of precorneal lipid film in the inferior cornea of eyes with ATD. As a result, lipid film is deficient in the superior cornea and unevenly distributed, further destabilizing the tear film. The fact that PO significantly improves lipid spread, evenness, and thickness suggests that the performance of lipid film is also dictated by the amount of aqueous tear fluid. These findings provide new insight into the interaction between the lipid film and the aqueous tear fluid.
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