Diagnosis and treatment of dry eye syndrome

Dry eye syndrome is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms. Tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles. Symptom screening with the Five-item Dry Eye Questionnaire or Ocular Surface Disease Index can be used to identify the possibility that a patient might have DED dry eye syndrome and triggers. The results of these screening tools can lead to performing diagnostic tests of (ideally non-invasive) breakup time, osmolarity and ocular surface staining with fluorescein and lissamine green (observing the cornea, conjunctiva and eyelid margin). Meibomian gland dysfunction, lipid thickness/dynamics and assessments of the volume and severity of tear allow the subclassification of dry eye syndrome as predominantly evaporative or aqueous deficient, which informs the management of dry eye syndrome. A staged management algorithm was derived that presents a stepwise approach to implementing the various management and therapeutic options according to disease severity.

The pathogenesis of dry eye disease and trends in treatment

Dry eye disease (also known as keratoconjunctivitis sicca) is a multifactorial disease of the tear film and ocular surface. It results in various symptoms of discomfort such as pain, tearing, fatigue, and headache. Visual function can also deteriorate, and quality of life is negatively affected. Tear film instability which may lead to damage to the ocular surface with an inflammatory reaction is key to the pathogenesis of dry eye disease. This review discussed the classification, pathogenesis, diagnostic approaches, and treatment options of dry eye disease.

Higher Order Aberrations of the Corneal Surface after Laser Subepithelial Keratomileusis

PURPOSE: To evaluate the changes of higher order aberrations (HOAs) before and after laser subepithelial keratomileusis (LASEK) and to analyze the influence of tear film instability on HOAs of the corneal surface after LASEK. METHODS: In this cross-sectional study, 31 patients who underwent LASEK were divided into dry eye (16 patients, 32 eyes) and non-dry eye groups (15 patients, 30 eyes). Uncorrected distance visual acuity, spherical equivalent refraction, ablation depth, tear film parameters and Ocular Surface Disease Index (OSDI) questionnaire scores were evaluated in both groups. Total HOA root mean square (RMS), third-order coma, third-order trefoil and fourth-order spherical aberration (SA) of the corneal surface immediately and at 10 seconds after blinking were measured before and after surgery. RESULTS: The total HOA RMS, coma, trefoil and SA significantly increased after LASEK compared with preoperative values in both groups. In the dry eye group, total HOA RMS, coma and trefoil significantly increased except for SA at 10 seconds after blinking compared with those measured immediately after blinking. In addition, the changes of total HOA RMS, coma and trefoil were negatively correlated with tear film break-up time (R = -0.420, -0.473 and -0.439, respectively), but positively correlated with OSDI score (R = 0.433, 0.499 and 0.532, respectively). In the non-dry eye group, there were no significant differences between HOAs measured at 10 seconds after blinking and those measured immediately after blinking. CONCLUSIONS: The HOAs including coma, trefoil and SA significantly increased after LASEK. The tear film instability in the dry eye can be associated with more deterioration of the optical quality after LASEK, due to more significant increase of total HOA RMS, coma and trefoil.