TFOS DEWS II Report Executive Summary

Dry eye disease (DED) affects millions of people worldwide and is a common reason for patient visits. TFOS launched TFOS DEWS II in 2015, involving 150 experts and taking over two years to complete the report, the executive summary of which is presented in this article.

Definition and Classification^[1]: The new definition describes DED as a multifactorial disease characterized by tear film instability and ocular symptoms.The classification is based on pathophysiology and divides DED into aqueous-deficient dry eye (ADDE) and evaporative dry eye (EDE), which exist on a continuum, and clinical management requires considering both.

Fig. 1. Classification of DED.[1]

Epidemiology^[2]: The prevalence of DED varies widely due to a lack of standardized criteria, ranging from 5% to 75%. Age, gender, and ethnicity are risk factors, and the economic burden is substantial. Future studies should focus on prevalence, incidence, and modifiable risk factors in different populations, including younger individuals.

Fig. 2. The prevalence of DED signs by age and sex.[2]

Sex, Gender and Hormones^[3]: The incidence of DED is higher in females than in males, influenced by sex, Gender, hormones and other factors. Gender and sex affect various aspects of health and DED.

Fig. 3. Hormones from the hypothalamic-pituitary axis.[3]

Pathophysiology^[4]: The core mechanism involves evaporation leading to hyperosmolarity of the tear film, triggering inflammation and creating a vicious cycle. ADDE results from reduced tear production, while EDE is caused by excessive tear evaporation, with Meibomian Gland Dysfunction (MGD) being a major cause of EDE.

Fig. 4. The Vicious Circle of DED.[4]

Tear Film^[5]: The tear film is a two-phase model, with a lipid layer covering the mucin-water layer. Tear osmolarity correlates with the severity of DED, but research on the tear film has been hindered by a lack of standardized parameters and a limited understanding of its structure.

Fig. 5. The tear film structure.[6]

Pain and Sensation^[7]: DED pain is nociceptive and neuropathic, transmitted via the trigeminal nerve. Inflammation and dryness affect neural activity, leading to pain, altered tear secretion, and blinking behavior.

Fig. 6. Peripheral and central neural mechanisms involved in the sensory and autonomic responses evoked by ocular surface dryness.[7]

Iatrogenic Dry Eye^[8]: Several medical interventions can cause DED, including medications, contact lenses, and surgeries. Further research is needed to investigate risk factors and develop low-toxicity medications and minimally invasive techniques.

Diagnostic Methods^[9]: It is recommended to first rule out similar conditions, and then use questionnaires for screening. Diagnosis should rely on tear film stability, osmolarity, and other indicators, followed by relevant tests for subtyping.

Fig. 7. DED diagnostic test battery.[9]

Management and Treatment^[10]: The goal is to restore ocular surface and tear film homeostasis. Due to individual variability in DED, treatment should be comprehensive and progress from conventional therapies to more advanced treatments. Treatment efficacy should be assessed over a period of 1-3 months.

Fig. 8. Diagrammatic representation of the process associated with the management of DED.[10]

Clinical Trial Design^[11]: It is recommended to follow Good Clinical Practice (GCP). Study designs should align with the treatment, research objectives, and stages, and outcome measures should include minimally invasive objective indicators. Exploring new assessment methods will help optimize clinical trials.

References

[1] Craig JP, Nichols KK, Akpek EK, Caffery B, Dua HS, Joo CK, et al. TFOS DEWS II definition and classification report. Ocul Surf 2017;15:276e83.

[2] Stapleton F, Alves M, Bunya VY, Jalbert I, Lekhanont K, Malet F, et al. TFOS DEWS II epidemiology report. Ocul Surf 2017;15:334e65.

[3] Sullivan DA, Rocha EM, Aragona P, Clayton JA, Ding J, Golebiowski B, et al. TFOS DEWS II sex, gender, and hormones report. Ocul Surf 2017;15:284e333.

[4] Bron AJ, dePaiva CS, Chauhan SK, Bonini S, Gabison EE, Jain S, et al. TFOS DEWS II pathophysiology report. Ocul Surf 2017;15:438e510.

[5] Willcox MDP, Argüeso P, Georgiev G, Holopainen J, Laurie G, Millar T, et al. TFOS DEWS II tear film report. Ocul Surf 2017;15:366e403.

[6] Craig JP, Willcox MD, Argueso P, Maissa C, Stahl U, Tomlinson A, et al. The TFOS International Workshop on Contact Lens Discomfort: report of the contact lens interactions with the tear film subcommittee. Invest Ophthalmol Vis Sci 2013;54. TFOS123e56.

[7] Belmonte C, Nichols JJ, Cox SM, Brock JA, Begley CG, Bereiter DA, et al. TFOS DEWS II pain and sensation report. Ocul Surf 2017;15:404e37.

[8] Gomes JAP, Azar DT, Baudouin C, Efron N, Hirayama M, Horwath-Winter J, et al. TFOS DEWS II iatrogenic dry eye report. Ocul Surf 2017;15:511e38.

[9] Wolffsohn JS, Arita R, Chalmers R, Djalilian A, Dogru M, Dumbleton K, et al. TFOS DEWS II diagnostic methodology report. Ocul Surf 2017;15:539e74.

[10] Jones L, Downie LE, Korb D, Benitez-del-Castillo JM, Dana R, Deng SX, et al. TFOS DEWS II management and therapy report. Ocul Surf 2017;15:575e628.

[11] Novack GD, Asbell P, Barabino B, Bergamini MVW, Ciolino JB, Foulks GN, et al. TFOS DEWS II clinical trial design report. Ocul Surf 2017;15:629e49.

journal homepage: https://pubmed.ncbi.nlm.nih.gov/28797892/