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The first Tear Film and Ocular Surface Society Dry Eye Workshop (TFOS DEWS), published in 2007, brought much-needed attention to the complex disease we call dry eye. The report emphasized the significant morbidity associated with an inflammatory process and recognized the quality of life issues that pose a tremendous burden to most patients with dry eye. As a result, DEWS sparked much interest in the research community and generated additional questions that beg to be answered.
This past July, TFOS released the second DEWS report (DEWS II), which expands on everything learned from the past 10 years of research. The updated definition of dry eye stresses its multifactorial nature as a disease. Also, the loss of homeostasis in the tear film is the central pathophysiological notion that defines dry eye disease (DED).1 Here are some important aspects of DEWS II and the clinical implications they bring.
The Top Two
I find two aspects of the report most intriguing: the new classification scheme and the exhaustive discussion on the neurosensory component of dry eye and neuropathic pain in general.
One way in which DEWS II expands upon its predecessor is with the introduction of a slightly different classification system that allows us to identify the essential component to effectively treat a patient’s condition.2,3 Rather than taking a shotgun approach to treating DED, clinicians can now directly address an individual’s specific problems. This may help explain why traditional treatment strategies have not worked for some patients in the past.
Additionally, DEWS II reflects current research by establishing biomarkers that are critical in DED pathogenesis.2,4 It retains the two major divisions in DED—evaporative and aqueous deficient—but stresses that both play a role the majority of time, with one likely driving the other.2 Cosmetics, contact lenses and the use of medications, both topical and oral, remain significant contributors in iatrogenic dry eye.2
According to DEWS II, neurosensory abnormalities also play a crucial role in DED, and the discussion includes neuropathic pain.4 For some patients with significant symptoms but no signs of true DED, pain management would likely be the most appropriate treatment option.
Pain Under the Microscope
An increase in ocular surface inflammation and osmolarity results in peripheral nerve damage.1,4 This propels additional sensitizing of the corneal nerves, causing the neurons to experience a decreased threshold and increased responsiveness to stimulation (i.e., wind or cold).4 Differentiating nociceptive pain from neuropathic pain in DED is fundamentally essential for successful treatment. A key component of neuropathic pain is the lack of objective signs in patients with severe DED-like symptoms.2-4 These patients don’t respond with appropriate relief when topical anesthetics are applied to the eye. They also often have pain elsewhere in their body.2,4
Beyond DEWS II, further research is needed to expose all the components in the development of neurosensory changes seen in dry eye.
Standard treatments for neuropathic pain consist of increased intake of antioxidants and off-label use of anticonvulsants, tricyclic antidepressants, opioids or neuromodulators.4 In particular, the use of topical lacosamide 1% has received some attention along with the use of scleral lenses for drug retention. However, guidelines on how to best manage neuropathic pain that manifests with dry eye-like symptoms are still sparse.
Kudos to the consensus team for their fabulous work with TFOS DEWS II. We look forward to further research in our quest to better understand the tear film’s ecosystem and new strategies to help us manage this complex disease.
1. Craig JP, Nichols KK, Akpek EK, et al. TFOS DEWS II definition and classification report. Ocular Surf. 2017;15(3):276-83. |
