Managing dry eye disease (DED) can be frustrating for patients and eyecare practitioners alike, because there are often discrepancies between the clinical presentation and patient-reported symptoms (Nichols et al, 2004).

Lemp’s (1995) Report of the National Eye Institute/Industry Workshop on Clinical Trials in Dry Eyes described four commonly found features of DED: symptoms, interpalpebral surface damage, increased osmolarity, and tear film instability. The report stated that “in some patients in whom the diagnosis is strongly suggested on the basis of signs, symptoms could be absent.”

Schein et al (1977) assessed the association between signs (Schirmer test and rose bengal staining) and symptoms as reported in a standardized dry eye questionnaire. The authors found weak association between increased rose bengal staining and symptoms and no association between reduced Schirmer scores and increased frequency of symptoms. Other studies have reported a similar “disconnect” between clinical findings and patient perception (Rentka et al, 2017).

Why Discrepancies Exist

One possible explanation for these discrepancies is the failure of the lacrimal functional unit (LFU), which includes the cornea, conjunctiva, lacrimal and meibomian glands, and the lacrimal drainage system connected by afferent and efferent nerves responsible for crucial communications (Bron et al, 2014). Compromise of any component of the LFU including innervation may lead to dysregulation of the ocular surface (Bron et al, 2014). In vivo confocal microscopy (IVCM) has emerged as a powerful noninvasive means of evaluating superficial structures such as the cornea.

Cruzat et al (2017) performed an extensive literature review of IVCM studies evaluating diseased and healthy ocular surface components. They found strong evidence that alterations in corneal nerve function, density, and morphology play a vital role in the pathogenesis of DED. The study authors postulated that the discrepancy between signs and symptoms in DED may be due to inflammation-induced alterations in corneal nerve endings that ultimately lead to impaired corneal sensation.

A multi-center, international study by Sullivan et al (2014) evaluated 344 subjects to determine the relationship between signs and symptoms of DED. They found very poor correlations; in subjects who had definitive signs of DED, only 57% reported any symptoms.

They postulated that failure to assess asymptomatic patients who have clinical signs could result in a failure to identify patients who have mild disease and to intervene early in the course of the disease (Sullivan et al, 2014).

The Impact

How might this information impact our approach to diagnosing and managing DED? Is it feasible to rely less on, but not ignore, patient symptoms and consider putting more emphasis on signs?

A prime example of this is a study by Shah and Jani (2015) that evaluated 400 subjects for DED. Patients underwent a routine ophthalmological examination and a single objective dry eye test.

The overall prevalence of DED was 54%, and it was higher in older individuals (67%), diabetics (67%), and individuals who had meibomian gland dysfunction (95%). The single objective test that afforded these results was fluorescein-based tear breakup time.

Conclusion

Numerous simple and not-so-simple objective tests for DED are available; they range in complexity from Schirmer test strips and vital dye staining to tear film osmolarity. This might be a good time to re-evaluate the relative value and importance of each of these tests in terms of the clinical diagnosis of DED. CLS

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