Aqueous deficiency is a contributor to evaporation-related dry eye disease

Abstract

Dry eye disease aetiologies can be classified dichotomously into aqueous deficient and evaporative types although many cases involve combinations of both. Differential diagnosis can be confounded by some features of dry eye disease being common to both aetiologies. For example, short tear break-up times are prime diagnostic findings of tear instability due to lipid and/or mucin deficiencies, but thin tear layers in aqueous deficient eyes also shorten tear break-up times, even at normal range rates of evaporation in eyes without lipid and/or mucin deficiencies. Because tear instability and short tear film break-up times due to thin tear layers can be independent of lipid and/ or mucin deficiency, aqueous deficiency can be another form of evaporation-related dry eye. Conversely, tear layers which are thickened by punctal occlusion can be less susceptible to tear break-up. An inflamed lacrimal gland producing reduced quantities of warmer tears can be a basis for thin tear layers and tear instability demonstrated by shorter tear break-up times. Commonly used clinical tests for aqueous deficiency can be unreliable and less sensitive. Consequently, failure to detect or confirm aqueous deficiency as a contributor to short tear break-up times could result in too much weight being given to a diagnosis of meibomian gland deficiency. Less successful treatment outcomes may be a consequence of failing to detect aqueous deficiency. Refining disease classification by considering aqueous deficiency as a contributor to, or even a form of evaporation-related dry eye, could be the basis for more comprehensive and appropriate treatment strategies. For example, some treatment methods for evaporation-related dry eye might be appropriate for aqueous and mucin-deficient as well as lipid-deficient dry eyes. Anti-inflammatory treatment for the lacrimal gland as well as the conjunctiva, may result in increased aqueous production, reduced tear temperature, tear instability and evaporation rates as well as lower osmolarity.

Comparative study of tear film evaluation among healthy pregnant women and gestational diabetes: a cross-sectional study

“…The prime diagnostic findings of tear instability were TBUT and Schirmer's. 24 The OSDI combined with TBUT and Schirmer's were the best tests to detect the dry eyes. 7 Our study expressed reduced TBUT values, mild range of OSDI scores as obvious signs directing towards EDE in the GDM group.…”

Transdermal anti‐inflammatory therapy for aqueous deficiency

“…The difficulties for a topically applied anti-inflammatory drug to reach and treat aqueous deficiency suggests that transdermal drug delivery to the lacrimal gland through the temporal superior upper eyelid and eyebrow might be a more successful treatment for aqueous deficiency associated with lacrimal gland inflammation. 2 For example, therapeutic benefits from transdermal therapy may be derived from a reduction in lacrimal gland inflammation and an associated reduction in inflammatory mediators being delivered in a greater volume of aqueous from the lacrimal gland to the ocular surface, or perhaps from a reduction in aqueous tear osmolarity and an associated reduction in ocular surface inflammation. It appears to be unknown to what degree a transdermally applied drug which is applied at the site of localised subcutaneous inflammation, can reach that site directly, or if that drug is absorbed into the systemic circulation to reach that site circuitously.…”

“…11 Short tear breakup time findings should arouse suspicion of aqueous production deficiency, and failure to assess and detect aqueous deficiency could result in too much weight being given to other contributions to tear instability such as Meibomian gland dysfunction. 2…”

“…2 Thus, deficiency in aqueous production can be a feature of many categories of dry eye; primarily in the case of main lacrimal gland aqueous deficiency and secondarily as a contributor to cases of aqueous loss by faster evaporation due to lipid and/or mucin deficiencies. 2 Our understanding of the destructive inflammatory process that occurs in the lacrimal glands of aqueous deficient patients is partly inferred from the study of labial minor salivary gland biopsies. 3…”

Why the symptoms and objective signs of dry eye disease may not correlate

“… 18 The sensory component of pain is described as a nociceptive physiological response which is the progenitor of the experience of pain. 19 About 10%–15% of corneal nociceptors are cold sensitive and able to detect tear temperature changes such as occur with tear evaporation 20 Abnormally high stimulation of these nociceptors might occur when lipid layer deficiencies and/or a thin tear layer, 21 result in more rapid evaporation and associated tear cooling. About 20% of nociceptors respond exclusively to mechanical stimuli 20 which might include friction sensations associated with blink-related lid wiper movements over a desiccated ocular surface such as occurs in areas of tear break up.…”