Break vicious cycle of MGD, dry eye disease with targeted heat, expression
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The health and vitality of the ocular surface are largely dependent on the protective and lubricating properties of a good quality tear film.
One such challenge to the production of a good quality tear film layer lies within the obstructive nature of meibomian gland dysfunction (MGD), which is caused by poor quality meibum lipid secretions forming blockages in the glands. This prevents optimal balance of lipid in the tear film, thereby resulting in disruption of the optical and protective properties of the tears. Consequently, the tear film evaporates at an increased rate, leading to an exacerbation of dry eye disease (DED) signs and symptoms.
As such, the lipid layer is the most critical tear film component in the prevention of so-called “evaporative DED.” In destabilizing this important protective layer of the tear film, evaporative DED launches a cyclic disruptive cascade across the ocular surface and further negatively affects MGD progression.
Without the protective benefits of a quality, lipid-enriched tear film, the ocular surface is subjected to an accelerated evaporative process that leads to ocular symptoms, decreased visual acuity and ocular surface damage susceptibility. Clinically, this means that a patient’s tear film begins to dissipate or break up soon after each blink, leaving the ocular surface exposed until the patient blinks again to refresh the tear film. This reduced tear film break-up time (TBUT) is a hallmark sign of evaporative DED.
Such repeated — and eventually chronic — exposure of the cornea in tear film-deficient eyes leads to the development of objective clinical signs, such as superficial punctate keratitis and hyperemia as well as subjective irritating and visual symptomatology.
Assessment, treatment options
The greater the interval between TBUT and the following blink, the greater potential for damage of the ocular surface. This interaction between TBUT and the time between blinks, known as the interblink interval (IBI), helps regulate the integrity or health of the ocular surface. In an ideal system, the TBUT would match or exceed the IBI, ensuring that the ocular surface is protected.
The relationship between TBUT and IBI has been quantified by the Ocular Protection Index (OPI), which is calculated by dividing TBUT by IBI. If the OPI is less than 1.0, the patient is at risk for an exposed ocular surface, whereas if the OPI is 1.0 or greater, the patient’s tear film protects their ocular surface. The OPI has proven to be useful in assessing causative and associated factors for DED.
Ultimately, a consequently and consistently unprotected ocular surface results in DED signs and symptoms, creating the MGD-DED cycle. To reduce the insidiously vicious MGD-DED cycle, treatment attempts should alleviate meibomian gland obstruction by liquefying the glands’ secretory contents. Successfully treating such obstruction can restore the lipid layer of the tear film, reduce the likelihood of future MGD progression and improve DED symptoms and clinical signs.
Removing MGD obstruction
However, treating MGD by removing gland obstruction does not come without difficulties. A primary challenge is that MGD alters the molecular composition of the meibum, increasing the melting point relative to normal body temperature. This increase results in the need for higher temperatures within the gland to liquefy obstructive material.
Previous in vitro and in vivo studies have demonstrated that although the temperatures required to melt obstructive secretions range from 32°C to 45°C, more severely obstructed glands require temperatures greater than 40°C for effective liquefaction (Borchman et al.).
Achieving this temperature within the meibomian glands is concerning for a few reasons. One obstacle is that there is approximately a 5°C difference in temperature between heat applied on the external eyelid surfaces and that which reaches the internal eyelid tissue surface where the meibomian glands are located (Blackie et al.). Achieving this desired internal tissue temperature of 40°C requires heating the outer lid surface to 45°C, potentially risking thermal injury to the skin as well as the underlying cornea, which also has a threshold heat tolerance of approximately 40°C.
The overarching goal of all MGD therapies is to improve the flow of meibomian gland secretions. Thus, beyond the traditional approaches of heat and lid hygiene, efforts must be specifically targeted to relieve meibomian gland secretory obstruction. While warm compresses and lid hygiene have long been proven effective for MGD, they do not constitute a cure, especially at advanced stages of disease. Massage of the eyelid provides only partial and temporary obstructive relief, while conventional external warm compresses apply heat only to the outer surface of the eyelid with limited internal effectiveness.
Therefore, it is suggested that the ideal treatment approach for patients with MGD should involve targeted heat for improving meibomian gland secretion lubricity, coupled with obstruction-clearing expressive measures. Ultimately, given the impact of obstruction on the ocular surface, alleviating secretory obstruction with targeted heat and expression represents the most robust strategy to successfully treat MGD while also minimizing concomitant DED signs and symptoms.
References:
- Baudouin C, et al. Br J Ophthal. 2016;doi:10.1136/bjophthalmol-2015-307415.
- Begley C, et al. Ocul Surf. 2019;doi:10.1016/j.jtos.2019.01.004.
- Blackie CA, et al. Optom Vis Sci. 2008;doi:10.1097/OPX.0b013e318181adef.
- Borchman D, et al. Invest Ophthalmol Vis Sci. 2011;doi:10.1167/iovs.10-6514.
- Bron AJ, et al. Ocul Surf. 2004;doi:10.1016/s1542-0124(12)70150-7.
- Knop E, et al. Invest Ophthalmol Vis Sci. 2011;doi:10.1167/iovs.10-6997c.
- Ousler GW III, et al. Cornea. 2008;doi:10.1097/ICO.0b013e31816583f6.
- Qiao J, et al. Clin Ophthalmol. 2013;doi:10.2147/OPTH.S33182
For more information:
Kenneth R. Kenyon, MD, is a clinical professor of ophthalmology at the New England Eye Center at Tufts Medical Center in Boston. He also is a faculty member at Harvard Medical School, Schepens Eye Research Institute and New England College of Optometry and medical director at Eye Health Vision Dartmouth.
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