Beyond the Meibomian Glands

Bacterial overpopulation can exacerbate MGD, but treatment with Avenova can help.

■ By Arthur B. Epstein, OD, FAAO

I’ve been fascinated by dry eye and ocular surface disease for many years, and I’ve watched its definition change over time to reflect our growing understanding of tear structure and function. Today, my practice focuses intensely on dry eye patients and I’m surprised at how rapidly my own approach to managing this growing segment of patients continues to evolve.

Although we continue to see a significant number of older and middle-aged patients with dry eye, we’re also seeing an increasing number of younger patients with severe dry eye and ocular surface disease. I typically see at least one 20-something or teenage dry eye patient per week, many of whom are barely functional. I attribute this change to a massive shift in the use of electronic devices, which interferes with normal blinking patterns that, in turn, contribute to meibomian gland dysfunction (MGD). In essence, the blink is the weak link in the eyes’ ability to maintain a normal healthy tear film.

» Figure 1. MGD with lid inflammation and inspissated glands.

Thankfully, as the number of patients with dry eye grows, so does our armamentarium of options for diagnosing and treating what is among the most common problems seen in eye care practice.

Modern Tear Film Model

In perhaps the most important shift in our understanding of dry eye, we now know that the vast majority of what we call dry eye is caused by MGD and resulting tear lipid deficiency. This leads to excessive evaporation, tear instability and the cascade of signs and symptoms that our patient’s describe as dry eye.

The traditional view of a discrete three-layer tear film dates back to the early 1950s, despite it being overly simplistic and clinically inept by today’s standards. The tear layer exists to provide a smooth and stable optical surface and is essential to survival. A functional tear film defies gravity and remains largely immune to the wide environmental variations to which humans are exposed. The tears are exquisitely complex with a structure that is a feat of brilliant engineering.

The tears transform the normally hydrophobic outer epithelial cell wall into a hydrophilic glycocalyx that allows the tears to adhere to the surface regardless of our orientation. The bulk of the tears consist of a protective viscoelastic gel formed by aqueous from the lacrimal and accessory glands and gel-forming mucins. Finally, non-polar lipids create the “roof ” of the tear structure, tacked in place by polar phospholipids, protecting the eye’s healthy, moist environment. MGD compromises the structure and function of that “roof,” leading to tear instability and ultimately collapse of the entire tear structure.

The Underlying Problem: MGD

Despite the dogma of past dry eye perspectives, MGD is the primary cause of most dry eye. Literature reports that 86% of dry eye patients have MGD as a primary or contributory cause of dry eye.¹ In my practice, in arid Arizona, I find that percentage to be even higher. As the importance of MGD as a cause of dry eye disease became increasingly apparent, many clinicians examined the lids with increased interest. Despite this, the diagnosis of MGD often remains elusive because not all MGD is obvious — even on slit lamp exam.

Although we use a battery of sophisticated equipment as part of our dry eye work up, MGD can be identified simply by expressing the meibomian glands. Normal, functional glands will produce copious, clear, unsaturated oil with just gentle pressure applied (emulating the force of a blink). Patients with healthy meibomian glands tend to be comfortable and relatively asymptomatic.

However, most of the patients I see have significant MGD. As MGD progresses, the glands become increasingly obstructed and lipids stagnate — becoming thick, saturated and stagnant. Glands may have obvious plugs or dilated orifices, and expressing them produces a cheesy or toothpaste-like substance, if anything. This secretion isn’t simply non-functional or sparse — the highly saturated oils also can contaminate the normal lipids within the tear film.

» Figure 2. Highly saturated, thick meibum on lid margins.

» Figure 3. Frothing in tear meniscus caused by saponification.

Non-obvious MGD (NOMGD) is common. In some patient populations, it’s more common than MGD. With NOMGD, the examiner won’t see anything on casual observation, but blink-like expression produces no clear oil. A more forceful manual expression produces white, toothpaste-like, filamentous secretions. This suggests the patient’s meibomian glands aren’t functioning properly.

Undiagnosed, MGD can contribute to dry eye, as well as bacterial colonization and surgical and contact lens complications.

MGD Diagnostic Technologies

To enhance our ability to diagnose MGD and obtain as much information as possible about the disease state, we’ve adopted several advanced diagnostic technologies in my practice.

We perform meibography using the Keratograph 5 (Oculus) on every dry eye patient. In a normal patient, meibography shows straight intact glands inside the upper and lower eyelids. Gland structure is well defined with individual acini visible. In contrast, meibography of a patient with MGD reveals that some of the glands may be absent. Remaining glands can be thinner, thready and tortuous. Because of chronic blockage, central ducts become more visible and with increased inflammation, glands can be damaged or destroyed. Some believe this damage is irreversible, which makes early treatment essential.

The LipiView II (TearScience) with dynamic meibomian imaging (DMI) adds a new dimension to meibography — increasing the clarity and resolution over conventional meibography, the DMI technology uses a number of different light sources to maximize the resolution. Gland structure, dropout, truncation and dilation are quite visible in the images. Lipiview also allows for measurement of lipid layer thickness down to nanometer levels as well as an analysis of blink patterns, which is critical in staging MGD to determine therapy.

Tear stability is another key measure of MGD. Traditionally, to gauge the stability of a patient’s tear film, we instilled fluorescein drops and measured tear breakup time. With the Keratograph 5, my technicians can easily, effectively, noninvasively measure tear breakup time before I even see the patient.

In a normal patient, tear breakup begins after 6 or 7 seconds. Patients with MGD and unstable tear films will show breakup over a wide area of the cornea very quickly — in some cases, in just 1 or 2 seconds.

MGD & Bacterial Colonization

We’ve come to recognize that MGD is the driver of dry eye and that MGD is an obstructive disease. But there’s a significant bacterial component to MGD that tends to be under-recognized and clinically overlooked. Similar to smoke and fire, where there is MGD, there is often significant bacterial overpopulation of the lids.

Bacteria grow best when easy sources of food are available. The saturated oils (toothpaste-like secretions) that result from MGD are an excellent food source. With a warm moist environment and readily available food, bacteria — particularly staph, overpopulate the lid margins.

Bacteria also tend to be very competitive. After colonizing the eyelids, they secrete exotoxins to kill off their neighbors. It’s a battle that both causes and extends inflammation and infection.

Finally, bacteria are gluttonous. They secrete enzymes to help pre-digest their food and in other cases, to better penetrate tissues to extend infection. Staphylococcus, is well known for its ability to secrete lipases, enzymes that break down lipids. We see the effects of lipase on meibomian gland secretion as foamy soap bubbles at the lower lid margin. This is the result of saponification from the combination of lipases breaking down meibomian lipids and alkaline tears.

Like any soap, this can disrupt the lipid layer, as can the lipases themselves. Not only does a patient with MGD produce an inferior, insubstantial lipid component, but also, with significant Staphylococcus overpopulation, that patient’s already ineffective lipids are degraded by saponification and lipase activity. Because bacteria are a key but often invisible driver of the MGD pathology, it’s extremely important to evaluate bacteria populations on patients’ lids and take steps to prevent colonization.

Treating MGD’s Bacterial Component

To manage lid disease, I address the bacterial component with pure hypochlorous acid (Neutrox, the active ingredient in Avenova by NovaBay). Solution testing confirms that Neutrox is effective against a wide range of bacteria and degrades enzymes such as lipase.^2,3 In vitro testing also demonstrates the inactivation of bacterial toxins, which are a source of inflammation and irritation for MGD patients.

As a substance that naturally occurs in the body as the chief line of defense used by neutrophils, pure hypochlorous acid has quieted some of my concerns that we’re running out of antibiotic options. Although hypochlorous acid has been overlooked as a therapeutic agent, it can act against bacteria in a very effective, comfortable and well-tolerated way. It’s an exciting new treatment approach.

I’ve never been a big fan of eyelid cleansers. So when I first received samples of Avenova, I initially dismissed it as just another eyelid cleanser. I prefer to approach lid scrubs with washcloths and warm water, and I think bacteria lipase activity produces sufficient soaps, so I didn’t try it.

My wife, who practices with me and is often far more astute, had a number of patients with blepharitis at the time, and she gave Avenova samples to some of them. A few weeks later, she told me, “I don’t understand what’s going on, but patients go crazy over this stuff. For some of them, it’s the best thing that’s ever happened. They’re afraid they won’t be able to get more, and they want to order more immediately.”

I was surprised and curious, so I started using Avenova for my dry eye patients and I’ve had phenomenal success. Patients are happy, their symptoms are reduced and, most importantly, I see better overall ocular health in patients with MGD who use Avenova. It has fundamentally changed the way we manage dry eye and blepharitis patients. ●

REFERENCES

ARTHUR B. EPSTEIN, OD, FAAO, is the Director of Cornea External Disease and Clinical Research at the Dry Eye Center of Arizona in Phoenix.

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