Dry eye/ocular surface disease is the single most misunderstood and overcomplicated disease state that optometrists see. It can’t be fixed by wetting the eye because, in most cases, “dry” isn’t the problem. This is clarified in the new definition from the Dry Eye Workshop (DEWS), which describes “loss of homeostasis of the tear film as a central concept.”¹ Fundamental to the loss of homeostasis is that the ocular environment struggles to maintain balance in the face of myriad challenges and that MGD drives much of the dysfunction of the tears and ocular surface. Lemp and colleagues reported that 86% of patients diagnosed with dry eye demonstrate signs of MGD.² I actually find that to be a significant underestimation in my patient population. Dear friend and mentor Donald Korb hit the nail on the head with his seminal paper “‘Dry Eye’ Is the Wrong Diagnosis for Millions.”³ As he wrote, an “MGD-first approach has the potential to revolutionize the timing of diagnosis and the choice of frontline therapy in most patients with dry eye.”

Tears form a perfect refractive surface, and our ability to see is so fundamental to survival that the eye is equipped with incredible mechanisms to maintain homeostasis and function of the tear film. The system is elegant and beautiful in both its simplicity and complexity. The lipid layer of the tear film consists of numerous species of lipids, produced by the meibomian glands, that create a coherent, tense outer surface that gives the tear film structure. And the blink, a beautifully choreographed movement, actively contributes to the integrity of that structure. I believe that the blink itself doesn’t directly express meibum; it pressurizes the meibomian glands as the orbicularis muscles contract with the blink. Gland expression is controlled by the muscle of Riolan (Figure 1) at the distal end of the gland. Riolan’s muscle prevents lipid expression, except when the eyelids touch as the blink completes. In a sweeping movement, the upper eyelid sweeps down, out, and around, squeegeeing tears off of the ocular surface. The lower eyelid pulls these spent tears toward the lacrimal drainage system, which is under negative pressure during the blink. The spent tears are sucked out of the system, and lipid is metered out in a concise amount and evenly spread on up-blink.

When homeostasis breaks down, many factors associated with dry eye come into play, including tear hyperosmolarity, ocular surface inflammation, and apoptosis, but, as I see it, tear film instability is the root of all the problems. We use the term “dry eye” largely because it’s historical. But it is the structure of the tears and the ability of the tears to create a stable surface that are really important. Christophe Baudouin’s Proposed Vicious Circle of the Pathology of Dry Eye Disease⁴ is an apt distillation of this, and it places MGD at the center of dysfunction (Figure 2).

IDENTIFY THE PATIENTS

There are two ways to build a viable dry eye practice based on either a primary care or a specialty care model. The former is proactive, whereby dry eye symptoms and meibomian gland function and structure are routinely screened in all patients. With this approach, dry eye and MGD — including gland obstruction — are identified early, with the short- and long-term goals being ocular surface health. Similar to how we approach glaucoma, this is a disease-preventative strategy. A specialty care approach is more reactive. The signs and symptoms of dry eye are managed as they present. Although a proactive approach is good, and likely where the field is headed, it can be difficult to implement because many patients are asymptomatic, unaware of the problem, and resistant to treatment, adhering to the old mentality, “If it ain’t broke, don’t fix it.” As a result, focusing on symptomatic patients may be a better way to start.

The good news is that symptomatic patients are already in the waiting room of every optometric practice, and their symptoms are or will soon be making them miserable. In more advanced cases, many feel frustrated and invalidated with prior care, and most are willing to do anything for relief. The best way to identify these patients is by using a validated questionnaire, such as the Ocular Surface Disease Index (OSDI) or the Standardized Patient Evaluation of Eye Dryness (SPEED). To keep practice flow efficient, a technician or other staff member should sit with each patient and administer the questionnaire. This also works well because patients typically feel more at ease with a staff member than they do with the physician. The staff member should review the results with the patient and, if the scores are high, have them explain that the doctor will evaluate and discuss further. (For more information on patient communication, see “Understanding the Psychology of Dry Eye” on Page 7. )

DIAGNOSTIC TECHNOLOGY

Is investing in advanced technology a requirement for building a dry eye practice? Not necessarily, but I did so early on. I purchased the Oculus Keratograph 5M, which is an advanced corneal topographer optimized for external imaging. It includes many useful features, such as the ability to evaluate the meibomian glands, non-invasive tear film break-up time, tear meniscus height, and lipid layer thickness. We also have a LipiView II (Johnson & Johnson Vision), which includes blink evaluation and interferometry, both of which can be very helpful.

Meibography clearly reveals the signs of MGD — gland obstruction, convolution, tortuosity or dropout, and dilated ducts — that are caused by the glands not emptying properly and meibum stagnation (Figure 3). Functionally, the glands are pressurized to release lipid with every blink; but when the blink is inhibited — for example when one stares at a digital device for too long — they don’t release, and back pressure can lead to structural changes. In addition, when lipid stays resident in the glands for too long, it eventually becomes rancid. The body doesn’t like anything rancid, so it directs inflammatory cells to remove it. But the inflammatory response can’t discriminate between rancid lipid and tissue, and glands are attacked and begin to drop out. I use a simple categorization scheme to group my patients based on prognosis (Figure 4). In group I, the glands are mostly intact but obstructed. The lipid layer has diminished thickness and coherence, i.e., the tear film is unstable. In group II, 20% to 80% of the glands have been lost, but the patients are still reasonably easy to manage. In group III, relatively few glands remain. These patients can be managed but usually require a great deal of adjunctive treatment. In conjunction with gland assessment on the Oculus Keratograph 5M, I utilize its non-invasive tear break-up time measurement. With this feature, it’s easy to see the difference between a perfectly smooth, intact tear structure and a surface with a depleted dysfunctional lipid layer, which leads to exposure to the dry atmosphere, inflammation, and all the damage that ensues from that (Figure 5).

Many other diagnostic instruments, some more expensive than others, are available to aid in dry eye diagnosis. Point-of-care testing has also become popular, although my use is somewhat limited except in clinical trials. By my analysis [Clinical Benefit ÷ (Time + Cost) = Value], I don’t use tests that don’t change my treatment decision-making. Again, the most efficient and cost-effective way to gather diagnostic data that’s automatically generated is to utilize technicians. Once a technician has gathered the data, patients can transition to the exam room to see the optometrist.

Whether or not a practice chooses to purchase equipment specific to diagnosing dry eye, the external exam and the slit lamp are invaluable. Bell’s phenomenon, for example, can be tested by holding the eyelids open and having the patient try to forcibly close his or her eyes. The eyes should turn up and out. If they don’t, and this protective reflex is failing, any exposure due to poor lid closure during sleep will cause corneal and conjunctival damage and worsen dry eye symptoms because the ocular surface won’t get a chance to recuperate during the night. In any dry eye patient, findings at the slit lamp may include saponification (Figure 6), which occurs as a result of bacterial lipase activity on tear lipids. (More on saponification in “Simplified Treatment Flow Chart Drives Successful Outcomes.”) The clinician should always look closely at the eyelids for signs of disease (Figure 7). Fluorescein, in addition to providing a picture of corneal health via staining, including specific patterns such as the inferior staining typically seen with exposure, helps to highlight the regularity of the eyelids. It may reveal, for example, notching in eyes with chronic MGD (Figure 8). Fluorescein can also be used to determine tear break-up time and break-up patterns. Breakup in the same area repeatedly indicates the underlying surface has become hydrophobic due to chronic damage. Breakup sporadically in different areas generally indicates that the lipid layer is insufficient.

A useful, and free-of-charge, instrument is the clinician’s finger. To evaluate meibum, healthy and clear or otherwise, use the finger to apply pressure to the eyelids slightly greater than the force of a blink. With practice, doing this effectively becomes second nature. Finally, I find that my most sensitive instrument is listening to patients. I listen, and they tell me what’s wrong with them and, thus, how to fix it. For example, a patient says, “I wake up in the morning and my eyes feel terrible, like sandpaper. I can barely get them open.” What’s wrong? Without even examining this patient, I am confident he has exposure.

THE HEART OF THE MATTER

I spend most of my time with patients listening and explaining to them what’s wrong. I can afford to do this because I charge appropriately for the time and the diagnostic testing. It’s time well spent because it’s what leads me to the best management plan, which motivates patients to follow it. •