Dry eye disease (DED) is challenging to define. Rather than being a single disorder, DED represents a spectrum of ocular surface conditions, all characterized by a loss of tear film and ocular surface homeostasis.1
Patients with DED can present with any of a variety of symptoms, including dryness, burning, fluctuating vision, light sensitivity, tearing, or pain, and these symptoms may or may not be consistent with objective clinical signs such as corneal and conjunctival staining or tear breakup time.2
Regardless of its presentation, DED is a massive and growing issue facing our modern, screen-focused world. It is estimated that anywhere between 5 to 50% of individuals worldwide suffer from some form of DED,2 and patients with moderate-to severe DED can experience a reduction in quality of life similar to patients who experience severe heart disease or a mobility-limiting hip fracture.2
In our practices, we treat DED in patients of all ages and backgrounds, and we have personally seen how it can have a deleterious, and even life-altering, impact on patients’ ability to read, drive, sleep, use screens, work productively, and even interact socially with family and friends.
Customizing your approach to DED
Due to its multifactorial and biologically complex nature, there is no “one-size-fits-all” approach to treating DED; in each case, the root causes of DED must be teased out and addressed individually, such as aqueous deficiency, meibomian gland dysfunction (MGD), blepharitis, inflammation, and altered nerve function.2
Successfully treating a patient with DED requires an individualized approach that utilizes a combination of treatments to combat each of a patient’s underlying drivers of disease. However, because of the seriousness of DED’s effects on wellbeing and ability to complete activities of daily living, patients often demand immediate relief.
While most therapies for DED are designed as long-term treatments that take effect gradually, several options can help reduce symptoms in the short term while longer-term therapies are introduced; together, these approaches can address the full range of factors contributing to an individual’s DED.
To learn more about treating all subtypes of DED check out, From Symptoms to Solutions: Appropriate Prescribing for Inflammatory Versus Evaporative Dry Eye Disease.
Quick-acting therapies for DED
Inflammation is often one of the main factors driving the “vicious cycle” of DED, both contributing to its initial development and exacerbating it over time.3 As such, acutely addressing inflammation on the ocular surface with fast-acting therapies can be one of the most important first steps for both quickly relieving symptoms and interrupting chronic processes that drive long-term disease.
Cryopreserved amniotic membranes
Cryopreserved amniotic membranes (CAMs) have emerged as one of the most useful tools in our armamentarium for quickly combating inflammation and desiccation in these patients.
We often explain to patients that using CAM is like applying a “vitamin-infused band-aid” due to the presence of heavy chain-hyaluronan/pentraxin 3 (HC-HA/PTX3), which is retained during cryopreservation but not in other preservation methods and provides the CAM with its natural anti-inflammatory, anti-scarring, and wound-healing properties.4
This makes CAM uniquely able to calm a severely desiccated ocular surface and restore normal homeostasis while promoting epithelial healing and providing a biological scaffold for epithelial regrowth.5
The role of CAMs in DED management
One of the major benefits of CAM is the wealth of data showing its rapid efficacy; in one multicenter, retrospective study, placement of CAM for only 2 days led to significant improvements in both signs and symptoms of DED that persisted for up to 3 months.6
In another multicenter, randomized controlled trial, patients who were treated with CAM for 3 to 5 days experienced significant improvements in signs and symptoms of DED for up to 3 months, as well as significant increases in corneal sensitivity and topography due to CAM’s ability to help regrow damaged nerves.7
Because of these regenerative properties, CAM is especially useful for cases of DED where neurotrophic keratitis is suspected. In fact, cenegermin, a topical recombinant nerve growth factor, can be initiated while these patients begin treatment with CAM to optimally re-innervate the cornea.8
Topical steroids
Another option for quickly treating inflammation in patients with DED is the use of topical corticosteroids. While topical corticosteroids are commonly used short-term for this condition and have demonstrated the ability to improve signs and symptoms of DED, longer-term use may carry a risk for increased intraocular pressure and cataract formation.9
Topical antiparasitics
In patients where Demodex blepharitis is a contributing factor, a 6-week course of lotilaner can be helpful for controlling their infestation and improving MGD and erythema.10
Fast-acting long-term therapies for DED
A subset of emerging therapies may help bridge the gap between rapid symptom relief and sustained disease control. Acoltremon (TRYPTYR, Alcon) has demonstrated an onset of action as early as 3 minutes,11 while perfluorohexyloctane (MIEBO, Bausch + Lomb) has shown symptom reduction within approximately 5 minutes.12
Both agents are notable in that they provide rapid relief while also being suitable for long-term use, positioning them as distinct options within the DED treatment paradigm for patients who desire both immediate and sustained improvement.
Long-term treatments for DED
Among treatments that work over a longer term, intense pulsed light (IPL) therapy is one option for reducing inflammation in DED, especially if MGD is a contributing factor.
Data from multiple studies have shown that treatment with IPL, which generally involves 3 to 4 sessions spaced 2 to 4 weeks apart, demonstrated improvements in both symptoms and clinical signs of DED with an excellent safety profile.13
Long-term lid hygiene
For patients where blepharitis is a contributing factor, lid hygiene measures like warm compresses, lid wipes, eyelid scrubs, or products that contain manuka honey, tea tree oil, or other over-the-counter compounds can be used indefinitely to provide relief.10
Long-term inflammation management
Immunomodulators, like cyclosporine and lifitegrast, can also be helpful as longer-term therapies to address ocular inflammation and have demonstrated the ability to improve signs and symptoms of DED; however, these treatments may take anywhere from 2 weeks to 6 months to start showing efficacy.14
Addressing evaporative DED
For patients where excessive tear film evaporation plays a role in their disease formation, lubricating drops can provide temporary relief, and, depending on the formulation, some therapeutic benefits such as osmoprotection or lipid supplementation.15 As mentioned before, perfluorohexyloctane is an option for evaporative dry eye that also has the benefit of providing rapid relief.16
Lubricating ointments may be useful for those with evaporation driven by incomplete lid closure or nocturnal lagophthalmos. However, it should be noted that these treatments are palliative in nature and do not address the underlying factors driving the disease.
For patients with evaporative DED, punctal occlusion—including intracanalicular placement of cross-linked hyaluronic acid gel—can serve as a longer-term strategy to reduce tear drainage and alleviate DED symptoms.17,18
Counseling patients with DED
DED can have a profound impact on patients’ daily functioning and overall quality of life. When seeing a patient with DED for the first time, it is essential that we listen to them and make them feel heard.
Far too often, patients with DED are told that “their eyes look fine” despite battling severe symptoms that leave them despondent. By listening to our patients and validating their experiences, we can build buy-in for treatment adherence while also gaining insight into their goals, allowing us to tailor therapy to their individual needs.
However, communication is a two-way street—talking to your patients and managing their expectations is also critical for treatment success. We must explain the rationale behind each therapy we initiate, which options provide rapid symptom relief versus long-term disease control, and what patients should expect from each.
Providing patients with a handout to take home can be another helpful tool, as many patients are overwhelmed when presented with medical information in the office. Furthermore, proactive follow-up scheduling can strengthen rapport and trust with patients, demonstrating an ongoing commitment to their care and eye health.
Conclusion
Successfully treating DED is a journey, not a quick jaunt; it requires commitment from both providers and patients, and no single prescription will act as a magic bullet or cure-all.
However, by using multiple complementary therapies simultaneously to calm inflammation and help restore ocular surface homeostasis, we can efficiently provide meaningful relief to the many patients suffering from this condition.
