- History taking
- Point of care diagnostic testing and imaging
- Clinical Examination
- Individualized treatment plan
- Meeting with dry eye educator
Published in Ocular Surface
How My Ophthalmology Practice Successfully Incorporated Dry Eye Therapy
This is editorially independent content
As our understanding of dry eye disease grows and dry eye therapies become more mainstream, you might be wondering how to incorporate these treatments into your ophthalmology practice. Here's one MD's tips on incorporating dry eye therapy into your practice!
If even a handful of years ago one had inquired about dry eye therapies in ophthalmology, there would only have been a few interventions from which to choose. The ‘basics’ including artificial tears, possibly topical cyclosporine or punctal plugs if symptoms were recalcitrant. However, there was a limit to what physicians had available to offer patients for relief of their symptoms. This, coupled with a limited understanding of dry eye disease (DED) as a disease process, caused ophthalmologists to shy away from embracing these patients. Luckily, there has been a steady increase in the peer-reviewed literature on DED pathophysiology as well as multiple new therapies that we have to offer patients. Our understanding of this complex disease is rapidly growing, and so are opportunities to incorporate DED therapies that benefit both the patient and generate revenue for the practice.
My approach is algorithmic in nature and follows the following protocol:
The best way to begin incorporating DED therapies into your practice is to ensure you are identifying all potential DED patients. Approximately 30% of all eye care visits are related to DED symptoms, and a high proportion of patients seeking cataract surgery have co-existing DED and other ocular surface diseases which may impact their visual outcomes after surgery. It is well known that signs and symptoms of DED do not always correlate, which is why careful history taking along with clinical examination is vital. The approach should first begin with the technician obtaining either a standardized DED questionnaire or by asking directed questions about DED symptoms including fluctuating vision, tired/irritated eyes, redness, etc. Inquire about prior medical or ocular diagnoses, concurrent medications that can exacerbate DED, makeup and skincare regimens (including topical retinol), and contact lens wear; all of which may contribute to DED.
Don't forget to check out our tips on educating your staff on dry eye disease!
The technician then performs point of care in office DED testing including tear osmolarity and matrix metalloproteinase-9 (MMP-9) before any eye drop application occurs. When osmolarity is abnormal (at least 300 mOsm/L in either eye or an inter-eye difference of at least 8 mOsm/L) DED is likely present, the severity of which may be linearly related to the osmolarity itself (300-320=mild, 320-340=moderate, >340=severe DED). When MMP-9 is elevated, ocular surface inflammation is suspected (DED-related or other cause) and treatment will often require anti-inflammatory medications. If available, the technician may also obtain meibography imaging at this time.
Armed with the above information, the clinician can then begin the clinical examination including vital dye staining of the cornea and conjunctiva, meibomian gland expression, and tear breakup time (TBUT). Eyelid and eyelash examinations are also important to rule out Demodex (classical ‘cylindrical scurf’ present at the base of the eyelashes). Other objective tools including non-invasive tear breakup time, tear meniscus height, lipid layer thickness, and other advanced metrics if available.
Universally, the underlying pathophysiology for any DED or ocular surface disease subtype is inflammation. This is among the most important information to understand about the treatment of DED: it is necessary to break the cycle of inflammation on the ocular surface in order to restore homeostasis and improve both signs and symptoms of DED.
Once DED is diagnosed, the patient is presented with an individualized therapeutic plan. I often illustrate that there are many treatment options available and that some patients respond well to certain therapies while others may respond differently, and it is about finding a regimen that is specific to their DED state. I also discuss that DED is a chronic inflammatory condition that may have flares and exacerbations (environmental, hormonal, situational). Therefore we need a daily regimen as well as a regimen for flare-ups. I also emphasize that because this is a chronic condition, the goal of treatment is to allow for more good days than bad days in regards to their symptoms. Setting expectations with your DED patients is paramount to treatment success.
Based on patient symptoms and clinical findings, recommendations are made for prescription therapies and in-office procedures. It is important to acknowledge that many external factors also play a role in determining treatment options including cost, patient preference, and the ability to comply with certain therapies. Treatment options should be presented and individualized for each patient.
My treatment approach centers around 3 classes of therapies: The Basics (all patients), Prescription Medications, and In-Office Procedures.
This class of therapy is recommended to all patients, regardless of the severity of DED. Examples include artificial tears (preferably oil-based and preservative-free), hydration and nutritional support (+/- omega-3 supplementation), warm compresses, and eyelid hygiene. Environmental modifications such as the use of a humidifier and stressor avoidance (wearing sunglasses to protect from wind, and avoiding allergens) are also discussed. Offering recommended products for sale at the office has been beneficial for patient compliance and ease of use.
Immunomodulators (cyclosporine 0.05%, cyclosporine 0.09%, lifitegrast 5%) provide long-term control of ocular surface inflammation which is often required for DED patients. Topical anti-inflammatories such as loteprednol etabonate 0.25% (recently FDA approved for dry eye flares) is the preferred medication for short-term control of inflammation and for flare-ups. It is also effective when started concurrently with immunomodulators for 2 weeks for more immediate relief of symptoms. Oral anti-inflammatories include doxycycline and minocycline long-term (3 months or longer) and are beneficial when ocular rosacea or blepharitis is present. If a patient has persistent symptoms despite immunomodulator use, I next recommend serum-based tears. Lastly, secretagogues and prescription medications for neuropathic pain (ex: Gabapentin) associated with DED can also be prescribed when symptoms are recalcitrant to other therapies.
Punctal plugs are extremely useful once ocular surface inflammation is under control. If inflammation is present, I prefer to start a topical anti-inflammatory first and will add plugs at a future visit if needed. If patients tolerate plugs and require a more long-term solution, punctal cautery can be useful. I frequently use microblepharoexfoliation in-office in combination with thermal pulsation with great success, especially in patients that may find daily compresses difficult to do, or those looking for immediate relief. Amniotic membrane can provide rapid reversal of punctate epithelial erosions for severe DED and are reimbursed by most insurances. Specialty contact lenses such as scleral lenses are offered in conjunction with optometry and can help with pain and fluctuating vision associated with DED. Lastly, if Demodex is present, I recommend in-office microblepharoexfoliation and 2 months of tea tree oil-based eyelid cleansing; however, topical prescription therapy is currently under investigation with promising results.
As mentioned, all patients are instructed on dry eye basics, and this is done with a dry eye educator. Having a dedicated person sit with the patient and explain how to apply eye drops and how to do effective warm compresses and other therapies has greatly increased patient compliance as well as physician efficiency in clinic. The extra time allowed for education has also increased conversion to in-office procedures such as thermal pulsation.
Lastly, I advise follow-up 3 months after initial therapies are introduced in order to assess response to therapies both symptomatically and clinically, and changes to therapies are made as needed.
As new research, diagnostics and therapeutic options emerge, the incorporation of many treatments may vary. But having an algorithmic approach to the diagnosis and treatment of DED patients can help in their management.