Many factors involved in diagnosis, treatment of dry eye syndrome
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Ocular surface disease includes dry eye syndrome, blepharitis/meibomian gland dysfunction, conjunctivitis, keratitis and episcleritis/scleritis.
Surveys suggest that nearly 40% of patients seen by an eye care professional (ECP) have some type of ocular surface disease (OSD). That makes the accurate diagnosis and treatment of OSD an everyday challenge. The cover story in this issue of Healio | OSN focuses on dry eye syndrome (DES).
According to a recently published survey in Market Scope, the core diagnostic evaluation performed by a U.S.-based ECP for OSD is an external and slit lamp examination. While the lights-out slit lamp examination is critical, much can be learned with a room lights-on external examination. This can be completed while talking with the patient. Useful findings include lid abnormalities such as ptosis, ectropion, entropion, scarring, abnormal lashes or lash loss, tumors and masses, blink rate abnormalities including reduced rate and partial blinks, evidence of acne rosacea or rhinophyma, lid and bulbar erythema, and many others. During the external examination, look at the patients’ hands for evidence of arthritic changes, which can be diagnostic and may suggest that a patient will not manage eye drops well. Look, lift, pull and push on the lids to look for localized injection, masses, evidence of lid laxity, floppy lid syndrome and meibomian gland dysfunction.
The preferred slit lamp examination utilizes the neutral density filter and broad beam illumination when examining the lids and conjunctiva. Look at the superior limbus for signs of superior limbal keratoconjunctivitis and the upper lash margin with the patient looking down to identify lash margin collarettes diagnostic of Demodex blepharitis, greasy scurf suggestive of seborrheic blepharitis, or the flat ulcerations and eyelid margin erythema consistent with infectious blepharitis.
Surveyed U.S. ECPs responded that a slit lamp examination with evaluation of the lid margin, meibomian glands, lashes, a vital dye-assisted screen for corneal staining, measurement of tear breakup time and measurement of the lower lid tear meniscus vertical size in millimeters were the preferred diagnostic signs. Other diagnostics utilized by many ECPs included Schirmer’s test, topography, meibography and tear film osmolarity. Biomarkers including MMP-9, lactoferrin, lacritin and IgE were less commonly employed.
Many ECPs have adopted a dry eye questionnaire for DES screening and to objectively monitor symptom improvement with therapy. There are many available. I personally favor the visual analog scale, the UNC Dry Eye Management Scale or the Dry Eye Questionnaire-5.
There are “lumpers” and “splitters” among ECPs regarding DES diagnosis and therapy. I am a “splitter,” and in the following paragraphs, I will share a few personal thoughts.
Most ECPs divide DES into evaporative, aqueous deficient and combined mechanism DES. This to me is the minimal subcategorization required as it impacts therapeutic decision-making. I find the DEWS level 1 to 4 classification useful as well.
DEWS level 1 DES has symptoms only, and many of these patients are manageable with artificial tears, lid hygiene and, if you are a believer, omega-3 supplementation. I call level 1 DES “pharmacist DES” as most of these patients simply go to the drug store and treat themselves with over-the-counter supplements. DEWS levels 2 to 4 DES patients have symptoms and signs. The core signs are corneal staining (punctate epithelial erosion and punctate epithelial keratitis), inflammation and hyperosmolarity. Other findings include reduced or fluctuating visual acuity, conjunctival or lid margin hyperemia, lash abnormalities, abnormal meibomian gland expression with the push test, a rapid tear breakup time, a reduced Schirmer’s test, elevated or asymmetric tear film osmolarity, or an abnormal topography, meibography or biomarker. I classify patients with level 2 or greater DES as “physician DES” and believe these patients deserve to be under the care of an ECP. Unfortunately, most of them are not. In my opinion, level 2 and greater DES patients deserve an ECP’s care as this level of DES has a significant impact on visual performance/quality of life and if left untreated can result in permanent vision-threatening pathology. Therapy of level 2 to 4 DES in addition to the level 1 treatment includes topical steroids, immunosuppressant eye drops, lacrimal outflow occlusion, serum or platelet-rich plasma eye drops, and office-based DES procedures. In severe DES, tarsorrhaphy or amniotic membrane placement may be required.
To carry the “splitter” story further, much DES is associated with surgery, whether in the surgery suite or office based including intravitreal injections. Every patient undergoing a surgical procedure deserves to be screened for DES. In patients who have ocular discomfort and corneal staining, or “pain and stain,” ocular surface preparation before surgery will enhance post-procedural comfort and visual recovery. In addition, during the procedure, a surgeon can take extra care to protect the ocular surface. It is also important to provide postoperative therapy to rehabilitate the ocular surface.
Finally, these patients deserve to be under an ECP’s care long term to maintain their ocular surface health. I call this subcategory of DES “surgery-associated dry eye syndrome.” Others have named it “surgical transient ocular discomfort syndrome.” Under either name, it is an important subcategory of DES and deserves preoperative diagnosis with appropriate ocular surface preparation, intraoperative ocular surface protection, and postoperative ocular surface rehabilitation with lifelong maintenance therapy.
Every year we have better DES diagnostics and therapeutics with more to come. We and our patients are fortunate that OSD diagnosis and therapy are well supported by investment of human and financial capital to the benefit of every ECP and their patients.
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