Keeping dry eye in the differential diagnosis and management plan when suspecting allergic conjunctivitis

Allergic conjunctivitis (AC) and dry eye disease (DED) are 2 of the most prevalent ocular surface disorders encountered in clinical practice, with affected patients seeking relief from bothersome ocular signs and symptoms that negatively impact visual function and quality of life. With the onset of spring and throughout summer and fall, optometrists may see an increasing number of patients presenting with complaints of eye irritation, redness, watering eyes, itchiness, and visual disturbances associated with AC. Appropriate care, however, hinges on an accurate diagnosis and requires recognition that AC shares signs and symptoms with other ocular surface disorders, particularly DED, and that AC and DED often coexist and can aggravate each other through bidirectional mechanisms.^1,2

Understanding AC/DED comorbidity

The epidemiology of both AC and DED has been changing, with increases in prevalence overall and in various age groups. Studies show that AC is persisting or even first presenting later in adulthood and that DED is being increasingly diagnosed in school-age children.^3-7 In addition, features of AC and treatments used to manage it can cause or worsen DED. Inflammation and tear film instability are features of AC and are also findings in DED, and they are core factors in its pathogenesis. In addition, oral and topical antihistamines used by patients with AC affect DED by reducing tear production. Furthermore, preservatives in some topical ophthalmic medications may also worsen ocular surface disease and further aggravate DED. Conversely, AC is exacerbated when DED is present because the disrupted tear film and cornea compromise the normal barrier to the inciting environmental allergens.

Diagnostic strategy

As always, obtaining a good history and performing a directed clinical examination are the keys to making an accurate diagnosis that guides effective management. Fortunately, every optometrist has the essential tools needed to diagnose both AC and DED.

Patient-reported signs and symptoms alone cannot reliably distinguish AC from DED, as the 2 conditions have many overlapping features. Nevertheless, itching is the hallmark symptom of AC, and when patients complain of itch, particularly if it is intense and not relieved or worsens with eye rubbing, I investigate potential triggers for AC. Recognizing that AC is often seasonal but may also be perennial, I ask about exposure to tree or grass pollen, mold spores, animal dander, or dust mites. Other clinical findings consistent with AC include marked bilateral conjunctival redness and papillae, tearing, stringy discharge, and chemosis, as well as concurrent systemic allergic symptoms, such as sneezing and nasal congestion.

My evaluation for DED begins by considering demographics, followed by a careful patient history and a review of symptoms. History aims to identify triggers for DED that both support its diagnosis and can offer modifiable targets for management. Common triggers include prolonged digital screen use, occupational demands, environmental factors (eg, exposure to ceiling fans or dry air), presence of certain systemic diseases, contact lens wear, use of various topical and systemic medications, and a history of ocular surgery.

Common symptoms of DED include burning, fluctuating vision, foreign body sensation, scratchiness, and sandiness. I do not routinely use formal questionnaires in my practice for eliciting symptoms. However, I believe that clinicians who are beginning to manage DED can find it helpful to use validated symptom questionnaires, such as the Ocular Surface Disease Index-6.

Although demographics, clinical history, and symptoms help identify patients at risk for DED, at least one positive objective clinical sign must be present to confirm the diagnosis. In most cases, only a slit lamp and a fluorescein stripare required to identify key clinical signs of DED, including mild conjunctival redness, decreased tear break-up time (TBUT), and ocular surface staining. To assure reliable results, I instill fluorescein and wait at least 1 minute before measuring TBUT and assessing corneal staining. In addition to evaluating the tear film, cornea, and conjunctiva at the slit lamp, I assess blink rate and completeness, eyelid malposition, the lashes, lid margins, and meibomian gland expression.

I also evaluate corneal sensitivity to identify neurosensory abnormalities that contribute to DED. A Schirmer test without an anesthetic is often performed to help guide the diagnosis toward aqueous tear deficiency. When there is suspicion of a systemic disease underlying aqueous tear deficiency, I may order serologic testing or refer the patient to rheumatology to evaluate for conditions such as Sjögren syndrome.

If TBUT is decreased or fluorescein staining is present, further staining may not always be necessary; however, lissamine green or rose bengal staining may be considered when additional information about the ocular surface is needed. Additional diagnostic tools for DED, including meibography, matrix metalloproteinase-9 testing, noninvasive tear breakup time, tear osmolarity, and other advanced ocular surface assessments, can enhance the diagnostic evaluation when available. Although these technologies can provide valuable information, a careful history, symptom assessment, and slit-lamp examination remain the foundation of diagnosis.

A practical guide to managing DED

Management for both AC and DED includes identifying and addressing triggers and contributing factors. Artificial tears can be recommended for both conditions for their lubricating effects on the ocular surface and their ability to help clear allergens. When AC is present, a dual-action topical medication providing antihistaminic activity and mast cell stabilization will provide both immediate and ongoing relief. Preservative-free artificial tears and topical medications are preferred when possible, and advising patients to refrigerate their eye drops may enhance treatment comfort and symptom relief.

Then, whether the diagnostic evaluation identifies DED alone or coexisting with AC, effective management of DED is important because DED can be a chronic, progressive disease. Inflammation control is essential in the management of DED to break the self-perpetuating pathophysiologic cycle that sustains the disease and drives its progression.⁸ When AC and DED coexist, management becomes more challenging because AC destabilizes the tear film, while DED amplifies allergic inflammation. Therefore, a treatment that addresses inflammation and increases tear production/tear film stability can have particular benefit in cases of comorbid AC/DED.

Multiple available modalities are used for controlling inflammation in patients with DED. A short course of a topical corticosteroid can be considered for rapid control of more severe DED-related inflammation, especially in individuals with a concomitant flare of AC. Among available corticosteroids, loteprednol is a good choice because of its low potential to increase intraocular pressure.⁹

A topical nonsteroidal immunomodulatory agent, however, should be used for ongoing management of inflammation in DED, and options include various cyclosporine formulations and lifitegrast (Xiidra; Table 1). While all have been shown to be safe and effective, my preference is for cyclosporine ophthalmic solution, 0.09% (Cequa).

Cequa is an aqueous, clear, preservative-free ophthalmic formulation that is distinguished from other cyclosporine products by its use of proprietary nanomicellar technology that improves cyclosporine physicochemical stability and its bioavailability at target sites.^10,11 The nanomicellar system encapsulates cyclosporine inside hydrophobic cores, each surrounded by a hydrophilic shell that facilitates cyclosporine penetration through the tear film’s aqueous layer and its delivery to the cornea and conjunctiva.

Clinical trials show Cequa increases natural tear production and improves key signs and symptoms of DED, with statistically significant improvements in corneal higher order aberrations, Standard Patient Evaluation of Eye Dryness score, conjunctival hyperemia, TBUT, mean corneal staining score, and the percentage of patients with grade 0-1 corneal staining achieved as early as 7 days after treatment initiation (Table).^12-16Importantly, Cequa was also proven to be safe and well tolerated, which is important for achieving early treatment adherence and long-term persistence. In clinical trials, 95% of patients using Cequa experienced no worse than mild instillation pain.^13,16 An induction course or concomitant use of a topical corticosteroid may be considered to minimize stinging and burning and/or hasten inflammation control when starting other topical immunomodulatory agents.^17,18 I have found that a combined approach is often not necessary when prescribing Cequa because of its comfort and early onset of benefit.

Conclusion

As primary eye care providers, optometrists are uniquely positioned to diagnose and effectively manage AC and DED. Differential diagnosis should not overlook the changing epidemiology of both conditions and the fact that these 2 common ocular surface disorders are not mutually exclusive. Guided by accurate diagnosis, appropriate management of AC and DED will improve patient comfort, visual stability, and long-term ocular surface health as well as increase patient satisfaction with care. Use of a topical immunomodulator for inflammation control plays an integral role in the long-term management of DED.

Financial disclosure 

Rodriguez serves as a paid speaker for Sun Pharma and has received honoraria for educational presentations.

References:

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