Article

CLINICAL: DRY EYE

MAKE THE CONNECTION

A look at the diseases and medications that cause dry eye

In Olivia Newtown-John’s “Physical,” the singer croons, “Let me hear your body talk.” This line fits well with our role as optometrists. After all, we can often evaluate the body’s health through the eye, enabling us to play a role in diagnosing conditions, such as diabetes, hypertension and, for the purpose of this month’s column, auto-immune diseases by way of the presence of dry eye disease (DED).

Here’s a look at the autoimmune diseases that cause DED, how to differentiate them from one another and how to manage them.

ACNE ROSACEA

This appears as facial acne, skin flushing or redness and dry, red eyes. Ocular rosacea typically involves one or more of the following clinical signs: interpalpebral conjunctival hyperemia, lid margin erythema, telangiectasias of the conjunctiva and redness. Further, blepharitis, chalazia, conjunctivitis, meibomian gland dysfunction, iritis and superficial punctate keratitis may occur as complications of the condition. Note: Diagnosing ocular rosacea can be tough because ocular changes can appear non-existent when accompanied by acne rosacea or facial dermatosis.

ATOPIC DERMATITIS

Also known as eczema, this condition can appear anywhere on the body, but often shows up as itchy, red, dry, swollen and sore skin patches on the face, behind the ears, the elbows’ insides, hands and feet and bottom. Further, bumps or hives can be present as well as an additional fold of skin under one’s eyes.

GRAPH VS. HOST DISEASE

In addition to keratoconjunctivitis sicca, the most common clinical sign, according to the literature, other signs include scleroderma-like eyelid changes, entropion, lagophthalmos, madarosis, poliosis, vitiligo, corneal ulcers, filamentary keratitis, superficial punctate keratitis, peripheral corneal melting (can lead to perforation), anterior or posterior scleritis, mononuclear cell infiltration of the lacrimal glands and, in severe cases of DED, conjunctival scarring, keratinization and cicatrization of the conjunctiva.

Scleroderma-like eyelid changes appear in patients who have graft vs. host disease.
Photo courtesy of Dr. Hsauser

GRAVES’ OPHTHALMOPATHY

Stemming from hypothyroidism, this auto-immune disease presents as chemosis, exophthalmos (causing DED and irritation, if lids cannot close), scleral injection and periorbital edema.

LUPUS ERYTHEMATOSUS

Along with keratoconjunctivitis sicca, the condition’s most common ocular manifestation, according to the literature, the other clinical signs are adnexa and eye lid abnormalities, choroidopathy, iridocyclitis, optic neuropathy, retinal vasculitis and vaso-occlusive disorder. In addition, Sjögren’s syndrome is known to accompany this auto-immune disease.

RHEUMATOID ARTHRITIS

Following in the footsteps of graph vs. host disease and Lupus erythematosus, this auto-immune disease’s most prevalent ocular manifestation is keratoconjunctivitis sicca as well. Also, similar to Lupus erythematosus, Sjögren’s syndrome is associated with this condition. Its other ocular signs are corneal changes, episcleritis, scleritis and retinal vasculitus.

MANAGEMENT

The patients with the aforementioned diseases tend to have more of an aqueous-deficient vs. an evaporative DED. In fact, over half of newly presenting DED cases to a tertiary center were secondary to a known (48%) or undiagnosed (5%) inflammatory disease, primary thyroid disorder, Sjögren syndrome or rheumatoid arthritis, reports the Tear Film and Ocular Surface Society (TFOS) Dry Eye Workshop (DEWS) II. Sjögren syndrome is considered a sub-classification of DED, but requires specific diagnostic differentiation from other forms of DED to facilitate appropriate interdisciplinary treatment and allow for the monitoring of potentially life-threatening complications, such as lymphoma. Unfortunately the average time to diagnose primary Sjögren syndrome from symptom onset is 6.5 years, despite being an independent risk factor for non-Hodgkin lymphoma and the most highly associated risk factor among all rheumatic diseases for malignancy, reveals the TFOS DEWS II Report.

Refrain from prescribing aqueous-deficient DED treatment without regarding systemic conditions. Interprofessional communication helps (a) the patient unaware of her disease acquire a definitive diagnosis (refer the unaware patient back to her internist) and (b) provides consultation with the diagnosed patient’s primary care doctor or specialist.

Finally, I would be remiss if I didn’t mention the systemic drugs that cause DED. They are: anticholinergics, antidepressants, antihistamines, anxiolytics, beta-blockers, botulin toxin injections, contraceptives, diuretics, isotretinoin and multivitamins. When patients develop DED from these drugs, discuss with their other care givers the possibility of decreasing or switching the drugs, and prescribe treatment, which is based on the condition’s severity. You’ve heard your patients’ bodies talk, now intervene. OM