Why So Dry?
Why So Dry?
To treat dry eye effectively, we must first understand the many factors that can cause or aggravate the condition.
Katherine Mastrota, O.D., M.S., F.A.A.O. New York, N.Y.
I must confess, along with Drs. Bloomenstein and Nichols, I start my day not only with a cup, but a with a pot of coffee — freshly ground "Park Slope Blend" beans brewed for exactly four minutes and pressed in a Bodum pot.
My colleagues and I are not alone in our coffee rituals. The National Coffee Associations' 2009 National Coffee Drinking Trends (NCDT) market-research survey estimates 54% of the adult population partakes in coffee consumption: The average American coffee drinker consumes three- to four cups a day. Caffeine, as found in coffee, colas or in popular "energy drinks," stimulates the central nervous system in humans, temporarily warding off drowsiness and restoring alertness. Interestingly, a recent study suggests that caffeine ingestion also increases intraocular pressure in patients who have glaucoma or ocular hypertension.1 Further, caffeine has diuretic properties when administered in sufficient doses to individuals who don't have a tolerance for it.2
Although a study suggests that caffeine intake can protect an individual from dry eye, most agree that chemicals or medications, including alcohol, that have a diuretic effect will contribute negatively to the balance of the pre-ocular tear film.3 In fact, nocturia (the need to get up during the night to urinate) is associated with a significant increase in the occurrence of dry eyes among the elderly.4
Caffeine is presumed to be added to the long list of medications that are associated with dry eye. Of course, such medications aren't the only culprits. Dry eye is a multifactorial disease that also presents with a wide range of symptoms. To treat it effectively, we first must understand the many factors that can induce or aggravate dry eye and dry eye symptoms.
I often recount the case of a nurse who took oxybutynin to manage her urinary incontinence. Her conjunctiva stained so brilliantly and completely with lissamine green that she rivaled the Grinch in her caliber of viridity.
Your patients' medications are an integral player in the multifactorial disease that is dry eye. Antihistamines, antihypertensives, anticholinergics, antiarrhythmics, diuretics, hormone replacement therapy and oral contraceptives are some of the medications that can become the bane of ocular comfort and clear vision.
Although dry eye is more common with advancing age, remember that medications associated with dry eye are prescribed across all age groups broadening the scope of patients we consider dry eye suspects.
Along with systemic medication, systemic disease puts patients at risk for dry eye or more aptly, ocular surface disease (OSD). Autoimmune diseases, such as thyroid disease, rheumatoid arthritis, Sjogren's syndrome and systemic lupus erythematosus, place the ocular surface at risk for malfunction.
In the neurologic disease category, the ocular surface of Parkinson's disease patients is challenged by the triad of autonomic and motor dysfunction combined with the ill-effects of the anti-cholinergic medications prescribed to ameliorate the other symptoms of the disease. These patients suffer from reduced tear production and a reduced blink rate. The combined detrimental effects of reduced tear volume and reduced inter-blink interval are compounded by the drying effects of medication in these patients.
Diabetic patients are also at risk for dry eye as a concomitant pathology of the disease. The connection between the two ailments is confirmed in numerous studies:
► More than half of patients who have diabetes experience dry eye symptoms, such as burning and foreign body sensation, and suffer from ocular dryness.5,6
► A Brazil study reveals that dry eye signs and symptoms in diabetic patients include transient visual acuity due to tear film reduction, lower goblet cell density, reduced corneal sensitivity and reduced lipid layer.7
► Diabetes is possibly linked to blepharitis.8
► A study of comorbidities of dry eye disease shows that compared with non-diabetic patients, patients who have dry eye were more likely to have diabetes.9 In another study, patients who self-reported diabetes had higher levels of dryness than those who didn't have diabetes.10
Corneal sensitivity, smoking and environmental factors
Reduced corneal sensitivity also becomes a significant source of OSD in patients other than diabetics. Contact lens wearers, post-surgical patients (particularly refractive surgery patients), pregnant patients, and patients who have been afflicted with herpetic corneal disease can also suffer a loss in corneal sensitivity.11
Additionally, smokers have the dual risk of reduced corneal sensitivity and reduced quality and quantity of their tear films as demonstrated by a study of non, light and heavy smokers.12 An early study corroborates the harmful effects of cigarette smoking, revealing chronic irritative effects of cigarette smoking may lead to defects in ocular surface defense.13
Certainly cigarette smoke can be bundled into the environmental conditions that can challenge the ocular surface. September 2010's issue of Toxicology Letters reviews the salient environmental, occupational and personal risk factors that alter the precorneal tear film. Irritants to the ocular surface/tear film included aggressive odors and aerosols, pollutants, combustion products, low humidity, high temperatures and drafts.14 Occupational environments/demands requiring visual tasking, such as computer work, can lead to computer vision syndrome (CVS). CVS, in part, is associated with ambient lighting, glare, screen display quality, increased ocular surface exposure and a decreased blink rate during long hours of focusing on computer screens.15
The gender connection
Apart from the above-mentioned challenges in the work/world environment for dry eye, the complex goal of simply "looking good" in and of itself, can become an overlooked contributor to OSD. It has been established that the female gender, primarily due to declining hormonal support of the tear film with advancing age, is more at risk for the development of OSD signs and symptoms.
Generally, but not exclusively, it is this same gender that goes to great lengths to enhance their appearance, particularly the eye and adnexal area, with a multitude of cosmetics, creams, gels, abrasives, cleaners, solvents, tattoos, glues, onabotulinumtoxin A (Botox, Allergan) injections and cosmetic surgery. Allergy to or toxicity from eye products, perfumes, particles of makeup pigments and minerals or oils that make their way to the tear film can be a source of disruption to the tear film and/or the ocular surface and its surroundings.16 Still popular, micropigmentation of the eyelid margin (tattooed permanent eyeliner) may be associated with extensive meibomian gland dropout, leading to tear film instability from lipid layer abnormalities.17
Botox has proven effective in smoothing the appearance of lateral canthal rhytids (crow's feet) and glabellar rhytids (brow furrows or "11 lines"). Although unusual, complications of periocular Botox injection include temporary decreased tear production and paralytic lagophthalmos.18,19
Lagophthalmos is but one of the causes of inadequate mechanical spread of the tears, or ocular surface exposure problems. The inability to blink and effectively close the eyes leads to corneal exposure and excessive evaporation of the tear film. A variety of causes of lagophthalmos exist, grouped as proptosis/eye exposure etiologies and palpebral insufficiency etiologies.20 The main cause of lagophthalmos is facial nerve paralysis. It can also occur after trauma or cosmetic surgery, or, oft overlooked, during sleep (nocturnal lagophthalmos). Paralytic lagophthalmos is most often caused by a Bell's palsy, but can be due to infection, tumors or other conditions.21 Each lagophthalmos patient's blink should be examined for rate, excursion and completeness; any gap or drift in eyelid closure will set the stage for evaporative surface problems.
The ocular surface is dependent on the physiological and anatomical integrity of the eyelids and associated adnexal structures. The lid malposition in entropion and ectropion each pose a risk to the ocular surface.22 Entropion can cause irritative symptoms from the lid margin turning in to rub against the ocular surface, and ectropion allows for exposure, desiccation, inflammation and epidermalization of the inferior tarsal conjunctiva.23,24 Floppy eyelid syndrome can contribute to ocular surface damage.25 Other lid-related considerations in dry eye syndrome are the potential sequela of blepharoplasty, which includes corneal exposure, scleral show and lid malposition.26
Conjunctivochalasis, or redundant conjunctiva, can cause a spectrum of patient symptoms, ranging from aggravation of a dry eye at the mild stage, to disturbance of tear outflow at the moderate stage, and exposure problems at the severe stage.27 Additionally, inflammatory mediators in the tear film are over-expressed in conjunctivochalasis, suggesting a relationship between this disorder and molecular inflammation.28
New finding on blepharitis
Blepharitis must also be considered as a contributing factor to dry eye. The 2009 Executive Summary of the ICare in America Survey (www.icareinamericasurvey.com) suggests that as many as 28 million U.S. adults are affected by symptoms associated with blepharitis. Blepharitis is generally categorized as anterior blepharitis or meibomian gland dysfunction (MGD)/posterior blepharitis, although these forms rarely present independently. Generally, anterior and posterior blepharitis are comorbidities that interact to perpetuate the overall disease state of the eyelid.
Anterior blepharitis, including angular blepharitis, can result from an overpopulation of bacterial lid commensals or Demodex (a ubiquitous mite) and from seborrheic changes of the lid margin. By causing inflammation, irritation, and/or hyperkeratinization of the lid margin, bacterial exotoxins and Demodex contribute to obstruction of the meibomian gland orifices. Chronic inflammation from meibum stasis and keratinization of the meibomian gland's ducts and orifices ultimately leads to obstructive MGD, a loss of gland clusters and atrophic nonfunctional glands.
In non-obstructive MGD — sometimes referred to as seborrheic MGD — copious amounts of abnormal meibum are delivered to the tear film. Additionally, bacterial lipases, acting upon meibum, create irritating free fatty acids that are released into the tear film. MGD can occur as a primary disorder or secondary to acne rosacea.
Less documented associations
Finally, less-documented associations with dry eye/MGD include dyslipidemia (suggesting the role of diet and dry eye), pseudoexfoliation syndrome (this seems to alter basic features of goblet cell morphology), pterygium, glaucoma, radiation complications and ciguatera fish poisoning.29-33 Ciguatera fish poisoning is one of a variety of non-bacterial forms of seafood (from tropical reefs) poisoning.34 The clinical picture of ciguatera fish poisoning is characterized by a variety of gastrointestinal, neurologic and cardiovascular symptoms.35 It can also include dry eye.
Indeed, dry eye is a dynamic, multifactorial disease. OM
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Dr. Mastrota is secretary of the newly formed Ocular Surface Society of Optometry (OSSO). E-mail her at firstname.lastname@example.org, or send comments to email@example.com.|
Optometric Management, Issue: November 2010