The tear film is made up of an outer oily component, a middle watery layer, and a deep mucous layer (Fig. 152). A decrease in the oily, mucous, or watery tear could cause symptoms such as dryness, stinging, grittiness, sore eyes, blurry vision, and tearing from irritations. Dry eye disease (DED) is reported to affect 5% of the general population, 9% of menopausal women, and 34% of the elderly. With most external eye infections, the tear film is highly infectious. In AIDS, only bloody tears are so far considered infectious. In any case, wash your hands between patient examinations.

The oily, superficial layer is secreted by the meibomian glands in the upper and lower lids (Fig. 153) and prevents desiccation and lubricates the eyelids as they pass over the globe. Dysfunction of these glands occurs in almost half of Americans and often manifests with a toothpaste‐like discharge (Fig. 154) with occasional infection, referred to as posterior blepharitis. It is the most common reason for dry eye disease. In my practice, not a day goes by without seeing patients with blepharitis.

Watery tears provide anti‐infective defenses, wash away debris, and smooth surface irregularities. Seventy percent is tonically secreted by the accessory lacrimal glands of Krause and Wolfring in the conjunctiva (Fig. 149). The lacrimal glands’ (Fig. 149) contribution to watery tears is mostly a reflex response to emotion and ocular irritations. The corneal reflex arc has the trigeminal nerve (CN V) as its afferent pathway and the facial nerve as the efferent branch. Damage to the sensory CN V nerves can cause dry eye and other ocular surface changes (neurotrophic keratitis). It may result from LASIK and PRK surgery, diabetes, and herpes simplex or zoster keratitis. Damage to the efferent CN VII, as in Bell’s palsy, causes desiccation due to incomplete blink reflex and inability to close the eye completely, especially at night. Corneal sensitivity (CN V) may be tested by touching a sterile cotton tip applicator to each eye and comparing blink reflexes. A wide variety of medications reduce watery tear production. They include diuretics and beta‐blockers used to treat blood pressure, tranquilizers, antidepressants, antihistamines, anti‐Parkinson disease drugs, bladder anti‐spasmotics, and gastroprotective and gastric motility agents. A decrease in the watery or mucous component could be due to aging or inflammation associated with systemic autoimmune diseases such as Sjögren’s disease (dry eye, dry mouth, and arthritis). The resulting inflammatory ocular surface epithelial disease is called keratoconjunctivitis sicca. Fifty percent of Sjögren’s patients have rheumatoid arthritis or lupus, both of which may also cause dry eye independent of Sjögren’s. All three of these autoimmune diseases are often treated with hydroxychloroquine.

Mucous is secreted by goblet cells which account for 5–20% of the conjunctival cells. The mucous traps exfoliated cells, bacteria, and other foreign bodies and washes them into the nose. Goblet cells decrease after menopause; or from any condition that damages the conjunctiva, such as Stevens–Johnson syndrome (Fig. 10), ocular pemphigoid (Fig. 303 and 304), trachoma (Fig. 308), alkali burns (Figs 254 and 255), or vitamin A deficiency (Fig. 155). The latter could cause dysfunction of the conjunctival epithelial cells (Fig. 240) reducing both tears and mucous. Vitamin A deficiency could be due to poor diet or malabsorption which is surging due to the popularity of gastric bypass surgery used to treat obesity. Loss of vision from vitamin A deficiency may result from desiccation of the cornea due to dryness or from decreased function of the rod receptors in the retina, which requires this vitamin to produce the visual pigment rhodopsin. Paradoxically, excess vitamin A is toxic and can cause elevated intracranial pressure with loss of vision (Figs 475–478).

Dry eye may cause intermittent haziness of the cornea resulting in transient blurring of vision. This blur must be distinguished from the transient ischemic attacks (TIAs—ministrokes) especially in seniors who may be predisposed to both conditions.

The diagnosis of DED may be confirmed by seeing punctate haziness of corneal epithelial cells (Figs 156, 248, and 249) and fluorescein staining of underlying stroma when illuminated by cobalt blue light. The integrity of the tear film layer is estimated by testing tear breakup time (TBUT) (Fig. 156). The Schirmer test measures tears on the surface of the eye. A drop of anesthetic is instilled, and a strip of folded filter paper is placed on the surface of the conjunctiva (Fig. 157). Less than 10 mm of moist paper in 5 minutes is presumptive of a dry eye. Patients with dry eye have an abnormal Schirmer test 21% of the time, corneal staining with fluorescein 50% of the time, conjunctival staining with lissamine green, and an abnormal TBUT in 60% of cases. Lissamine green specifically stains devitalized conjunctival epithelium (Fig. 158).

Dry eye is treated in the daytime with artificial tears and at night with ointments. There are many on the market and vary mostly by their viscosity, cost, and whether they have preservatives. Viscous agents, especially ointments, maximize duration of action but interfere with vision and are therefore preferred during sleep. Symptoms of dry eye are more common in eyes that do not close at night, as with lagophthalmos (Fig. 251); Bell’s palsy (Fig. 111); Grave’s disease (Figs 1 and 177); and ectropion (Fig. 174). It is further aggravated by those with sleep apnea due to chronic obstructive lung disease using a continuous positive airway pressure (CPAP) that might blow on their eye. Unfortunately, the effect of lubricating drops may last less than an hour, often leading to excessive use. Benzalkonium chloride (BAK)—the most common preservative in most eye drops—could cause surface toxicity, especially in glaucoma patients using other drops. Preservative‐free (PF) drops in individual ampules are then indicated. If annoying symptoms persist, the puncta may be closed with absorbable or permanent punctal plugs (Figs 159 and 160). If temporary plugs are shown to improve chronic symptoms, the puncta may be permanently closed with a cautery. Room humidifiers may be tried, and oral flaxseed oil (1000 mg BID) may increase meibomian gland secretions. Computer use and reading suppress blinking, and desiccation of surface tears aggravates DED. Intentional blinking during computer use should be encouraged. Restasis (cyclosporine ophthalmic emulsion) or Xiidra (lifitegrast) eye drops reduce inflammation of tear producing cells and either can be used twice a day to increase tear production by suppressing lymphocyte T‐cell‐induced inflammation. Low dose steroid eye drops, such as fluorometholone (FML, 0.19%) are infrequently added. DED may cause corneal changes, resulting in fluctuating vision. It is critical to document its presence before corneal refractive or cataract surgery, which could aggravate the condition and thus cause patient disgruntlement. The intermittent blurring should not be confused with circulatory disturbances in older patients.

Tearing (epiphora)

Tearing is a very common complaint and is often minor enough so as not to require the workup and treatment discussed below.

There are two causes of tearing (epiphora):

1. increased tear production due to emotion and eye irritation; paradoxically, dry eye stimulates reflex tearing;
   
2. tears that are produced normally but which cannot flow properly into the nose.