Miscellaneous Ocular Disorders

Almost any disorder that affects the eyes can occur in the elderly; however, some (eg, acute diplopia, diabetic ophthalmoplegia, intracranial tumors, myasthenia gravis) are more common among the elderly.

Binocular Diplopia

The fusion of images from each eye into a single image requires intact, bilaterally coordinated, extraocular movements. Diplopia (double vision) may be monocular, which occurs when only one eye is open, or binocular, which disappears when either eye is closed. Causes of monocular diplopia include cataracts, refractive error (most often astigmatism), corneal scarring, a dislocated lens, keratoconus, and retinal detachment. Binocular diplopia almost always suggests disconjugate alignment of the eyes. Causes of intermittent binocular diplopia include myasthenia gravis and latent eye deviation (phoria) that becomes uncompensated. Causes of constant binocular diplopia include palsy of the 3rd, 4th, or 6th cranial nerve (eg, due to diabetic ophthalmoplegia); orbital disorders (eg, due to thyroid disorders, tumor, or pseudotumor); and CNS disorders (eg, vertebrobasilar insufficiency, internuclear ophthalmoplegia).

Third cranial nerve palsy may result from an intracranial aneurysm, trauma, diabetic neuropathy, or an intracranial space-occupying mass. Fourth cranial nerve palsy is caused by a hemorrhage in the roof of the midbrain (usually due to arteriosclerosis) or closed head trauma. Sixth cranial nerve palsy is caused by meningitis, skull fracture, and increased intracranial pressure. If patients have any combination of palsies with a normal pupillary response to light and a history of fatigue that waxes and wanes during the day, myasthenia gravis should be suspected; the diagnosis can be confirmed with an edrophonium chloride test.

History should determine whether diplopia affects one or both eyes, whether diplopia is intermittent or constant, and whether the images are separated vertically, horizontally, or both. Diplopia must be distinguished from blurriness; patients are often unaware of the onset of diplopia and may mistake it for blurred vision or difficulty seeing on one side.

Vision in each eye should be checked with the other eye covered to determine whether the diplopia is monocular or binocular. The presence of eyelid droop, pupillary abnormalities, or disconjugate eye movement during extraocular muscle testing should be noted.

Ocular motility is checked by keeping the patient's head steady and having the patient track the examiner's finger, which is moved to the extreme gaze--right, left, upward, downward, diagonally to either side, and inward toward the patient's nose. However, this examination may miss paresis of ocular motility that is mild but sufficient to cause diplopia. If diplopia occurs in one direction of gaze, the eye that produces each image can be determined by repeating the examination with a red glass placed over one of the patient's eyes and asking the patient to look at a white light (eg, penlight). The image that is most peripheral originates in the paretic eye; if the most peripheral image is red, the red glass is covering the paretic eye. If a red glass is not available, the paretic eye can sometimes be identified by having the patient alternately close each eye; the eye that eliminates the most peripheral image when closed is paretic. If the paretic eye is identified but whether the eye is esotropic (crossed in) or exotropic (crossed out) is unclear, a red glass can be placed in front of the paretic eye. If the paretic eye is esotropic, the red light appears to the right of the white light. If the paretic eye is exotropic, the red light appears to the left of the white light.

Specific tests can be done to identify the affected muscle or muscles or cranial nerve or nerves. The Parks 3-step test compares eye alignment in different positions. The Hess screen and Lancaster red-green tests assess patient responses to dissimilar images produced by special glasses. The double Maddox rod test assesses the degree of rotation patients need to make the lines on striated lenses appear parallel.

Follow-up testing may include corneal topography to measure corneal shape and identify keratoconus; phorometry to assess ocular muscle balance and detect phoria, exophthalmometry to measure the degree of eyeball protrusion (exophthalmos); CT or MRI to detect orbital or CNS disorders; and blood testing for thyroid disorders and diabetes, which cause some cranial nerve palsies.

Treatment is management of the underlying disorder.

Dry Eyes

Dry eyes (keratoconjunctivitis sicca) is chronic, bilateral desiccation of the conjunctiva and cornea caused by an inadequate tear film. The cause is accelerated tear evaporation or inadequate tear volume. Symptoms include itching, burning, irritation, and photophobia. Diagnosis is clinical; the Schirmer test may be helpful. Treatment is with topical tear supplements and blockage of the punctal openings; sometimes oral tetracyclines, topical antibiotics, or both or topical cyclosporine is used.

Etiology

The cause is most commonly accelerated tear evaporation because of poor tear quality (called evaporative keratoconjunctivitis sicca) but may be inadequate tear volume (called aqueous tear-deficient keratoconjunctivitis sicca). Rarely, an insufficient blink rate causes exposure and drying.

Evaporative keratoconjunctivitis sicca is caused by loss of the tear film due to abnormally rapid evaporation from an inadequate oil layer on the surface of the aqueous layer of tears. Symptoms may result from abnormal oil quality (due to meibomian gland dysfunction) or from a degraded normal oil layer (due to seborrheic blepharitis). Patients frequently have acne rosacea.

Aqueous tear-deficient keratoconjunctivitis sicca is usually an isolated idiopathic disorder in postmenopausal women; it is caused by age-related changes in goblet cells, lacrimal glands, or meibomian glands. This disorder is also commonly part of Sjögren's syndrome. Less commonly, it is secondary to disorders that scar the lacrimal ducts (eg, cicatricial pemphigoid, Stevens-Johnson syndrome, trachoma). Other causes include damage to or malfunction of the lacrimal gland due to graft-vs-host disease, HIV infection (diffuse infiltrative lymphocytosis syndrome), local radiation therapy, or familial dysautonomia.

Symptoms and Signs

Patients report itching, burning, photophobia, and pressure behind the eye or a gritty, pulling, or foreign-body sensation. Other symptoms include a sharp, stabbing pain and eye strain or fatigue; vision may be blurred. Some patients note a flood of tears after severe irritation, and some have nocturnal lagophthalmos (inability to completely close the eye).

Typically, symptoms fluctuate in intensity. They may be intermittent, aggravated by prolonged visual efforts (eg, reading, working on the computer, driving, watching television) or by local dry, dusty, or smoky environments. Certain systemic drugs (eg, antihypertensives, oral contraceptives, isotretinoin, diuretics, sedatives, all anticholinergic drugs including antihistamines and many GI drugs) can aggravate symptoms. Symptoms lessen on cool, rainy, or foggy days or in other high-humidity environments (eg, the shower). Although keratoconjunctivitis sicca rarely decreases vision, irritation can be intense.

In both forms, the conjunctiva is hyperemic, and scattered, fine, punctate loss of corneal epithelium (superficial punctate keratitis), conjunctival epithelium, or both often occurs. When the disorder is severe, the affected areas, mainly between the eyelids (intrapalpebral or exposure zone), stain with fluorescein dye. Patients often blink at an accelerated rate because of irritation. In the evaporative form, abundant tears and foam may be present at the eyelid margin. In the aqueous tear-deficient form, the conjunctiva can appear dry and lusterless with redundant folds.

Very rarely, severe, advanced, chronic drying leads to substantial vision loss because the ocular surface is keratinized or corneal epithelium is lost. Scarring, vascularization, infections, ulceration, and perforation then result.

Diagnosis

Diagnosis is based on characteristic symptoms and clinical appearance.

Schirmer's test determines whether tear production is normal. After a topical anesthetic is used, a strip of filter paper is placed at the junction of the middle and lateral 1/3 of the lower eyelid. If tearing is < 10 mm after 5 min on 2 successive occasions, aqueous tear-deficient keratoconjunctivitis sicca is diagnosed. In patients with evaporative keratoconjunctivitis sicca, Schirmer's test results are usually normal.

The tear breakup test provides information on tear quality. A small volume of highly concentrated fluorescein is instilled; it makes the tear film visible under the cobalt blue light of the slit lamp. A blink reapplies a complete tear film. The patient then stares, and the length of time until the first dry spot develops is determined. An accelerated rate of intact tear film loss (< 10 sec) is characteristic of both forms keratoconjunctivitis sicca.

Once aqueous tear-deficient keratoconjunctivitis sicca is diagnosed, Sjögren's syndrome should be suspected, especially if xerostomia is also present. Diagnosis is by serologic tests and labial salivary gland biopsy. Patients with primary or secondary Sjögren's syndrome are at increased risk of several serious disorders, (eg, biliary cirrhosis, non-Hodgkin lymphoma). Therefore, appropriate evaluation and monitoring are essential.

Treatment

Frequent use of artificial tears can be effective for both forms. Viscous artificial tears, which coat the ocular surface longer, are particularly useful in the evaporative form. Artificial tear ointments applied before sleep benefit patients who have nocturnal lagophthalmos or irritation when they awake. Such treatment is adequate for most patients throughout their life. Using humidifiers and avoiding dry, drafty environments often helps. Also, patients should not smoke and should avoid secondary smoke. In recalcitrant cases, occlusion of the punctum may be indicated. In severe cases, a partial tarsorrhaphy can reduce tear loss through evaporation. Topical cyclosporine may be a useful adjunct for some patients.

Patients with the evaporative form often benefit from treatment of concomitant blepharitis and associated rosacea. Treatment includes warm compresses plus eyelid margin scrubs and intermittent topical eyelid antibiotic ointments (eg, bacitracin at bedtime), systemic doxycycline 50 to 100 mg po once/day or bid, or both.

Excessive Tearing

Excessive tearing (epiphora) may be caused by excess production or decreased drainage of tears.

Excess production most commonly results from the following:

• Irritation: Causes include a foreign body (including turned-in eyelashes), a corneal epithelial defect, and desiccation of the ocular surface (dry eyes) as a reflex reaction.
• Allergic rhinitis or conjunctivitis
• The common cold

Decreased drainage may result from the following:

• Acquired nasolacrimal duct obstruction: The most common cause is age-related stenosis of the nasolacrimal duct. Other causes include past nasal or facial bone fractures or sinus surgery (which disrupts the nasolacrimal duct), inflammatory disorders (eg, sarcoidosis, Wegener's granulomatosis), and dacryocystitis.
• Punctal and canalicular stenosis: Stenoses physically prevent tears from entering the canalicular system, causing the tears to drain down the cheek. Causes include chronic conjunctivitis (especially herpetic), certain types of chemotherapy, adverse reactions to eye drops (especially topical echothiophate iodide), and radiation therapy.
• Eyelid abnormalities: Ectropion and entropion can cause tearing; with both, the punctum inverts or everts with the eyelid and no longer drains tears normally. Irritation caused by entropion also stimulates excessive tear production. Ectropion or entropion may prevent the upper and lower eyelid margins from touching during a blink, exposing the cornea and causing tearing or a foreign-body sensation.

Symptoms and Signs

Symptoms that accompany tearing vary depending on the cause. They include itching (suggesting an allergic cause), nasal pain (suggesting dacryocystitis), and a foreign-body sensation (commonly described as a scratchy or gritty feeling). Foreign-body sensation may be constant (suggesting a corneal foreign body, corneal abrasion, corneal ulcer, or trichiasis) or intermittent (suggesting dry eyes). Other symptoms (eg, photophobia) suggest uveitis or keratitis.

Diagnosis

Diagnosis is usually obvious from the history and physical examination. The examiner should look for signs of underlying disorders, such as foreign bodies, sinus pain, canthal swelling or mass, and eyelid abnormalities.

If dacryocystitis is suspected, pressure is applied over the lacrimal sac; if reflux of mucoid material is observed, nasolacrimal duct obstruction is diagnosed.

Schirmer's test may be used to quantify tear production. Saline irrigation of the lacrimal drainage system with and without fluorescein dye (an adjunctive test done by an ophthalmologist) may be needed to diagnose specific causes of tearing. Reflux through the opposite punctum and canaliculus indicates fixed obstruction; reflux and nasal drainage indicate stenosis.

Imaging procedures (eg, scintigraphy, dacryocystography, CT, nasal endoscopy) are sometimes used to delineate abnormal anatomy when surgery is being considered.

Treatment

Treatment varies by cause. Foreign bodies should be removed, and allergies should be treated. Using artificial tears paradoxically leads to improvement when dry eyes or corneal epithelial defects are the cause.

For acquired nasolacrimal duct obstruction, irrigation of the nasolacrimal duct may be therapeutic when underlying disorders do not respond to treatment. As a last resort, dacryocystorhinostomy can be done to create a passage between the lacrimal sac and nasal cavity.

Ectropion and entropion typically require surgery. For punctal or canalicular stenosis, dilation is usually curative. If canalicular stenosis is severe or bothersome, surgical placement of a tube leading from the caruncle into the nasal cavity can be considered.

Dacryocystitis

Dacryocystitis is infection of the lacrimal sac, usually resulting from nasolacrimal duct obstruction.

Acute dacryocystitis manifests with pain, redness, and edema around the lacrimal sac. An abscess may form (see Figure 127-5). Chronic dacryocystitis usually manifests with chronic conjunctivitis and a mass under the medial canthal tendon.

For the acute form, initial treatment is warm compresses and oral antibiotics (cephalexin 500 mg po q 6 h) for mild cases or IV antibiotics (cefazolin 1 g q 6 h) for severe cases. Antibiotics can be changed based on culture results if the initial antibiotic is ineffective. An abscess can be drained.

Definitive treatment of resolved acute or chronic dacryocystitis is usually with surgery (eg, external or transnasal laser dacryocystorhinostomy). Chronic dacryocystitis must be treated before elective intraocular surgery.

Pinguecula and Pterygium

Pinguecula (see Figure 127-6) is an accumulation of degenerated collagen at the nasal and temporal junction of the sclera and cornea. Its significance is cosmetic; the tissue may be white or yellow. Pinguecula rarely requires removal; if excised, it tends to recur.

Pterygium (see Figure 127-6) is connective tissue that becomes vascularized and invades the cornea. If a pterygium continues to grow and reaches the center of the cornea, it can interfere with vision. Pterygia usually occur in people who spend a lot of time outdoors, especially in dusty, windy environments. At the first sign of central corneal involvement, pterygia should be surgically excised. Artificial tears every 4 h may help halt growth.

Foreign-body Sensation

Foreign-body sensation may be caused by dry eyes, entropion, poor health, latent eye muscle imbalance, excessive use of close vision, or chronic fatigue of the eye muscles due to lack of sleep. All of these conditions may lead to incomplete blinking of the eyelids and fewer blinks per minute, causing the eyeball to dry and a foreign-body sensation to occur. Counseling patients about these possibilities usually increases blinking, improving visual comfort and performance and relieving the foreign-body sensation. However, an actual foreign body must be ruled out.

Fuchs' Endothelial Dystrophy

Fuchs' endothelial dystrophy is degeneration of the endothelial cells lining the inner surface of the cornea.

Fuchs' endothelial dystrophy is very common; it affects more women than men. Transmission may be autosomal dominant or sporadic. Onset is after age 50.

The endothelium of the cornea degenerates, leading to accumulation of extracellular fluid in the cornea. Corneal edema results, and collagen and extracellular matrix are deposited in Descemet's membrane. Epithelial edema may develop, leading to microcystic edema and later to epithelial bullae, which may rupture and cause pain. Chronic edema may lead to subepithelial fibrosis.

Some patients do not develop symptoms, and most do not know they have this disorder until fluid has accumulated in the cornea, causing blurred vision. Symptoms are rare before age 50. They are worse when patients awaken because surface evaporation decreases while the eyelids are closed during sleep. Pain due to ruptured bullae may subside once subepithelial fibrosis occurs.

If this disorder is suspected, referral to an ophthalmologist for diagnosis and treatment is necessary.

Diagnosis is by slit-lamp examination. Specular microscopy and corneal pachymetry are useful in determining the relative safety of cataract or other intraocular surgery. Caution is required if the number of endothelial cells is decreased or corneal thickness is increased because corneal stromal edema, subepithelial fibrosis, and epithelial bullae (cornea decompensation) may develop after intraocular surgery.

Treatment is first aimed at reducing corneal edema and relieving pain. Using NaCl drops, ointment, and drugs to lower intraocular pressure may temporarily relieve the edema. Lubricating drops and a soft-bandage contact lens are useful in treating ruptured bullae. In advanced cases, a conjunctival flap may be considered, but corneal transplantation is required to restore vision. Surgery should be done before the entire cornea becomes edematous. Likelihood of corneal graft survival is good.

This topic was last updated May 2006.