Figure 4-1: Internal hordeolum, left upper eyelid, pointing on skin side. This should be opened by a horizontal skin incision. (Courtesy of A Rosenberg.)

Figure 4-2: Chalazion, right lower eyelid. (Courtesy of K Tabbara.)

Figure 4-3: Entropion. (Courtesy of M Quickert.)

Figure 4-4: Ectropion. (Courtesy of M Quickert.)

Figure 4-5: Epicanthus tarsalis.

Figure 4-6: Blepharochalasis.

Figure 4-7: Dermatochalasis of upper lids and herniation of orbital fat of lower lids. (Courtesy of M Quickert.)

Table 4-1: Beard's revised classification of ptosis.

Levator maldevelopment Simple With superior rectus weakness Other myogenic ptosis Blepharophimosis syndrome Chronic progressive external ophthalmoplegia Oculopharyngeal syndrome Progressive muscular dystrophy Myasthenia gravis Congenital fibrosis of the extraocular muscles Aponeurotic ptosis Senile ptosis Late-developing hereditary ptosis Stress or trauma to levator aponeurosis Following cataract surgery Following other local trauma Blepharochalasis Associated with pregnancy Associated with Graves' disease Neurogenic ptosis Ptosis caused by lesions of the oculomotor nerve Posttraumatic ophthalmoplegia Misdirected third nerve ptosis Marcus Gunn jaw-winking syndrome Horner's syndrome Ophthalmoplegic migraine Multiple sclerosis Mechanical ptosis Apparent ptosis Due to lack of posterior eyelid support Due to hypotropia Due to dermatochalasis

A. Levator Maldevelopment:

Ptosis from levator maldevelopment-formerly classified as true congenital ptosis-is the result of an isolated dystrophy of the levator muscle affecting both contraction and relaxation of the fibers. Ptosis is present in the primary position of gaze, and there is reduced movement of the lid in upgaze and impaired closure on downgaze. Lid lag on downgaze is an important clue to diagnosis of levator maldevelopment. Other ocular abnormalities such as strabismus are sometimes associated with this form of congenital ptosis. In 25% of cases, the superior rectus muscle shares the same dystrophic changes as the levator, resulting in weakness of upgaze. It is important to identify this finding. Successful surgical outcome in the presence of superior rectus weakness requires the resection of an additional length of levator.

The distinction between levator maldevelopment and other forms of ptosis is an important one that cannot always be made by the history. Neurologic and other myogenic ptosis may be present at birth. Application of the surgical principles intended for levator maldevelopment to these types of ptosis patients would result in a gross overcorrection.

B. Other Types of Myogenic Ptosis:

Blepharophimosis accounts for 5% of cases of congenital ptosis. Poor levator function and severe ptosis are accompanied by telecanthus, epicanthal folds, and cicatricial ectropion of the lower lids. The condition is familial.

Chronic progressive external ophthalmoplegia is a slowly progressive hereditary neuromuscular disease that begins in mid life. All extraocular muscles including the levator and the muscles of facial expression gradually become affected. Other neurodegenerative disorders may be present. In the form known as oculopharyngeal dystrophy, myopathy of the laryngeal muscles produces dysphagia. In Kearns-Sayre syndrome, ophthalmoplegia is associated with retinitis pigmentosa and heart block.

Ptosis and facial weakness may also be found in myotonic dystrophy. Other findings include cataract, pupillary abnormalities, frontal baldness, testicular atrophy, and diabetes.

Ptosis associated with the rare and sometimes familial congenital fibrosis of the extraocular muscles may be unilateral.

Ptosis and diplopia are often the initial manifestations of myasthenia gravis. The orbicularis oculi muscles are also frequently involved. Cogan's lid twitch is sometimes present-on rapid movements of the eyes from downgaze to the primary position, the upper lid twitches upward. Demonstration of lid fatigue, however, is more consistent. The diagnosis can be confirmed by intravenous administration of edrophonium, which temporarily reverses the weakness. Another useful test is the detection of circulating anti-acetylcholine receptor autoantibodies.

Medical management is usually effective initially, but ptosis surgery often becomes necessary. Thymectomy may be helpful in refractory cases. When lid closure and Bell's phenomenon have been impaired, difficult problems with exposure keratitis may complicate ptosis surgery.

C. Aponeurotic Ptosis:

A common form of myogenic ptosis occurs late in life and results from partial disinsertion or dehiscence of the levator aponeurosis from the tarsal plate. Typically, there are sufficient residual attachments to the tarsus to maintain full excursion of the lid with upgaze. Retention of the attachment of the retracted levator aponeurosis to the skin and orbicularis muscle creates an unusually high lid fold. Thinning of the lid may also occur, and on occasion the image of the iris may be seen through the skin of the upper lid. Trauma is often a precipitating cause of disinsertion of the levator. Ptosis following cataract surgery is thought to be due to this mechanism. A hereditary variant is known as "late-developing hereditary ptosis." The mechanism of ptosis associated with ocular surgery, blepharochalasis, pregnancy, and Graves' disease is usually damage to the aponeurosis.

D. Neurogenic Ptosis:

In Marcus Gunn syndrome (jaw-winking phenomenon), the eye opens when the mandible is opened or is deviated to the opposite side. The ptotic levator muscle is innervated by motor branches of the trigeminal nerve as well as the oculomotor nerve.

Partial or complete oculomotor palsy due to trauma is often complicated by aberrant regeneration, resulting in bizarre movements of the globe, eyelid, and pupil. Congenital oculomotor nerve paralysis, however, is not associated with aberrant regeneration. If the lid is completely closed, deprivational amblyopia will develop unless the ptosis is corrected. Visually immature children with oculomotor nerve paralysis, even after successful ptosis repair, are almost certain to develop strabismic amblyopia without vigorous and early treatment.

Paralysis of Müller's muscle is almost always associated with Horner's syndrome and is usually acquired. Rarely is there more than 2 mm of ptosis, and amblyopia is never a threat.

E. Mechanical Ptosis:

The upper lid may be prevented from opening completely because of the mass effect of a neoplasm or the tethering effect of scar formation. Excessive horizontal shortening of the upper lid is a common cause of mechanical ptosis. Another form is that seen following enucleation, when absence of support to the levator by the globe permits the lid to drop.

F. Apparent Ptosis:

Hypotropia may give the appearance of ptosis. When the eye looks down, the upper lid drops more than the lower lid. The narrowed palpebral fissure and the ptotic upper lid are much more apparent than the hypotropic globe. Occlusion of the opposite eye, however, reveals the true condition. In severe dermatochalasis, a fold of pretarsal orbicularis and skin may conceal the lid margin and give the appearance of blepharoptosis.

Treatment (  Figure 4-8)

With the exception of myasthenia gravis, all types of ptosis are treated surgically. In children, surgery can be performed when accurate evaluation can be obtained and the child is able to cooperate postoperatively. Astigmatism and myopia may be associated with childhood ptosis. Early surgery might be helpful in preventing anisometropic amblyopia, but this has not been proved. Deprivational amblyopia probably occurs only with complete ptosis, as in oculomotor nerve palsy.

Symmetry is the goal of surgery, and symmetry in all positions of gaze is possible only if levator function is unimpaired. In most cases, the best result that can be achieved is to balance the lids in the primary position. With unilateral ptosis, achievement of symmetry in other positions of gaze is proportionate to levator function.

Most ptosis operations involve resection of the le-vator aponeurosis or superior tarsal muscle (or both). The superior portion of the tarsus is often resected for additional elevation. Many approaches, from both skin and conjunctiva, are currently in use. In recent years, emphasis has been placed on the advantages of confining the operation to advancement and resection of the levator aponeurosis, especially in acquired ptosis.

Patients with little or no levator function require an alternative elevating source. Suspension of the lids to the brow allows the patient to elevate the lids with the natural movement of the frontalis muscle. Autogenous fascia lata is usually considered the best means of suspension.

COSMETIC MICROPIGMENTATION OF THE LIDS

Tattooing the lids of women is a controversial procedure whose purpose is to eliminate the need for applying eyeliner. The procedure is also occasionally used to simulate cilia following reconstruction of the lid margin. It is performed under local anesthesia using a power-driven handpiece to implant various pigments adjacent to the eyelashes or eyebrow. Because subcutaneous impregnation of certain mercury-based dyes can cause a local inflammatory reaction, these dyes have been abandoned. Carbon particle tattooing appears to be harmless, but the long-term consequences of dye impregnation at the lid margin are unknown.

As is true also of tattoos elsewhere on the body, the intensity and crispness of the image tends to fade with time. Complete removal of the pigmentation because of misplacement or change in fashion is difficult.

TUMORS OF THE EYELIDS

BENIGN LID TUMORS

Benign tumors of the lids are very common and increase in frequency with age. Most are readily distinguished clinically, and excision is done for cosmetic reasons. However, it is often impossible to recognize malignant lesions clinically, and biopsy should always be performed if there is any doubt about the diagnosis.

Nevus

Melanocytic nevi of the eyelids are common benign tumors with the same pathologic structure as nevi found elsewhere. They initially may be relatively unpigmented, enlarging and darkening during adolescence. Many never acquire visible pigment, and many resemble benign papillomas. Nevi rarely become malignant.

Nevi may be removed by shave excision if desired for cosmetic reasons.

Papillomas

Papillomas are the most common benign eyelid tumors. Two types occur: squamous cell papillomas and seborrheic keratoses (basal cell papillomas, senile verrucae). In both, fibrovascular cores permeate thickened (acanthotic and hyperkeratotic) surface epithelium, giving it a papillomatous appearance. Seborrheic keratoses occur in middle-aged and older individuals. They have a friable, verrucous surface and are often pigmented because melanin accumulates in the keratocytes.

Verruca Vulgaris

Another papillomatous, hyperkeratotic nodule that may occur on the skin of the face and eyelids is due to the wart virus, a deoxyribonucleic acid (DNA) virus in the papovavirus group.

Molluscum Contagiosum (Figure 4-9)

This tumor, due to a poxvirus, is a small, dome- shaped nodule, often umbilicated centrally. Lid margin lesions may be minute and partially hidden in the cilia but may produce conjunctivitis and even keratitis if the lesion sheds into the conjunctival space.

Cure can usually be achieved by curettement, cautery, or excision.

Keratoacanthoma

Keratoacanthomas are benign inflammatory tumors occurring in sun-exposed skin of adults. Occasionally they are associated with immunodeficiency, xeroderma pigmentosum, or the Muir-Torre syndrome. Many will undergo spontaneous involution, but excisional biopsy is often indicated for cosmetic reasons or to rule out the possibility of squamous cell carcinoma, which they may mimic both clinically and histologically.

Xanthelasma (Figure 4-10)

Xanthelasma is a common disorder that occurs on the anterior surface of the eyelid, usually bilaterally near the inner angle of the eye. The lesions appear as yellow, wrinkled patches on the skin and occur most commonly in elderly people. Xanthelasma represents lipid deposits in histiocytes in the dermis of the lid. They occur in patients with hereditary hyperlipidemia and in diabetics and other patients with secondary hyperlipidemia, but approximately two-thirds of patients with xanthelasma have normal serum lipids.

Treatment is indicated for cosmetic reasons. Lesions can be excised, cauterized, or treated with laser surgery. Recurrence following removal is not unusual.

Cysts

Cysts in the eyelids are common. Keratinous cysts, lined by epithelium and filled with cheesy-looking keratin and debris, are the result of obstruction of pilosebaceous structures (milia and pilar cysts), or congenital and traumatic subepithelial implantation of surface epithelium (epidermal inclusion cysts).

Dermoid cysts, with adnexal structures such as hair follicles and sebaceous glands in the walls and with hair as well as keratin in the lumen, are congenital but may not become apparent until later in life, when they increase in size or rupture, eliciting a granulomatous inflammatory response. Most are located near the orbital rim superotemporally, and many are associated with a defect in the bone that may communicate with the intracranial cavity.

Hidrocystomas (sudoriferous cysts) arise from the sweat ducts and are filled with a watery material.

Hemangioma(Figure 4-11)

The most common congenital vascular tumor of the eyelids is the capillary hemangioma (strawberry nevus) composed of proliferating capillaries and endothelial cells. They arise at or shortly after birth, often grow rapidly, and usually involute spontaneously by age 7 years. If superficial, they may be bright red (strawberry nevus); deeper lesions may be bluish or violet. Secondary anisometropia, refractive amblyopia, and strabismus are common and must be appropriately treated. Treatment of the tumor is rarely indicated unless it blocks the pupil. If it does, intralesional injection of steroids may produce rapid resolution; if this fails, partial surgical excision is indicated.

Capillary hemangiomas should be differentiated from the much rarer nevus flammeus (port wine stain), which is more purple in hue than the bright red of capillary hemangiomas. The nevus flammeus is composed of dilated, cavernous vascular channels. It is always present at birth, does not grow or regress as does a capillary hemangioma, and is often associated with Sturge-Weber syndrome. The cosmetic defect can be treated with laser surgery.

A third type of angioma is the cavernous hemangioma, composed of large, endothelium-lined vascular channels with smooth muscle in their walls. They are developmental rather than congenital and tend to arise after the first decade. Unlike capillary hemangiomas, they do not usually regress.

PRIMARY MALIGNANT TUMORS OF THE LIDS

Carcinoma (Figures 4-12 and 4-13)

Basal cell and squamous cell carcinomas of the lids are the most common malignant ocular tumors. These tumors occur most frequently in fair-complexioned individuals who have had chronic exposure to the sun. Ninety-five percent of lid carcinomas are of the basal cell type. The remaining 5% consist of squamous cell carcinomas, meibomian gland carcinomas, and other rare tumors such as Merkel cell carcinomas and carcinomas of the sweat glands.

Treatment of all these carcinomas is by complete excision, which is best achieved by controlling the surgical margins with frozen sections. Many of these malignant tumors and many benign ones as well can have the same appearance; biopsy is usually required to establish the correct diagnosis.

A. Basal Cell Carcinoma:

Basal cell carcinoma usually grows slowly and painlessly as a nodule that may or may not become ulcerated. It slowly invades adjacent tissues but rarely metastasizes. A less common type-sclerosing or morphea basal cell carcinoma-tends to extend insidiously and surreptitiously beneath the surface, sometimes producing ectropion, entropion, lid notching or retraction, dimpling of the overlying skin, or loss of eyelashes.

Frozen section study of the surgical margins is particularly important for sclerosing basal cell carcinomas, since the tumor margins are seldom clinically apparent. Microscopically controlled excision (a modified Mohs technique) is used by some dermatologists to achieve complete excision. Selected cases may be treated by other methods such as radiotherapy or cryotherapy with liquid nitrogen.

B. Squamous Cell Carcinoma:

Squamous cell carcinomas also grow slowly and painlessly, often starting as a hyperkeratotic nodule that may become ulcerated. Benign inflammatory tumors such as keratoacanthomas may closely resemble carcinomas. The correct diagnosis may depend on biopsy. Like basal cell carcinomas, these tumors can invade and erode through adjacent tissue; they can also spread to regional lymph nodes via the lymphatic system.

C. Sebaceous Gland Carcinoma:

Sebaceous gland carcinomas most often arise from the meibomian glands and the glands of Zeis but can also occur in the sebaceous glands of the eyebrow or caruncle. About half resemble benign inflammatory lesions and disorders such as chalazia and chronic blepharitis. They are more aggressive than squamous cell carcinomas, often extending into the orbit, invading lymphatics, and metastasizing.

Carcinoma Associated With Xeroderma Pigmentosum

This rare disease is characterized by the appearance of a large number of freckles in sun-exposed areas of the skin. These are followed by telangiectases, atrophic patches, and eventually a warty growth that may undergo carcinomatous degeneration. The eyelids are frequently affected and may be the first area to show degenerative changes, causing atrophy and ectropion with secondary inflammatory changes of the conjunctiva, symblepharon, corneal ulceration, and carcinoma of the lids. Malignant tumors include basal cell carcinomas, squamous cell carcinomas, and malignant melanomas. This condition is inherited as an autosomal recessive trait and is due to a defect in the repair of DNA damaged by ultraviolet light. Carriers can often be identified by excessive freckling.

The disease appears early in life and in most cases is fatal by adolescence as a result of metastasis. Life may be prolonged by carefully protecting the skin from actinic rays and treating carcinomatous tumors as rapidly as they appear.

Sarcoma

Soft tissue sarcomas of the lids are rare and usually are anterior extensions of orbital tumors. Rhabdomyosarcomas involving the lids and orbit are the most common primary malignant tumors found in these tissues in the first decade of life. The lid tumor may be the first sign. A combination of radiotherapy and chemotherapy is usually effective in preserving ocular function and preventing death.

Malignant Melanoma

Malignant melanomas of the eyelids are similar to those elsewhere in the skin and include three distinct varieties: superficial spreading melanoma, lentigo maligna melanoma, and nodular melanoma. Not all malignant melanomas are pigmented. Most pigmented lesions on the eyelid skin are not melanomas. Therefore, biopsy should be used to establish the diagnosis. The prognosis for melanomas of the skin depends upon the depth of invasion or the thickness of the lesion. Tumors less than 0.76 mm in thickness rarely metastasize.

METASTATIC TUMORS

Metastatic tumors to eyelids are rare. Because they frequently mimic benign lesions such as chalazions, cysts, and granulomas, the diagnosis is often not suspected. Not infrequently, the lid lesion appears before the primary tumor is discovered.

II. LACRIMAL APPARATUS

The lacrimal system incorporates structures involved in the production and drainage of tears. The secretory component consists of the glands that produce the various ingredients of tear fluid. The nasolacrimal ductules form the excretory element of the system, depositing these secretions into the nose. The tear fluid is distributed over the surface of the eye by the action of blinking.

LACRIMAL SECRETORY SYSTEM

The largest volume of tear fluid is produced by the major lacrimal gland located in the lacrimal fossa in the superior temporal quadrant of the orbit. This almond-shaped gland is divided by the lateral horn of the levator aponeurosis into a larger orbital lobe and a smaller palpebral lobe, each with its own ductule system emptying into the superior temporal fornix (Chapter 1). The palpebral lobe can sometimes be visualized by everting the upper lid. The secretions from the main lacrimal gland are triggered by emotion or physical irritation and cause tears to flow copiously over the lid margin (epiphora). Innervation of the main gland is from the pontine lacrimal nucleus through the nervus intermedius and along an elaborate pathway of the maxillary division of the trigeminal nerve. Denervation is a common consequence of acoustic neuroma and other tumors of the cerebellopontine angle.

The accessory lacrimal glands, although only one-tenth the mass of the major gland, have an essential role. The glands of Krause and Wolfring are identical to the major gland but lack a ductile system. These glands are located in the conjunctiva, mainly in the superior fornix. Unicellular goblet cells, also scattered throughout the conjunctiva, secrete glycoprotein in the form of mucin. Modified sebaceous meibomian and zeisian glands of the lid margin contribute lipid to the tears. The glands of Moll are modified sweat glands that also add to the tear film.

The accessory glands are known as the "basic secretors." Their emissions are sufficient to maintain the cornea without those of the main lacrimal gland. Loss of goblet cells, however, leads to drying of the cornea despite profuse tearing from the lacrimal gland.

DISORDERS OF THE SECRETORY SYSTEM

Alacrima

Congenital absence of tearing occurs in Riley-Day syndrome (familial dysautonomia) and anhidrotic ectodermal dysplasia. Although initially asymptomatic, patients may develop signs typical of keratoconjunctivitis sicca. Absence of tears may also occur after disruption of the lacrimal secretory nerve by acoustic neuroma or following surgery of the cerebellopontine angle. Tumors or inflammation of the lacrimal gland may reduce tear production.

Lacrimal Hypersecretion

Primary hypersecretion is rare and must be distinguished from tearing due to obstruction of the excretory ductules. Secondary hypersecretion may be psychogenic or reflex from irritation of surface epithelium or retina. It is possible to stop hypersecretion by blocking the lacrimal secretory nerve in the sphenopalatine ganglion.

Paradoxic Lacrimation ("Crocodile Tears")

This condition is characterized by tearing while eating. Although it may be congenital, it is usually acquired after Bell's palsy and is the result of aberrant regeneration of the facial nerve.

Bloody Tears

This is a rare clinical entity attributed to a variety of causes. It has been associated with menstruation ("vicarious menses"). Blood-tinged tears may be secondary to conjunctival hemorrhage due to any cause (trauma, blood dyscrasia, etc) or to tumors of the lacrimal sac. They have also been reported in a hypertensive patient suffering from epistaxis with extension through the nasolacrimal duct.

Dacryoadenitis

Acute inflammation of the lacrimal gland is a rare condition most often seen in children as a complication of mumps, measles, or influenza and in adults in association with gonorrhea. Chronic dacryoadenitis may be the result of benign lymphocytic infiltration, lymphoma, leukemia, or tuberculosis. It is occasionally seen bilaterally as a manifestation of sarcoidosis. When combined with parotid gland swelling, it is called Mikulicz's syndrome.

Considerable pain, swelling, and injection occur over the temporal aspect of the upper eyelid, which often imparts to it an S-shaped curve. If bacterial infection is present, systemic antibiotics are given. It is rarely necessary to surgically drain the infection.

LACRIMAL EXCRETORY SYSTEM

The excretory system is composed of the puncta, canaliculi, lacrimal sac, and nasolacrimal duct (see Chapter 1). With each blink, the eyelids close like a zipper-beginning laterally, distributing tears evenly across the cornea, and delivering them to the excretory system on the medial aspect of the lids. Under normal circumstances, tears are produced at about their rate of evaporation, and for that reason few pass through the excretory system. When tears flood the conjunctival sac, they enter the puncta partially by capillary attraction. With lid closure, the specialized portion of pretarsal orbicularis surrounding the ampulla tightens to prevent their escape. Simultaneously, the lid is drawn toward the posterior lacrimal crest, and traction is placed on the fascia surrounding the lacrimal sac, causing the canaliculus to shorten and creating negative pressure within the sac. This dynamic pumping action draws tears into the sac which then pass by gravity and tissue elasticity through the nasolacrimal duct into the inferior meatus of the nose. Valve-like folds of the epithelial lining of the sac tend to resist the retrograde flow of tears and air. The most developed of these flaps is the "valve" of Hasner at the distal end of the nasolacrimal duct. This structure is important because when imperforate in infants it is the cause of congenital obstruction and chronic dacryocystitis.

DISORDERS OF THE EXCRETORY SYSTEM

1. DACRYOCYSTITIS(Figure 4-14)

Infection of the lacrimal sac is a common disease that usually occurs in infants or postmenopausal women. It is most often unilateral and always secondary to obstruction of the nasolacrimal duct. In many adult cases, the cause of obstruction remains unknown. Dacryocystitis is uncommon in the intermediate age groups unless it follows trauma or is caused by a dacryolith. Spontaneous improvement follows passage of a dacryolith, but recurrence is the rule.

In infants, chronic infection accompanies nasolacrimal duct obstruction, but acute dacryocystitis is uncommon. Acute dacryocystitis in children is often a result of Haemophilus influenzae infection. Prompt and aggressive treatment should be instituted because of the risk of orbital cellulitis.

Acute dacryocystitis in adults is usually caused by Staphylococcus aureus or occasionally -hemolytic streptococci. In chronic dacryocystitis, Streptococcus pneumoniae or, rarely, Candida albicans is the predominant organism-mixed infections do not occur. The infectious agent can be identified microscopically by staining a conjunctival smear taken after expression of the tear sac.

Clinical Findings

The chief symptoms of dacryocystitis are tearing and discharge. In the acute form, inflammation, pain. swelling, and tenderness are present in the tear sac area. Purulent material can be expressed from the sac. In the chronic form, tearing is usually the only sign. Mucoid material can usually be expressed from the sac. It is curious that dacryocystitis is seldom complicated by conjunctivitis even though the conjunctival sac is constantly being bathed with pus exuding through the lacrimal puncta. Corneal ulcer occasionally occurs following minor corneal trauma in the presence of pneumococcal dacryocystitis.

Treatment

Acute dacryocystitis usually responds to appropriate systemic antibiotics, and the chronic form can often be kept latent with antibiotic drops. However, relief of obstruction is the only cure.

In adults, the presence of a mucocele is evidence that the site of obstruction is in the nasolacrimal duct and that dacryocystorhinostomy is indicated. The patency of the canalicular system is ensured if mucus or pus is regurgitated through the puncta on compression of the sac. Examination of the nose is important to ensure adequate drainage space between the septum and the lateral nasal wall. Dacryocystorhinostomy consists of forming a permanent anastomosis between the lacrimal sac and the nose. Exposure is gained by an incision over the anterior lacrimal crest. A bony opening is made in the lateral wall of the nose, and the nasal mucosa is sutured to the mucosa of the lacrimal sac. An endoscopic approach through the nose using lasers to help form the opening between the lacrimal sac and the nasal cavity is under investigation. Transluminal balloon dilation of the distal nasolacrimal system may also be useful for patients not suitable for surgery.

Excessive tearing (epiphora) is occasionally due to canalicular stenosis (see below) or obstruction at the junction of the common canaliculus and lacrimal sac. In either case, compression of the sac does not cause regurgitation of fluid, mucus, or pus through the puncta, and no mucocele is present. Intubation and irrigation of the canalicular system with a lacrimal cannula and x-ray studies with contrast media (dacryocystography) will identify the site of obstruction. Common canalicular obstruction may be treated by intubation of the passages with silicone stent for 3-6 months. A thick obstructing scar, however, will necessitate dacryocystorhinostomy and canaliculoplasty with silicone intubation of the canalicular system.

In infantile dacryocystitis, the site of stenosis is usually at the valve of Hasner. Failure of canalization is a common occurrence (4-7% of newborns), but normally the duct opens spontaneously within the first month. Forceful compression of the lacrimal sac will sometimes rupture the membrane and establish patency. If stenosis persists more than 6 months or if dacryocystitis develops, probing of the duct is indicated. One probing is effective in 75% of cases. In the remainder, cure can almost always be achieved by repeated probing, by inward fracture of the inferior turbinate, or by a temporary silicone lacrimal splint. Probing should not be attempted in the presence of acute infection.

2. CANALICULAR DISORDERS

Congenital anomalies of the canalicular system include imperforate puncta, accessory puncta, canalicular fistulas, and, rarely, agenesis of the canalicular system. Most cases of canalicular stenosis are acquired, usually the result of viral infections-notably varicella, herpes simplex, and adenovirus infection. Obstruction-even obliteration-may occur with Stevens-Johnson syndrome, pemphigoid, and other conjunctival shrinkage diseases. Systemic chemotherapy with fluorouracil and topical idoxuridine may also cause obstruction. Canaliculitis is an uncommon chronic unilateral infection caused by Actinomyces israelii (Figure 4-15), Candida albicans, or Aspergillus species. It affects the lower canaliculus more often than the upper, occurs exclusively in adults, and causes a secondary purulent conjunctivitis that frequently escapes etiologic diagnosis. Untreated, it will result in canalicular stenosis. The patient complains of a mildly red and irritated eye with a slight discharge. The punctum usually pouts, and material can be expressed from the canaliculus. The organism can be seen microscopically on a direct smear taken from the canaliculus. Curettage of the necrotic material in the involved canaliculus, followed by irrigation, is usually effective in establishing patency. Canaliculotomy is sometimes necessary. Tincture of iodine may be applied to the lining of the canaliculus after canaliculotomy. Recurrence is common.

Total canalicular obstruction necessitates use of an artificial tear duct for relief of epiphora (conjunctivodacryocystorhinostomy). A Pyrex glass tube is placed between the conjunctival sac and the nasal cavity.

Closure of the punctum is sometimes performed in patients with keratitis sicca to allow tears to remain in the conjunctival sac. Temporary closure may be done with silicone or collagen plugs in the canaliculi or by sealing the punctum with a hot cautery. The temporary obstruction will provide an opportunity to evaluate the effect. Permanent closure may be accomplished by deep cautery within the ampulla with thermal, electrocautery, or laser energy or by dividing the canaliculus surgically.

III. TEARS

Tears form a thin layer approximately 7-10 m thick that covers the corneal and conjunctival epithelium. The functions of this ultrathin layer are (1) to make the cornea a smooth optical surface by abolishing minute surface epithelial irregularities; (2) to wet and protect the delicate surface of the corneal and conjunctival epithelium; (3) to inhibit the growth of microorganisms by mechanical flushing and antimicrobial action; and (4) to provide the cornea with necessary nutrient substances.

LAYERS OF THE TEAR FILM

The tear film is composed of three layers (Figure 4-16): (1) The superficial layer is a monomolecular film of lipid derived from meibomian glands. It is thought to retard evaporation and form a watertight seal when the lids are closed. (2) The middle aqueous layer is elaborated by the major and minor lacrimal glands and contains water-soluble substances (salts and proteins). (3) The deep mucinous layer is composed of glycoprotein and overlies the corneal and conjunctival epithelial cells. The epithelial cell membranes are composed of lipoproteins and are therefore relatively hydrophobic. Such a surface cannot be wetted with an aqueous solution alone. Mucin is partly adsorbed onto the corneal epithelial cell membranes and is anchored by the microvilli of the surface epithelial cells. This provides a new hydrophilic surface for the aqueous tears to spread over which is wetted by a lowering of surface tension.

COMPOSITION OF TEARS

The normal tear volume is estimated to be 7 ± 2 L in each eye. Albumin accounts for 60% of the total protein in tear fluid. Globulin and lysozymes are divided equally in the remainder. Immunoglobulins IgA, IgG, and IgE are present. IgA predominates, and differs from serum IgA in that it is not transudated from serum only but is produced by plasma cells located in the lacrimal gland. In certain allergic conditions such as vernal conjunctivitis, the IgE concentration of tear fluid increases. Tear lysozymes form 21-25% of the total protein and-acting synergistically with gamma globulins and other nonlysozyme antibacterial factors-represent an important defense mechanism against infection. Other tear enzymes may also play a role in diagnosis of certain clinical entities, eg, hexoseaminidase assay for diagnosis of Tay-Sachs disease.

K⁺, Na⁺, and Cl^- occur in higher concentrations in tears than in plasma. Tears also contain a small amount of glucose (5 mg/dL) and urea (0.04 mg/dL), and changes in blood concentration parallel changes in tear glucose and urea levels. The average pH of tears is 7.35, though a wide normal variation exists (5.20-8.35). Under normal conditions, tear fluid is isotonic. Tear film osmolality ranges from 295 to 309 mosm/L.

DRY EYE SYNDROME (Keratoconjunctivitis Sicca)

Dryness of the eye may result from any disease associated with deficiency of the tear film components (aqueous, mucin, or lipid), lid surface abnormalities, or epithelial abnormalities. Although there are many forms of keratoconjunctivitis sicca, those connected with rheumatoid arthritis and other autoimmune diseases are commonly referred to as Sjögren's syndrome.

Etiology

Many of the causes of dry eye syndrome affect more than one component of the tear film or lead to ocular surface alterations that secondarily cause tear film instability. Histopathologic features include the appearance of dry spots on the corneal and conjunctival epithelium, formation of filaments, loss of conjunctival goblet cells, abnormal enlargement of nongoblet epithelial cells, increased cellular stratification, and increased keratinization. The etiology and diagnosis of keratoconjunctivitis sicca are summarized in Table 4-2.

Table 4-2: Etiology and diagnosis of dry eye syndrome.

I. Etiology Conditions Characterized by Hypofunction of the Lacrimal Gland: 1. Congenital-     a. Familial dysautonomia (Riley-Day syndrome)     b. Aplasia of the lacrimal gland (congenital alacrima)     c. Trigeminal nerve aplasia     d. Ectodermal dysplasia 2. Acquired-     a. Systemic diseases-         (1)Sjögren's syndrome         (2)Progressive systemic sclerosis         (3)Sarcoidosis         (4)Leukemia, lymphoma         (5)Amyloidosis         (6)Hemochromatosis     b. Infection-         (1)Mumps     c. Injury-         (1)Surgical removal of lacrimal gland         (2)Irradiation         (3)Chemical burn     d. Medications-         (1)Antihistamines         (2)Antimuscarinics: atropine, scopolamine         (3)General anesthetics: halothane, nitrous oxide         (4)Beta-adrenergic blockers: timolol, practolol     e. Neurogenic Neuroparalytic (facial nerve palsy) Conditions Characterized by Mucin Deficiency: 1. Avitaminosis A 2. Stevens-Johnson syndrome 3. Ocular pemphigoid 4. Chronic conjunctivitis, eg, trachoma 5. Chemical burns 6. Medications-Antihistamines, antimuscarinic agents, beta-adrenergic blocking agents (eg, practolol) 7. Folk remedies, eg, kermes Conditions Characterized by Lipid Deficiency: 1. Lid margin scarring 2. Blepharitis Defective Spreading of Tear Film Caused by the Following: 1. Eyelid abnormalities-     a. Defects, coloboma     b. Ectropion or entropion     c. Keratinization of lid margin     d. Decreased or absent blinking         (1)Neurologic disorders         (2)Hyperthyroidism         (3)Contact lens         (4)Drugs         (5)Herpes simplex keratitis         (6)Leprosy     e. Lagophthalmos-         (1)Nocturnal lagophthalmos         (2)Hyperthyroidism         (3)Leprosy 2. Conjunctival abnormalities-     a. Pterygium     b. Symblepharon 3. Proptosis II. Diagnostic Tests: Schirmer test without anesthesia Tear break-up time Ocular ferning test Impression cytology Fluorescein staining Rose bengal staining Tear lysozyme Tear film osmolality Tear lactoferrin

Clinical Findings

Patients with dry eyes complain most frequently of a scratchy or sandy (foreign body) sensation. Other common symptoms are itching, excessive mucus secretion, inability to produce tears, a burning sensation, photosensitivity, redness, pain, and difficulty in moving the lids. In most patients, the most remarkable feature of the eye examination is the grossly normal appearance of the eye.The most characteristic feature on slitlamp examination is the interrupted or absent tear meniscus at the lower lid margin. Tenacious yellowish mucus strands are sometimes seen in the lower conjunctival fornix. The bulbar conjunctiva loses its normal luster and may be thickened, edematous, and hyperemic.

The corneal epithelium shows varying degrees of fine punctate stippling in the interpalpebral fissure. The damaged corneal and conjunctival epithelial cells stain with 1% rose bengal (Figure 4-17), and defects in the corneal epithelium stain with fluorescein. In the late stages of keratoconjunctivitis sicca, filaments may be seen-one end of each filament attached to the corneal epithelium and the other end moving freely (Figure 4-18).

Figure 4-17: Rose bengal staining of corneal and conjunctival cells in a 54-year-old woman with keratoconjunctivitis sicca.

Figure 4-18: Corneal filaments in a 56-year-old patient with keratoconjunctivitis sicca.

In patients with Sjögren's syndrome, conjunctival scrapings may show increased numbers of goblet cells. Lacrimal gland enlargement occurs uncommonly in patients with Sjögren's syndrome. Diagnosis and grading of the dry eye condition can be achieved with good accuracy using the following diagnostic methods:

A. Schirmer Test:

This test is done by drying the tear film and inserting Schirmer strips (Whatman filter paper No. 41) into the lower conjunctival cul-de-sac at the junction of the mid and temporal thirds of the lower lid. The moistened exposed portion is measured 5 minutes after insertion. Less than 10 mm of wetting without anesthesia is considered abnormal.

When performed without anesthesia, the test measures the function of the main lacrimal gland, whose secretory activity is stimulated by the irritating nature of the filter paper. Schirmer tests performed after topical anesthesia (0.5% tetracaine) measure the function of the accessory lacrimal glands (the basic secretors). Less than 5 mm in 5 minutes is abnormal.

The Schirmer test is a screening test for assessment of tear production. False-positive and false-negative results occur. Low readings are sporadically found in normals, and normal tests may occur in dry eyes- especially those secondary to mucin deficiency.

B. Tear Film Break-Up Time:

Measurement of the tear film break-up time may sometimes be useful to estimate the mucin content of tear fluid. Deficiency in mucin may not affect the Schirmer test but may lead to instability of the tear film. This causes the film's rapid break-up. "Dry spots" (Figure 4-19) are formed in the tear film, and exposure of the corneal or conjunctival epithelium follows. This process ultimately damages the epithelial cells, which can then be stained with rose bengal. Damaged epithelial cells may be shed from the cornea, leaving areas susceptible to punctate staining when the corneal surface is flooded with fluorescein.

Figure 4-19: Baring of the corneal epithelium following formation of a dry spot in the tear film. (Modified and redrawn from Dohlman CH: The function of the corneal epithelium in health and disease. Invest Ophthalmol 1971;10:383.)

The tear film break-up time can be measured by applying a slightly moistened fluorescein strip to the bulbar conjunctiva and asking the patient to blink. The tear film is then scanned with the aid of the cobalt filter on the slitlamp while the patient refrains from blinking. The time that elapses before the first dry spot appears in the corneal fluorescein layer is the tear film break-up time. Normally, the break-up time is over 15 seconds, but it will be reduced appreciably by the use of local anesthetics, by manipulating the eye, or by holding the lids open. The break-up time is shorter in eyes with aqueous tear deficiency and is always shorter than normal in eyes with mucin deficiency.

C. Ocular Ferning Test:

A simple and inexpensive qualitative test for the study of conjunctival mucus is performed by drying conjunctival scrapings on a clean glass slide. Microscopic arborization (ferning) is observed in normal eyes. In patients with cicatrizing conjunctivitis (ocular pemphigoid, Stevens-Johnson syndrome, diffuse conjunctival cicatrization), ferning of the mucus is reduced or absent.

D. Impression Cytology:

Impression cytology is a method by which goblet cell densities on the conjunctival surface can be counted. In normal persons, the goblet cell population is highest in the infranasal quadrant. Loss of goblet cells has been documented in cases of keratoconjunctivitis sicca, trachoma, cicatricial ocular pemphigoid, Stevens-Johnson syndrome, and avitaminosis A.

E. Fluorescein Staining:

Touching the conjunctiva with a dry strip of fluorescein is a good indicator of wetness, and the tear meniscus can be seen easily. Fluorescein will stain the eroded and denuded areas as well as microscopic defects of the corneal epithelium.

F. Rose Bengal Staining:

Rose bengal is more sensitive than fluorescein. The dye will stain all desiccated nonvital epithelial cells of the cornea as well as conjunctiva

G. Tear Lysozyme Assay:

Reduction in tear lysozyme concentration usually occurs early in the course of Sjögren's syndrome and is helpful in the diagnosis of that disorder. Tears can be collected on Schirmer strips and assayed. The most common method is spectrophotometric assay

H. Tear Osmolality:

Hyperosmolality of tears has been documented in keratoconjunctivitis sicca and in contact lens wearers and is thought to be a consequence of decreased corneal sensitivity. Reports claim that hyperosmolality is the most specific test for keratoconjunctivitis sicca. It can occur even with a normal Schirmer test and normal rose bengal staining

I. Lactoferrin:

Tear fluid lactoferrin is low in patients with hyposecretion of the lacrimal gland. Testing kits are commercially available.

Complications

Early in the course of keratoconjunctivitis sicca, vision is slightly impaired. As the condition worsens, discomfort can become disabling. In advanced cases, corneal ulceration, corneal thinning, and perforation may develop. Secondary bacterial infection occasionally occurs, and corneal scarring and vascularization may result in marked reduction in vision. Early treatment may prevent these complications.

Treatment

The patient should understand that dry eyes is a chronic condition and complete relief is unlikely except in mild cases when the corneal and conjunctival epithelial changes are reversible. Artificial tears are the mainstay of treatment. Ointment is useful for prolonged lubrication, especially when sleeping. Additional relief can be achieved by using humidifiers, moisture chamber spectacles, or swim goggles.

The primary function of these measures is fluid replacement. Restoration of mucin is a more formidable task. In recent years, high-molecular-weight water-soluble polymers have been added to artificial tears in an attempt to improve and prolong surface wetting. Other mucomimetic agents include sodium hyal- uronate and solutions of the patient's own serum as eye drops. If the mucus is tenacious, as in Sjögren's syndrome, mucolytic agents (eg, acetylcysteine 10%) are helpful.

Patients with excessive tear lipids require specific instructions for removal of lipid from the eyelid margin. Antibiotics topically or systemically may be necessary. Topical vitamin A may be useful in reversing ocular surface metaplasia.

All chemical preservatives in artificial tears induce a certain amount of corneal toxicity. Benzalkonium chloride is the most damaging of the commonly used preparations. Patients who require frequent drops fare better with nonpreserved solutions. Preservatives can also cause idiosyncratic reactions. This is most common with thimerosal.

Patients with dry eyes from any cause are more likely to have concurrent infections. Chronic blepha-ritis is common and should be treated with hygiene and topical antibiotics. Acne rosacea is associated with keratoconjunctivitis sicca, and treatment with systemic tetracycline may be helpful.

Surgical treatment for dry eyes includes insertion of temporary (collagen) or extended (silicone) punctal plugs to retain lacrimal secretions. Permanent closure of the puncta and canaliculi can be done by thermal, electrocautery, or laser treatment.

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List of Figures

	Figure 4-1: Internal hordeolum, left upper eyelid, pointing on skin side. This should be opened by a horizontal skin incision. (Courtesy of A Rosenberg.)
	Figure 4-2: Chalazion, right lower eyelid. (Courtesy of K Tabbara.)
	Figure 4-3: Entropion. (Courtesy of M Quickert.)
	Figure 4-4: Ectropion. (Courtesy of M Quickert.)
	Figure 4-5: Epicanthus tarsalis.
	Figure 4-6: Blepharochalasis.
	Figure 4-7: Dermatochalasis of upper lids and herniation of orbital fat of lower lids. (Courtesy of M Quickert.)
	Figure 4-8: Surgical correction of ptosis. Left: Before operation, ptosis of the upper lid was present. Right: After the operation (levator resection), the ptosis was well corrected and a natural-appearing upper lid fold produced. (Courtesy of C Beard.)
	Figure 4-9: Molluscum contagiosum. Note central umbilication.
	Figure 4-10: Xanthelasma. (Courtesy of M Quickert.)
	Figure 4-11: Cavernous hemangioma of left upper lid.
	Figure 4-12: Squamous cell carcinoma of upper lid. (Courtesy of A Rosenberg.)
	Figure 4-13: Basal cell carcinoma of left lower lid. (Courtesy of S Mettier, Jr.)
	Figure 4-14: Acute dacryocystitis.
	Figure 4-15: Actinomyces israelii canaliculitis, left eye. (Courtesy of P Thygeson.)
	Figure 4-16: The three layers of the tear film covering the superficial epithelial layer of the cornea.
	Figure 4-17: Rose bengal staining of corneal and conjunctival cells in a 54-year-old woman with keratoconjunctivitis sicca.
	Figure 4-18: Corneal filaments in a 56-year-old patient with keratoconjunctivitis sicca.
	Figure 4-19: Baring of the corneal epithelium following formation of a dry spot in the tear film. (Modified and redrawn from Dohlman CH: The function of the corneal epithelium in health and disease. Invest Ophthalmol 1971;10:383.)

List of Tables

	Table 4-1: Beard's revised classification of ptosis.
	Table 4-2: Etiology and diagnosis of dry eye syndrome.

 
 
 
 

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