Section I: Nasolacrimal Duct System

The nasolacrimal duct system of the dog is similar to that of most domestic mammals. It is a walled conduit that drains the tear film from the eye into the nasal passages. The first section of this chapter reviews the embryology, anatomy, physiology, and diagnostic procedures as well as the clinical manifestations for both congenital, developmental, and acquired diseases and their appropriate medical and surgical management (Figure 7.1).

Embryology

The nasolacrimal duct system develops from surface ectoderm within the nasolacrimal groove (i.e., furrow), which separates the lateral nasal fold and the maxillary process (Figure 7.2a). Ectodermal cells grow along this groove, sink into mesenchyme, and become buried. These cells form a cord as the maxillary process fuses with the lateral nasal fold between days 22 and 26 of gestation in the dog (Figure 7.2b). The ectodermal cords grow toward the nasal cavity and the eye, and eventually, they extend from the eyelid to the inferior nasal passage. The upper end of this cord develops two buds, which grow into the upper and lower eyelids near the medial canthus (Figure 7.2c) and develop into the superior and inferior canaliculi and puncta. The cord becomes a duct through a process of canalization and normally is patent at birth.

Anatomy

The superior and inferior lacrimal puncta are oval‐to‐slit‐like openings that measure approximately 1 mm by 0.3 mm, with their long axis parallel to the lid margin. They are located on the palpebral conjunctiva at the edge of the upper and lower eyelids 2–5 mm from the medial canthus, approximately where the tarsal glands end (Figure 7.3a). The lacrimal puncta open into the superior and inferior canaliculi. The canaliculi are approximately 4–7 mm in length and 0.5–1.0 mm in diameter. They extend through the orbicularis oculi muscle, and they join together ventral to the medial canthus to form the lacrimal sac, which lies within a slight depression (i.e., the lacrimal fossa) in the lacrimal bone. The lacrimal sac is simply a slight dilation at the beginning of the nasolacrimal duct, not a distinct sac. The proximal nasolacrimal duct itself is constricted as it traverses the lacrimal bone, and the most frequent site for retention of foreign bodies and development of dacryocystitis in the dog. The duct, then enlarged in diameter, passes through a canal on the medial surface of the maxillary bone, and it ends in a nasal punctum. The nasal puncta are usually located in the ventral lateral nasal meatus, opening approximately 1 cm inside the external nares (Figure 7.3b). They can be accessed with the dog under general anesthesia and the nares dilated. In approximately 50% of dogs, the nasolacrimal duct has a second opening in the oral mucosa of the central hard palate, behind the incisors at the level of the canine teeth. The nasolacrimal duct is approximately 1 mm in diameter, and the length varies considerably between brachycephalic, mesocephalic, and dolichocephalic dogs. Brachycephalic breeds often have very short nasolacrimal ducts, and they often drain the tears into the pharynx.

Physiology

The sole purpose of the nasolacrimal duct system is to drain tears from the surface of the eye to the nasal passages. Evaporation, which varies with environmental conditions and whether the eyelids are open or not, removes a significant portion (approximately 25%) of tears from the ocular surface. Most (60%) of the tear volume is normally drained through the inferior puncta and canaliculi. Tears flow ventrally in response to gravity, and they are pulled into the canaliculi during eyelid closure because of reduced intracanalicular pressure. This reduced pressure develops as these thin‐walled ducts are compressed by contraction of the orbicularis oculi muscle. Capillary action and siphon effect from the lacrimal sac pull tears through the canaliculi and duct.

Mucosa‐associated lymphoid tissue (MALT) has been reported in human nasolacrimal drainage systems. This lacrimal drainage‐associated lymphoid tissue is part of the common mucosal immune system, and T cells, B cells, and plasma cells were confirmed with immunohistochemistry within the walls of the nasolacrimal ducts and canaliculi. MALT and production of natural peptide antibiotics have not been reported in the dog, but they are likely present in animals.

Clinical Manifestations of Nasolacrimal Disease

Disorders of the nasolacrimal duct system in the dog may be congenital, developmental, or acquired, and they are limited to a lack of patency or inflammation. The clinical manifestations of nasolacrimal system disease include epiphora; mucopurulent punctal, conjunctival, and nasal discharge; swelling of the ventral medial canthal region; punctal foreign bodies; and draining fistula in the medial canthal region.

Diagnostic Procedures

Several diagnostic procedures allow clinicians to establish an accurate diagnosis of obstruction or inflammation of the nasolacrimal duct system or epiphora secondary to increased lacrimation. These include the Schirmer tear test (STT), cytology and microbial culture, fluorescein dye passage test, normograde punctal and canalicular cannulation and lavage, nasal punctal cannulation and retrograde flushing, dacryocystorhinography, ultrasonography, computed tomography (CT), magnetic resonance imaging (MRI), and lacrimal scintigraphy (see Chapter 4).

Congenital Diseases

Reported congenital anomalies of the nasolacrimal duct system include punctal atresia and micropuncta, canalicular and nasal lacrimal duct atresia, misplacement of the punctum and canaliculus, displacement of the punctum secondary to medial ventral entropion, dacryops, and canaliculops. Of these anomalies, lacrimal punctal atresia is presented.

Lacrimal Punctal Atresia

Punctal atresia is the most frequently diagnosed congenital anomaly. It may affect the superior, inferior, or both puncta, and it may be either unilateral or bilateral (Figure 7.4). It occurs in numerous breeds and is commonly seen in American Cocker Spaniels, Bedlington Terriers, Golden Retrievers, Miniature and Toy Poodles, and Samoyeds.

The diagnosis is confirmed by biomicroscopic examination and normograde or retrograde nasolacrimal duct flushing. Superior punctal atresia is usually asymptomatic and is diagnosed incidentally during routine biomicroscopic examinations. When inferior punctal atresia is present, epiphora is usually present in puppies, and nasolacrimal flushing is warranted. The conjunctiva over the punctum will bulge during flushing. Ventral punctal atresia is treated by surgical excision of the ballooning conjunctiva (Figure 7.5a and b). The affected eye is then treated with topical antibiotic and corticosteroid solutions four times a day for 7–10 days until the punctum is patent and epiphora is absent.

Atresia of the Canaliculus, Nasolacrimal Sac, and Nasolacrimal Duct

Atresias of the canaliculus, nasolacrimal sac, or duct are rare. Congenital anomalies of the nasolacrimal duct have been reported in cattle and the horse, but not in the dog. When the ventral canaliculus, nasolacrimal sac, or nasolacrimal duct is missing, epiphora will be present, and the diagnosis is confirmed with a dacryocystorhinograph. Therapeutic options are limited to surgery, and include conjunctival rhinostomy, conjunctival‐maxillary sinusotomy, or conjunctival buccostomy. These procedures attempt to create a permanent fistula from the conjunctiva directly to the nasal turbinates, maxillary sinus, or mouth, respectively.

Developmental Disorders

Many brachycephalic and toy dogs have epiphora related to multiple anomalies of the medial canthal region and inferior lacrimal punctum. These anomalies are inherited as part of the facial development in these breeds of dogs, and epiphora usually manifests in the first year of life. The inferior lacrimal puncta and canaliculi are commonly displaced inward and ventrally by a subtle, medioventral entropion, which rolls the medial eyelid margin into the cornea and partially obstructs the lacrimal puncta and narrows the canalicular lumen (Figure 7.6). This displacement is integral to the tear‐staining syndrome, commonly seen in the toy and brachycephalic breeds. The lacrimal puncta are usually normal in these dogs, and the clinical signs relate to multiple factors, including displacement of the ventral lacrimal puncta and compression of the canaliculi by the medioventral entropion. In addition, tight medial canthal ligaments displace the medial canthus ventrally and, in combination with medial canthal trichiasis and eyelid trichiasis, exacerbate tear spillage in these dogs. Oral tetracycline and metronidazole have been reported as a therapy for tear staining, but neither has any appreciable effect on tear production or excretion. Their success relates to reduced staining of the medial canthal region by bacteria rather than to control of the epiphora. Therefore, they are used infrequently as therapy today.

The treatment of choice for this condition is a Hotz–Celsus repair of the medial ventral entropion in which a triangular piece of skin is excised with the apex of the triangle opposite the lower lacrimal punctum or, preferably, a bilateral medial canthoplasty to correct the caruncular trichiasis and tight medial canthal ligaments.

Acquired Diseases

Acquired nasolacrimal disorders of the dog include traumatic lacerations, dacryocystitis and obstruction with foreign bodies, and invasion or compression by neoplasms.

Lacerations

Facial trauma may result in lacerations of the lacrimal puncta, canaliculi, medial canthus, and eyelids. Lacerations of the canaliculi are diagnosed with use of biomicroscopic examination and the bubble test, which involves cannulation of both lacrimal puncta and injection of air. The resultant bubbling allows the surgeon to detect and cannulate the lacerated canalicular ends with a silastic tube. The lacerated eyelid surfaces are then repaired by microsurgical apposition of the tissues around the cannulated duct. The eye is treated with topical antibiotic solutions four times a day until the cannula is removed (at approximately three weeks). These surgeries require the operation microscope and are best left to the specialist.

Dacryocystitis and Foreign Bodies

Dacryocystitis, with or without foreign bodies, occurs infrequently in the dog, and must be differentiated from abscesses secondary to the canine carnassial tooth. Clinical manifestations of dacryocystitis and nasolacrimal duct foreign bodies include epiphora, purulent conjunctival discharge, punctal foreign bodies (Figure 7.7), and late developing draining skin fistulas ventral to the medial canthus. These foreign bodies must be removed for effective therapy.

The diagnosis of dacryocystitis is confirmed by (i) the nasolacrimal flush performed through the upper lacrimal punctum, (ii) the dacryocystorhinography, and (iii) cytological examination of the contents from a nasolacrimal lavage or from biopsies from tissues excised during surgical exploration. Foreign bodies may be flushed from the nasolacrimal duct system by retrograde or normograde lavage, or they may be removed via a dacryocystotomy. The skin incision for a dacryocystotomy is ventral to the medial canthus over the lacrimal fossa. After removal of the foreign body, the nasolacrimal duct system is then cannulated with a silastic tube and treated with topical broad‐spectrum antibiotics while catheterized for approximately three weeks postoperatively.

Neoplasia of the Nasolacrimal Duct

Primary neoplasia of the nasolacrimal duct is rare in all species. Lymphoma is reported to have invaded the lacrimal sac and to have induced dacryocystitis. Pseudotumors of the lacrimal canaliculus have been reported in a dog. Tumors of nasal turbinates and the maxillary sinus, however, may compress or invade the nasolacrimal ducts and spread into the orbit via the nasolacrimal foramen and cause epiphora, mucopurulent, or serosanguineous ocular and nasal discharge, masses ventral to the medial canthus, and orbital signs, including prolapse of the third eyelid, enophthalmos, and conjunctival hyperemia. The diagnosis of nasal neoplasia with involvement of the nasolacrimal duct system is established by clinical examination, plain and contrast radiography, and advanced multisectional imaging, and it is confirmed through light microscopic evaluation of nasal biopsies.

Section II: Lacrimal Secretory System: Disease and Surgery

The “headwater” of the tear system is the lacrimal glands, located dorsolateral of the globe and within the nictitating membrane. Tear abnormalities are among the most common causes of canine ocular surface disease. Medical and surgical procedures for treatment of tear‐deficient ocular surface diseases are frequently performed in both general and small animal practices as well as in veterinary ophthalmology clinics.

Formation and Dynamics of Tear Components

The precorneal tear film (PTF) is crucial for the maintenance of ocular surface health and clear vision, as it is the first refractive surface of the eye. Its functions include primary oxygen source to the avascular cornea, lubricant between the lids and ocular surface, source of protective antimicrobial proteins, and removal of debris and exfoliated cells through drainage. The PTF is classically described as a superimposition of three structurally and functionally unique layers consisting of lipid, aqueous, and mucin components and, in some references, a fourth innermost layer of glycocalyx extending from the superficial layer of the ocular surface epithelia (see Chapters 1 and 2). Tear film thickness is a key variable in the study of normal tears and dry eye diseases. In humans, currently accepted PTF thickness is estimated to be 3.4 ± 2.6 μm.

The lacrimal glands of the orbit and the nictitating membrane are tubuloacinar and histologically similar. Ductules from these glands deliver aqueous tear secretions into the conjunctival fornices. In the dog, three to five ductules from the orbital lacrimal gland open into the dorsolateral conjunctival fornix, whereas the nictitans gland delivers aqueous tears onto the corneal surface through multiple ducts opening between lymphoid follicles on the posterocentral (bulbar) third eyelid (Figure 7.8).

The relative contributions by each of the main lacrimal glands to reflex tear secretion have been investigated in the dog by surgical removal of either one or both glands and measurement of the resulting tear production. Removal of both glands resulted in near‐total absence of secretions, thereby suggesting that accessory conjunctival glands may not be present in the dog, or that they play an inconsequential role in aqueous secretions. The role of each gland (i.e., orbital or nictitans glands) in the production of basal secretions versus reflex tear secretions in the dog has been investigated using the STTs I and II. Surgical removal of either the lacrimal or the tear gland of the nictitans does not significantly lower STT I measurements (total tear production), but reduces by about 50% of the basal tear measurements (STT II).

The tear film, lacrimal glands, and eyelids act together with the ocular surface as a functional unit to preserve the quality of the refractive surface of the eye and to protect the globe from injury. Important to any discussion of the homeostasis of this functional unit is the mucosal immune system. The conjunctiva forms a continuous mucosal surface from the eyelid margin to the cornea and continuously contacts airborne antigens as well as those on adjacent eyelid skin and in the PTF. Conjunctival lymphoid follicles, routinely identified on the bulbar surface of the nictitans in dogs, will undergo hyperplasia upon stimulation by a variety of pathogens. In addition to innate defense mechanisms, an increasing body of evidence supports the role of conjunctival lymphoid cells in the normal homeostasis of the ocular surface as part of the body’s larger MALT.

Pathogenesis of Tear Film Disease

Ocular surface health is ensured by a close relationship between the PTF and normal adnexal conformation and function. Normal tear production in dogs fluctuates slightly during the day (differences of less than 2 mm/min) in a predominantly nocturnal acrophase and decreases with age. Tear production in puppies reaches normal levels by 9–10 weeks of age. Abnormalities in either the quantity or quality of any tear component (lipid, aqueous, mucus) may alter tear fluid dynamics and compromise tear function. Hypertonicity and dehydration of conjunctival and corneal epithelia are initial pathophysiological events associated with tear deficiency. Hypoxia of the corneal epithelium and subepithelial corneal stroma also occurs early in the course of tear film disease. Lack of appropriate lubrication results in frictional irritation of the ocular surface by the eyelids and third eyelid. Potentially toxic tissue metabolites (i.e., lactic acid, desquamated cells, denatured mucus, and other “micro” debris) may accumulate on the ocular surface as well. In tear‐deficient patients, microorganisms more readily colonize affected eyes, thereby resulting in increased incidence of ocular surface infections. Whatever the underlying cause of tear film disease, ocular surface inflammation results, which in turn becomes the cause and consequence of cell damage, creating a self‐perpetuating cycle of external ocular tissue deterioration.