Ophthalmology

Chapter 19


Ophthalmology





Chapter contents



INTRODUCTION


THE ORBIT



THE EYELIDS



THE NICTITATING MEMBRANE



THE CONJUNCTIVA



THE LACRIMAL/NASOLACRIMAL SYSTEM



THE CORNEA



THE ANTERIOR UVEAL TRACT



GLAUCOMA



THE LENS



THE POSTERIOR SEGMENT



NEOPLASIA OF THE EYE AND ADNEXA



OCULAR TRAUMA



NEURO-OPHTHALMOLOGY




INTRODUCTION


Equine ophthalmology has always been, and continues to be, an interesting and challenging aspect of equine practice. For both esthetic and functional reasons, disorders of the eye are of great concern to the horse owner. The horse, perhaps more so than other domestic species, can have devastating complications from ocular trauma or inflammations.


Management of ophthalmic disorders in the horse requires knowledge of the anatomy of the structures involved, an understanding of the pathophysiology of the disease process, and an appreciation of the therapeutic options available. This section is designed to aid the practitioner through the diagnosis and management of the common, and not so common, ocular disorders encountered in practice.


Over the 10 years since the first edition of this volume significant advances have been made in equine ophthalmology, as documented in this chapter. And yet, as will be shown below, there are all too many areas where our understanding of the pathobiology of the equine eye is not sufficient to allow rapid and successful diagnosis and treatment of equine ophthalmic disorders from herpetic keratitis at the very front of the eye to retrobulbar neoplasia behind it.



THE ORBIT



ANATOMY


The orbit is the bony fossa that surrounds and supports the eye. It is composed of the frontal, lacrimal, zygomatic, sphenoid, temporal and palatine bones. The supraorbital process of the frontal bone forms the dorsal rim of the orbit, and provides a complete orbital rim. The ventral floor of the orbit is composed of soft tissue, which, along with a large amount of orbital fat, serves to support the globe.


The orbit is in close proximity to the paranasal sinuses. The frontal sinus is located medial to the orbit and extends dorsally and ventrally along the orbit. The maxillary sinus is ventral and medial to the orbit. The medial canthus of the eye serves as a reference point for trephination of the maxillary sinus. A third smaller sinus, the sphenopalatine, which communicates with the maxillary sinus, is also located ventral and medial to the orbit.


Orbital foramina allow for nerve and blood vessel entry into the orbit. These include, with their associated vessels and nerves, the rostral alar foramen (the maxillary artery and nerve), the orbital fissure (the abducens, ophthalmic, trochlear and oculomotor nerves), the optic foramen (the optic nerve and internal ophthalmic artery), the ethmoidal foramen (ethmoidal nerve and vessels), and the supraorbital foramen (the supraorbital nerve and vessels). The first four of these foramina are clustered on the ventromedial wall of the orbit near its apex, and are important when performing retrobulbar injections for anesthesia. The supraorbital foramen is located medially in the supraorbital process of the frontal bone, and serves as a landmark for injection for regional anesthesia of the upper eyelid. It can be easily found by grasping the supraorbital process, at the point where it begins to widen, between the thumb and middle finger, and palpating with the first finger.


The orbit also contains the extraocular muscles. The dorsal and ventral rectus muscles rotate the eye around a horizontal axis, while the lateral and medial rectus muscles rotate the eye on a vertical axis. The dorsal and ventral oblique muscles rotate the eye on an anteroposterior axis. The retractor bulbi muscle lies within the cone formed by the rectus muscles and extends posteriorly around the optic nerve. The main diagnostic importance of the extraocular muscles is in neurologic examination, as the position of the globe may indicate lesions of certain cranial nerves.


A sheet of connective tissue, the periorbita, lines the orbit. It is reflected to sheathe the extraocular muscles, and extends onto the globe as Tenon’s capsule.



ORBITAL DISEASES



Congenital anomalies



Microphthalmia/anophthalmia

Microphthalmia is an abnormally small eye. True anophthalmos (the absence of any ocular tissue) is rare, with most cases having some remnants of eye present. Microphthalmia, which results from degeneration or abnormal growth of the optic vesicle, may be pure (nanophthalmia), with a normal but small eye, colobomatous, or complicated with other ocular anomalies. There can also be associated systemic anomalies. The absence of a normal-sized eye may result in the failure of the orbit to develop, with subsequent cranial asymmetry.






Orbital cellulitis


Unlike the dog, the horse rarely develops orbital cellulitis. When it occurs, it is frequently an extension of inflammation from sinusitis, guttural pouch infection, blunt trauma or penetrating orbital wound, dental disease, or an extension of panophthalmitis (q.v.).







Enophthalmos


The eye may appear sunken in horses that are dehydrated or debilitated, due to shrinkage of the orbital fat pads. The eye will be actively retracted in cases of ocular pain. Loss of sympathetic tone (Horner’s syndrome) will create an enophthalmos. Orbital fractures may also present with a sunken globe, due to displacement of bone fragments or orbital fat.






THE EYELIDS




ANATOMY AND FUNCTION


The eyelids serve to protect the globe and have important roles in the production, distribution and removal of tears. The outer, oily layer of the tears is produced by the Meibomian glands. This oily film decreases tear evaporation and coats the eyelid margins thus preventing epiphora (watering of the eye) (q.v.). Eyelid closure moves the precorneal tear film toward the nasolacrimal puncta, the first components of the tear drainage pathway.


The vibrissae are long, tactile hairs of the dorsal and ventral orbit. Eyelashes, or cilia, are always present on the upper eyelids but may not be present on the lower eyelids. Both vibrissae and cilia serve a protective role supplying sensory input for the blink response.


The Meibomian (tarsal) glands are positioned perpendicular to the eyelid margins. These glands excrete their sebaceous product onto the globe through openings that lie in a furrow at the mucocutaneous junction of both the superior and inferior eyelids.


The superior and inferior lacrimal puncta and respective canaliculi are located within the nasal aspect of the upper and the lower eyelids and serve as the normal route for tear removal.


The eyelids have a profuse vascular network. The primary muscles of the eyelid include the orbicularis oculi, levator palpebrae superioris and Müller’s muscles. The orbicularis oculi muscle completely encircles the palpebral fissure and is responsible for eyelid closure. The upper eyelid is more mobile than the lower eyelid and thus is responsible for most of the blink response. The levator palpebrae superioris muscle elevates the upper eyelid. The upper and lower eyelids also contain smooth muscle tissue, Müller’s muscle, which serves to open the palpebral fissure.


The sensory innervation of the eyelids is derived from branches of the trigeminal (fifth cranial) nerve. The upper eyelid is innervated by the lacrimal, supraorbital and infratrochlear nerves, which are branches of the ophthalmic nerve. The lower eyelid is innervated by the zygomatic and infratrochlear nerves, which are branches of the maxillary and ophthalmic nerves, respectively. The orbicularis oculi muscle is innervated by dorsal and ventral palpebral nerves, which are distant branches of the facial (seventh cranial) nerve. The oculomotor (third cranial) nerve innervates levator palpebrae superioris, and the sympathetic component of the autonomic nervous system innervates the smooth muscle of Müller via the trigeminal nerve. A normal palpebral reflex demonstrates intact trigeminal (sensory) and facial (motor) nerve pathways.



CONGENITAL ANOMALIES


The eyelids of foals are normally open at birth. Ankyloblepharon is a persistent fusion of the eyelid margins. The eyelids can usually be separated manually, however insertion of scissors between the eyelids and globe may be necessary to “unzip” the adhesions, without closing the scissor blades. Scarring can occur with adhesion of the lid margin to conjunctiva, resulting in symblepharon. Frequent massage and hot compresses should thus be used over the days following separation of lids in a case of ankyloblepharon.


Many other congenital eyelid defects may occur but are very rare. Eyelid agenesis may be characterized by epiphora, conjunctivitis and possibly keratitis (q.v.). Surgical correction, blepharoplasty, may be required.


An imperforate nasolacrimal punctum is uncommon in Equidae, but may cause chronic epiphora. If the canaliculus is present but a membrane obstructs the punctum, the membrane can be surgically removed thus opening the tear outflow pathway.



ABNORMAL EYELID POSITION AND CLOSURE


Entropion is inversion of the eyelid margin toward the eye and usually involves the lower eyelid. Entropion is rare in adult horses but not uncommon in foals. Entropion does not appear to be a familial disease process, but Thoroughbreds may have an increased prevalence. The cause is unknown, but affected newborn foals may be slightly enophthalmic (q.v.) at birth thus predisposing to the condition. The abnormal eyelid position may resolve as the foal gains body weight and retrobulbar fat.


The eyelid margin may rub against the conjunctiva and cornea causing a painful keratoconjunctivitis characterized by epiphora, blepharospasm (involuntary closure of the eyelids), conjunctival hyperemia and possibly corneal ulceration (q.v.). Treatment of entropion is by eversion of the eyelid margin. An everting suture pattern (e.g. interrupted Lembert pattern using 4-0 or 5-0 non-absorbable monofilament suture material) placed in the eyelid skin is a temporary measure but may be sufficient for permanent correction. Surgical removal of a wedge of skin is reserved for severe cases with recurrent entropion following the skin eversion technique or in adults with acquired entropion. A skin incision is made approximately 3–4 mm from and parallel to the eyelid margin. The second incision is spaced as needed to correct the defect. The wedge of skin is removed and the cut edges are opposed with a small diameter, non-absorbable suture material in a simple interrupted pattern.


Ectropion is an eversion of the eyelid margin that is usually secondary to a wound that heals improperly. Surgical intervention is required if the defect causes chronic epiphora, conjunctivitis or exposure keratitis (q.v.).


Symblepharon is an abnormal adhesion of the inner conjunctival surface of the eyelid (palpebral conjunctiva) to the conjunctiva overlying the sclera (bulbar conjunctiva). This is a rare condition that may restrict eyelid movement and necessitate surgical intervention.


Ptosis is a drooping of the upper eyelid due to loss of oculomotor innervation to levator palpebrae superioris or loss of sympathetic innervation to Müller’s muscle (Horner’s syndrome) (q.v.). Absence of oculomotor nerve function is also associated with lateral strabismus. Horner’s syndrome is not commonly diagnosed in horses because the clinical signs may be subtle. In addition to ptosis, loss of sympathetic tone can produce ipsilateral miosis, slight enophthalmia and passive elevation of the nictitating membrane, conjunctival and nasal mucosal hyperemia, and an increase in skin temperature with sweat production on the face and neck. If a specific cause is identified, appropriate treatment should be initiated.


Lagophthalmos is an inability to close the eyelids completely. Lagophthalmos may be caused by marked buphthalmos, exophthalmos or facial nerve paralysis. Secondary exposure keratitis is common.



EYELASH DISORDERS






BLEPHARITIS


Inflammation of the eyelid, blepharitis, may be caused by blunt trauma, an allergic reaction (e.g. insect bites), exposure to intense solar radiation, and infectious agents (e.g. fungal organisms, mites and parasitic larvae).


Solar-induced blepharitis is an inflammatory condition that generally affects horses with minimal periocular pigmentation and may be a precursor to squamous cell carcinoma. Solar-induced blepharitis can be reduced and its recurrence prevented by decreasing exposure to high levels of UV radiation. An affected horse can be housed indoors during peak hours of sunlight or, if prevention is not feasible, the susceptible tissues can be tattooed.





Cutaneous habronemiasis


Habronema are parasitic gastric nematodes of horses (q.v.). Aberrant larval migration of Habronema muscae, H. microstoma and Draschia megastoma causes rapidly developing, raised, non-healing ulcerative granulomas containing caseated and calcified particles. Lesions may be pruritic and painful. The medial canthus and/or nictitating membrane are usually affected since the infective larvae are carried by flies (Musca domestica or Stomoxys calcitrans), which are attracted to moisture at the medial canthus. Definitive diagnosis is by histopathology, which usually reveals granulation tissue, eosinophils, mast cells, neutrophils and intact or fragmented larvae. Ivermectin is the treatment of choice and may be administered in conjunction with a topical antibiotic–corticosteroid ointment.



TRAUMA


Trauma caused by sharp objects such as barbed wire and nails is common in horses. A complete ophthalmic examination, including palpation of the facial bones, should be performed in order to ensure that additional ocular or periocular structures are not damaged. The therapeutic goal is the re-establishment of a functional and cosmetic eyelid. Attaining the desired outcome usually requires surgical intervention, which may include debridement and primary closure.


Tetanus prophylaxis should be administered prior to corrective surgical procedures. In addition, systemic antibiotics and NSAIDs are indicated pre- and postoperatively. If corneal ulceration or secondary uveitis is present, treatment with topical antibiotic and atropine ophthalmic ointments should be initiated.


If the presenting wound is >12 h old, contaminated or severely edematous, surgical closure should be delayed. The open wound should be managed medically for 12–24 h with application of a dressed bandage which will cleanse the laceration, soften the traumatized tissue and decrease swelling. Nitrofurazone ointment can be used for this purpose as it is well tolerated by the eye and inexpensive.


Following induction of general anesthesia (q.v.), the surgical site is prepared in a routine manner and the wound thoroughly cleansed. Excessive suture and tissue tension is avoided by conservative debridement and a two-layer closure. The deep, connective tissue layer should be apposed with absorbable suture (e.g. 5-0 or 6-0 chromic gut or polyglactin). Non-absorbable suture should be used in the skin (e.g. 4-0 or 5-0 monofilament nylon, polypropylene or silk) beginning at and restoring the eyelid margin. Small suture material in a simple interrupted pattern will yield the best results. A bandage and stockinette or protective hood with eye cup may be beneficial for 3–5 days postoperatively, especially during the fly season.


Severe tissue loss may necessitate reconstructive grafting procedures, e.g. sliding H-blepharoplasty, to re-establish an eyelid margin. Because of the absence of readily moveable facial skin in horses, extensive reconstructive procedures are difficult to perform. Blepharoplastic procedures are more successful when performed on the lower than the upper eyelid since the lower eyelid normally has limited motility. In addition, the surgeon should restrict dissection of tissue immediately beneath the orbicularis oculi muscle of the upper eyelid since levator palpebrae superioris function is necessary to prevent secondary postoperative ptosis (q.v.). A split-thickness eyelid tarsorrhaphy (q.v.) (in which the outer parts of the upper and lower lids are joined) may promote uncomplicated healing by relieving postoperative tension.



THE NICTITATING MEMBRANE



ANATOMY AND FUNCTION


The nictitating membrane, or third eyelid, serves to protect the globe, distribute tears, and produce immunoglobulins and part of the precorneal tear film. The caruncle is a small, finely haired prominence within the nasal canthus that may or may not be pigmented. The nictitating membrane has an exposed, palpebral conjunctival surface and a bulbar conjunctival surface that is in contact with the underlying globe. Superficial lymphoid follicles are located on the bulbar conjunctival surface and presumptively produce IgA, which becomes a component of the tear film. The nictitating membrane has an internalized T-shaped section of cartilage that serves as structural support. The gland of the nictitating membrane, located at its base, produces a portion of the aqueous part of the tear film and possibly immunoglobulins. The gland’s excretory ductules empty their products onto the bulbar conjunctival surface. Movement of the nictitating membrane is passive. As the globe is pulled deeper into the orbit by the retractor bulbi muscles, the nictitating membrane moves across the corneal surface. Sensory innervation of the nasal canthus, caruncle and nictitating membrane is supplied by the infratrochlear nerve, a distant branch of the trigeminal nerve.





FOLLICULAR CONJUNCTIVITIS


Follicular conjunctivitis is uncommon in horses. However, the nematode Thelazia lacrimalis (q.v.) commonly infests the conjunctival sac and nasolacrimal system. Depending upon the parasitic load, their active serpentine movement may cause secondary conjunctivitis or dacryocystitis (inflammation of the lacrymal sac) (q.v.). Treatment with topically administered, long-acting organophosphorus anticholinesterase compounds is reportedly effective (0.03–0.25% echothiophate [ecothiopate] iodide q 12 h, or 0.1% isoflurophate [dyflos] q 12 h for 7–10 days). The anthelmintic treatment should be administered in conjunction with an antibiotic–corticosteroid ophthalmic ointment. Since the intermediate host is believed to be the face fly, Musca autumnalis, fly control may prevent recurrence.



PROTRUSION (ELEVATION) OF THE NICTITATING MEMBRANE


One or both nictitating membranes may protrude more than normal. The specific etiology should be sought and appropriate treatment initiated. Concomitant clinical signs, diagnostic work-up, treatment and prognosis vary considerably depending upon the actual cause. Protrusion may be associated with enophthalmia (q.v.), due to passive elevation over a retracted eye, or with exophthalmia (q.v.), due to displacement of the nictitating membrane by a space-occupying lesion. Some causes of unilateral protrusion of a nictitating membrane include pain, Horner’s syndrome, phthisis bulbi (shrinking of the eyeball), microphthalmia, orbital fractures and a retrobulbar mass (e.g. neoplasia, abscess, cyst, cellulitis or foreign body granuloma) (q.v.). Bilateral protrusion of the nictitating membranes can be caused by dehydration, cachexia (loss of retrobulbar fat), tetanus (Clostridium tetani) and hyperkalemic periodic paralysis.



THE CONJUNCTIVA



ANATOMY


The conjunctiva is the mucous membrane that lines the eyelids (palpebral conjunctiva) and is reflected onto the surface of the globe (bulbar conjunctiva). The junction between the palpebral and bulbar conjunctiva is called the fornix. Ventrally, a fold in the conjunctiva covers the nictitating membrane. Palpebral conjunctiva is adherent to the underlying tissue, but the bulbar and fornix conjunctiva is mobile, to permit free movement of the globe.


The conjunctiva is composed of a non-keratinizing stratified columnar epithelium and an underlying layer of loose connective tissue, the substantia propria. The fornices and palpebral conjunctival epithelium are rich in goblet cells, which produce mucin. This allows for adhesion of the tear film to the ocular surface. The epithelium also contains melanin pigment. This is frequently most pronounced in the limbal and temporal bulbar conjunctiva and on the nictitating membrane. The bulbar conjunctival epithelium is continuous with the corneal epithelium and changes at the limbus, the corneoscleral junction.


The substantia propria contains many small superficial and deep blood vessels, allowing for the red appearance of the inflamed conjunctiva. The superficial portion of this layer contains lymphoid tissue that becomes active with antigen stimulation. This is particularly prominent on the bulbar surface of the nictitating membrane, adjacent to the limbus and in the ventral fornix. Lymphatic drainage is through the parotid lymph node.




CONJUNCTIVITIS


Inflammation of the conjunctiva may be caused by bacterial, viral, fungal or parasitic infections, or due to dacryocystitis or environmental factors, such as trauma, or irritants such as foreign bodies or solar irradiation (q.v.). Conjunctivitis must be distinguished from the ciliary flush, or deep hyperemia associated with uveitis or glaucoma (q.v.). The normal equine conjunctival flora consists of many bacteria, particularly staphylococci, as well as a variety of fungi.



Bacterial conjunctivitis


Frequently secondary to trauma, local irritants or systemic disease, compromised resistance may allow overgrowth of normal flora or opportunistic pathogens. Moraxella spp. may be associated with a primary conjunctivitis.


Diagnosis is based on conjunctival hyperemia and purulent ocular discharge. Culture is indicated in persistent cases or in outbreaks.


Treatment consists of removing the primary cause, if identified. Topical broad-spectrum antibiotics, such as gentamicin or triple antibiotic, 3–4 times daily, are usually sufficient to control the infection. Corticosteroids may also speed the resolution of the clinical signs, but should be used with caution if a specific cause of the conjunctivitis has not been identified, and are contraindicated in the presence of corneal ulcers. With uncomplicated bacterial conjunctivitis, prognosis is good with appropriate therapy.



Viral conjunctivitis


Generally seen in association with upper respiratory infections, viral conjunctivitis may be caused by rhinopneumonitis, influenza, adenovirus or viral arteritis infections (q.v.). The conjunctivitis is usually not a serious component of the disease, although an ocular examination should be carried out to rule out concurrent uveitis (q.v.). A severe hyperemic conjunctivitis can be the presenting sign in equine viral arteritis (q.v.), and this differential diagnosis of conjunctivitis is thus particularly important in countries free of the disease where early diagnosis of an infected animal is critical.


Diagnosis is usually best accomplished with serology. Treatment is non-specific. Topical broad-spectrum antibiotics may be used if secondary bacterial infection occurs. Prognosis for the eyes is good, as the conjunctivitis is usually self-limiting.




Parasitic conjunctivitis



Habronemiasis

The eye is a common site for habronemiasis (q.v.), as the moisture of the medial canthus attracts the flies that act as vectors. Larvae of Habronema muscae, H. microstoma or Draschia megastoma deposited by the flies migrate into the conjunctiva, skin and nasolacrimal system, where they incite an intense granulomatous reaction.


Granulomatous conjunctivitis/blepharitis, often at the medial canthus, is typically seen. Nodules are frequently ulcerated, with caseous, often mineralized “sulfur granules” being characteristic. Secondary corneal abrasions are common. Diagnosis may be confirmed by demonstrating larvae in the exudate or in a biopsy of the granuloma. The presence of a marked eosinophilic and mast cell infiltrate is supportive of the diagnosis.


Systemic ivermectin (0.02 mg/kg PO, single dose) is the treatment of choice. Echothiophate 0.03% solution applied topically twice daily is larvicidal. Antibiotics and corticosteroids are helpful in controlling secondary infection and inflammation. The latter is important since an immune reaction against dead larvae can cause severe reactive signs. Fly control will reduce re-infestation. Surgical excision of granulomas may be required.


Chronic granuloma formation and re-infestation are possible. However, resolution of conjunctival lesions is generally good.



Onchocerciasis

The adult Onchocerca cervicalis nematode (q.v.) lives in the ligamentum nuchae and produces microfilaria that migrate to subcutaneous tissues. Microfilaria are spread from horse to horse by biting midges (Culicoides spp.). Migrating microfilaria frequently reach the eye and adnexal structures. The disease, which includes conjunctivitis, keratitis, uveitis and chorioretinitis (q.v.), results from the inflammatory response to dying microfilaria.


Although demonstration of microfilaria in bulbar conjunctival biopsy may support the diagnosis, microfilaria may be found in many normal horses. Therefore, diagnosis should also be based on the finding of characteristic lesions. These include depigmentation of the lateral limbal conjunctiva, perilimbal keratitis and follicular perilimbal conjunctivitis.


As the dead microfilaria are more pathogenic than the living microfilaria, treatment with microfilaricidal drugs may exacerbate the condition. Therefore active inflammation should be controlled prior to antiparasitic treatment, using topical or subconjunctival corticosteroids. Specific therapy includes ivermectin (0.02 mg/kg PO, single dose), diethylcarbamazine (4.4–6.6 mg/kg PO daily for 21 days), or echothiophate (0.25% q.i.d. in both eyes for 21–28 days). Ivermectin may be the preferred drug as it is associated with less local inflammatory response.


Prognosis is good for conjunctival lesions. Corneal lesions and uveitis (q.v.) may be more chronic and are potentially recurrent problems.



Thelaziasis

Thelazia is a nematode found in the conjunctival fornix. Infections in horses have been attributed to T. lacrimalis, T. skrjabani, T. gulosa and T. californiensis. Infection may be common in some areas, but is frequently subclinical. Larger numbers of worms are found in younger horses. The face fly, Musca autumnalis, serves as the intermediate host.


Most infections show no clinical signs. However, epiphora, photophobia and keratitis (q.v.) may be seen along with the conjunctivitis. A seromucoid discharge and follicular conjunctivitis is seen in chronic cases. Nasolacrimal duct obstruction and keratoconjunctivitis sicca (q.v.) may also be seen. The worms are large (10–25 mm long) and are readily seen when they are moving. Topical anesthesia will immobilize them, making diagnosis more difficult.


Many anthelmintics may be ineffective for treatment. Topical anesthetics immobilize the worms and may allow for mechanical removal of some of the worm burden. Echothiophate may also be effective, given as 0.03% t.i.d. in both eyes. Fly control will reduce re-infestation and spread.


Prognosis is good, as most cases are asymptomatic.





THE LACRIMAL/NASOLACRIMAL SYSTEM



ANATOMY


The precorneal tear film consists of three layers: the inner mucin layer, produced by conjunctival goblet cells; the middle aqueous tear layer; and the outer oily layer, produced by the Meibomian glands at the eyelid margin. The mucin serves to bond the aqueous film to the hydrophobic epithelial surface, improving wetting ability. The outer oily layer reduces evaporation and prolongs the surface tension of the tear film, stabilizing its distribution. The aqueous portion, which makes up the bulk of tear film, is produced from the orbital lacrimal gland and the gland of the nictitating membrane. The orbital gland is located in the dorsolateral orbit and empties into the dorsal conjunctival fornix through multiple small ducts.


The action of the eyelids during blinking moves the tear film toward the medial canthus, and actively moves tears into the nasolacrimal puncta. There are two puncta, one on each eyelid. The dorsal and ventral puncta are approximately 8 and 5 mm from the medial canthus, respectively.


The puncta open into the canaliculi, which run medially and ventrally under the palpebral conjunctiva. The canaliculi drain into the lacrimal sac, located in the lacrimal fossa. The sac is drained by the nasolacrimal duct, which runs rostrally to the distal nasal meatus. The proximal one third of the duct runs through the lacrimal and maxillary bones. Distally, the duct runs through the lacrimal groove, a sulcus in the nasal wall of the maxilla, then turns ventrally to open on the floor of the nasal vestibule at the mucocutaneous junction. Multiple openings may be present in some animals and all may or may not connect with the nasolacrimal duct.



CONGENITAL ATRESIA


Atresia may occur at any point of the nasolacrimal duct, but is most frequent at the distal meatus.





Treatment

Atresia requires surgical correction under general anesthesia. Distal atresia can be corrected by approach through the nostril, or through a paramedian incision through the dorsal nostril wall. The duct is identified by catheterization through the dorsal punctum, or by distending the duct with fluid. The nasal mucosa is incised through into the duct and the catheter is advanced through the incision. The catheter is sutured in place and left for 3–4 wk to maintain patency. A topical ophthalmic antibiotic–corticosteroid solution will also reduce stenosis during healing.


More proximal atresia may necessitate a conjunctivorhinostomy by which a silicone tube is passed from the ventral conjunctival recess into the nasal passage after production of a stoma using a Steinman pin. After several weeks the new canaliculus becomes endothelialized and the tube can be removed. Postoperative management is as described for distal atresia repair.


Prognosis is fair to good, with distal atresia having a better prognosis for long-term cure after surgery than cases requiring conjunctivorhinostomy.



ACQUIRED DISEASES




Dacryocystitis


Inflammation, or infection, of the nasolacrimal duct may be unilateral or bilateral and can result from a variety of causes. Foreign bodies such as plant matter or sand, parasites such as Habronema spp. or Thelazia spp., adnexal neoplasia (most frequently squamous cell carcinoma) and infections of the upper respiratory tract or sinuses are all possible differential diagnoses (q.v.). A wide variety of secondary bacteria may be involved and cultures of exudate are indicated.




Treatment

After collection of exudate from the duct for cultures and cytology, the duct should be flushed thoroughly to remove the maximum amount of debris and exudate, and to restore patency if possible. It may help to pass a size 5 French catheter to provide optimal flushing. If the catheter can be passed in its entirety, it should be sutured in place for several weeks to maintain patency. If patency cannot be restored, plain radiographs and dacryocystorhinography (q.v.) should be performed to identify the obstruction and to find any bony changes. Treatment with an appropriate ophthalmic antibiotic–corticosteroid solution will frequently lead to resolution after patency is restored. Systemic antibiotics may also be indicated. If an obstruction resists flushing, treatment with an antibiotic–corticosteroid may reduce the swelling sufficiently to allow flushing of the duct after a few days of treatment.


Prognosis is generally good, depending on the primary cause, although recurrence is possible. Stenosis is possible in chronic cases and may necessitate surgical intervention.




Keratoconjunctivitis sicca


Inadequate tear production resulting in corneal or conjunctival inflammation is termed keratoconjunctivitis sicca (KCS). KCS is rare in the horse. It may be idiopathic or result from head trauma causing skull fractures, facial paralysis or parasitic infection of the lacrimal gland, or occur transiently during general anesthesia. Certain toxins, such as locoweed (Astragalus mollissimus), may also cause KCS. It should be noted that tear film deficiencies can be related either to reduced production of the aqueous phase of the tear film or to increased evaporation secondary to a reduction in the lipid layer that exists to reduce evaporation. Meibomitis (inflammation of the Meibomian glands, q.v.) may result in this evaporative form of dry eye. While differentiation of aqueous deficiency versus evaporative dry eye has been discussed in the literature, it is difficult to achieve in practice, and tear replacement is the treatment of choice in both.


< div class='tao-gold-member'>

Related posts:

  1. Oncology
  2. Fundamentals of the equine pre-purchase examination
  3. The stallion and mare reproductive system
  4. Perinatology

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 8, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Ophthalmology

Full access? Get Clinical Tree
Get Clinical Tree app for offline access