Chapter 13
Orbit and Globe

Anatomy of the orbit

Orbital structure differs somewhat between the various species, but basically is one of two types: open or closed orbital rim. Many of the facial and cranial bones are involved in the formation of the orbit. Adjacent to the bony wall of the orbit is modified connective tissue known as the periorbita which is continuous with the periosteum of the bones. Within or at junctions of these bones are found the various foramina through which pass the nerves and blood vessels to the eye and peribulbar structures.

Dog, cat, pig, birds

These species have an open orbit. In the dog, cat and pig, the bony orbital rim is discontinuous laterally. A thick, dense fibrous ligament (orbital ligament) spans the gap between the frontal and zygomatic bones. This ligament is an important landmark, especially for the administration of retrobulbar medications.

Horse, cattle, sheep, goat

These species have a continuous bony orbital rim. However, as with the other species above, the orbit is continuous posteriorly with the temporal fossa.

Humans and many other primates

These species have completely enclosed orbits which do not communicate with other portions of the head except by way of the various foramina.

Diagnostic considerations (McCalla and Moore, a, b)

When there is any change in the amount of tissue in the orbit, there will be concomitant displacement of the globe. If there is a reduction in orbital tissue, the globe will be displaced caudally giving a sunken appearance. When there is an increase in orbital tissue, a space-occupying effect is seen and the degree and direction of globe displacement are dependent upon the amount and location of the tissue. In general, the displacement of the globe will be to the opposite side of the space-occupying mass. For example, if the space-occupying mass is located ventromedially, the globe will be displaced dorsolaterally . In almost all cases, regardless of location, the space-occupying mass will cause a protrusion of the third eyelid. This is because even a slight increase in orbital tissue will displace orbital fat which in turn displaces the third eyelid. Therefore, you need to carefully evaluate the position of the globe to determine where is the space-occupying lesion.

If there is a space-occupying lesion in the orbit which not only displaces the globe, but also impinges upon it, there may be changes visible in the ocular fundus. Because the posterior eyewall will be indented, this will change the optical quality of the retina. Like a piece of clear plastic membrane which is being twisted or folded, the indented retina will appear opaque gray. You often can accentuate this by pressing gently on the globe through the upper eyelid while you do ophthalmoscopy. In cases where the orbital mass is not directly attached to the globe, it will impinge upon different regions of the caudal part of the globe as the eye moves. This will make the opaque region appear stationary while the globe is moving.

Congenital Abnormalities

Anophthalmia

This is complete absence of the eye and is extremely rare (Mausolf and Wunder). Most cases of clinical anophthalmia turn out to be severe microphthalmia because the individual has ocular vestiges of various sizes, sometimes demonstrable only histologically.

True anophthalmia often is associated with other severe, usually lethal, deformities of the head.

Microphthalmia

This condition is not uncommon and can be unilateral or bilateral. In severe cases the microphthalmic eye may be represented only by a tiny, melanotic cyst which is deeply embedded in the orbit and hidden from view by permanently closed eyelids. In less severe forms, there may be a small, but well developed eye with normal vision; this is called nanophthalmia.

Microphthalmia is most common in the collie and also is seen in the Australian shepherd, Pekingese, poodle, miniature schnauzer and Chihuahua. It occasionally is seen in other species (Fulton, et al.) and may be heritable in shorthorn cattle.

Strabismus and exophthalmos

These two conditions often are seen together when they occur congenitally. Exophthalmos, which simply means a protruding globe, can occur with numerous acquired conditions and needs to be evaluated carefully in each patient. The remainder of this subsection is primarily about the congenital occurrence of strabismus and exophthalmos.

In dogs, these conditions are most common in Pekingese, Pugs, Boston terriers and Chihuahuas.

In cats, strabismus alone is most pronounced in the Siamese in whom it is believed to be the result of abnormal retinal projections to the brain (the individual develops a convergent strabismus to compensate).

In cattle, these conditions may be heritable in Jerseys and shorthorns; not uncommon to see some degree of exophthalmos in Jerseys, Ayrshires and some Holsteins as a normal finding.

Appaloosa horses sometimes have a rotatory strabismus . This does not seem to be associated with any visual or behavioral problems.

Treatment is not necessary. Surgical intervention to reposition extraocular muscles usually fails.

Acquired Abnormalities

Orbital cellulitis (retrobulbar abscess)

This is one of the major diseases of the orbit.

Signs

Exophthalmos - this is one of the major signs.

Pain upon opening the mouth - due to mandibular movement which impinges upon orbital tissue.

Conjunctival discharge - may be serous or mucopurulent with blood.

The patient may be systemically ill - fever, lethargy and anorexia.

The globe itself usually is unaffected, but optic neuritis is a most serious complication.

Cause

Usually the cause is obscure. Many are due to foreign bodies (such as ingested bones or foxtail awns) which invade the orbit by way of the mouth (behind last upper molar teeth). The original wound seals, abscessation occurs, and the material cannot escape; exophthalmos follows.

Inflammation of orbital musculature, polymyositis, also can occur as a syndrome different from the typical orbital cellulitis (Carpenter, et al.).

Treatment

The best method, as with any abscess, is to create drainage (Rosenthal). This should be done with the patient under general anesthesia. The soft tissue just behind the last upper molar tooth (there may be a reddened zone) is entered with a large-gauge needle; the needle should be directed up into the orbit to make a track. Then, a hemostat can be used to enter this track and enlarge it. Purulent material then may escape into the mouth as the hemostat is removed. The orbit may be irrigated through this wound and then treated with potassium penicillin.

Often there will be little escape of material because the inflammatory reaction is diffuse. However, the production of a drainage track still is beneficial.

The patient also should be treated with broad spectrum antibiotics systemically.

If there is evidence of optic neuritis (loss of pupillary responses in the affected eye), then systemic steroids may be indicated. This is a difficult decision to make because the steroids may compromise resolution of the orbital cellulitis if there is a bacterial infection; on the other hand, the optic neuritis may lead to permanent blindness. Each case needs to be decided as it is presented; there are no hard-and-fast rules.

Prognosis

Prognosis is good if the disease is diagnosed early and treated properly. If the optic nerve becomes involved this may lead to optic nerve degeneration and blindness.

Proptosis

This is most common in the brachycephalic breeds of dogs in whom it occurs without a great deal of trauma. Proptosis in other canine breeds or other species usually is the result of severe head trauma, and often the proptosis is the least of the patient's problems.

The client should be told to keep the eye moist on the way to the hospital; can use gauze pads or a washcloth soaked in water into which has been added a small amount of salt or sugar (to create an osmotic differential to reduce some of the edema).

Initial assessment of the globe

If the eye has ruptured with extrusion of intraocular contents, enucleate the eye rather than try heroic measures to repair the globe. Rupture of the posterior segment of the globe will be suggested by an extremely soft eye with no visible lacerations.

The pupillary light reflex should be assessed. A response in the opposite eye when the affected eye is stimulated with strong light may indicate the retina and optic nerve are intact in the affected eye (to some degree at least); this would suggest that replacing the globe might be feasible. A lack of response, however, should be considered with caution. Although it probably means the prognosis for return of a functioning eye is poor, the lack of response could be from local tissue shock from which there may be recovery. If you are in doubt, and the globe is otherwise in good shape, replace it.

In severe cases, the optic nerve may be severed or avulsed from the globe; these globes should be enucleated . Even if the transection cannot be visualized, it may be inferred if the globe protrudes further than what may reasonably be guessed as the length of the optic nerve, or if the globe is markedly rotated laterally or medially.

In most cases, there is considerable optic neuritis even if the nerve is not severed. This situation may benefit from treatment as will be described.

If feasible, the pupil should be dilated with 1% tropicamide (Mydriacyl®) so that the ocular fundus can be examined. If the eye is kept moist and the globe is not being strangulated, this exam is worthwhile because it may provide you with information about the optic nerve and retina, and thereby give you a reasonable idea of the prognosis.

Vascular strangulation and glaucoma may occur in an intact globe due to closure of the eyelids behind it. These conditions usually are relieved when the globe is replaced.

Replacement of the globe

This usually should be done with the patient under general anesthesia. The longer the globe has been out, the more difficult will be its replacement. The globe must be kept moist from the time of initial trauma until treatment.

After routine cleansing, the globe should be moistened thoroughly (saline or ocular lubricant). Gentle pressure should be used to replace it within the orbit. Once the globe is replaced, a temporary tarsorrhaphy should be done.

If the globe cannot be replaced easily, several temporary tarsorrhaphy sutures should be preplaced. Then insert the handle end of a scalpel handle between the globe and the sutures passing over it. At that point, pull all the sutures upward (outward) while applying gentle pressure to the globe with the scalpel handle. Once the globe is in place, remove the scalpel handle and tie the sutures to keep the palpebral fissure closed. The sutures should be left for at least a week. If the globe cannot be replaced easily, a lateral canthotomy should be done.

If the eye cannot be replaced or the eyelids adequately closed over it, the globe should be enucleated.

Medical therapy after replacement of the globe

Systemic steroids and antibiotics should be used.

Topical steroids and antibiotics should be administered through the closed eyelids four times a day (ointments are best for this). If the cornea is ulcerated, use only an antibiotic until the ulcer has healed.

Topical iridocycloplegics such as atropine ointment should be administered once a day.

Retrobulbar steroids may be indicated, but you should seek the assistance of a specialist before instituting this type of therapy.

Complications

When the tarsorrhaphy sutures are being removed, the globe may tend to prolapse in which case the sutures should be left in another week or more. If after that time the globe still has a tendency to prolapse, a permanent partial tarsorrhaphy may be required.

If vascular strangulation was present for some time, infarction of the ocular anterior segment may occur which will lead to corneal and conjunctival necrosis. Some of these eyes may remain functional if there is re-vascularization with regeneration of tissue after incomplete infarction.

After successful repair, the eye may be deviated due to extraocular muscle damage. This often will spontaneously correct itself in time.

Various ocular problems may be anticipated in severe cases and include: corneal scarring, cataract, retinal separation (detachment) and optic nerve degeneration. If the globe remains comfortable to the patient and is cosmetically acceptable, these complications may be ignored.

Prognosis

Because of optic neuritis and other potential problems, the prognosis for continued vision in the affected eye is guarded (Gilger, et al.).

Glaucoma

Glaucoma is an increase in intraocular pressure and the pathologic changes produced by this increased pressure (Brooks and Dziezyc; Gwin). It occurs in virtually any species (Heywood; Kinnear, et al.; Kolker, et al.; Martin and Wyman; Miller, et al.; Wilcock, et al.).

It is extremely important to bear in mind that as such, glaucoma should be considered only a sign of ocular disease rather than a specific disease. Many different conditions can lead to an increase in intraocular pressure. Knowing which is involved in a particular case can be a critical factor in successful treatment. On the other hand, there are certain pathological processes that are independent of the cause of the glaucoma and these may continue to have a deleterious effect even if intraocular pressure is reduced to what is considered a normal value (Weinreb and Levin). Therefore, neuroprotection of the ganglion cells and optic nerve axons, although not clinically feasible at the time of writing these notes, may become an important consideration in properly managing a patient with glaucoma.

The disturbance of aqueous humor flow is the major factor involved in glaucoma. Aqueous humor not only maintains intraocular pressure (and part of the shape of the eye), but also serves as a carrier of metabolites to, and waste products from, the lens and cornea.

Normal aqueous humor pathway

Before you can appreciate the reasons for glaucoma, you must understand the normal sequence of events:

Aqueous humor is secreted by the ciliary epithelium into the posterior chamber. Formation of aqueous humor is by passive diffusion or ultrafiltration, and by active secretion against a concentration gradient.

From the posterior chamber, aqueous humor passes through the pupillary aperture into the anterior chamber where it circulates.

Aqueous humor leaves the anterior chamber through the ciliary cleft (also known as filtration or drainage angle). It passes between the pectinate ligaments, through the trabecular meshwork, and then into the scleral collecting vessels which empty into scleral veins.

The process by which aqueous passes from the trabecular meshwork into the collecting vessels is not fully understood, but it is not by simple diffusion alone. Evidence indicates that active transport across cell membranes occurs.

Sites of aqueous humor outflow blockage

Pupil - e.g., extensive posterior synechiae.

Anterior chamber - e.g., cellular debris, luxated lens.

Chamber angle - e.g., extensive anterior synechiae, especially peripherally.

Trabecular meshwork - e.g., cellular debris, post-inflammatory scarring.

Unknown.

Types of glaucoma

Glaucoma generally is considered to be one of two types: primary or secondary. Another term which is used is absolute glaucoma, which means glaucoma which is not treatable.

Primary glaucoma: Cause is unknown; block in aqueous humor outflow is due to inherent defect in the globe. Of the two types, primary glaucoma is less common in domestic animals.

Open ciliary cleft (angle) - glaucoma in the presence of an open and normal appearing chamber angle. This type of glaucoma is common in humans, but has not been well documented in others, although it may be the type of heritable glaucoma which occurs in beagles (Gelatt).

Narrow ciliary cleft (angle) - reduction in aqueous humor outflow due to forward displacement of the iris. This also is more common in humans than others, but is a heritable problem in American cocker spaniels (Lovekin and Bellhorn) and some other canine breeds.

Mesodermal dysgenesis - the angle has not developed normally so that sheets of mesodermal tissue block the flow of aqueous humor. Most of these patients have so-called flow holes in the mesoderm so that aqueous humor outflow may occur. Whether mesodermal dysgenesis alone is a true cause of glaucoma is debatable because this condition is seen frequently in certain breeds of dogs with no increase in intraocular pressure. It may be that it has no effect on aqueous humor outflow or that it predisposes the eye to glaucoma. This condition is seen in at least American cocker spaniels (Bedford), basset hounds (Martin and Wyman), and certain strains of rabbits.

Secondary glaucoma: Blockage of aqueous humor outflow is secondary to other intraocular disease processes. This is the most common form of glaucoma seen in domestic animals. In fact, when a diagnosis of glaucoma is made in a domestic animal you should assume it is secondary (until proven otherwise), and search for a cause.

Some of the conditions in which an increase in intraocular pressure (glaucoma) occurs include:

Luxation or subluxation of the lens - glaucoma due to blockage of the ciliary cleft, pupillary block or unknown reasons.

Anterior uveitis - glaucoma due to formation of synechiae (peripheral anterior or posterior with iris bombé), or clogging of the ciliary cleft with inflammatory debris.

Lens intumescence - glaucoma due to forward displacement of iris and narrowing of ciliary cleft.

Surgery or trauma leading to scarring of the ciliary cleft.

Resorbing cataractous lens - this may lead to anterior uveitis with secondary changes that result in glaucoma; may be complicated by lens material-laden macrophages which may clog the ciliary cleft.

Intraocular neoplasia - glaucoma secondary to inflammation, or by neoplasm physically blocking aqueous humor outflow.

Canine breeds predisposed to glaucoma

In many cases, the reason behind this predisposition is unknown.

Terrier breeds, cocker spaniels (American and English) (Bedford; Lovekin and Bellhorn), basset hound, poodles, beagle (Gelatt), Siberian husky, Norwegian elkhound, to name a few.

Diagnosis of glaucoma

Early: Increased intraocular pressure - this is the only way of verifying the diagnosis and differentiating this condition from others which cause similar signs; this means it is mandatory that you have a tonometer of some type available in your practice. If the pressure is very high, the patient temporarily may be blinded. See elsewhere for information on tonometry.

The pupil may be dilated with little or no response to light, unless there is uveitis, in which case the pupil may be miotic. However, dilated pupils alone are not a sign of glaucoma.

Episcleral vascular congestion .

Corneal opacification due in part to edema, and in part to change in arrangement of collagen fibers , particularly with pressures above 55 mm Hg.

Pain or discomfort manifested by blepharospasm or pawing at eye.

Cupping of optic disk - the degree depends on the amount of rise in intraocular pressure as well as the duration; this may not occur in acute glaucoma where pressures are only moderately elevated.

Retinal degeneration - as with optic disk cupping, amount and duration of pressure increase are important considerations; the ganglion cells and their axons (optic nerve) are affected first, and may be the only part affected; this may be very difficult to demonstrate clinically. The reason for predilection of the ganglion cells is unknown.

Gonioscopy (Gelatt and Ladds; Martin) may reveal various abnormalities of the chamber angle : narrowing, closure, scarring, neoplastic invasion, etc. (Compare with normal angle .) When unilateral glaucoma is diagnosed, gonioscopy of the normal eye should be done to determine its status. A narrow or abnormal angle would warrant preventive medical therapy of indefinite duration in the so-called normal eye, regardless of the outcome of the obviously abnormal eye.

An important part of the evaluation of a glaucoma patient for prognostic purposes is the pupillary light response. With unilateral glaucoma, presence of a response in the opposite eye when the affected eye is stimulated with strong light indicates that the optic nerve still is functioning and offers a somewhat better prognosis. Lack of this consensual response suggests severe damage to the optic nerve in the affected eye.

Late: Buphthalmia - this is due to stretching of the fibrous coat of the eye. It is prominent in young individuals due to scleral elasticity (therefore, may be an early sign in very young individuals); it may not occur in horses and is less prominent in cats.

Striate keratopathy due to linear breaks in, or stretching of, Descemet's membrane; often appear as deep, parallel, white or gray lines .

Lens luxation secondary to buphthalmia (due to zonular rupture).

Pronounced optic disk cupping and optic nerve degeneration .

Advanced retinal degeneration.

Permanent blindness.

Intraocular pressure may be lower than normal if ciliary body function has been compromised.

Treatment

Because glaucoma is a very difficult condition to manage, the best thing you can do for the patient is to start her or him on nonspecific therapy to reduce intraocular pressure and refer her or him to a specialist immediately. I strongly suggest you not attempt to manage the situation yourself without at least consultation with a specialist. Nonspecific therapy would include osmotic agents such as glycerol or mannitol, and carbonic anhydrase inhibitors.

If the cause of the glaucoma is not due to an acquired problem, the opposite eye, even if apparently normal, may benefit from being treated prophylactically. This is another reason why you should seek the help of a specialist. Proper management of the 'unaffected' eye may extend vision in that eye (Slater and Erb). Nevertheless, the prognosis in the case of heritable predisposition to glaucoma is very poor because, even with prophylactic therapy, the 'unaffected' eye eventually may become glaucomatous.

If for some reason you cannot refer the patient to a specialist, you first must try to determine the reason for increased intraocular pressure or else rational therapy cannot be initiated.

Generally, mydriatics are contraindicated in glaucoma because they tend to further narrow or obstruct the ciliary cleft. Although epinephrine compounds are used, their mydriatic effect usually is not problematical.

Treatment is aimed at reducing intraocular pressure and maintaining it within normal range. This can be accomplished by decreasing the amount of aqueous humor produced, increasing the aqueous humor outflow, osmotically reducing the pressure, or combinations of the three. The actual cause of the pressure increase also must be treated if there is to be long term success.

In the future, additional therapy may be aimed at protecting surviving retinal ganglion cells and optic nerve axons from destruction by neurotoxic compounds which are released by those which are damaged (Weinreb and Levin).

Reducing aqueous humor production: By using a carbonic anhydrase inhibitor, you can block aqueous humor production up to a maximum of about 50% (carbonic anhydrase is an enzyme necessary in aqueous humor production). One of the best of these agents is dichlorphenamide at 4-8 mg/kg body weight two or three times a day. Because these agents deplete potassium, the patient must be receiving adequate nourishment.

This also can be done by surgically destroying portions of the ciliary body (cyclodialysis, cyclodiathermy, cyclocryotherapy). These procedures should be done only by a specialist.

Increasing aqueous humor outflow with or without reduction in production: Various combinations of sympathomimetic and parasympathomimetic medications may be used topically, usually for primary glaucoma. One percent pilocarpine and 1% epinephrine may be used together two to four times a day depending upon the response of the patient. Dipivefrin, an epinephrine prodrug, can be used at the rate of one drop twice a day. Timolol maleate has questionable efficacy in dogs and cats unless given at higher concentrations than commercially available (at least in dogs (Gum, et al.)).

Surgical procedures may be employed to increase aqueous humor outflow by creating artificial openings in the globe to allow filtering of aqueous (iridencleisis or iridocyclectomy). These procedures should be done only by a specialist; they have a high failure rate regardless.

Osmotic reduction of intraocular pressure: This method is dependent upon an intact blood-ocular barrier so that the osmotically active molecules (glycerin and mannitol are most popular) can produce the desired effect. Mannitol is given intravenously at 1-2 gm/kg body weight and is an excellent, quick method of reducing intraocular pressure in acute cases (it also reduces vitreous volume, which is helpful). Glycerin is given orally as a 50% aqueous solution at 1-2 cc/kg body weight.

These osmotic agents are used initially to reduce pressure, but should not be continued as part of the definitive therapy.

Other methods: Cryosurgery or laser (Nasisse and Davidson) therapy is used to destroy portions of the ciliary body in an attempt to reduce the production of aqueous humor. These methods are not universally effective.

Prognosis

Generally, the prognosis for vision in domestic animals with glaucoma must remain guarded to poor. This stems, in part, from the patients being brought for diagnosis after irreversible damage has occurred, or due to incorrect diagnosis and treatment initially.

Pressures greater than 60 mmHg for 24-48 hours may lead to permanent impairment of vision or blindness.

Once buphthalmia occurs, return of vision is unlikely. The more advanced the glaucoma, the more difficult it is to control.

Panophthalmitis

This term is used to describe ocular inflammation involving all coats of the eye (fibrous, vascular and neural). It usually is used to designate widespread ocular inflammation although it technically could be used for a focal involvement of all three layers.

The signs shown by affected patients are not specific. The eye is markedly inflamed usually with prominent corneal edema, debris in the anterior chamber, marked congestion of the superficial and deep vessels of the conjunctiva and episclera, moderate to marked swelling of the conjunctiva, and a mucopurulent discharge. Blepharospasm usually is severe due to the amount of pain the patient experiences.

Panophthalmitis is not a specific disease; it is a pathologic condition which can be caused by numerous insults. Some of the causes are: 1) perforating corneal ulcer with intraocular contamination, 2) systemic bacterial or fungal infection with ocular involvement, and 3) proptosis of more than few hours' duration.

One of the important factors in panophthalmitis is the potential for spread of the inflammatory process to the brain by way of the optic nerve meninges. This must be considered when attempting therapy. Generally, diffuse panophthalmitis is not amenable to medical therapy and enucleation is the treatment of choice. Even if the inflammation subsided, the damage to internal ocular structures usually results in blindness.

Endophthalmitis

This term describes inflammation present within the ocular cavities and adjacent structures. As with panophthalmitis, it is a pathologic condition with many potential causes, and not a specific disease.

The signs seen in endophthalmitis are similar to those seen with moderate to severe uveitis. There may be leukocoria due to inflammatory exudate in the vitreous.

Much of the discussion on panophthalmitis is applicable to endophthalmitis although, if the specific cause of inflammation is determined, the prognosis is somewhat better with endophthalmitis.

Surgical procedures involving orbit and globe

It is hoped that removal of an eye is not frequently necessary, but sometimes it is inevitable and you must decide which of the following procedures is best suited for the condition at hand.

Enucleation

This involves removing the globe and conjunctiva. Extraocular muscles and other orbital structures are left behind. Some conditions for which enucleation is justified include intraocular neoplasms, absolute glaucoma, severe panophthalmitis, and severe endophthalmitis, if the inflammatory or neoplastic process does not extend beyond the globe into Tenon's capsule or conjunctiva.

For small animals and horses, general anesthesia is necessary. Chemical (with analgesic qualities) and physical restraint can be used in cattle and sheep along with local anesthesia. The latter can be local infiltration of the eyelid margins and subconjunctival and retrobulbar regions. An auriculopalpebral block for akinesia can be used if the sedation is insufficient for preventing eyelid movement.

Caution: When removing an eye, regardless of the method chosen, you should apply very little traction on the optic nerve. Particularly in the cat and the bird, even mild tugging on the optic nerve may cause damage to the optic chiasm. This can lead to permanent blindness in the remaining eye. Although not published as a documented series of cases at the time of writing this paragraph, several cats and at least one bird have had unilateral enucleation and awakened from anesthesia blind in the remaining eye. The signs in these eyes indicated severe damage to the optic nerve and the only feasible conclusion was that traction on the optic nerve of the eye being removed resulted in damage to the chiasm.

Technique for enucleation (subconjunctival approach (Kuhns)): A lateral canthotomy is done. The bulbar conjunctiva is incised 360 degrees around the globe leaving at least 5 mm attached to the globe for manipulation. The conjunctiva not attached to the globe is undermined with curved scissors (preferably Metzenbaum scissors), and the attachments of the extraocular muscles (and other tissue), to the globe are severed. This dissection is carried out until the globe is freed enough to rotate within the orbit. A clamp (curved hemostat, or tonsil snare), is placed around the optic nerve and associated blood vessels. Curved scissors are used to sever the final attachments distal to the clamp, and the eye is removed and placed in appropriate fixative prior to submitting it for histologic evaluation.

Absorbable suture material may be used in an attempt to place a ligature proximal to the clamp, and the clamp removed; realistically, you may simply leave the clamp in place for several minutes for hemostasis, and not use a ligature. The nictitating membrane then is excised (if it was not removed along with the globe) along with the remainder of the bulbar and palpebral conjunctiva. Absorbable suture material is used to appose the subconjunctival tissues across the orbit.

The eyelid margins (about the distal 3 mm), are removed around the entire circumference (exercise extra care medially: here it is more difficult to adequately excise the tissue; you must remove all skin, the caruncle, and the medial canthal ligament; if not adequately excised, healing will be impaired). The incised edge of the upper eyelid then is apposed to the lower using non-absorbable skin suture in an interrupted fashion (either simple or horizontal mattress).

For a few days after surgery, there may be a bloody discharge from the nostril on the side of the surgery due to passage down the nasolacrimal duct. The client should be told about this.

Regardless of how the surgery is done, there usually is a certain amount of permanent invagination of the skin overlying the orbit after healing occurs; the client must be warned about this. Fortunately, with time, regrowth of hair helps improve the appearance.

On occasion, glandular secretions (conjunctival or lacrimal), may persist after surgery so that a fluid-filled cyst forms. This easily is corrected by re-entering the orbit and dissecting out the cyst.

Birds present special problems when enucleation is necessary (Murphy, et al.). Because of the shape of the orbit and because the globe is tightly encased, removal of the globe is difficult. In addition, the bones of the orbit are very thin and easily fractured.

Exenteration

This procedure involves removing the entire orbital contents. Some indications for exenteration would include retrobulbar neoplasms, unresponsive orbital inflammation, and orbital extension of an intraocular neoplasm.

The technique is essentially the same as for enucleation, except that the extraocular muscle cone, orbital fat, and other tissues also are removed.

Evisceration

This is a special procedure which involves removal of all intraocular contents leaving behind the sclera and cornea. It usually is not indicated except for cosmetic purposes where an intrascleral implant is to be used, such as with absolute glaucoma. I am not in favor of using such implants because they extend the painful period of the patient, they have potential for causing serious problems due to rejection and they are done only for cosmetic reasons with no benefits to the patient.

Sarcoma of globe in cats

Cats who have had ocular trauma resulting in phthisis bulbi appear to be at risk for developing intraocular sarcoma (Dubielzig, et al.). Besides a history of trauma, a common feature in these cases is rupture of the lens. It may be that the lens epithelial cells undergo malignant transformation, or the neoplastic process may be from activated retinal epithelial cells.

These neoplasms can be aggressive and spread locally and grow into the brain along the optic nerve. Therefore, you should enucleate phthisical eyes in cats rather than leave them in the orbit even if there appear to be no problems for the individual. This should be done as soon as possible after phthisis bulbi is recognized, and as much of the optic nerve as possible should be removed with the globe, with appropriate care not to apply too much traction or else there may be damage to the optic chiasm. If a traumatized cat eye is not yet phthisical, but the eye is blind and you cannot see the intraocular structures due to opacification of the ocular media, it would be prudent to remove the affected globe. If there is any question about the propriety of removing the globe, consult a specialist.

The syndrome of ocular sarcoma following trauma appears to be a problem primarily of cats. Although it has not been reported in dogs and other nonhuman animals, it would be prudent to remove phthisical eyes from any patient in whom there is a history of a penetrating or perforating wound to the globe.

Orbital neoplasia

Neoplasia of the orbit is relatively uncommon. Most neoplasms causing signs relating to orbital disease stem from other than ocular sources, or they may be extensions of intraocular neoplasms (Dukes and Pettit; Kern).

Signs of orbital neoplasia

The most prominent feature is exophthalmos of slow onset. Deviation of the globe occurs when the neoplasm is other than directly retrobulbar (the deviation is away from the neoplastic invasion). The globe often is fixed in position.

Other signs include protrusion of the nictitating membrane; edema of the eyelids, conjunctiva and retina may occur; pain; exposure keratitis; loss of vision due to optic nerve involvement. Always examine the fundus; there often is indentation of the globe that can be visualized as a zone of color or reflection alteration . You can sometimes accentuate this by gently pressing on the globe as you view the fundus .

Diagnosis

Any patient showing signs of a space-occupying lesion within the orbit should be suspected of having a neoplasm.

Particular attention should be paid to the history because this will help in differentiating neoplastic from other diseases causing similar signs: neoplastic changes usually progress slowly.

As part of a diagnostic workup, you may want to sample tissue from the orbit. Depending on the condition of the eye, you could use needle aspiration (Boydell), explore the orbit to get the specimen (if the globe is in good condition), or exenterate the orbit (if the eye is in poor condition and there is no hope of continued visual function).

Orbital angiography also can be useful in demonstrating unusual vascular patterns, but findings in domestic animals usually are difficult to interpret. Other radiographic contrast techniques also are available (Gelatt, et al.).

Ultrasonography and magnetic resonance imaging (Grahn, et al.) are increasingly becoming more important in evaluating orbital disease. These procedures, like angiography, usually is limited to large specialty practices or teaching institutions.

If you believe that orbital cellulitis (retrobulbar abscess) is not the problem, but believe some other inflammatory process is present, you may want to institute a short course of systemic steroid therapy, with antibiotic if susceptible infection is suspected, to see if there is a response. Sometimes idiopathic inflammation of the orbital contents (so-called pseudotumor, a poor term), may mimic a neoplasm. However, improvement with therapy does not rule out neoplasia because there may have been an inflammatory component to the neoplasm, which responded temporarily to treatment. If this is the case, signs will return shortly.

If physical examination, radiography of the orbit, needle biopsy and trial therapy are inconclusive, and other diagnostic modalities are unavailable to you, it would be best to refer the patient to a specialist. If this is impractical, you may have to enucleate the globe or exenterate the orbit to reach a diagnosis or treat the condition.

Neoplasms involving the orbit

Melanoma extending from the uveal tract.

Nasal and sinus cavity carcinomas extending through floor of orbit.

Squamous cell carcinoma.

Lymphosarcoma (Rebhun).

Meningioma.

Other less common ones: angiosarcoma (Hacker, et al.), rhabdomyosarcoma, zygomatic gland carcinoma ( Buyukmihci, et al.), chondrosarcoma and osteosarcoma.

Treatment

Generally, enucleation or exenteration is the only practical treatment. Rarely, a neoplasm will be well-localized or encapsulated so that it can be removed completely by exploring the orbit surgically. In some instances, radiation therapy must be combined with surgery.

In those cases where the neoplasm is metastatic (e.g., lymphosarcoma), treatment is not practical.

Footnotes:

Lateral approach to enucleation: There also is a lateral approach to enucleation (see Bistner, et al. or article by Bellhorn). This method may provide better visualization of the orbital structures, an opportunity for better control of hemorrhage, and less chance of rupture of the globe.