Orbit

The orbit is a bony fossa that encompasses the eye, associated muscles, nerves, and vasculature. It protects the eye as well as separates it from the cranial cavity. All vertebrate orbits are of two types: (1) the enclosed orbit, which is completely surrounded by bone (e.g., horses, sheep, cattle, and goats), or (2) the open or incomplete orbit, which is only partially surrounded by bone (e.g., dogs, cats, and pigs) [1,2]. The bones that form the orbit in dogs, cats, cattle, and sheep are the lacrimal, zygomatic, frontal, sphenoid, palatine, and maxillary. In horses, goats, and pigs, there is no involvement of the maxillary bone. Instead, the temporal bone and the ethmoid bone contribute to the orbit in horses and pigs, respectively. The orbital foramen is differently structured in the horse and is therefore referred to as the “orbital fissure” in this species. In cattle and pigs, the orbital fissure and foramen rotundum are typically fused to form the foramen orbitorotundum [1,2].

Ocular adnexa

The orbital fascia is a thin, tough connective tissue layer that lines all the structures within the orbit. This fascia encompasses three anatomic structures: the periorbita, Tenon’s capsule, and the extraocular muscles (EOM). The orbital fat fills up the spaces between these structures and acts as a protective cushion for the eye. The EOMs suspend the globe in the orbit and provide ocular mobility. The seven orbital muscles that control the movement of the globe are the dorsal rectus, ventral rectus, medial rectus, lateral rectus, dorsal oblique, ventral oblique, and retractor oculi (Table 67.1) [1,2]. The retractor oculi muscle is absent in birds and snakes [3]. The eyelids are two musculo‐fibrous folds of the skin. The space between the upper and lower eyelids is called the “palpebral fissure.” Closure of the palpebral fissure is achieved by contraction of the orbicularis oculi muscle. Opening of the eyelids is mediated by the relaxation of the orbicularis oculi muscle as well as contraction of the levator palpebrae superioris muscle (Table 67.1) [2,4].

The conjunctiva is the clear thin mucous membrane that lines the inner aspect of the eyelids, the nictitating membrane, and the exposed sclera. The nictitating membrane is a thin translucent sheet of ocular tissue situated ventromedial to the globe, which is actively retracted across the cornea to provide protection and lubrication. It is well developed in domestic animals, while in higher primates, it is a vestigial structure. In most domestic animals, the movement of the nictitating membrane occurs due to contraction of the retractor oculi muscle. However, in cats, since the retractor oculi muscle is less developed, adjacent smooth muscle bundles may contribute to its movements [2].

Globe

The globe is made of three tunics that surround the transparent ocular media, which are the aqueous humor, the lens, and the vitreous humor. The outermost fibrous tunic is further divided into the cornea and sclera. The avascular cornea protects the internal structures of the eye, contributes to the refractive power of the eye, and forms a retinal image via focusing of light rays. The sclera is a tough, opaque layer filled with a dense network of collagen and elastic fibers. There is also a cartilaginous component seen in fish, lizards, chelonians, certain amphibians, and birds [3]. It is the supporting wall of the globe and helps maintain the structure of the eyeball and protects it from injury.

The thick middle layer is the vascular tunic, commonly referred to as the “uvea” or “uveal tract.” It is interposed between the retina and the sclera and is heavily pigmented and vascularized. The iris, ciliary body, and choroid are three subparts of the uvea. The pigmented iris controls the quantity of light entering the eye through the pupil, as well as influences the pupil size. The heavily pigmented ciliary body provides nourishment and removes waste from the cornea and lens and participates in lens accommodation. The choroid is composed of blood vessels and pigmented support tissues, and it nourishes the outer retinal layers.

The innermost layer is the nervous tunic, consisting of the retina and optic nerve. The ten‐layered neurosensory retina is connected to the brain by the optic nerve and the optic tracts. The rods and cones (i.e., retinal photoreceptors) transform light stimuli from the external environment into nerve impulses and transmit these signals to the brain where they are converted to visual images. The optic nerve extends from the globe to the optic chiasm, and forms optic tracts. The transparent, avascular, and crystalline lens focuses light rays on the sensory retina, providing optimal focusing power for visual clarity.

Ocular circulation

In domestic animals, branches of the external carotid artery (i.e., the internal maxillary and external ophthalmic arteries) form the primary blood supply to the eye and its adnexa. The internal ophthalmic artery is a smaller artery that arises from the rostral cerebral artery at the level of the optic chiasm, providing blood supply for the optic nerve. The long and short posterior ciliary arteries are derived from the external ophthalmic artery, and they supply most of the blood to the anterior segment of the eye, including the retina and the choroid. The retinal arteries are derived from the short posterior ciliary arteries as they pass through the sclera at the periphery of the optic nerve [2,4].

There is significant variation within domestic animals with respect to the venous drainage of the eye. In dogs, the two main venous channels are the supraorbital and the inferior orbital veins. The supraorbital vein further unloads into two prominent veins, the orbital vein entering intracranially, and the internal maxillary vein connecting with the external jugular vein. The cat has an external rete, which is drained by a large ophthalmic vein connecting to the external jugular vein. Also, the supraorbital vein drains into the facial vein, finally emptying into the internal jugular vein. In horses, the principal ocular venous channels are the ophthalmic, orbital, supraorbital, and reflex veins [2,4].

Ocular innervation

The eye and its adnexa are innervated by the optic, oculomotor, trochlear, trigeminal, abducens, and facial nerves (Table 67.2, Fig. 67.3).

Assessment of palpebral and the corneal reflexes is considered standard monitoring during general anesthesia in animals to characterize the anesthetic depth. The palpebral reflex is tested by lightly touching the lateral and medial canthi, which results in eyelid closure. The afferent pathway is via the ophthalmic and maxillary branches of the trigeminal nerve, for medial and lateral stimulation, respectively. The efferent arm is the facial nerve. The corneal reflex is assessed by touching the cornea with a wisp of cotton wool or a swab tip or a drop of sterile water, which should result in retraction of the globe and eyelid closure. The afferent arm of the corneal reflex is mediated by the ophthalmic branch of the trigeminal nerve, and the efferent arm is mediated by the abducens nerve (globe retraction) and facial nerve (eyelid closure) [9].

Aqueous humor

Aqueous humor (AH) is a transparent, colorless liquid that fills the anterior and posterior chambers including the pupil. It nourishes the cornea and the lens, removes waste products, and maintains the intraocular pressure and globe shape. The mean AH turnover rate among several species is approximately 1–2% of the anterior chamber volume per minute, with cats having a lower turnover rate (0.7%/min) when compared to dogs and humans [10]. Two‐thirds of AH is produced in the posterior segment of the ciliary body via active mechanisms such as the sodium pump, carbonic anhydrase‐catalyzed reaction of CO₂ hydration, and the cytochrome oxidase systems. These active processes lead to a higher AH osmotic pressure than the plasma, and this disparity promotes a continuous production of AH. The remaining one‐third is passively formed at the iris capillaries by diffusion of lipid‐soluble substances moving down a concentration gradient, as well as ultrafiltration from plasma in response to an osmotic gradient or hydrostatic pressure.

The AH exits the eye through two pathways. In the conventional or trabecular route, aqueous fluid passes from the posterior chamber, through the pupillary aperture into the anterior chamber. From there it flows through the trabecular meshwork into the angular aqueous plexus, finally draining into the episcleral veins, conjunctival veins, and vortex venous system that join the systemic venous circulation. The majority of the AH (i.e., ~50% in horses, 85% in dogs, and 97% in cats) leaves the eye via this route [11]. The unconventional or uveoscleral pathway excludes the trabecular meshwork. The AH bathes the iris and the ciliary muscle to reach the supraciliary space or the suprachoroidal space. From here, it seeps through the sclera and is absorbed into the orbital vasculature. Uveoscleral outflow drains the remainder of the AH (i.e., ~15% in dogs [12] and 3% in cats [13]). Horses appear to have a higher dependency on this pathway [14].

Vitreous humor

The vitreous humor (VH) is a transparent elastic hydrogel that comprises a portion of the clear ocular media, and accounts for up to two‐thirds of globe volume. It occupies the space between the lens and sensory retina and maintains structural integrity of the posterior portion of the globe. It is part of the optical pathway through which light passes as it travels to the retina. The VH is 99% water, and the remaining 1% is a network of polygonal, hydrated fibrils consisting of type II collagen and hyaluronic acid [11]. The collagen provides plasticity and hyaluronic acid contributes to the viscoelasticity of the VH.

Intraocular pressure

The pressure exerted by ocular contents against the globe is termed “intraocular pressure” (IOP). In the healthy eye, IOP is generated by a delicate balance between rates of AH inflow and outflow, keeping it at a steady state when the rates are equivalent. The most important influence on AH formation is the difference in osmotic pressure between AH and plasma [15]. The relationship is illustrated as:

where K is coefficient of outflow, OP_aq is osmotic pressure of AH, OP_pl is osmotic pressure of plasma, and CP is capillary pressure. This equation explains why mannitol, due to its hypertonicity, can lower IOP by influencing AH production. The normal IOP range in dogs, cats, and rabbits is 15–20 mmHg, while in cows and horses, IOP ranges from 20–30 mmHg and 17–28 mmHg, respectively [11]. The IOP can be theoretically determined by the Goldmann equation:

where Q represents the aqueous inflow (in μL/min), U represents the uveoscleral outflow (in μL/min), C represents conventional aqueous outflow facility through the trabecular meshwork (μL/min/mmHg), and EVP is the episcleral venous pressure [11].

The primary factors impacting IOP are: (1) pressure on the eyeball; (2) muscle tone of EOM and orbicularis oculi muscle; (3) AH production and drainage, (4) corneal and scleral rigidity; (5) volume of intraocular contents; and (6) episcleral venous pressure (Table 67.3).

Muscle tone of extraocular and orbicularis oculi muscles

The central nervous system (CNS) impacts IOP directly through neurogenic control of extraocular muscle tone by central diencephalic centers, and indirectly via hormonal and hemodynamic effects. Increased tone or contracture of EOM and the orbicularis oculi muscle can markedly increase IOP, which is observed during rapid blinking, forced eyelid closure, inadequate plane of anesthesia, and with drugs like ketamine and succinylcholine. In contrast, general anesthesia lowers IOP partly by depressing the central control centers.

Aqueous humor production and drainage

The rate of AH formation by the ciliary epithelium is influenced by sympathetic and parasympathetic innervation, as well as humoral mechanisms. Topical β‐adrenergic receptor antagonists (e.g., timolol) and α₂‐adrenergic receptor agonists (e.g., brimonidine) may lower IOP by decreasing AH production. During sleep, AH formation decreases by about 50%. Further, depending on whether animals are nocturnal or diurnal, variations in AH production and IOP may follow a circadian rhythm [16]. Acute break down of the blood–aqueous barrier during ocular trauma can lead to plasma leakage into the anterior chamber, thus mimicking AH overproduction and increasing IOP.

Outflow of AH can be impacted by increases in jugular venous pressure and central venous pressure (CVP). Collection of debris or blood in the anterior chamber and abnormalities of the iridocorneal angle can cause impeded AH outflow and glaucoma. The most significant factor controlling AH outflow is the diameter of Fontana spaces (i.e., spaces within the trabecular meshwork), as explained by the Hagen–Poiseuille law [17]:

where A is the volume of AH outflow per unit of time, r is the radius of Fontana spaces, P_iop is the IOP, P_v is the venous pressure, η is the viscosity, and L is the length of Fontana spaces. During pupillary dilation, the Fontana space narrows, resistance to flow increases, and a marked rise in IOP is seen. Hence, during glaucoma, patients are treated with topical miotics.

Ocular rigidity

Resistance offered by the sclera and cornea to a change in intraocular volume is termed “ocular rigidity.” Changes in intraocular volume will affect ocular rigidity. Also, scleral and corneal compliance decreases with age, increasing IOP in older animals.

Volume of the intraocular contents

When ocular tumors or systemic malignancies that spread to the eye occur, IOP can escalate. Ocular circulation autoregulates in response to changes in the ocular perfusion pressure via metabolic and myogenic mechanisms. Hyperoxia, hypocapnia, and alkalosis induce vasoconstriction in the retinal and choroidal arterioles, thus reducing IOP. The opposite effect on IOP occurs with hypoxia, hypercapnia, and acidosis [17]. Disorders associated with substantially decreased blood flow to the eye (e.g., dehydration, hypovolemic shock, and cardiogenic shock) can result in lower mean ocular perfusion pressure, retinal ischemia, and decreased IOP. During chronic arterial hypertension, IOP returns to normal due to adaptive mechanisms triggered by compression of choroidal vessels. This feedback mechanism reduces the total ocular blood volume, with IOP staying fairly constant. However, acute increases in blood pressure may lead to transient elevations in IOP.

Episcleral venous pressure

Episcleral venous pressure (EVP) is the “backpressure” created by the episcleral veins of the conventional pathway near the angular aqueous plexus. The pressure gradient between the anterior chamber and the episcleral veins has a significant effect on the rate of aqueous flow through this route and constitutes approximately 50–75% of the resistance that determines IOP. Increases in jugular venous pressure and CVP can augment EVP and IOP. This can happen during jugular compression, the Trendelenburg position [18], and other postural changes as seen in dogs [19], cats [20], and horses [21–24].

Pupil size

Variation in the pupil size is regulated by a balance between the iris sphincter (constrictor) and iris dilator muscle groups. The iris sphincter is a ring of smooth muscle cells connected by gap junctions and is located within the pupillary border. The oculomotor nerve provides parasympathetic innervation to the sphincter muscle, thus causing miosis. In contrast, the iris dilator is a myoepithelial layer extending from the iris root, where muscle fibers are also interconnected with gap junctions. The dilator muscle is innervated by sympathetic nerves and is responsible for mydriasis. This sympathetic activity in the dilator muscle is mediated by a combination of α‐ and β‐adrenergic receptors [11]. Prostaglandins are involved in maintaining the muscle tone of iris sphincter muscles and can cause miosis. Thus, prostaglandin analogs like latanoprost possess IOP‐lowering activity and are used for glaucoma treatment in dogs [26]. Pupillary diameter is a primary factor affecting the success of cataract surgery and the likelihood of complications. Hence, sympathomimetics and anticholinergics can be useful mydriatics during cataract surgeries. The exception is the avian eye, where the constrictor and dilator muscles are mainly striated and, as such, the pupil is not affected by traditional mydriatics [27].

Tear production and drainage

The precorneal tear film (PTF) is a complex blended three‐layered structure comprised of an outer lipid layer, middle aqueous layer, and deep mucin layer. The PTF serves multiple functions such as: (1) maintaining an optically uniform cornea; (2) removing debris and foreign material from the ocular surface; (3) lubricating the conjunctiva and cornea; (4) providing nutrients and oxygen to the avascular cornea; (5) controlling local bacterial flora; and (6) preserving ocular immunity. Fibers from the ophthalmic division of the trigeminal nerve (i.e., lacrimal nerve), facial nerve, pterygopalatine ganglion, and sympathetic fibers from the carotid plexus provide innervation to the lacrimal gland. Parasympathetic innervation of the lacrimal gland results in reflex tearing [28].

In animals, the aqueous portion of the tear film is routinely measured by the Schirmer tear test. Schirmer I does not need topical anesthesia and evaluates both basal and reflex tearing. Schirmer II is carried out with topical anesthesia and measures only basal tearing. Results of studies in humans [29], dogs [30–32], cats [33], and horses [34] report significant reductions in tear flow during general anesthesia. Dryness in the corneal epithelium predisposes patients to painful postanesthetic abrasions or corneal ulcers. These sequelae can be prevented with periodic ocular lubrication during the anesthetic period. Larger dogs demonstrate greater wetting per minute than smaller dogs [35]. Additionally, canine neonates have lower tear production than adults [36]. Hence, special care needs to be taken in these patients presented for anesthesia.

Ocular barriers

There are two primary ocular barriers, the blood–aqueous barrier (BAB) and the blood–retinal barrier (BRB). In combination, these maintain homeostasis by protecting the eye and preventing entry of lethal substances into internal ocular components. The BAB is the anterior barrier of the eye and is composed of capillary endothelial cells of the iris and non‐pigmented epithelial cells of the ciliary body. This barrier can be altered during ocular inflammation, intraocular surgery, trauma, or vascular diseases. The BRB is the posterior barrier comprised of retinal pigment epithelium and retinal vascular endothelium equipped with non‐leaky tight junctions. This restricts intercellular permeation of drugs after systemic and periocular application to the retina. Although these barriers offer protective functions, they can also impede entrance of many drugs into the eye, diminishing therapeutic efficacy [37]. Variations in the BRB may lead to the development of retinal diseases such as diabetic retinopathy and age‐related macular degeneration.

Oculocardiac reflex

The oculocardiac reflex (OCR) (i.e., Aschner reflex or trigeminovagal reflex) induces reflexive slowing of the heart rate and cardiac dysrhythmias such as atrioventricular blockade, ectopic atrial rhythm, junctional rhythm, multifocal ventricular premature contractions, ventricular bigeminy, ventricular ectopy, asystole, and ventricular fibrillation [38]. This reflex is more commonly encountered in pediatric human patients during strabismus surgery [39] as compared to adults. The OCR has been reported in dogs [40], cats [41], horses [42], rabbits [40], and birds [43]. The incidence of the OCR may be increased by hypercapnia [44], hypoxemia [38], a light plane of anesthesia [39], and drugs such as short‐acting opioids (e.g., sufentanil and remifentanil) [45] and dexmedetomidine [46].

The triggers for the OCR include external pressure on the eyeball, ocular manipulation, traction on the EOM, conjunctiva and orbital structures, orbital injections, retrobulbar block, ocular trauma, ocular pain, ocular hematomas, and facial trauma [7,8,47]. As a fatigable reflex, the intensity of the OCR may diminish with repeated stimulation. Upon activation of stretch receptors in the eye, short and long ciliary nerves conduct sensory impulses to the ciliary ganglion. From there, the impulses are transported via the ophthalmic division of the trigeminal nerve to the Gasserian ganglion and trigeminal nucleus. This afferent pathway continues along short internuncial fibers in the reticular formation to connect with the efferent limb. Signals are returned via the visceral motor nucleus of the vagus nerve to the sinoatrial node in the heart [38] (Fig. 67.4). There are also oculo‐respiratory [7] and oculo‐emetic [48] reflexes characterized by a similar afferent pathway, but which carry different efferent signals.

Immediate management of the OCR includes (1) communication with the surgeon and temporary cessation of surgical manipulation until heart rate and rhythm normalize; (2) confirmation of optimum ventilation, oxygenation, and anesthetic depth; (3) administration of a systemic anticholinergic, if warranted, due to significant or persistent bradycardia; (4) possible infiltration of local anesthetic around the ocular muscles (e.g., rectus muscles), which may abolish the afferent pathway; and (5) initiation of cardiopulmonary resuscitation in the event of asystole. Various maneuvers to abolish or obtund the OCR have been suggested but warrant further investigation. In dogs undergoing enucleation, preoperative administration of an anticholinergic drug was not associated with a lower prevalence of the OCR [50]; thus preemptive anticholinerigc use should be determined on a case‐by‐case basis depending on patient needs. Preoperative retrobulbar anesthesia can blunt the afferent pathway and help reduce incidence of OCR in dogs [50] and horses [51]. Use of a nondepolarizing muscle relaxant may also attenuate this reflex by reducing extraocular muscle tone [52].