ANATOMY

The orbit is a unique bony structure that has the primary purpose of housing and protecting the globe. By age 5 years, orbital growth is 85% complete; growth is finalized between 7 years of age and puberty. The orbit is a four-sided pyramid with its apex at the optic foramen; anteriorly, its base is formed by the orbital rim ( Figure 13-1 ). The orbital rim consists of dense cortical bone that protects the orbital contents from direct trauma. Seven bones contribute to the formation of the orbit: maxillary, zygomatic, frontal, ethmoidal, lacrimal, palatine, and sphenoid. These bones form a socket for the globe, provide insertions for the extraocular muscles, and are intimately associated with the surrounding sinuses and cranial fossae. Numerous nerves and vessels course through foramina, fissures, and canals of the orbital bones ( Table 13-1 ).

Right orbit. A , Anterior orbital fissure; G , inferior orbital groove; I , inferior orbital fissure; O , optic foramen (formed by lesser wing of sphenoid); P , posterior lacrimal crest (lacrimal bone); S , superior orbital fissure.

The orbital walls vary in thickness and strength. Fractures of the anterior and middle thirds of the orbit are common, with the maxillary sinuses and ethmoid air cells serving as shock absorbers and acute volume expansion compartments. As a result, globe perforation and acutely increased intraocular pressure (>20 to 25 mm Hg) are relatively infrequent following midfacial trauma. Except in severe life-threatening trauma, fractures occurring in the posterior one third of the orbit are rare. It is these fractures that can more commonly result in blindness.

The roof of the orbit consists largely of the orbital plate of the frontal bone, with the lesser wing of the sphenoid contributing only a minor portion posteriorly. The roof of the orbit is thin and separates the orbit from the anterior cranial fossa. In the elderly, the orbital roof may become resorbed, resulting in areas where the periorbita becomes fused to the overlying dura. The anterior portion of the roof is occupied by the supraorbital extension of the frontal sinus. Anterolaterally is a smooth, broad fossa for the lacrimal gland. Medially, approximately 4 mm behind the rim, lies the trochlear fovea, where the cartilaginous pulley inserts for the superior oblique muscle tendon. At the junction of the medial one third and lateral two thirds of the superior rim lies the supraorbital notch, which is often converted to a foramen (in 25% of individuals) by ossification of the ligament crossing it, thus encasing the supraorbital nerve and vessels.

The thin orbital floor is defined posterolaterally by the sphenomaxillary fissure. However, there is no distinct border medially. The bones of the floor consist of the orbital process of the maxilla; anterolaterally, a portion of the zygomatic bone; and posteriorly, a small portion of the palatine bone. The infraorbital groove originates from the middle of the infraorbital fissure approximately 2.5 to 3 cm from the infraorbital rim and converts to a canal halfway forward. The infraorbital groove and canal carry the infraorbital nerve and vessels, which innervate the soft tissues of the upper lip, the mucosa over the anterior maxilla, and the anterior maxillary teeth. The canal opens 5 mm below the rim of the maxilla as the infraorbital foramen. The floor of the orbit is often only 0.5 mm thick and separates the maxillary sinus from the orbital contents. The thinnest portion of the floor is just medial to the infraorbital groove and canal.

The lateral wall of the orbit is composed of the greater wing of the sphenoid bone and the frontal process of the zygoma. This is the strongest wall, but it may be fractured along its thinnest portion of the suture line, where the greater wing of the sphenoid and zygoma join. This wall separates the orbit from the temporalis muscle. The lateral wall is angled 45 degrees with respect to the medial wall and 90 degrees with respect to its other counterpart. The lateral wall and roof of the orbit, as well as the greater and lesser wing of the sphenoid, are separated by the superior orbital fissure. At the orbital apex, the lesser wing of the sphenoid forms the lateral wing of the optic canal. Internally, just behind (5 mm) the lateral orbital rim, is Whitnall’s tubercle. The tubercle is approximately 1 cm below the frontozygomatic suture. This slight projection functions as the attachment for lateral retinacular structures, namely, the lateral horn of the levator aponeurosis, lateral canthal tendon, inferior suspensory (Lockwood’s) ligament, and check ligament of the lateral rectus muscle. These soft tissue attachments are found anatomically in this order as one proceeds inferiorly and posteriorly, and they become confluent to form the lateral retinaculum, which actually attaches to the tubercle.

The medial wall of the orbit is by far the most complex. Arranged anteriorly to posteriorly, it consists of a portion of the frontal, lacrimal, ethmoid, and sphenoid bones. The maxilla contributes slightly at the anterior and inferior boundaries. The orbital surface of the ethmoid, or lamina papyracea , is extremely thin (0.2 to 0.4 mm) and forms the largest section of the medial wall. At the most anterior extent of the medial wall is the anterior lacrimal crest, which is formed by the frontal process of the maxilla. Proceeding posteriorly, the lacrimal fossa is then defined by the posterior lacrimal crest, a part of the lacrimal bone. Approximately 20 to 25 mm behind the medial orbital rim is the anterior ethmoidal foramen, and 12 mm further back is the posterior ethmoidal foramen. These foramina appear two thirds of the way up the medial wall within the frontoethmoidal suture and mark the level of the cribriform plate. The anterior ethmoidal foramen contains the anterior ethmoidal artery and anterior ethmoidal branches from the nasociliary nerve. The posterior ethmoidal foramen transmits the posterior ethmoidal artery and inconsistently a sphenoethmoidal nerve from the nasociliary nerve.

The surgeon must be aware of the limits of safe subperiosteal dissection ( Figure 13-2 ). A subperiosteal dissection can be safely extended 25 mm posteriorly from the inferior and lateral rims. An exploration distance of 30 mm from the superior orbital border or anterior lacrimal crest can be performed. The surgeon must bear in mind that these safe distances are referenced from intact adult orbital rims. When a traumatic force has displaced a portion of the rim, it is generally in a direction (posterior and medial) that effectively reduces these distances. At all times the surgeon must be aware of the orbital bony anatomy and the vital structures that course through it. Care must be taken to avoid disruption of the medial canthal tendon, lacrimal apparatus, and pulley of the superior oblique muscle; supraorbital nerves and vessels; structures attached to Whitnall’s tubercle; and the origin of the inferior oblique muscle. Rontal and colleagues arrived at mean distances for locating vital structures in relationship to identifiable fine bony landmarks ( Table 13-2 ).

Potential site of visual impairment, with traumatic etiologies.

The eyelids and fibrous orbital septum form the anterior boundary of the orbit. The upper and lower eyelids are similar in anatomic composition, except for the lid retractors, so they are discussed jointly ( Figure 13-3 ). The lids are surfaced by a very thin keratinized epithelium. The skin is loosely attached to the orbicularis oculi muscle ( Box 13-1 ), which is innervated by cranial nerve VII. The closing action of the orbicularis oculi muscle is chiefly opposed in the upper lid by the levator palpebrae superioris, which is innervated by cranial nerve III. The resting tone of the upper eyelid is partly determined by the amount of sympathetic input to Müller’s muscle. The orbicularis oculi is divided into the orbital portion, outer superficial fibers, and the palpebral section (central most deep fibers). The palpebral section medially has intricate insertions and envelops the lacrimal sac by dividing into intertwined deep and superficial heads. The superficial heads insert into the medial canthal ligament; the deep heads insert into the fascia of the lacrimal sac and posterior lacrimal crest. The medial canthal tendon or ligament is formed by the confluence of thickened fibrous insertions. The medial canthal tendon has a thin, deep head that inserts into the posterior lacrimal crest and a thick, superficial head that tenaciously inserts into the anterior lacrimal crest. Laterally, the more superficial fibers of the orbicularis oculi form an indistinct raphe, and the deeper fibers insert as the lateral canthal tendon onto Whitnall’s tubercle. The lids form a 30- to 40-degree angle at the lateral canthus, usually 1 cm below the frontozygomatic suture. The lateral canthus is usually 2 mm above the level of the medial canthus.

Cross-sectional anatomy of lower eyelid, with surgical approaches identified. C , Capsulopalpebral fascia (inferior lid retractors); F , extraconal fat (orbital); O , orbicularis oculi; S , orbital septum; T , tarsal plate; W, Whitnall’s inferior suspensory ligament.

Deep to the orbicularis oculi is the fibrous orbital septum, which is confluent with the periorbita (orbital periosteum) and the periosteum of the facial bones composing the rims. In the lower lids, this junction is thickened and is termed the arcus marginale . It is located 1 to 2 mm below the edge of the inferior rim. At the distal edges, the orbital septum is confluent and inserts into the underlying levator aponeurosis (upper lid) and the capsulopalpebral fascia (lower lid). Preaponeurotic orbital fat is retained by the septum in both lids and is divided into several pads above (central and medial) and three below (medial, central, and lateral). With aging and increased connective tissue laxity of the orbital septum, these preaponeurotic orbital fat pads may bulge externally, creating “baggy lids.” Severe sagging of the lower lids is referred to as “festooning.”

The levator palpebrae superioris muscle (primary elevator of the upper lid) consists anteriorly of an aponeurosis that attaches broadly over the superficial anterior two thirds of the tarsal plate and subcuticular tissue. Approximately 15 to 20 mm above the tarsal plate, the aponeurosis consists of a fascial condensation called Whitnall’s ligament. This ligament acts as a suspensory ligament of the globe. Müller’s muscle arises beneath Whitnall’s suspensory ligament. Müller’s muscle is a smooth muscle that relies on sympathetic input for its tone and regulates the resting position of the upper lids while the eyes are open. The lower lid retractors are known as the capsulopalpebral fasciae, which extend from the inferior rectus and inferior oblique muscles to fuse with the inferior suspensory ligament of Lockwood. The tarsal plate is dense, fibrous tissue that largely maintains the convex form of each lid. The border of the tarsus is next to the free margin of each lid. The length of each tarsus is approximately 45 mm, and its width and thickness are greatest midway on the lid. The width of the upper tarsus (11 mm) is about twice that of the lower (5 to 6 mm). Within the tarsal plates are embedded many slender meibomian (sebaceous) glands. When these glands become chronically obstructed and inflamed, they form a cystlike mass termed a chalazion .

Tears or lacrimal secretions accumulate at the medial inferior aspect of the eye. The fluid is then picked up by the lacrimal puncta, which are two small (0.2 to 0.3 mm in diameter) openings in the upper and lower lids. The upper punctum is usually slightly medial in relation to the lower punctum ( Figure 13-4 ). The upper and lower canaliculi travel within the lids first vertically (2 mm), and then horizontally, paralleling the lid margin for 8 to 10 mm, where they join to form the common canaliculus (3 to 5 mm). The common canaliculus enters the lacrimal sac on the lateral aspect of the junction of the upper and middle thirds. The lacrimal sac, which is approximately 1 cm in length and 5 mm in diameter, is encased by a dense, adherent fascia. The nasolacrimal duct has a 12-mm intrabony canal and eventually opens below the inferior turbinate into the inferior meatus, usually 30 to 35 mm from the external nares. At the opening of the duct is a mucosal fold called the valve of Hasner. This valve helps prevent fluid and air reflux when high intranasal pressure is generated by blowing one’s nose. With epiphora it is important to establish where the mechanical obstruction exists within the lacrimal drainage system. Canalicular irrigation may relieve temporary obstruction caused by dried, thickened secretions. A Jones’ dye test or dacryocystography can help determine the point of obstruction and thus guide surgical planning. Also, epiphora may be due to hypersecretion. Following trauma, corneal abrasion, a foreign body, lash ptosis, or entropion may serve as the stimulus for the lacrimal gland’s overproduction.

Right medial eyelid anatomy and landmarks. C , Caruncle; G , gray line; M , medial canthus; P , inferior puncta; S , plica semilunaris.

FRACTURE PATTERNS

Isolated orbital fractures constitute 4% to 16% of facial fractures. If one includes orbital fractures that extend outside the confines of the orbit into the facial skeleton, the incidence approaches 30% to 55%. Fractures involving the orbit can be classified as zygomatic complex, naso-orbital-ethmoid (NOE), or internal orbital fractures.

Zygomatic complex fractures are the most commonly occurring facial fracture, second only to nasal fractures. These fractures are also the most commonly occurring fractures of the orbit. Zygomatic complex fractures are often displaced in an inferior, medial, and posterior direction, and the complex fulcrums about the frontozygomatic suture. Various classification systems have been reported; however, the system proposed by Jackson is most notable ( Figure 13-5 ). It classifies the fracture based on severity: type I (nondisplaced), type II (segmental fracture of the orbital rim), type III (tripod fracture), and type IV (fragmented).

Classification of orbitozygomatic fracture patterns. A, Type II segmental fracture of the orbital floor, involving the infraorbital rim. B, Type III. The zygoma is fractured in a single piece, in a typical “tripod” fashion with inferior medial displacement.

NOE fractures most often occur following blunt trauma to the midface. These fractures result primarily in cosmetic deformities such as flattening of the nasal dorsum and widening of the intercanthal distance. This can occur as a result of disruption of one or both medial canthal ligaments. Lacrimal drainage problems can also arise from NOE fractures. The severity of these fractures can range from minimal displacement of a large segment of the medial orbital rim to severe comminution with complete avulsion of the canthal ligament from the bone ( Figure 13-6 ).

Type III naso-orbital-ethmoid fracture with medial displacement.

Internal orbital fractures can occur in numerous patterns. They are often described by their location and the size of the defect. Three patterns of internal orbital fractures have been described : linear, blow-out, and complex ( Figure 13-7 ). Linear fractures maintain periosteal attachments and therefore do not result in a defect; however, they can result in significant enlargement of the orbit. Blow-out fractures are the most commonly occurring injury and are limited to one wall, with a defect of less than 2 cm in diameter. Blow-out fractures most commonly occur in the anterior or middle part of the floor; however, they can also occur in the medial or superior walls, where they can present as blow-in fractures ( Figure 13-8 ). Exploration, repair, and/or reconstruction of orbital roof fractures may be indicated if a dural tear is suspected or to prevent a “pulsatile globe.” This inward and outward movement of the eye is due to arterial pulsations and respiratory fluctuations that occur in the overlying cerebral hemisphere. This phenomenon often manifests after resolution of edema and hematoma in unrepaired roof defects and causes persistent blurred or double vision. Complex fractures consist of extensive fractures that affect two or more orbital walls; they often involve the posterior orbit and may involve the optic canal. Complex fractures are usually associated with fractures of the facial skeleton outside the orbital frame (LeFort II and III fractures or frontal sinus fractures), which are classified as combined fractures.

A, Linear orbital floor fracture. B, Orbital floor blow-out or blow-in fracture, typically occurring in the medial half. C, Complex fracture of the internal orbit. The defect involves more than one wall and typically extends back to the orbital cone, making repair and graft support difficult.

Noncontrasted coronal computed tomography scan demonstrating isolated blow-in fracture of the right orbital roof. The patient presented with mild diplopia and no firm restricted gaze (negative forced duction test). Treatment was observation only, and the fracture healed without sequelae.

CLINICAL EXAMINATION

A brief history of the mechanism of injury and direction of force should be ascertained before performing a clinical examination of the orbit and globe. A systematic approach assessing both orbits will further define functional and anatomic defects associated with orbital injuries. The initial ophthalmologic evaluation should include periorbital examination, visual acuity, ocular motility, pupillary responses, visual fields, and funduscopic examination.

Visual acuity is independently tested for each eye using a Snellen chart at a standard 20-foot distance or a near card (standard-type print at 14 inches) if a Snellen chart is unavailable. If the patient wears corrective lenses, these should be worn during the examination.

The eyelids and periorbital area should be inspected for edema, ecchymosis, lacerations, ptosis, asymmetric lid drape, canalicular injury, and canthal tendon disruption. When traumatic forces have produced lid ecchymosis, there should be heightened awareness of the possibility of an occult ocular injury or an orbital wall fracture. A lid retractor (Desmarres) is useful in separating edematous eyelids to examine the globe and can be used to inspect the inner aspect of the lid. Upper lid lacerations with fat herniations below the level of the brow should alert the examiner to potential full-thickness lid injury or underlying penetrating globe injury ( Figure 13-9 ). If the pleural conjunctiva has been violated, it is prudent to consult an ophthalmologist to assess for ocular penetration. Gentle lateral traction on the lower lids can reveal medial canthal disruption.

A, Isolated upper and lower eyelid laceration. Fat herniation through the upper eyelid laceration should alert the examiner to the potential of a full-thickness injury and penetrating globe injury. B, Slit-lamp examination of the right eye demonstrating full-thickness corneal laceration extending superiorly to the edge of the limbus. Note the asymmetric pupil pointing superiorly. C, After ophthalmologic repair of the corneal laceration with 10-0 nylon suturing, the patient maintained full normal visual acuity.

Extraocular movements are evaluated to rule out mechanical entrapment or paresis. Any diplopia and the field of gaze in which it occurs should be noted. Mild (<5 degrees) restriction in extreme fields of gaze is common in the face of severe orbital edema. After topically anesthetizing the eye, forced ductions with fine-toothed forceps can be performed in the direction of limitation to determine a mechanical (entrapment) versus a neurologic origin ( Figure 13-10 ).

The patient presented with moderate limited gaze in the upward and medial directions in the right eye. Forced duction testing demonstrated free passive motion both superiorly and medially. The isolated nondisplaced orbital floor fracture (anterior half) was not repaired.

Pupillary size, shape, and symmetry should be evaluated, as well as light reactivity. In any patient with anisocoria (unequal pupils) or an irregular pointing pupil, a history of previous ocular trauma or eye surgery (cataract) should be elicited. An irregular pupil often points toward the site of globe penetration or injury (see Figure 13-9, B ). The globe should also be evaluated for acute enophthalmos or proptosis, which can be ascertained by viewing directly from above or below. In addition, the vertical position of the globe should be noted.

Visual fields are tested for each eye, one at a time, by confrontation. This involves directly aligning the patient’s and examiner’s faces 2 feet apart (both maintaining direct forward gaze) and asking the patient to detect movement at the extremes of the examiner’s own visual field. Quadratic defects may indicate ocular, optic nerve, or optic pathway damage.

A funduscopic examination should be performed in a dimly lit room. Lens dislocation, vitreous hemorrhage, retinal hemorrhage, retinal detachment, and foreign bodies can be noted. If history and initial findings warrant a dilated funduscopic examination, neurologic status and clearance should first be obtained. An ophthalmologist is best qualified to perform a dilated funduscopic examination, searching for more occult ocular injuries. Also, when the history or initial examination warrants further evaluation, tonometry and a slit-lamp examination can be performed, usually by an ophthalmologist.

Tonometry measures intraocular pressure in both eyes by surface readings. Although normal (10 to 20 mm Hg) or equal readings are reassuring, they do not rule out a penetrating injury. A relatively low pressure reading in an injured eye suggests scleral rupture. An abnormally high or unequal reading may be indicative of a retrobulbar hematoma, which may require acute evacuation via a lateral canthotomy.

A slit-lamp examination is performed with the patient in an upright position. If the patient is confined to bed, a modified examination with a penlight can be performed. The examiner can rule out conjunctival chemosis, hemorrhage, emphysema, and foreign bodies. Fluorescein dye and a cobalt blue light (Wood’s lamp) facilitate corneal assessment for abrasion, laceration, and foreign body. The anterior chamber is assessed for depth, clarity, and hyphema (blood in the anterior chamber). The shape and reactivity of the iris are also noted.

Last, the bony orbital rim should be palpated for evidence of a bony step, bony crepitus, or mobility. Neurologic sensory testing can also be performed to evaluate the supraorbital, supratrochlear, and infraorbital nerves. Once a complete ophthalmologic examination has been performed, additional studies such as a computed tomography (CT) scan or magnetic resonance imaging (MRI) can be selectively ordered, with meaningful results.

VISUAL DISTURBANCES

Visual impairment or loss can occur at various levels of the optic pathway, such as the globe or optic nerve (see Figure 13-2 ). Direct injury or forces transmitted to the globe can result in retrobulbar hematoma formation, rupture of the globe, hyphema, lens displacement, vitreous hemorrhage, and retinal detachment.

Retrobulbar hematoma is often manifested as visual loss with severe ocular pain. It causes an elevation in the intraorbital pressure, leading to central retinal artery compression or ischemia of the optic nerve ( Figure 13-15 ). Increased intraorbital pressure may also raise intraocular pressure, thereby compromising ocular circulation. Immediate surgical management is necessary and consists of a lateral canthotomy (with or without cantholysis) and blunt dissection along the lateral orbital walls to evacuate the hematoma. Often a drain is left in place for 24 to 48 hours to ensure that the bleeding has access to the surface. If necessary, intravenous mannitol and acetazolamide, along with a topical beta blocker, can be administered to lower intraocular pressure. In our experience, orbital volume reduction as a result of blow-in or compressive wall fractures does not typically cause increased intraorbital pressures leading to visual loss, because the fractures are often accompanied by some degree of “compensatory disruption” of the medial wall (ethmoid air cells) and floor (maxillary sinus). Through these drainage pathways and volume expansion, some degree of protection is provided against critical increases in intraorbital pressures.

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